View Full Version : The traditional diet of Greece and cancer.
THIS THREAD IS PRIMARILY ABOUT THE THE EVIDENCE THAT EXCESS OMEGA 6 AND LACK OF OMEGA 3S SIGNIFICANTLY INCREASES THE RISK OF BREAST CANCER.
(I apologise for the "shout" but I think this is something worth shouting about - figures as high as a 70% for reduction in BC risk deserve a hearing)
WE NEED 1/2-2% OF CALORIES AS OMEGA 6 1-4 GRAMS FOR A 2000 CALORIE DIET WE EAT 8-13% OF CALORIES.
WE ARE SERIOUSLY OVERLOADING ON OMEGA 6.
THE BIGGEST CULPRIT OF EXCESS OMEGA 6 ARE HIGH OMEGA SIX VEGETABLE OILS,WHICH ARE MOST OF THE COMMON ONES FOUND THROUGHOUT THE FOOD CHAIN.
WE FEED LIVESTOCK ON GRAIN WHICH DISTORTS THEIR OMEGA 3/6 BALANCE BY A FACTOR AS HIGH AS 10 TIMES, AND THAT INCLUDES THEIR PRODUCTS EGGS, AND DAIRY. GRAIN FEEDING ALSO REDUCES ANTIOXIDANTS AND SOME VITAMINS eg K.
WE HAVE DEPLETED THE MINERAL CONTENT OF LIVESTOCK AND VEGETABLES OF MINERALS BY BETWEEN 20% AND 70% IN THE LAST 50 YEARS. http://www.mineralresourcesint.co.uk/pdf/Mineral_Depletion_of_Foods_1940_2002.pdf
WE ARE AGAIN SEEING IODINE DEFICIENCIES IN SIGNIFICANT PARTS OF WESTERN POPULATIONS (EG AUSTRALIA 2005).
IODINE HAS A SPECIAL ROLE IN THE BREAST, AND DEFICIENCY MAY HAVE A ROLE IN BREAST CANCER.
EXCELLENT VIDEO http://her2support.org/vbulletin/showthread.php?t=37340
USEFUL PAPER http://www.articlearchives.com/medicine-health/diseases-disorders-endocrine-system/2297945-1.html Iodine and iodide: functions and benefits beyond the thyroid.
By: Rheault, Shana,Olmstead, Stephen,Ralston, Janet,Meiss, Dennis
EXCELLENT SOURCE OF INFORMATION ON IODINE - http://www.iodine4health.com/index.htm
VITAMIN D PLAYS A ROLE IN CANCER PREVENTION. VITAMIN D DEFICIENCIES ARE INCREASING DUE TO LACK OF MODEST SUN EXPOSURE. FACTOR 15 SUNCREAMS BLOCK 90% OF UVB. UVB IS NEEDED TO MAKE VITAMIN D.
EXCELLENT VIDEOS ON VITAMIN D. http://her2support.org/vbulletin/showthread.php?t=37448 and another on melanoma, sunscreen, ozone etc http://www.youtube.com/watch?v=eeXtGHSt-5o&eurl=http%3A%2F%2Fvitamind3.blogspot.com%2F&feature=player_embedded and one on the risk of cancer including BC with reductions of risk of up to 80% http://www.uctv.tv/search-details.aspx?showID=15767 .
(Caucasians who have not seen the sun for a while can make up to 50,000 IU of vitamin D in half an hour of full body exposure to sunshine, which suggests to me we were intended to get more than a few hundred units a day.)
AND THIS WILL MAKE YOU THINK ABOUT BEING TOO LIBERAL WITH THE SUNSCREEN
The Chemical Sunscreen Health Disaster http://www.skinbiology.com/toxicsunscreens.html
WE REMOVE OMEGA3S FROM THE FOOD CHAIN BECAUSE THEY DO NOT KEEP.
WE DO NOT EAT ENOUGH LONG CHAIN OMEGA 3. LONG CHAIN OMEGAS 3S ARE FOUND PRIMARILY IN OILY FISH. FISH AND SHELLFISH ARE ALSO GOOD SOURCES OF MINERALS AND IODINE.
I will try and revisit this thread for the first time since I wrote it in the next few days and amend it where my knowledge has moved on. I am removing the numerous appalling spelling errors with the assistance of an online spell checker. I am definitely a little word blind I think, as it is only with the spell checker that the errors stand out, or maybe it is the way I read - anyway my sincere apologies I had no idea there were so many spelling errors.
I have recently (2008) found I had a large jaw abscess which has now been removed. A capped tooth had died and caused an asymptomatic abscess. It must have been there some time, several years I would guess.They found the tooth abscess but not the jaw abscess about a year ago. I had complained about discharges and bad tastes, periodic worries about bad breath to doctors and dentists, but nobody had suggested a jaw abscess, or asked if it had ever been suggested that filling/caps were close to tooth nerves etc. It turns out the abscess had been leeching into the sinuses, which may explain a slightly fuzzy brain, anxiety etc . . . Fuzzy brain may have contributed to the above. It is minor compared with what you all go through, but does emphasise the importance of dental health. I have just had a CT scan, as I am not certain they have yet got all the infection. Update - the CT scan disclosed more infection where I said I believed it was; all of which has taken more than a year. Two further infections, one of which had resulted in a significant area of infected jaw bone, were found (late 2009), and both related to root filled teeth; a subject on their own. In summary all three of my root filled teeth had resulted in bone infection in the jaw.
[Since I started this thread I have written a book (2008) on Omega 6 and 3. It looks at a wide range of health issues including mental health. It only has a short section on breast cancer. It will be updated fairly soon with a simple summary and how to section.
It is called Omega Six The Devils Fat because EXCESS Omega six as well as having huge health implications arguably promotes societal changes in behaviour in the "Seven deadly sins" (extravagance later lust, gluttony, greed, sloth, wrath, envy, and pride - wikipedia). Fish (a source of Omega 3 and minerals) has been promoted in many cultures for 1000s of years. Those following Christian teachings would have eaten fish about 180 day a year. All of which is dealt with in less than a page.
Omega 6 arguably controls our ability to breed and links that ability to the fertility of the environment. Excess Omega 6 and lack of Omega 3, combined with a lack of vitamin D minerals and iodine, is arguably one of the greatest threats to human survival because all these nutrients are essential to brain function, and because excess Omega 6 subtly alters our behaviour towards more male characteristics, including, aggression, impulsiveness, and acquisitiveness as in territoriality, which are all seen in the breeding behaviour of male animals.
These nutrients are equally essential to wider health.
The book is a serious work with over 900 references
www.Omegasixthedevilsfat.com
RB
[added 26th Feb 2010]
More on food fats omega three and six.
RB
ABSTRACT
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15167223&query_hl=24&itool=pubmed_docsum
1: Eur J Cancer Prev. 2004 Jun;13(3):219-30. Related Articles, Links
Click here to read
The traditional diet of Greece and cancer.
Simopoulos AP.
The Center for Genetics, Nutrition and Health, 2001 S Street, N.W., Suite 530, Washington, DC 20009, USA. cgnh@bellatlantic.net
The term 'Mediterranean diet', implying that all Mediterranean people have the same diet, is a misnomer. The countries around the Mediterranean basin have different diets, religions and cultures. Their diets differ in the amount of total fat, olive oil, type of meat, wine, milk, cheese, fruits and vegetables; and the rates of coronary heart disease and cancer, with the lower death rates and longer life expectancy occurring in Greece. The diet of Crete represents the traditional diet of Greece prior to 1960. Analyses of the dietary pattern of the diet of Crete shows a number of protective substances, such as selenium, glutathione, a balanced ratio of n-6/n-3 essential fatty acids (EFA), high amounts of fibre, antioxidants (especially resveratrol from wine and polyphenols from olive oil), vitamins E and C, some of which have been shown to be associated with lower risk of cancer, including cancer of the breast. Epidemiological studies and animal experiments indicate that n-3 fatty acids exert protective effects against some common cancers, especially cancers of the breast, colon and prostate. Many mechanisms are involved, including suppression of neoplastic transformation, cell growth inhibition, and enhanced apoptosis and anti-angiogenicity, through the inhibition of eicosanoid production from n-6 fatty acids; and suppression of cyclooxygenase 2 (COX-2), interleukin 1 (IL-1) and IL-6 gene expression by n-3 fatty acids. Recent intervention studies in breast cancer patients indicate that n-3 fatty acids, and docosahexaenoic acid (DHA) in particular, increase the response to chemopreventive agents. In patients with colorectal cancer, eicosapentaenoic acid (EPA) and DHA decrease cell proliferation, and modulate favourably the balance between colonic cell proliferation and apoptosis. These findings should serve as a strong incentive for the initiation of intervention trials that will test the effect of specific dietary patterns in the prevention and management of patients with cancer.
Publication Types:More on food fats omega three and six.
A related article
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=10471132&query_hl=5&itool=pubmed_DocSum
1: Prostaglandins Leukot Essent Fatty Acids. 1999 May-Jun;60(5-6):421-9. Related Articles, Links
Evolutionary aspects of omega-3 fatty acids in the food supply.
Simopoulos AP.
The Center for Genetics, Nutrition and Health, Washington, DC 20009, USA. Lcgnh@bellatlantic.net
Information from archaeological findings and studies from modern day hunter-gatherers suggest that the Paleolithic diet is the diet we evolved on and for which our genetic profile was programmed. The Paleolithic diet is characterized by lower fat and lower saturated fat intake than Western diets; a balanced intake of omega-6 and omega-3 essential fatty acids; small amounts of trans fatty acids, contributing less than 2% of dietary energy; more green leafy vegetables and fruits providing higher levels of vitamin E and vitamin C and other antioxidants than today's diet and higher amounts of calcium and potassium but lower sodium intake. Studies on the traditional Greek diet (diet of Crete) indicate an omega-6/omega-3 ratio of about 1/1. The importance of a balanced ratio of omega-6:omega-3, a lower saturated fatty acid and lower total fat intake (30-33%), along with higher intakes of fruits and vegetables leading to increases in vitamin E and C, was tested in the Lyon Heart study. The Lyon study, based on a modified diet of Crete, confirmed the importance of omega-3 fatty acids from marine and terrestrial sources, and vitamin E and vitamin C, in the secondary prevention of coronary heart disease, and cancer mortality.
Publication Types:
* Review
PMID: 10471132 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=12442909&query_hl=12&itool=pubmed_docsum
A related article same author
1: Biomed Pharmacother. 2002 Oct;56(8):365-79. Related Articles, Links
The importance of the ratio of omega-6/omega-3 essential fatty acids.
Simopoulos AP.
The Center for Genetics, Nutrition and Health, Washington, DC 20009, USA. cgnh@bellatlantic.net
Several sources of information suggest that human beings evolved on a diet with a ratio of omega-6 to omega-3 essential fatty acids (EFA) of approximately 1 whereas in Western diets the ratio is 15/1-16.7/1. Western diets are deficient in omega-3 fatty acids, and have excessive amounts of omega-6 fatty acids compared with the diet on which human beings evolved and their genetic patterns were established. Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today's Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a low omega-6/omega-3 ratio) exert suppressive effects. In the secondary prevention of cardiovascular disease, a ratio of 4/1 was associated with a 70% decrease in total mortality. A ratio of 2.5/1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3 PUFA had no effect. The lower omega-6/omega-3 ratio in women with breast cancer was associated with decreased risk. A ratio of 2-3/1 suppressed inflammation in patients with rheumatoid arthritis, and a ratio of 5/1 had a beneficial effect on patients with asthma, whereas a ratio of 10/1 had adverse consequences. These studies indicate that the optimal ratio may vary with the disease under consideration. This is consistent with the fact that chronic diseases are multigenic and multifactorial. Therefore, it is quite possible that the therapeutic dose of omega-3 fatty acids will depend on the degree of severity of disease resulting from the genetic predisposition. A lower ratio of omega-6/omega-3 fatty acids is more desirable in reducing the risk of many of the chronic diseases of high prevalence in Western societies, as well as in the developing countries, that are being exported to the rest of the world.
Publication Types:
* Review
PMID: 12442909 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=10901194&query_hl=12&itool=pubmed_docsum
1: Poult Sci. 2000 Jul;79(7):961-70. Related Articles, Links
Human requirement for N-3 polyunsaturated fatty acids.
Simopoulos AP.
The Center for Genetics Nutrition and Health, Washington, DC 20009, USA. cgnh@bellatlantic.net
The diet of our ancestors was less dense in calories, being higher in fiber, rich in fruits, vegetables, lean meat, and fish. As a result, the diet was lower in total fat and saturated fat, but contained equal amounts of n-6 and n-3 essential fatty acids. Linoleic acid (LA) is the major n-6 fatty acid, and alpha-linolenic acid (ALA) is the major n-3 fatty acid. In the body, LA is metabolized to arachidonic acid (AA), and ALA is metabolized to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The ratio of n-6 to n-3 essential fatty acids was 1 to 2:1 with higher levels of the longer-chain polyunsaturated fatty acids (PUFA), such as EPA, DHA, and AA, than today's diet. Today this ratio is about 10 to 1:20 to 25 to 1, indicating that Western diets are deficient in n-3 fatty acids compared with the diet on which humans evolved and their genetic patterns were established. The n-3 and n-6 EPA are not interconvertible in the human body and are important components of practically all cell membranes. The N-6 and n-3 fatty acids influence eicosanoid metabolism, gene expression, and intercellular cell-to-cell communication. The PUFA composition of cell membranes is, to a great extent, dependent on dietary intake. Therefore, appropriate amounts of dietary n-6 and n-3 fatty acids need to be considered in making dietary recommendations. These two classes of PUFA should be distinguished because they are metabolically and functionally distinct and have opposing physiological functions; their balance is important for homeostasis and normal development. Studies with nonhuman primates and human newborns indicate that DHA is essential for the normal functional development of the retina and brain, particularly in premature infants. A balanced n-6/n-3 ratio in the diet is essential for normal growth and development and should lead to decreases in cardiovascular disease and other chronic diseases and improve mental health. Although a recommended dietary allowance for essential fatty acids does not exist, an adequate intake (AI) has been estimated for n-6 and n-3 essential fatty acids by an international scientific working group. For Western societies, it will be necessary to decrease the intake of n-6 fatty acids and increase the intake of n-3 fatty acids. The food industry is already taking steps to return n-3 essential fatty acids to the food supply by enriching various foods with n-3 fatty acids. To obtain the recommended AI, it will be necessary to consider the issues involved in enriching the food supply with n-3 PUFA in terms of dosage, safety, and sources of n-3 fatty acids.
Publication Types:
* Review
PMID: 10901194 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=10479232&query_hl=12&itool=pubmed_docsum
1: Am J Clin Nutr. 1999 Sep;70(3 Suppl):560S-569S. Related Articles, Links
Click here to read
Comment in:
* Am J Clin Nutr. 2004 Mar;79(3):523-4.
Essential fatty acids in health and chronic disease.
Simopoulos AP.
Center for Genetics, Nutrition and Health, Washington, DC 20009 cgnh@bellatlantic.net
Human beings evolved consuming a diet that contained about equal amounts of n-3 and n-6 essential fatty acids. Over the past 100-150 y there has been an enormous increase in the consumption of n-6 fatty acids due to the increased intake of vegetable oils from corn, sunflower seeds, safflower seeds, cottonseed, and soybeans. Today, in Western diets, the ratio of n-6 to n-3 fatty acids ranges from approximately 20-30:1 instead of the traditional range of 1-2:1. Studies indicate that a high intake of n-6 fatty acids shifts the physiologic state to one that is prothrombotic and proaggregatory, characterized by increases in blood viscosity, vasospasm, and vasoconstriction and decreases in bleeding time. n-3 Fatty acids, however, have antiinflammatory, antithrombotic, antiarrhythmic, hypolipidemic, and vasodilatory properties. These beneficial effects of n-3 fatty acids have been shown in the secondary prevention of coronary heart disease, hypertension, type 2 diabetes, and, in some patients with renal disease, rheumatoid arthritis, ulcerative colitis, Crohn disease, and chronic obstructive pulmonary disease. Most of the studies were carried out with fish oils [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)]. However, alpha-linolenic acid, found in green leafy vegetables, flaxseed, rapeseed, and walnuts, desaturates and elongates in the human body to EPA and DHA and by itself may have beneficial effects in health and in the control of chronic diseases.
Publication Types:
* Review
PMID: 10479232 [PubMed - indexed for MEDLINE]
marymary
06-30-2006, 08:42 AM
This is all Greek to me! What would be most helpful to me is recipies, and foods that are especially beneficial and should be emphasized in my diet.
Currently I go to Farmer's Market as often as possible, at least once and sometimes twice a week. The only problem is that foods there are entirely seasonal. By January it's onions and chard.
Right now I am consuming blueberries like a bear. I ate big bowls of broccoli all winter. Right now it's salad with the following olive oil dressing:
Minced garlic
Salt
Pepper
Curry Powder
Cayenne Pepper
Pinch of ground Cloves
Dash of tabasco
Extra virgin locally grown olive oil
Lemon juice (from the tree in my backyard)
Balsamic vinegar
Dijon mustard as an emulsifier
I read on Web MD that olive oil fights HER 2 and also it just tastes so good, although I know it does pack some calories. I try and eat half an avocado daily, fattening, yes, but also a good cancer fighter.
Right now it's salad, salad, salad and my husband eats lunch out daily, yesterday it was a BLT for him!
I am trying to lose a few pounds, stay off the sugar, etc. and I do believe eating fruits & veggies has helped me live as long as I have. That & Herceptin/Arimidex!
Thanks.
Mary
mamacze
06-30-2006, 09:17 AM
Dear RB,
I think you are a genius in your own right and I am grateful for your laser focus on omega 3's and 6's. Clearly, the ratio of 3's to 6's is significant. For those of us who are intellectually challenged in this area; would you consider giving us a plain English summary of what you are gleaning from these studies;and also it would help me to know what some good food sources of 3's and 6's are. Finally, do you know of any food source where the 3's and 6's are found together and optimally balanced for people with auto immune problems and cancer?
Love Kim from CT
RhondaH
06-30-2006, 09:29 AM
here's a list of omega 3
http://www.whfoods.com/genpage.php?tname=nutrient&dbid=84
AND a list of omega 6
http://www.annecollins.com/dietary-fat/omega-6-fats.htm
AND an article on green tea and autoimmune disorders
http://www.nutraingredients.com/news/news-ng.asp?id=60691-green-tea-could
Rhonda
al from Canada
06-30-2006, 11:07 AM
RB,
For those of us on a non-junk food diet, cook only with olive oil, do you think that it is still neccessary to suppliment O-3? If so, how much?
Also, we all really appreciate the work you are doing to benefit all of us in this area, as I personally feel that diet is a hugh part of the problem!.
Al
Thank you for your kind comments and interest.
Thanks Rhonda for the links. The Mateljan site was particularly well laid out, and from a quick skim is informative.
Re the questions as to how much - as usual no easy answer but in essence from what I have read so far
1...**** BALANCE the Omega 3 and 6 plant based fats with a ratio between 1:1 and 1:2. We only need between 1/2 - 2% of calories (Issfal suggests 2-3%). There is not a simple way to do that except look up the fat content of the foods you eat and try and estimate your intake. The vast majority of processed food will contain vegetable fat even some processed dried fruit! - So check lablels.
2. Get at least a gram and up to 3 grams combined total of the long chain Omega 3s DHA and EPA from oily fish or fish oil. Women and men have different needs it appears. Women make DHA better than men and need more of it. (Our shore dwelling ancestors would have eaten more Omega 3 than 6 as fish and shell fish are much higher in Omega 3 than 6.)
Fish and shell fish are a good source of minerals and iodine.
Minerals in food have dropped by between 20 and 70% due to soil depletion in the last 50 years.
Do remember to have a look at the content of fish oil as it contains a whole range of fats which may help inform you other intake. Check the A and D content of fish oil and make sure you are neither overloading or getting too little. Some manufacturers remove D or A or both.
If you feel it appropriate to take GLA remember it usually comes with omega six and work that into the balancing act. As usual looking for a food source might be a better option. I am less certain as to where GLA sits in the pecking order, and less is written on the series one products and the extent to which the body will produce GLA.
http://cpmcnet.columbia.edu/dept/ihn/symposia/pdf/dr_arterburn_slides_2005.pdf
This link provides some graphs which seem to suggest 2 grams of DHA a day is the level at which take off drops off, BUT I would guess it would depend on what the omega six intake was, the composition of stored fats, individual metabolism etc. ( about 4 to 5 tps of a reasonable quality fish oil or equivalent in algae source). I am taking 2grams as a minimum some times more and just trying to assess how I feel changes in body function, fitness, weight, liver function etc.
I am afraid that there are simply no absolute answers and the research has not been done.
Side effects are limited but do exist at higher doses so check with your advisor particularly if on medication. Blood thinning is the most common issue.
Other than the fish oil, use maybe a little olive oil or other low Omega 6 oil maybe 1 tablespoon a day. Moderate use of grass fed butter is fine (vit A D K etc). I do not use any oils margarines etc, but it is very much a personal choice. In hunter gatherer terms our access to omega six was limited so my guess is less is better eg give up margarine etc. There are no easy answers and until they trial outcomes v changes in adipose fat content in a sufficient number of people we simply will not know.
I hope that helps I am sorry I cannot be more specific at this time.
I will post separately on sources of omega three and six in so far as I can.
RB
chrisy
06-30-2006, 03:45 PM
I just wanted to say I read your posts with interest - I really appreciate your efforts to convey this complex information in ways we can easily "digest" (pun intended). For those of us who have neither the time nor intellectual focus to dive into this pool, it's great to have such an awesome researcher on the team!
Thanks!
karenann
06-30-2006, 03:57 PM
R.B. and Rhonda,
Thanks a million for all of the information. I think I am finally, "getting it" when it comes to food and supplements.
Karen
Barbara H.
06-30-2006, 04:52 PM
I take one fish oil capsule each day. Should they be stored in the refrigerator?
Barbara H.
Hi Rb,
Always read your posts but I like to cause trouble.
When I look at historical precedence, I have to wonder. 100 years ago, I would not have made it through childbirth. I would not have made it to later become a BC statistic.
Grew up with Meditteranean Diet, alas on the wrong side of the Adriatic. I don't know any answers. I just want to help on your research path. BB
Thanks for the kind comments.
RE Progress.
I am not arguing with progress in medicine, access to good food and clean water, shelter, a warm space to live and sleep, better working conditions etc. although many in the world are not so lucky.
I applaud and am amazed by the advances in medicine, including greater understanding and knowledge. Staggering things have been achieved and there is huge future potential.
But are those reasons for not keeping the basics in view, as well as doing the more exotic financially rewarding research. - If these papers based on the research and work of others are well founded, and it looks increasingly as if they are, the Omega 3:6 fats imbalance is responsible for a chunk of western disease (or at least removal of the ability to delay them to the end of life). Is it justifiable to ignore the basics and start 12 year olds off in life with the early forms of vascular disease, depression, ADHD etc because we are ignoring prevention in favour of the development of commercial solutions.
Is it not time to find another funding model that ensures funding for research but not at a cost of ignoring the basics, because ignoring the basic creates increased commercial markets for medical drugs.
Ignoring the basics to effectively maintain ill health in order to create a market to provide funding for more research seems to me a dangerous path.
The researchers in this field I would guess must have coffee room discussions in this vein
RB
Re storage - fridge or cool place and do not store for too long.
DO NOT CONFUSE PLEASE !
Please do note that the graphs above are looking at DHA which is a component of fish oil. ONE gram of fish oil will only contain maybe 100mg DHA (guess) (A teaspoon holds about 5grams, so contains about 500 mg. of DHA) In fish oil terms I would guess you are looking at 20 grams a day (4 teaspoons) but you would need to look at the label and contents, as all products are different.
Usually they include antioxidants vit E, etc to prevent oxidisation.
You also need to check the amounts of Vitamin A and D the fish oil contains as they vary tremendously with brands.
From my reading/experience it is cheaper to buy in bottled form. Some of them have almost no taste. The quality of refining has increased hugely, and with quality products the days of fishy repeats all day are long gone. The cost savings at higher dosages are potentially significant for those on tight budgets. I take mine from a teaspoon - no back taste - no repeating etc - less flavour than olive oil (tastes of lemons).
RB
This post is out on a limb as I have not seen it suggested any where as cancer treatment adjunct but would have grounds for consideration if one takes the stance that the omega three six balance is relevant.
Thought provoking article.
An interesting area for a trial, or consideration by those running out of options.
One for discussion with your onc????
RB
http://www.jimmunol.org/cgi/content/full/171/9/4837
ABSTRACT from full trial write up
"Potential impact of {omega}-3 fatty acids, as contained in fish oil, on immunological function has been suggested because observations of reduced inflammatory diseases in Greenland Inuit were published. A fish oil-based lipid emulsion has recently been approved for parenteral nutrition in many countries. We investigated the influence of a short infusion course of fish oil-based ({omega}-3) vs conventional ({omega}-6) lipid emulsion on monocyte function. In a randomized design, twelve healthy volunteers received {omega}-3 or {omega}-6 lipid infusion for 48 h, with cross-over repetition of the infusion course after 3 mo. Fatty acid profiles, monocyte cytokine release and adhesive monocyte-endothelium interaction were investigated. Resultant {omega}-6 lipid emulsion increased plasma-free fatty acids including arachidonic acid, whereas the {omega}-3/{omega}-6 fatty acid ratio in monocyte membranes remained largely unchanged. It also caused a tendency toward enhanced monocyte proinflammatory cytokine release and adhesive monocyte-endothelium interaction. In contrast, {omega}-3 lipid emulsion significantly increased the {omega}-3/{omega}-6 fatty acid ratio in the plasma-free fatty acid fraction and in monocyte membrane lipid pool, markedly suppressing monocyte generation of TNF-{alpha}, IL-1, IL-6, and IL-8 in response to endotoxin. In addition, it also significantly inhibited both monocyte-endothelium adhesion and transendothelial monocyte migration, although monocyte surface expression of relevant adhesive molecules (CD11b, CD18, CD49 days, CCR2) was unchanged. Although isocaloric, {omega}-3 and {omega}-6 lipid emulsions exert differential impact on immunological processes in humans. In addition to its nutritional value, fish oil-based {omega}-3 lipid emulsion significantly suppresses monocyte proinflammatory cytokine generation and features of monocyte recruitment."
On the general thread and published in NEJM.
http://content.nejm.org/cgi/content/abstract/320/5/265?ijkey=1986443e7dcda4bad1a17ec7c475fd4cfa4af58c&keytype2=tf_ipsecsha
Interesting as to levels of supplementation 18grms fish oil (4tps ? assuming 5grms per tps. approx?)
Effect 61% reduction inflammatory factors.
Dependence on omega three. Supplementation stopped so did effect. Washout 2o weeks which is in ball park of other trials I have read (time was for DHA).
No mention of omega six. From what I have read elsewhere lowish and balancing threes and sixes further enhances effects of omega three.
On omega six intake
To particularly watch for
Concentrated plant reproductive vehicles - seeds and nuts (and their oil etc) generally contain significant amounts of omega six, and not many contain much three
Products of herbivores - the fat offal content etc of living things we eat reflect what they eat. So if chickens cattle etc are fed on grain they will have higher omega six which will be concentrated by them in fat offal eggs etc. It is difficult to be definitive is so is more of a "food for thought" than anything else, combined with noting suggestions that those who eat grass fed meat may be less prone to these inflammatory diseases. A whole subject on its own. http://www.nutritiondata.com/facts-B00001-01c20wT.html This is an example for beef, not on the same high level as nuts but still quite a lot of omega six and half as much three, if you are eating a lot of meat. This is a link for chicken liver pan fried. Corn fed? http://www.nutritiondata.com/facts-B00001-01c21sJ.html. The omega threes and sixes are totalled at the end of the column which helps.
Farmed fish. - as above they are what they eat - so high grain etc content will push up omega six content - of course better than some alternatives but it is important to be aware of the different fat profiles of grain fed and wild animals - grain fed animals also have lower vitamin D, and plant antioxidant levels in their fat - feeding fish to fish also does not seem a very productive use of a potentially scarce resource, it takes 4-5 tons of wild fish to grow a ton of farmed fish - time to start farming algae etc.
Nut are excellent sources of all sorts of things but that has to be balanced with the omega six factor if that is in your sights. As previously noted a number of dietary books suggest no more than a palmful about a day.
I cant think of any other "very high" (you get quite a lot in a small or very small portion) omega six sources I have come across but there may be others.
But at the end of the day we are all individual and have to make our own choices.
Please do talk to your advisers about significant dietary changes.
RB
Abstract
We examined whether the synthesis of interleukin-1 or tumor necrosis factor, two cytokines with potent inflammatory activities, is influenced by dietary supplementation with n-3 fatty acids. Nine healthy volunteers added 18 g of fish-oil concentrate per day to their normal Western diet for six weeks. We used a radioimmunoassay to measure interleukin-1 (IL-1 beta and IL-1 alpha) and tumor necrosis factor produced in vitro by stimulated peripheral-blood mononuclear cells. With endotoxin as a stimulus, the synthesis of IL-1 beta was suppressed from 7.4 +/- 0.9 ng per milliliter at base line to 4.2 +/- 0.5 ng per milliliter after six weeks of supplementation (43 percent decrease; P = 0.048). Ten weeks after the end of n-3 supplementation, we observed a further decrease to 2.9 +/- 0.5 ng per milliliter (61 percent decrease; P = 0.005). The production of IL-1 alpha and tumor necrosis factor responded in a similar manner. Twenty weeks after the end of supplementation, the production of IL-1 beta, IL-1 alpha, and tumor necrosis factor had returned to the presupplement level. The decreased production of interleukin-1 and tumor necrosis factor was accompanied by a decreased ratio of arachidonic acid to eicosapentaenoic acid in the membrane phospholipids of mononuclear cells. We conclude that the synthesis of IL-1 beta, IL-1 alpha, and tumor necrosis factor can be suppressed by dietary supplementation with long-chain n-3 fatty acids. The reported antiinflammatory effect of these n-3 fatty acids may be mediated in part by their inhibitory effect on the production of interleukin-1 and tumor necrosis factor.
Source Information
Department of Medicine, New England Medical Center Hospital, Boston, MA.
A table of EPA and DHA in fish
http://www.ncbi.nlm.nih.gov/gquery/gquery.fcgi?term=Fish+oil+OR+omega-3+OR+docosahexaenoic+OR+eicosapentaenoic
And this is the article it comes from
"Practical Applications of Fish Oil ({Omega}-3 Fatty Acids) in Primary Care
Robert Oh, MD
From the Department of Family Medicine, MCHJ-FP, Madigan Army Medical Center, Ft. Lewis, Washington "
http://www.jabfm.org/cgi/content/full/18/1/28#R4
It is more readable than most and deals with arthritis, heart disease etc.
RB
If you have questions check the manufacturers web site these trials are general and not specific and buy reputable brands I guess.
These trials below would suggest that as far as mercury etc goes that fish oils are low risk - possibly lower levels than whole fish which is comforting but no reason not to eat the original food source as well.
Little fish in general terms don't live as long and so have lower contaminates.
Big fish shark swordfish are reported as having "higher" levels, so are possibly not the best everyday menu item.
There are also other pollutants eg dioxins etc but the solution is to stop putting them into the environment. They will also be concentrated in land animals etc. However the trial below would suggest that the risks of organochlorines in fish oil are lower that those in fish.
As to species bottom feeders particularly, but other fish as well that come from potentially polluted inland waters or industrial outlet areas to the sea (e.g. Baltic) are reported as containing on average more pollutants.
Many of the heavy metals also have natural sources volcanoes etc but we are adding to them significantly industrial pollution, incineration, fossil fuels, metal production etc. So do amalgam fillings etc - dentists are reported as having higher mercury levels etc. so whilst not good the risk of pollutants has to be kept in perspective in balancing risks and benefits.
So one less thing to worry about may be fish oil.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=2718527&query_hl=13&itool=pubmed_docsum
1: Z Ernahrungswiss. 1989 Mar;28(1):76-83. Related Articles, Links
[Contaminating substances in 22 over-the-counter fish oil and cod liver oil preparations: cholesterol, heavy metals and vitamin A]
[Article in German]
Koller H, Luley C, Klein B, Baum H, Biesalski HK.
Institut fur Physiologische Chemie II, Johannes-Gutenberg-Universitat, Mainz.
Fish oil capsules are increasingly used by self-medicating patients. We studied 22 commercial fish oil and menhaden oil preparations in respect to accompanying substances that could be harmful. The substances measured were: cholesterol as determined by gas liquid chromatography, heavy metals measured by atomic absorption, and vitamin A as determined by high-performance liquid chromatography (HPLC). The contents of cholesterol and heavy metals were in ranges which can be regarded as negligible; the content of vitamin A in menhaden oils, however, was found in amounts which warrant that pregnant women do not exceed the dosage as recommended by the manufacturers.
PMID: 2718527 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=14632570&query_hl=13&itool=pubmed_docsum
1: Arch Pathol Lab Med. 2003 Dec;127(12):1603-5. Related Articles, Links
Click here to read
Measurement of mercury levels in concentrated over-the-counter fish oil preparations: is fish oil healthier than fish?
Foran SE, Flood JG, Lewandrowski KB.
Division of Laboratory Medicine, Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass 02114, USA.
CONTEXT: Fish consumption has been associated with a decreased risk of coronary artery disease. Recent studies have illustrated that the high mercury content in cold-water fish may negate the cardiovascular benefits of fish meals. Fish oils have similar antiatherogenic properties to fish, and similar studies should be performed to determine the level of mercury in fish oils. OBJECTIVE: To determine the concentration of mercury in 5 over-the-counter brands of fish oil. RESULTS: The levels of mercury in the 5 different brands of fish oil ranged from nondetectable (<6 microg/L) to negligible (10-12 microg/L). The mercury content of fish oil was similar to the basal concentration normally found in human blood. CONCLUSIONS: Fish are rich in omega-3 fatty acids, and their consumption is recommended to decrease the risk of coronary artery disease. However, fish such as swordfish and shark are also a source of exposure to the heavy metal toxin, mercury. The fish oil brands examined in this manuscript have negligible amounts of mercury and may provide a safer alternative to fish consumption.
PMID: 14632570 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=15628911&query_hl=13&itool=pubmed_docsum
1: Arch Pathol Lab Med. 2005 Jan;129(1):74-7. Related Articles, Links
Click here to read
Measurement of organochlorines in commercial over-the-counter fish oil preparations: implications for dietary and therapeutic recommendations for omega-3 fatty acids and a review of the literature.
Melanson SF, Lewandrowski EL, Flood JG, Lewandrowski KB.
Clinical Laboratories Division, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
CONTEXT: The consumption of fish high in omega-3 fatty acids is advocated by the American Heart Association to decrease the risk of coronary artery disease. However, fish contain environmental toxins such as mercury, polychlorinated biphenyls, and organochlorine pesticides, which may negate the beneficial cardiovascular effects of fish meals. Toxin levels vary depending on both the fish source and the specific toxin, and neither farm-raised nor wild fish are toxin free. Fish oil supplements also prevent the progression of coronary artery disease and reduce cardiovascular mortality. However, only sparse data exist on the level of toxins in fish oil. In a previous study we showed that the amount of mercury in 5 over-the-counter brands of fish oil was negligible. OBJECTIVE: To determine the concentrations of polychlorinated biphenyls and other organochlorines in 5 over-the-counter preparations of fish oil. DESIGN: The contents of 5 commercial fish oil brands were sent for organochlorine analysis. RESULTS: The levels of polychlorinated biphenyls and organochlorines were all below the detectable limit. CONCLUSIONS: Fish oil supplements are more healthful than the consumption of fish high in organochlorines. Fish oils provide the benefits of omega-3 fatty acids without the risk of toxicity. In addition, fish oil supplements have been helpful in a variety of diseases, including bipolar disorder and depression.
PMID: 15628911 [PubMed - indexed for MEDLINE]
"Farmed salmon had greater levels of total lipid (average 16.6%) than wild salmon (average 6.4%). The n-3 to n-6 ratio was about 10 in wild salmon and 3-4 in farmed salmon."
IN WILD FISH omega three to six 10:1
IN FARMED FISH omega three to six 3-4:1
as independently reflected on the nutritional data site
http://www.nutritiondata.com/facts-B00001-01c216F.html
http://www.nutritiondata.com/facts-B00001-01c216g.html
http://www.nutritiondata.com/facts-B00001-01c216F.html
So still a good source of omega three but less useful in balancing the threes and sixes.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=10479232&query_hl=12&itool=pubmed_docsum
1: Environ Sci Technol. 2005 Nov 15;39(22):8622-9. Related Articles, Links
Lipid composition and contaminants in farmed and wild salmon.
Hamilton MC, Hites RA, Schwager SJ, Foran JA, Knuth BA, Carpenter DO.
AXYS Analytical Services, Sidney, British Columbia, Canada, School of Public and Environmental Affairs, Indiana University, Bloomington, Indiana 47405, USA.
Levels of omega-3 (n-3) and omega-6 (n-6) fatty acids and lipid-adjusted concentrations of polychlorinated biphenyls (PCBs), dioxins, toxaphene, and dieldrin were determined in 459 farmed Atlantic salmon, 135 wild Pacific salmon, and 144 supermarket farmed Atlantic salmon fillets purchased in 16 cities in North America and Europe. These were the same fish previously used for measurement of organohalogen contaminants. Farmed salmon had greater levels of total lipid (average 16.6%) than wild salmon (average 6.4%). The n-3 to n-6 ratio was about 10 in wild salmon and 3-4 in farmed salmon. The supermarket samples were similar to the farmed salmon from the same region. Lipid-adjusted contaminant levels were significantly higher in farmed Atlantic salmon than those in wild Pacific salmon (F = 7.27, P = 0.0089 for toxaphene; F = 15.39, P = 0.0002 for dioxin; F > or = 21.31, P < 0.0001 for dieldrin and PCBs, with df = (1.64) for all). Levels of total lipid were in the range of 30-40% in the fish oil/fish meal that is fed to farmed salmon. Salmon, especially farmed salmon, are a good source of healthy n-3 fatty acids, but they also contain high concentrations of organochlorine compounds such as PCBs, dioxins, and chlorinated pesticides. The presence of these contaminants may reduce the net health benefits derived from the consumption of farmed salmon, despite the presence of the high level of n-3 fatty acids in these fish.
PMID: 16323755 [PubMed - indexed for MEDLINE]
AlaskaAngel
07-02-2006, 10:42 AM
RB,
My sincere appreciation for this unbiased distinction you provided.
An Alaskan Angel
Unregistered
07-02-2006, 12:36 PM
Rhonda ,
Thanks for the links on fatty acids.Could you please clarify why walnuts and soybeans are one of the best omega 3 sources on your first link and why soybean and walnut oil are referred to as omega 6 on the second link. It seems a little contradictory. What do you think?
Thanks!
Walnuts and soy are identified as they have some omega three which is you will see from the chart below is unusual. { there are many more rarefied members of these fat families but they are not commonly discussed and it starts getting very complicated - the subs bench might be a description.}
Many of the trials on omega three and six have only got as far as omega three and take no account of omega six intake as a factor. Omega six is not yet on the wider radar.
Hence they will look at say the impact of walnuts on a diet - so the subject is getting more three which is an improvement BUT misses the real point that six is the key and omega three the essential partner. Fred Aistaire without Ginger Rogers. This also can lead to suggestions that three has no impact, which may in fact be simply because the relatively low additional intake is being swamped by the impact of excess omega six already in the diet.
It is the mother fat linolenic acid 18:3 n3 soy and walnut etc contain which if your body is working ok, pathways not hindered by medication, not compromised by excess six....can be made into the longer and more flexible and influential children DHA and EPA.
BUT walnuts soy etc do not provide DHA or EPA which is even harder to find high level food sources for - there is only basically fish and meat with offal and particular fish providing higher levels - which is why scavengers etc prize the offal as a food source and it is first choice on the carnivore menu, why
bears like salmon etc. I guess.
In general terms the animals have collected the mother fat it from green things and made it into the children, and collected it and the children fats from littler living things, and we are making use of that.
There are vegetarian options but they are limited, which I guess makes balancing the threes and sixes and low level sources of the mother fat greens etc even more important for some. There are some algae products as well.
http://www.benbest.com/health/fpercent.gif
http://www.benbest.com/health/fcontent.gif
This site is useful to look up particular foods
http://www.nutritiondata.com/facts-B00001-01c20oc.html
http://www.nutritiondata.com/facts-B00001-01c20ob.html
http://www.nutritiondata.com/facts-B00001-01c20ob.html
So in the absence of any other omega three sources some walnut and soy is better than none. In a three six diet they would be included for variety and width of diet but factored into the omega six intake (and soy is a personal chioce given the issues that surround it for BC reasons).
AND they also have high levels of six, which as a nomad who fished so omega threes were no problem was good news too ( except soy is reported not to have been on the menu until the chinese found out how to cook it or ferment it to make it more digestible).
AND walnuts have lots of antioxidants and other things - soy products have lots of facets which are the subject of much ongoing discussion for BC sufferers good or bad is still under debate as noted above.
BUT whilst having more three than most things which is good news if you are short of sources of three, they are high sources of omega six which is an issue if you are trying to balance the threes and sixes.
HENCE the general observation if the three six is of interest to keep in mind that nut consumption is high six source in many instances, and nuts and seeds should be consumed in strict moderation. AGAIN CHECK ON NUTRITION DATA as some nuts like macademia and to a lesser extent cashew are much lower in Omega 6s, and some like sunflower are very high.
Levels of intake must be an individual choice but there are suggestion that low sensible is the most effective option keeping the three six balance in mind.
Flax perillia etc are some of the few high three vegetable seed source exceptions - but they too have some six but less six than three see above table.
I hope this helps.
Thanks for the comments. It is a pleasure to feel of some use hopefully, and questions / posts make me check and think about things from different perspective, and force a better understanding which is very helpful in my wanders.
RB
Another reason and a familiar cast of players.
RB
http://www.ajcn.org/cgi/content/abstract/81/4/934
ABSTRACT
There are a plethora of biologically plausible pathways whereby PUFAs may regulate the factors involved in bone metabolism, such as prostaglandins, cytokines, insulin-like growth factor I, and calcium. Reviewers have suggested that one or a combination of these factors may have an effect on bone (5, 6, 13, 23). For example, PGE2, the major prostaglandin involved in bone metabolism, is synthesized from n–6 fatty acids, whereas n–3 fatty acids inhibit its production (1, 13). Normal or moderate concentrations of PGE2 support bone formation, whereas greater quantities promote bone resorption (5). Fatty acids are also involved in calcium metabolism. Higher n–3 fatty acid intake enhances calcium absorption, decreases calcium loss, and increases bone calcium (13, 20,23). In addition, the inhibition of cytokine production has been implicated as a potential mechanism of the favorable effects of fatty acids on bone, with higher intakes of n–3 fatty acids inhibiting the synthesis of proinflammatory cytokines, such as interleukin 6, interleukin 1, and tumor necrosis factor {alpha} (24, 25). Kettler (6) suggested that bone loss is mediated by cytokines, and n–3 fatty acid supplementation in animals and humans reduces cytokine synthesis and increases calcium absorption.
In the present study, there was a significant interaction between hormone use and the ratio of dietary n–6 to n–3 fatty acids on BMD at the hip and spine. Fatty acids could potentiate the effect of HT on bone through increasing calcium absorption (26). A study in ovariectomized rats showed that estrogen plus a combination of n–6 and n–3 fatty acids increases bone formation and decreases bone resorption, whereas estrogen alone only increases bone formation (27).
To our knowledge, this is the first large epidemiologic investigation of the association between PUFAs and BMD in older, community-dwelling white men and women who had a wide range of dietary n–6 and n–3 fatty acid intake. The latest longitudinal study by Macdonald et al (11) investigated the association between total PUFAs and bone in women only and did not differentiate between various types of PUFAs (eg, n–3 versus n–6). Previous experimental studies had limited ability to assess a range of fatty acid intakes because of study design and small sample sizes.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=11207457&dopt=Abstract
1: Altern Med Rev. 2001 Feb;6(1):61-77. Related Articles, Links
Click here to read
Can manipulation of the ratios of essential fatty acids slow the rapid rate of postmenopausal bone loss?
Kettler DB.
Sky Park Wellness Center, Irvine, CA 92614, USA dr.debra@home.com
The rapid rate of postmenopausal bone loss is mediated by the inflammatory cytokines interleukin-1, interleukin-6, and tumor necrosis factor alpha. Dietary supplementation with fish oil, flaxseeds, and flaxseed oil in animals and healthy humans significantly reduces cytokine production while concomitantly increasing calcium absorption, bone calcium, and bone density. Possibilities may exist for the therapeutic use of the omega-3 fatty acids, as supplements or in the diet, to blunt the increase of the inflammatory bone resorbing cytokines produced in the early postmenopausal years, in order to slow the rapid rate of postmenopausal bone loss. Evidence also points to the possible benefit of gamma-linolenic acid in preserving bone density.
Publication Types:
* Review
PMID: 11207457 [PubMed - indexed for MEDLINE]
http://www.jacn.org/cgi/content/full/19/4/478S
ABSTRACT
Conjugated Linoleic Acid and Bone Biology
Bruce A. Watkins, PhD, FACN and Mark F. Seifert, PhD
Purdue University, Department of Food Science, Lipid Chemistry and Molecular Biology Laboratory, West Lafayette, Indiana, and Department of Anatomy, Indiana University School of Medicine, Indianapolis, Indiana
Address reprint requests to: Dr. B.A. Watkins, Department of Food Science, Lipid Chemistry and Molecular Biology Laboratory, Purdue University, W. Lafayette, IN, 47907. E-mail: watkins@foodsci.purdue.edu.
Osteoporosis, osteoarthritis and inflammatory joint disease afflict millions of people worldwide. Inflammatory cytokines inhibit chondrocyte proliferation and induce cartilage degradation for which part of the response is mediated by PGE2. Excess production of PGE2 is linked to osteoporosis and arthritis and is associated with bone and proteoglycan loss. PGE2 also influences the IGF-I/IGFBP axis to facilitate bone and cartilage formation. Recent investigations with growing rats given butter fat and supplements of CLA demonstrated an increased rate of bone formation and reduced ex vivo bone PGE2 production, respectively...............
Anti-inflammatory diets, including nutraceutical n-3 fatty acids, are associated with decreased pathogenesis of rheumatoid arthritis (secondary osteoporosis), reduced inflammatory diseases [66–68] and lowered cancer risk [69]. The common link between these diseases resides in the regulation/expression of COX-2. For example, multiple lines of evidence indicate that up-regulation of COX-2 contributes to tumorigenesis and inflammation, providing tissue levels of prostanoid precursors that influence formation of the pro-inflammatory PGE2. In addition, chronic aspirin users (COX inhibitor) have reduced incidence of colorectal cancer. Both COX-1 and COX-2 inhibitors suppress experimental mouse skin carcinogenesis, and permanent overactivation of arachidonic acid metabolism appears to be a driving force for tumor development [70]. Moreover, metastasis of cancer to bone is a frequent outcome of breast (about two-thirds of patients with metastatic breast cancer have bone involvement) and prostate malignancies. The metastasis is often associated with significant morbidity (severe bone pain and pathologic fractures) due to osteolysis, and metastatic target bone is continually being remodeled under the influence of factors produced locally and systemically [71].
Interestingly, recent investigations suggest that both COX-2 induction and an increase in the supply of arachidonic acid are needed to greatly increase prostanoid production [72]. Supplying arachidonic acid appears to increase prostanoids to reduce the effects of nonsteroidal anti-inflammatory drugs, including NS-398 a specific COX-2 inhibitor. Therefore, in our view, n-3 fatty acids and CLA isomers may act as potent anticancer nutrients because they not only directly/indirectly affect the activity and expression of COX-2, but may also reduce the supply of arachidonic acid to diminish prostanoid biosynthesis. In any case, one mode of action for CLA appears to be anti-inflammatory with respect to reducing PGE2 production.
The data presented in this review describe consistent and reproducible effects of CLA isomers on decreasing ex vivo PGE2 production in bone organ cultures [33,34] and in various cell culture systems [51]. The potent beneficial anticancer effect of CLA is likely linked, in part, to down-regulation of COX-2 activity. Future investigations on CLA should evaluate isomeric effects on COX-1 and COX-2, for which over-expression of the latter is associated with carcinogenesis and inflammation. This research would lead to 1) important discoveries for bone modeling and remodeling, 2) development of delivery systems in designed/functional foods and 3) opportunities to identify a synergism between nutraceuticals and drug therapies to reduce cancer risk and control inflammatory bone/joint disease.
Mr Menendez and Ruth Lupu are frequent authors on the subjects of fats and BC and have a particular expertise in the field.
This seems to be saying that the gene involved in the synthesis of fats by the body is key to aggressive cancers, and is suggesting that there should be a recognition that it relates to the body's metabolism (of which diet is an important factor in this case fats by implication of the FAS pathways my interpretation based on their previous studies).
Not the easiest to read but for me a "public" statement of some significance suggesting implicitly that fats and body "metabolism" have a significant role in aggressive cancers.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16778562&query_hl=15&itool=pubmed_DocSum
1: Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):346-357.Click here to read Links
Oncogenic properties of the endogenous fatty acid metabolism: molecular pathology of fatty acid synthase in cancer cells.
* Menendez JA,
* Lupu R.
aFoundation of the Recerca Bio-Medical Institute of Girona Dr Josep Trueta, University Hospital of Girona, Dr Josep Trueta, Girona, Catalonia, Spain bDepartment of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, Illinois, USA cNorthwestern University Feinberg School of Medicine, Chicago, Illinois, USA dRobert H. Lurie Comprehensive Cancer Center of Northwestern University, Chicago, Illinois, USA.
PURPOSE OF REVIEW: This review documents our rapidly changing perspectives on the function of fatty acid synthase-catalyzed endogenous fatty acid biogenesis in cancer biology. RECENT FINDINGS: Up-regulation of fatty acid synthase gene expression and fatty acid synthase biosynthetic activity are molecular events accompanying the pathogenesis and natural history of cancer disease. First, the increased fatty acid synthase gene expression in precursor, preinvasive and invasive cancer lesions appears to represent an indirect, early epiphenomenon, occurring in response to a microenvironment containing regions of poor oxygenation and high acidity due to, for example, lack of an adequate angiogenesis and/or nutritional supply. Second, aberrant transduction cascades driven by cancer-associated oncogenic changes subvert the downregulatory effects of circulating fatty acids. Third, fatty acid synthase-dependent endogenous fatty acid metabolism actively contributes to cancer evolution by specifically regulating the expression, activity and/or cellular localization of proteins closely related to malignant transformation and/or cancer progression. SUMMARY: Fatty acid synthase-catalyzed endogenous fatty acid metabolism appears to be an obligatory acquisition selecting a biologically aggressive sub-group of cancer cells capable of growth and survival upon stresses such as hypoxia, low pH and/or nutritional deprivation. Considering that an ever-growing body of evidence demonstrates that fatty acid synthase-driven signalling actively regulates key cancer-controlling networks, we may hereafter redefine fatty acid synthase as a metabolic oncogene in human cancer cells.
PMID: 16778562 [PubMed - as supplied by publisher]
RobinP
07-03-2006, 04:49 AM
Thanks for the precious, valued, VAST information on FA RB and for the answer to my unregistered post above about walnuts being both omega 3 and 6 FA.
The basis of many margarines and used in processed food to varying degrees.
Note potential inflammatory link.
RB
ABSTRACT
"Consumption of trans fatty acids (TFA) predicts higher risk of coronary heart disease, sudden death, and possibly diabetes mellitus. These associations are greater than would be predicted by effects of TFA on serum lipoproteins alone. Systemic inflammation and endothelial dysfunction may be involved in the pathogenesis of atherosclerosis, acute coronary syndromes, sudden death, insulin resistance, dyslipidemia, and heart failure. Evidence from both observational and experimental studies indicates that TFA are pro-inflammatory. Limited evidence suggests that pro-inflammatory effects may be stronger for trans isomers of linoleic acid (trans-C18:2) and oleic acid (trans-C18:1),"
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16713393&query_hl=15&itool=pubmed_DocSum
1: Atheroscler Suppl. 2006 May;7(2):29-32. Epub 2006 May 18.Click here to read Links
Trans fatty acids - Effects on systemic inflammation and endothelial function.
* Mozaffarian D.
The Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA.
Consumption of trans fatty acids (TFA) predicts higher risk of coronary heart disease, sudden death, and possibly diabetes mellitus. These associations are greater than would be predicted by effects of TFA on serum lipoproteins alone. Systemic inflammation and endothelial dysfunction may be involved in the pathogenesis of atherosclerosis, acute coronary syndromes, sudden death, insulin resistance, dyslipidemia, and heart failure. Evidence from both observational and experimental studies indicates that TFA are pro-inflammatory. Limited evidence suggests that pro-inflammatory effects may be stronger for trans isomers of linoleic acid (trans-C18:2) and oleic acid (trans-C18:1), rather than of palmitoleic acid (trans-C16:1), but further study of potential isomer-specific effects is needed. TFA also appear to induce endothelial dysfunction. The mechanisms underlying these effects are not well-established, but may involve TFA incorporation into endothelial cell, monocyte/macrophage, or adipocyte cell membranes (affecting membrane signaling pathway relating to inflammation) or ligand-dependent effects on peroxisome proliferator-activated receptor (PPAR) or retinoid X receptor (RXR) pathways. Activation of inflammatory responses and endothelial dysfunction may represent important mediating pathways between TFA consumption and risk of coronary heart disease, sudden death, and diabetes. Further study is indicated to define these effects of TFA and the implications of such effects for cardiovascular health.
PMID: 16713393 [PubMed - in process]
RobinP
07-03-2006, 05:26 AM
Recent investigations with growing rats given butter fat and supplements of CLA demonstrated an increased rate of bone formation and reduced ex vivo bone PGE2 production, respectively...............This taken with your above post on margarines certainly promotes butter over margarine and the trans fa. Of course, lets not forget to balance butter with the omega 3s and do butter in moderation.
StephN
07-03-2006, 12:04 PM
Living in the glorious great Northwest, we are blessed to have an abundance of healthy fresh fish. Much comes from Alaskan waters.
With a diabetic husband, fresh fish is a menu staple. We spend the extra money on the lovely fish and thoroughly enjoy our dinner meals. Had some fresh Ling Cod last night after the baseball game.
Now that the "cat is out" about the farmed salmon not having the right levels of the omega 3, as these fish do not develop the muscle tissue from swimming upstream, we have avoided this type. Also, the doubts I have about the feeding and living conditions of farmed fish, including shrimp from Asia, keep me away from these.
Since we eat fish more than once a week, I have not taken the fish oil separately. Not sure if I should anyway, but do get plenty of high quality olive oil, some grape seed and seasame oil in cooking.
Thanks a lot RB!
FARMED FISH
They do have omega three just not in the same proportions, and a trial raised questions as to levels of certain chemicals etc. But if you cant get wild fish or too expensive probably better than no fish.
VEGETABLE SEED OILS AND NUT OILS(with very limited exception)
***************THEY ARE HIGH IN OMEGA SIX*****************
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16713393&query_hl=15&itool=pubmed_DocSum
in 218 grams of oil GRAPESEED
Total omega-3 fats (est) 218 mg
Total omega-6 fats (est) 151,700 mg
IN 218 grams SESAME
http://www.nutritiondata.com/facts-B00001-01c208F.html
Total omega-3 fats (est) 654 mg
Total omega-6 fats (est) 90040 mg
IN 216 grams OLIVE ( this will be a virgin oil in cheap olis as much as 50% is omega six)
http://www.nutritiondata.com/facts-B00001-01c208D.html
Total omega-3 fats (est) 1644 mg
Total omega-6 fats (est) 21090 mg
THIS IS THE POINT I AM TRYING TO MAKE
NOT A LOT OF MOST VEGETABLE AND SEED OILS IS A LOT OF OMEGA SIX.- and it is everywhere in process foods, olives in oil (sunflower etc)
You need to check on fish to as you may be surprised how the amounts of omega three differ.
MY GUESS is that you would need fish oil to balance your omega threes.
MY SUGGESTION if omega three six is now on your radar is spend a week actually checking how much omega six and three you are getting - no need to be too fussy but in broad terms, and then consider the dietary iimplications.
Sorry to shout but I have been down this path of diet discovery too - a year a ago being pleased with my self for consuming lots of high polyunsaturated veg oils, cutting down, and then realising with a shock when I checked how far out my three six balance was.
Two Brazil nuts balance a teaspoon of fish oil in very approximate terms.
Essentially in balancing the threes and sixes vegetable oils are very high on the NO list - with the exception of flax (no good for cooking) and olive virgin (and virgin olive still has about 10% omega six).
I hope this helps.
RB
Whilst going back through Smart Fats ( latest version called Brain Building Nutrition) I noted the following comment in relation to fatty acids and brain tumour tissue.
I have not managed to find the original research.
" Indeed, intravenously administered fatty acids were more rapidly incorporated into the implanted tumour cells than the normal brain tissue." This was in respect of intralcerebrally implanted brain tissue.
The book suggests that brain tumours have higher omega six and lower omega three than healthy brain tissue.
The book asks the question could balancing the fats and oils prevent or treat brain tumours.
Very much on the edge and an area that is unresearched, but maybe a subject to discuss with advisers for those with brain tumours whose options are otherwise limited.
Trials referred in book to as to the composition of normal and tumorous brain tissue are copied below. I have been unable to find two.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=search&term=MArtin+dd+composition+of+human+gliomas
1: Lipids. 1996 Dec;31(12):1283-8. Related Articles, Links
The fatty acid composition of human gliomas differs from that found in nonmalignant brain tissue.
Martin DD, Robbins ME, Spector AA, Wen BC, Hussey DH.
Department of Radiology, University of Iowa Hospitals and Clinics, Iowa City 52242, USA.
To compare the fatty acid composition of tumor tissue from glioma patients with that of normal brain tissue, tissue samples were obtained from 13 glioma patients and from 3 nonmalignant patients. Following lipid extraction, total fatty acid composition was measured using gas-liquid chromatography. samples were further separated into phospholipids and neutral lipids. Representative samples were then separated into phospholipid classes by thin-layer chromatography and the fatty acid composition assayed. Levels of the polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA), were significantly reduced (P = 0.029) in the glioma samples compared with normal brain samples; mean values were 4.8 +/- 2.9% and 9.2 +/- 1.0%, respectively. This reduction in glioma DHA content was also observed in terms of phospholipids (4.6 +/- 2.1% vs. 9.6 +/- 0.8%, P = 0.002). The phosphatidylserine and phosphatidylethanolamine phospholipid classes were reduced in the glioma samples. Differences were also noted in the n-6 PUFA content between glioma and normal brain samples. The glioma content of the n-6 PUFA linoleic acid was significantly greater (P < 0.05) than that observed in the control samples in terms of total lipids. Thus, the fatty acid composition of human gliomas differs from that found in nonmalignant brain tissue.
PMID: 8972462 [PubMed - indexed for MEDLINE]
1: Acta Physiol Hung. 1992;79(4):381-7. Related Articles, Links
Phospholipids and fatty acids in human brain tumors.
Ledwozyw A, Lutnicki K.
Department of Pathophysiology, Veterinary Faculty of Agricultural Academy, Lublin, Poland.
Phospholipid and fatty acid composition of human brain tumors is presented. The white matter contains a greater amount of phosphatidylinositol and a very low level of lysophosphoglycerides, as compared to the grey matter. Glioma and meningioma tumors contain a greater amount of phosphatidylinositol, sphingomyelin, and lysophosphoglycerides, as compared to normal cortex tissue. A significant rise in oleic, linoleic and arachidonic acid content in tumor tissue was observed. It is suggested, that changes in lipid composition, may play a role in structural and functional membrane perturbations in neoplastic cells.
PMID: 1343190 [PubMed - indexed for MEDLINE]
A Mediterranean type non prescriptive diet with flaxseed etc.
In essence "serum testosterone and estradiol levels were decreased"
"These results suggest that the multi factorial dietary intervention applied in this study may prevent breast cancer if continued in the long term."
Reduction in BC risk etc
An interesting read.
RB
"We observed significant and favorable changes in hormonal indicators of breast cancer risk in a group of postmenopausal women living in northern Italy, initially with high serum levels of testosterone, who followed an ad libitum diet of radically modified composition for 4.5 months. The main results were that serum sex hormone-binding globulin levels were increased and serum testosterone and estradiol levels were decreased. We also found decreased body weight, decreased insulinemic response to oral glucose, decreased fasting glucose, and decreased cholesterol: all of these changes were anticipated by the study hypothesis. Minor changes in the same direction were observed also among women in the control group, who were blind to the dietary strategy of the study but may have slightly changed their diet following publicly available cancer prevention guidelines."
Reducing Bioavailable Sex Hormones through a Comprehensive Change in Diet: the Diet and Androgens (DIANA) Randomized Trial1
http://cebp.aacrjournals.org/cgi/content/full/10/1/25
Trans fat versions of DHA have been found to be incorporated into brain retina etc. in a study in mice.
There is also suggestion with a caveat of more research required that trans fats may adversely impact on aspect of brain, eye function etc.
Trans fat occur as the result of heat treatment of fats etc.
Trans fats are found in some food products margarines etc. Which and to what extent and which fats - an argument for better labelling ?
"Synaptosomes, brain microvessels and retina were shown to contain the highest levels (about 0.5% of total fatty acids) of the trans isomer of docosahexaenoic acid (22:6 delta 4c,7c,10c,13c,16c,19t). This compound was also observed in myelin and sciatic nerve, but to a lesser extent (0.1% of total fatty acids)."
"We conclude that long-term intake of small amounts of trans-isomers of alpha-linolenic acid could disturb visual function. However, further studies are required to determine the mechanisms responsible for this phenomenon."
Its those poor mice we have to thanks for this info again.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=7909911
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=12368410&query_hl=6&itool=pubmed_docsum
Thought provoking.
"The fatty acid composition, total trans content....human milk samples..........remarkably similar to that in partially hydrogenated soybean and canola oils, suggesting that partially hydrogenated vegetable oils are the major source of these trans fatty acids."
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=7760684
1: Lipids. 1995 Jan;30(1):15-21. Links
Trans fatty acid isomers in Canadian human milk.
* Chen ZY,
* Pelletier G,
* Hollywood R,
* Ratnayake WM.
Nutrition Research Division, Health Protection Branch, Health Canada, Ottawa, Ontario.
The fatty acid composition, total trans content (i.e., sum of all the fatty acids which may have one or more trans double bonds) and geometric and positional isomer distribution of unsaturated fatty acids of 198 human milk samples collected in 1992 from nine provinces of Canada were determined using a combination of capillary gas-liquid chromatography and silver nitrate thin-layer chromatography. The mean total trans fatty acid content was 7.19 +/- 3.03% of the total milk fatty acids and ranged from 0.10 to 17.15%. Twenty-five of the 198 samples contained more than 10% total trans fatty acids, and thirteen samples contained less than 4%. Total trans isomers of linoleic acid were 0.89% of the total milk fatty acids with 18:2 delta 9c,13t being the most prevalent isomer, followed by 18:2 delta 9c,12t and 18:2 delta 9t,12c. Using the total trans values in human milk determined in the present study, the intake of total trans fatty acids from various dietary sources by Canadian lactating women was estimated to be 10.6 +/- 3.7 g/person/d, and in some individuals, the intake could be as high as 20.3 g/d. The 18:1 trans isomer distribution differed from that of cow's milk fat but was remarkably similar to that in partially hydrogenated soybean and canola oils, suggesting that partially hydrogenated vegetable oils are the major source of these trans fatty acids.
PMID: 7760684 [PubMed - indexed for MEDLINE]
Hidden fats.
RB
"We defined a "high trans menu" as a large size serving of French fries and nuggets, 100g of microwave popcorn, and 100g of biscuits/wafers/cakes. "
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=7909911
1: Atheroscler Suppl. 2006 May;7(2):47-52. Epub 2006 May 19.Click here to read Links
A trans world journey.
* Stender S,
* Dyerberg J,
* Bysted A,
* Leth T,
* Astrup A.
Department of Clinical Biochemistry, Gentofte University Hospital, Copenhagen, Denmark.
A high intake of industrially produced trans fatty acids (IP-TFA) is associated with increased risk of coronary heart disease (CHD), and a daily intake as low as possible is required to minimize health risks. To achieve this at the individual level in Denmark, legislation limited IP-TFA in foods to a maximum of 2% of fat content from 2004. We assessed the potential exposure of consumers to IP-TFA by analysing popular foods in Denmark, and in 25 other countries. Fifty-five servings of French fries and chicken nuggets, 87 packages of microwave popcorn, and 393 samples of biscuits/cakes/wafers with "partially hydrogenated vegetable fat" listed high on the food label were bought between November 2004 and February 2006. The content of IP-TFA was analysed by standardized methodology. We defined a "high trans menu" as a large size serving of French fries and nuggets, 100g of microwave popcorn, and 100g of biscuits/wafers/cakes. The amounts of IP-TFA in a "high trans menu" was 30g in 2001 in Denmark, but was reduced to less than 1g in 2005. By contrast, a "high trans menu" provided more than 20g in 17 out of 18 countries, with Hungary, Czech Republic, Poland, Bulgaria, and USA, ranking highest with 42, 40, 38, 37, and 36g, respectively. The legislation in Denmark has reduced the exposure of IP-TFA at the individual level without noticeable effect on availability, price, and quality of foods previously containing high amounts of IP-TFA. The findings of high concentrations of IP-TFA in popular foods outside Denmark suggest that millions of people inside and outside EU have intakes of IP-TFA that may increase their risk of CHD. The Danish experience demonstrates that this risk can be eliminated.
PMID: 16713385 [PubMed - in process]
I have not checked this out but thought provoking.
Where there is a willl...?
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16674878
1: Ugeskr Laeger. 2006 Apr 24;168(17):1654-7. Links
[High levels of industrially produced trans fatty acids in popular fast food - but not in Denmark--secondary publication]
[Article in Danish]
* Stender S,
* Dyerberg J,
* Bysted A,
* Leth T,
* Astrup AV.
Amtssygehuset i Gentofte, Klinisk-biokemisk Afdeling, Hellerup. stst@gentoftehosp.kbhamt.dk
An intake of trans-fatty acids of 5 grams per day is associated with an increase of 25% in the risk of ischemic heart disease. In 2004 Denmark, as the first country in the world, introduced a limitation on the content of industrially produced trans-fatty acids in foods. The amount in a "high-trans menu" consisting of popular foods was, from 2001 to 2005, reduced in Denmark from 30 g to <1 g. The amount in the same menu bought in countries within and outside the European Union is 20-40 g. During a period of just a few years, Denmark has thus eliminated a risk factor for ischemic heart disease without noticeable side effects for consumers. This risk factor is, however, still present in many other countries.
PMID: 16674878 [PubMed - indexed for MEDLINE]
madubois63
07-06-2006, 12:20 PM
>>I take one fish oil capsule each day. Should they be stored in the refrigerator?
Barbara H.<<
Barbara - YES. Keep you fish capsules in the fridge. They cold keeps them from repeating on you and giving you that fishy taste later on.
Maryann
madubois63
07-06-2006, 12:32 PM
I am first generation Greek American. We fished for our dinner, grew our own vegies and fruits, cooked only with pure olive oil, garlic and beans were a mainstay. I never ate fast food until I was about 15. Frozen and canned foods were somewhat of a treat for me (weird but true). R.B. - Do you think the busy years in between 15 and now are what nearly killed me??? I don't blame anyone for what I am going through (except my ex husband - lol). I believe in supplements and eating right. I started with a good foundation and have always cooked healthy meals...the desserts are my downfall though. My ex eats butter by the pound, smokes 2 packs of camels a day and drinks enough alcohol to kill a horse each day. He's very healthy. A friend from my old gym - best body you ever saw, young, eats like a professional body builder..died from ovarian cancer. She died fairly quickly. I just have to wonder how much is just luck or lack of it.
..·´¨¨)) -:¦:-
¸.·´ .·´¨¨)) -:¦:-
((¸¸.·´ ¸.·´ -:¦:- -:¦:-
-:¦:- ((¸¸.Maryann -:¦:-´´
More straws in the wind.
Melanoma this time.
Another wild thought on the edge - As a short term measure? - Boost threes, NSAIDS to block six and force body to use up six reserves and at the same time cut down omega six intake ???
All significant changes to diet should be discussed with your medical advisor.
RB
Department of Biology, The Chinese University of Hong Kong, Shatin, China. chimingchiu@graduate.hku.hk
Recent studies have suggested the inhibition of cyclooxygenase-2 (COX-2) as strategy to prevent colorectal cancer. In this study, the cytostatic and cytotoxic effects of different non-steroidal anti-inflammatory drugs (NSAIDs), all of them are reported COX inhibitors, were investigated in human skin melanoma A-375 cells. Using BrdU-cell proliferation assay, we showed that 50 and 100 microM of celecoxib (CEL) reduced proliferation of the melanoma cells at 72-h incubations by 34.0% and 82.7%, respectively. As determined by Toxilight-cytotoxicity assay, the drug was only toxic to the cancer cells at 100 microM. Indomethacin (IND) also inhibited the cell proliferation by about 40% at 240 and 480 pM and was only slightly toxic to the melanoma. Neither aspirin (ASP) nor piroxicam (PIR) exhibited cytostatic or cytotoxic effect on the cancer cells. Combinatory effects of the above NSAIDs with dietary docosahexaenoic acid (DHA) on inhibiting growth of the melanoma cells were further elucidated. Each of the NSAIDs, at doses 10-480 pM, was incubated simultaneously with the melanoma cells and 160 pM of DHA for 72 h. Results from MTT assay showed that both CEL and IND, starting from 20 microM. exhibited additive effects on the DHA-induced growth inhibition. ASP also enhanced the DHA-induced growth inhibition by 42.8% at 480 microM. To our surprise, although PRX did not suppress the melanoma growth, the drug at 40-240 microM enhanced the DHA-induced growth inhibition by 15.9-66.4%, respectively. Results from these studies suggest that the anticancer effects of NSAIDs may not be explained solely by their COX-inhibitory activities. Further studies are therefore required to understand their modes of action, before they could be used alone or in combinations with other agents for cancer chemoprevention.
PMID: 16507396 [PubMed - indexed for MEDLINE]
The same principle DHA plus NSAID shows possibility in Prostate Cancer.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15703837
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY 10987, USA. nnarayan@env.med.nyu.edu
Epidemiological studies have provided evidence that high intake of saturated fat and/or animal fat increases the risk of prostate cancer, but on the other hand, diets rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs), present in fish oils were found to reduce the risk. There are indications of an increased expression of immunoreactive PPARgamma in prostatic intraepithelial neoplasia (PIN) and prostate cancer, suggesting that PPARgamma ligands may exert their own potent anti-proliferative effect against prostate cancer. The experimental evidence for the role of cyclooxygenase-2 (COX-2) in prostate carcinogenesis is well established through several investigations. It clearly suggests the need for development of strategies to inhibit COX-2 mediated prostate carcinogenesis. However, administration of high doses of COX-2 inhibitors, such as celecoxib, over longer periods may not be devoid of side effects. We assessed the efficacy of DHA and celecoxib individually and in combination at low doses in three prostate cancer cell lines (LNCaP, DU145 and PC-3) measuring cell growth inhibition and apoptosis, and on the levels of expression of COX-2, nuclear factor-kappaB (NF-kappaBp65), and nuclear receptors, such as PPARgamma and retinoid X receptors (RXR), all of which presumably participate in prostate carcinogenesis. A 48-h incubation of prostate cancer cells with 5 microM each of DHA or celecoxib induced cell growth inhibition and apoptosis, and altered the expression of the above molecular parameters. Interestingly, the modulation of these cellular and molecular parameters was more pronounced in cells treated with low doses of DHA and celecoxib (2.5 microM each) in combination than in cells treated with the higher doses of individual agents. In conclusion, the present study demonstrates for the first time that a combination of lower doses of the n-3 PUFA, and DHA with the selective COX-2 inhibitor celecoxib effectively modulates the above cellular and molecular parameters that are relevant to prostate cancer. This raises the intriguing prospect that the use of low doses of a COX-2 inhibitor in combination with an n-3 PUFA could be a highly promising strategy for prostate cancer chemoprevention while minimizing undesired side effects.
PMID: 15703837 [PubMed - indexed for MEDLINE]
And Colon Cancer...
A subject for for your oncs?
RB
Chemoprevention and Nutritional Carcinogenesis Program, Institute for Cancer Prevention, American Health Foundation-Cancer Center, Valhalla, NY, USA.
To develop efficient synergistic or additive combinations of chemopreventive and nutritional agents to reduce the risk of colon cancer, experiments were designed to test the application of a selective cyclooxygenase-2 (COX-2) inhibitor together with dietary omega-3 polyunsaturated fatty acids (PUFAs), such as decosahexaenoic acid (DHA). Thus, individual application of celecoxib, a COX-2 inhibitor, DHA, a omega-3 PUFA, and combinations of both were tested for their effectiveness using cell proliferation, apoptosis, and COX-2 expression as markers in the human colon cancer HCA-7 cell line. HCA-7 cells exposed to various subtoxic doses of celecoxib, DHA, or combinations of both were analyzed for inhibition of cell proliferation by trypan blue exclusion and proliferating cell nuclear antigen methods, induction of apoptosis by 4',6-diamidino-2-phenylindole method, and COX-2 by reverse transcription-PCR and Western blot analysis. In addition, we examined the inhibitory potential of celecoxib and DHA on (14)C-arachidonic acid metabolism mediated by COX-2 in the HCA-7 cell line. We found that treatment with celecoxib (50-150 micro M) or DHA (150-225 micro M) individually induces apoptosis and inhibits cell proliferation only at high concentrations in HCA-7 cell lines. A synergistic effect was observed on induction of apoptosis and inhibition of proliferation when cells were exposed to low doses of celecoxib (50-100 micro M) together with DHA (75 micro M). At high concentrations, celecoxib and DHA blocked the increase in COX-2 protein and mRNA expression in HCA-7 cells. Importantly, the inhibition of COX-2 expression was more pronounced in cells treated with low-dose combinations than with individual agents at high concentrations. In addition, celecoxib and DHA at low-dose levels inhibited (14)C-arachidonic acid metabolism (50-85%, P < 0.0001) leading to very low levels of type 2 series prostaglandin formation. These findings provide the basis for the development of combinations of low-dose regimens of a COX-2 inhibitor and omega-3 PUFAs such as DHA for the prevention and treatment of colon cancer. We are currently testing this concept in preclinical models.
PMID: 14985462 [PubMed - indexed for MEDLINE]
Combined with the above I think this might even merit a smiley.
Would omega three plus low dose COX blocker yield even better result.
Maybe deliver as intravenous lipid feed plus cox blocker ?
As ever changes to diet should be discussed with your medical advisor.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15772428&query_hl=19&itool=pubmed_docsum
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA. ydenkins@vetmed.lsu.edu
Cyclooxygenase-2 (COX-2) is important in the progression of epithelial tumors. Evidence indicates that omega-6 PUFAs such as arachidonic acid (AA) promote the growth of tumor cells; however, omega-3 fatty acids [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] inhibit tumor cell proliferation. We investigated the effects of omega-3 PUFA on the expression and function of COX-2 in 70W, a human melanoma cell line that metastasizes to the brain in nude mice. We show that 1) tumor necrosis factor-alpha upregulates the expression of both COX-2 mRNA and prostaglandin E2 (PGE2) production, and 2) omega-3 and omega-6 PUFA regulate COX-2 mRNA expression and PGE2 production. AA increased COX-2 mRNA expression and prostaglandin production in omega-6-stimulated 70W cells. Conversely, COX-2 mRNA expression decreased in cells incubated with EPA or DHA. AA increased Matrigel invasion 2.4-fold, whereas EPA or DHA did not. Additionally, PGE2 increased in vitro invasion 2.5-fold, whereas exposure to PGE3 significantly decreased invasion. Our results demonstrate that incubation of 70W cells with either AA or PGE2 increased invasiveness, whereas incubation with EPA or DHA downregulated both COX-2 mRNA and protein expression, with a subsequent decrease in Matrigel invasion. Taken together, these results indicate that omega-3 PUFA regulate COX-2-mediated invasion in brain-metastatic melanoma.
PMID: 15772428 [PubMed - indexed for MEDLINE]
Busy little things these n-3s ?
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15358633
Institute of General Pathology, Catholic University, L.go F. Vito, 1, 00168 Rome, Italy. g.calviello@rm.unicatt.it
n-3 Polyunsaturated fatty acids (PUFAs) inhibit the development of microvessels in mammary tumors growing in mice. Human colorectal tumors produce vascular endothelial growth factor (VEGF) whose expression is up-regulated in tumor cells by both cyclooxygenase-2 (COX-2) and PGE(2) and directly correlated to neoangiogenesis and clinical outcome. The goal of this study was to examine the capability of n-3 PUFAs to regulate VEGF expression in HT-29 human colorectal cells in vitro and in vivo. Constitutive VEGF expression was augmented in cultured HT-29 cells by serum starvation and the effects of eicosapentaenoic (EPA) or docosahexaenoic acid (DHA) on VEGF, COX-2, phosphorylated extracellular signal-regulated kinase (ERK)-1 and -2 and hypoxia-inducible-factor 1-alpha (HIF-1alpha) expression and PGE(2) levels were assessed. Tumor growth, VEGF, COX and PGE(2) analysis were carried out in tumors derived from HT-29 cells transplanted in nude mice fed with either EPA or DHA. Both EPA and DHA reduced VEGF and COX-2 expression and PGE(2) levels in HT-29 cells cultured in vitro. Moreover, they inhibited ERK-1 and -2 phosphorylation and HIF-1alpha protein over-expression, critical steps in the PGE(2)-induced signaling pathway leading to the augmented expression of VEGF in colon cancer cells. EPA always showed higher efficacy than DHA in vitro. Both fatty acids decreased the growth of the tumors obtained by inoculating HT-29 cells in nude mice, microvessel formation and the levels of VEGF, COX-2 and PGE(2) in tumors. The data provide evidence that these n-3 PUFAs are able to inhibit VEGF expression in colon cancer cells and suggest that one possible mechanism involved may be the negative regulation of the COX-2/PGE(2) pathway. Their potential clinical application as anti-angiogenic compounds in colon cancer therapy is proposed.
PMID: 15358633 [PubMed - indexed for MEDLINE]
Thought provoking.
Particularly when considered in light of Canadian trial on trans fats in breast milk etc above - implications for wider community - etc.
RB
Directly Quantitated Dietary (n-3) Fatty Acid Intakes of Pregnant Canadian Women Are Lower than Current Dietary Recommendations1
http://jn.nutrition.org/cgi/content/full/135/2/206
This is interesting in that it gives an idea as to dietary fat profiles, and underlines the low levels of DHA EPA.
From the previous post some of this will be trans.
There are suggestions that the preference given to the omega three pathway drops after the 3 6 ratio gets lower than 1:7.
IF women are getting insufficient DHA EPA to provide for their infants, and the pathway for fabrication are restricted by trans fats, poor three six ratios, cox blockers in some instances aspirin, any inherent deficiency etc they can only provide by drawing on their own reserves.
Trials suggests sources include the brain. (A factor in post natal depression?).
Other trials suggest that in the absence of replenishment this reduction in the mothers stores becomes a trend.
The table below is helpful in that it gives an indication of the long chain three six balance in meat eggs fish etc.
RB
Intakes of essential n-6 and n-3 polyunsaturated fatty acids among pregnant Canadian women1,2,3
http://www.ajcn.org/cgi/content/full/77/2/473
http://www.ajcn.org/cgi/content/full/77/2/473/T3
AA EPA DHA
mg/d
Fatty fish 3.5 ± 0.6 (0.0–16.0) 9.1 ± 3.3 (0.0–88.1) 83.5 ± 14.4 (0.0–384.4)
Lean fish 3.1 ± 0.3 (0.0–10.7) 14.9 ± 1.6 (0.0–51.6) 27.4 ± 3.0 (0.09–5.3)
Shellfish and crustaceans 7.6 ± 1.2 (0.0–38.8) 16.9 ± 2.7 (0.0–86.2) 14.7 ± 2.4 (0.0–75.0)
Total fish and seafood 14.2 ± 1.8 (0.0–50.8) 50.4 ± 6.1 (0.0–58.7) 125.7 ± 17.0 (0.0–426.5)
Chicken 34.6 ± 3.8 (0.0–120.1) 3.8 ± 0.4 (0.0–13.3) 6.7 ± 0.7 (0.0–23.2)
Turkey 24.3 ± 5.7 (0.0–188.9) 1.1 ± 0.2 (0.0–8.2) 3.8 ± 0.9 (0.0–29.1)
Total poultry 58.8 ± 6.5 (0.0–202.9) 4.9 ± 0.5 (0.0–13.3) 10.4 ± 1.1 (0.0–31.8)
Beef and beef products 20.5 ± 0.2 (0.0–63.1) 15.7 ± 1.6 (0.0–4.8) 2.7 ± 0.3 (0.0–8.5)
Pork and pork products 14.4 ± 1.8 (0.0–49.1) 1.4 ± 0.1 (0.0–4.9) 1.4 ± 0.1 (0.0–4.9)
Lamb and lamb products 1.5 ± 0.3 (0.0–8.7) 1.2 ± 0.3 (0.0–6.7) 0.4 ± 0.1 (0.0–2.2)
Total meat 36.4 ± 3.3 (0.0–97.4) 18.4 ± 1.8 (0.0–43.5) 4.6 ± 0.4 (0.0–11.9)
Eggs 32.7 ± 3.6 (0.0–82.7) 0.31 ± 0.04 (0.0–0.9) 14.6 ± 1.6 (0.0–37.0)
Total 112.0 ± 7.8 (0.5–275.8) 73.5 ± 6.3 (0.4–186.8) 153.6 ± 17.9 (17.7–518.6)
julierene
07-08-2006, 05:13 PM
I don't mean to be a bad girl here, but I hope to provoke thought on this issue of diet. Diet plagues me... I have had a very good diet for a long time, and still managed to get breast cancer at age 28 because of my genetics. Is it possible that people in other countries have better genetics because they are in a different gene pool - per say? Over time, I have heard that if you take a chinese woman to the US and feed her american foods, that she will develop the same risk for breast cancer, so I feel compelled that there may be genetic factors that supercede dietary factors. Meaning, if you have bad genetics, no matter what you do, you will get cancer. If you have good genetics, you may be able to sway your risk if you eat better. But do you have any way of knowing what your risk are if you could potentially get a bad genetic combination at conception? I think it's always a good idea to eat right, but I wouldn't hold out my hopes on it preventing cancer or curing our cancer.
From the little I have read on genetics there are clearly those who carry higher risks of particular diseases.
Dietary change is not going to eliminate disease but can be a significant modifier of risk. For example I have previously posted this tale but I have read that vascular / heart disease was so rare at the turn of the 1900s that students would rush to see a case as they did not want to miss the opportunity.
Around 70 % is the figure most generally quoted for the increase of western diseases over those with more culturally traditional diets, and lack of access to refined western food.
Diet can and does manipulate expression of genes by significant amounts. ("Expression" Our gene pool is largely similar but we use or expression different amounts according to environmental factors - Most have the same basic ingredients in the kitchen cupboard but they "express" it in their cooking in different quantities according to cultural factors. )
I have previously tried to formulate a scenario where those who considered themselves on a very healthy diet high in polyunsaturates low in fat etc in fact had high omega six compared to omega three. As I keep reiterating it is not about absolute quantities it is about balance.
All of the evidence is that diet does pay a large part in the overall risk factor when looking at issues on a population wide basis.
BC is a dreadful disease. I cannot begin to understand how you feel having contracted it so young. If you have been healthy it must feel like a double whammy.
I too have read lots of health books etc, juiced, etc for many years and it was only about a year ago that I realised that my avid pursuit of polyunsaturates was actually very bad news as it was pushing my omega three six balance way out from the ideal of somewhere around one to one ( or may be even 2:1). I suspect I was not the only one falling into this trap.
My limited field of knowledge relates to what I have read on fats. I would urge all to look VERY closely at their dietary intake in terms of balancing the omega threes and sixes. This can only be done by knowing or looking up the approximate fat contents of the foods you eat until you get to have an reasonable idea of what you are likely to be consuming. For most on a western diet omega three supplementation will be needed. Sources are limited so this is likely to include flax seed and oily fish or fish oil, or algae based products for vegetarians.
RB
Here is a link where change expression of genes in the brain for rate fed high fish oil or high perilla diets is shown by reference to a standard diet.
The trials are looking at the impact of fats on the brain ageing alzheimer's etc. This is one of many in the general subject area.
I have no idea as to the significance of various genes.
I just post the chart to try and illustrate the point that changes in diet and particularly fats can alter the ways our bodies work even in the way we use the genetic ingredients available to us.
Significantly
In numerous subtle ways
At very fundamental levels
Different recipe for different cakes some of which will work and some which will not. I suspect nature is no different from cookery - go beyond certain parameters and your cake mix will not work.
http://www.pnas.org/cgi/content/full/99/5/2619/T5
and the link to the trial
http://www.pnas.org/cgi/content/full/99/5/2619?ijkey=42a2d2f351981cad19aeb809157faf8fdb71664 5
julierene
07-09-2006, 03:21 PM
I guess my point was that I watched my mother "juice" herself to her grave - thinking it would extend her life. She got 4 months, and the doctors thought she would have had 6. She was a healthy 33 year old woman with a good BMI and on a healthy food kick like you wouldn't believe... Then her son died at age 12 from Stage 4 Rhabdomyosarcoma, that was originally Stage 2 when he was 5. Then I got cancer at 28, early stage 2a and I was healthy... Then my daughter got cancer at age 5, stage 2 Adrenal Cortical Carcinoma... then she had a local recurrance. She was our healthiest eater, and of course at a normal BMI. Then I had a recurrance, and BOOM stage 4 for me. Then we found out that we had Li-Fraumeni syndrome. Back in 1991, they told us our p53 gene was normal. Now they told us our p53 gene was mutated. The far end of the gene was where the mutation was, which they didn't know about in 1991. So I just hesitate to hear so many hold out hope that diets were the cause of their cancers. For years I tried to "do the right thing" to prevent cancer. I asked the doctor in tears, why I couldn't have prevented it when I was doing so many things to prevent it. He said "Your risk was 80% of developing cancer before the age of 50. In your family, I would guess that it would be more like 80% before the age of 30. With odds like that, diet wouldn't prevent your cancer. I've seen hundreds people try to prevent cancer with diet, knowing they had the 'cancer gene', and failure was almost 100%." His field of study was Brazilian children with adrenal cortical carcinoma with a p53 mutation called Arg337Cys. He also studies genetic retinal cancer that almost 100% get before the age of 5 with the gene. You can probably see now why I am on the other side of the fence. It failed for me, my mother, my brother, my daughter, and probably will fail for my other 2 children, and hundreds of patients of my daughter's doctor. We have all tried to eat the "right diet" and it has failed us all. I think the only case I know of is an author with stage 4 breast cancer, named Jane Plant, who has been cancer free for a while now after practically eliminating cow and dairy products. And then I guess I know about Lance Armstrong, but he ate like 5 apple fritters every day...
Mary Anne in TX
07-09-2006, 04:14 PM
My husband has made vast improvements in his "heart health" after a heart attack 10 years ago. I have watched him exercise, eat "amazing things", and take a handful of supplements.
Now, I am working hard to eat right, exercise everyday, and take some vitamins and fish oil.
But I must confess that I don't have a clue whether it will help with my cancer. I just know when I eat those veggies and fruit and drink my tons of water, I feel better to fight the next fight!
I'm so glad that I have access to so many who are learning so much and are willing to share. Thanks a million!
ma
Thank you for your post.
Life has certainly dealt you all a desperately difficult hand, and you appear to be dealing with it very bravely.
I very clearly understand your point and position.
I have never claimed diet will cure cancer. I have just suggested that on a population wide basis it will reduce risks for some, and that specifically that there are a significant number of trials implicating fat intake in cancer risk and inflammatory pathways etc.
I have also always said there that the commonly quoted figure of differential in "western" disease from non "western" populations is about 70%. This leaves a very large 30% for whom it would be reasonable to assume that diet if that is the factor has no effect.
I still hold to a position that there is evidence that balancing the omega threes and sixes will moderate the inflammatory pathways, and assist in maintaining the immune system, general health, and moderate risks based on the trials I have read.
Based on the trials being conducted research organisations are sufficiently interested to explore the impacts of lipids on health, and some products developed in consequence, some products being legislated against in some countries eg trans fats etc.
Again I understand your position, and can only begin to imagine your frustration. Please do not associate me with those that are holding diet as the only way to go, or who does not appreciate the huge advances in medicine.
There is room for both and it is important we do not lose sight that the body is immensely complex and has developed this complexity in relation to its environment and the limiting factors in that environment, and so much is simply not understood.
I wish I had the knowledge and expertise to relate what I have read over the last year to your very specific circumstances but I don't.
I have not begun to walk in your shoes and experience the see-saw of hurt and anguish that you must have been through and continue to face.
Thank you for your post. It is important for all of us to know and try and understand if that is ever possible the impossible difficulties in life that many have to face.
RB
PS please find below the results of a search on the ncbi site for "p53 gene and fats" which might suggest fats have a bearing on P53 activity which may or may not be relevant in your circumstances just in case of any interest to you or your doctor.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=search&DB=pubmed
1: Wu B, Iwakiri R, Ootani A, Tsunada S, Fujise T, Sakata Y, Sakata H, Toda S, Fujimoto K. Related Articles, Links
Free Full Text Dietary corn oil promotes colon cancer by inhibiting mitochondria-dependent apoptosis in azoxymethane-treated rats.
Exp Biol Med (Maywood). 2004 Nov;229(10):1017-25.
PMID: 15522837 [PubMed - indexed for MEDLINE]
2: Chi TY, Chen GG, Lai PB. Related Articles, Links
Abstract Eicosapentaenoic acid induces Fas-mediated apoptosis through a p53-dependent pathway in hepatoma cells.
Cancer J. 2004 May-Jun;10(3):190-200.
PMID: 15285929 [PubMed - indexed for MEDLINE]
3: Chung FL, Pan J, Choudhury S, Roy R, Hu W, Tang MS. Related Articles, Links
Abstract Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from omega-3 and omega-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation.
Mutat Res. 2003 Oct 29;531(1-2):25-36. Review.
PMID: 14637245 [PubMed - indexed for MEDLINE]
4: Hanibuchi M, Sone S. Related Articles, Links
No abstract [Causative agents for lung carcinogenesis]
Nippon Rinsho. 2002 May;60 Suppl 5:63-6. Review. Japanese. No abstract available.
PMID: 12101751 [PubMed - indexed for MEDLINE]
5: Shabany K, Chiu PC, Raghian A, Chang KW, Solt DB. Related Articles, Links
Abstract Rapid in vivo assay for topical oral cancer chemopreventive agents.
Int J Oncol. 2002 Jul;21(1):159-64.
PMID: 12063563 [PubMed - indexed for MEDLINE]
6: Perjesi P, Pinter Z, Gyongyi Z, Ember I. Related Articles, Links
Abstract Effect of rancid corn oil on some onco/suppressor gene expressions in vivo. A short-term study.
Anticancer Res. 2002 Jan-Feb;22(1A):225-30.
PMID: 12017293 [PubMed - indexed for MEDLINE]
7: Diggle CP, Pitt E, Roberts P, Trejdosiewicz LK, Southgate J. Related Articles, Links
Free Full Text N;-3 and n;-6 polyunsaturated fatty acids induce cytostasis in human urothelial cells independent of p53 gene function.
J Lipid Res. 2000 Sep;41(9):1509-15.
PMID: 10974058 [PubMed - indexed for MEDLINE]
8: Yano S, Sone S. Related Articles, Links
Abstract [Causative agents for lung carcinogenesis]
Nippon Rinsho. 2000 May;58(5):1017-22. Review. Japanese.
PMID: 10824542 [PubMed - indexed for MEDLINE]
9: Taylor DD, Gercel-Taylor C, Weese JL. Related Articles, Links
Abstract Modulation of colon tumor oncogene expression by cancer patient-derived lipids.
J Surg Oncol. 1996 Sep;63(1):46-51.
PMID: 8841466 [PubMed - indexed for MEDLINE]
mamacze
07-09-2006, 05:38 PM
A bit late Rhonda, but thank you for your nutritional links...teamed up with RB's data, it was extremely helpful. My sis in law has scleroderma and this information will be helpful to her as well. You and RB are sharing a real wealth of information and "food" for thought!
Love Kim from CT
Julierene.
Re P53 gene mutation and fats.
The technicalities are beyond me but the generality seems to be that oxidised fats and particularly omega 6 (AA archidonic acid is a product of omega six.) can induce gene mutation, AND it seems to suggest the body may have some ability to repair them...? (thanks I had not seen anything about this subject before)
"HNE-dG adducts were detected exclusively in incubations with AA."
"It has been reported that 4-HNE treatment in human cells induces a high frequency of G.C to T.A mutations at the third base of codon 249 (AGG*) of the p53 gene, a mutational hot spot in human cancers,"
"Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from omega-3 and omega-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation."
One for your doctor if of interest?
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=12820894&query_hl=2&itool=pubmed_docsum
1: Biochemistry. 2003 Jul 1;42(25):7848-54. Related Articles, Links
Click here to read
Mutational spectrum and genotoxicity of the major lipid peroxidation product, trans-4-hydroxy-2-nonenal, induced DNA adducts in nucleotide excision repair-proficient and -deficient human cells.
Feng Z, Hu W, Amin S, Tang MS.
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987, USA.
trans-4-Hydroxy-2-nonenal (4-HNE), a major product of lipid peroxidation, is able to interact with DNA to form 6-(1-hydroxyhexanyl)-8-hydroxy-1,N(2)-propano-2'-deoxyguanosine (4-HNE-dG) adducts, but its genotoxicity and mutagenicity remain elusive. It has been reported that 4-HNE treatment in human cells induces a high frequency of G.C to T.A mutations at the third base of codon 249 (AGG*) of the p53 gene, a mutational hot spot in human cancers, particularly in hepatocellular carcinoma. This G.C to T.A transversion at codon 249, however, has been thought to be caused by etheno-DNA adducts induced by the endogenous metabolite of 4-HNE, 2,3-epoxy-4-hydroxynonanal. We have recently found that 4-HNE preferentially forms 4-HNE-dG adducts at the GAGG*C/A sequence in the p53 gene including codon 249 (GAGG*C). Our finding supports the possibility that G.C to T.A mutations at codon 249 may be induced by 4-HNE-dG adducts. To investigate this possibility, we determined the mutational spectrum induced by 4-HNE-dG adducts in the supF gene of shuttle vector pSP189 replicated in human cells. We have found that 4-HNE-dG adducts are mutagenic and genotoxic in human cells, and that G.C to T.A transversions are the most prevalent mutations induced by 4-HNE-dG adducts. Furthermore, 4-HNE-dG adducts induce a significantly higher level of genotoxicity and mutagenicity in nucleotide excision repair (NER)-deficient human and Escherichia coli cells than in NER-proficient cells, indicating that NER is a major pathway for repairing 4-HNE-dG adducts in both human and E. coli cells. Together, these results suggest that 4-HNE-dG adducts may contribute greatly to the G.C to T.A mutation at codon 249 of the p53 gene, and may play an important role in carcinogenesis.
PMID: 12820894 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=11896684&query_hl=2&itool=pubmed_docsum
1: Chem Res Toxicol. 2002 Mar;15(3):367-72. Related Articles, Links
Click here to read
Formation of cyclic deoxyguanosine adducts from omega-3 and omega-6 polyunsaturated fatty acids under oxidative conditions.
Pan J, Chung FL.
Division of Carcinogenesis and Molecular Epidemiology, American Health Foundation, Valhalla, New York 10595, USA.
The discovery of the cyclic 1,N(2)-propanodeoxyguanosine adducts of acrolein (Acr), crotonaldehyde (Cro), and t-4-hydroxy-2-nonenal (HNE) as endogenous DNA lesions from lipid peroxidation has raised questions regarding the role of different types of fatty acids as sources for their formation. In this study, we carried out reactions at pH 7 and 37 degrees C with deoxyguanosine 5'-monophosphate and omega-3 polyunsaturated fatty acids (PUFAs), including docosahexaenoic acid (DHA), linolenic acid (LNA), and eicosapentaenoic acid (EPA); or omega-6 PUFAs, including linoleic acid (LA) and arachidonic acid (AA), each in the presence of ferrous sulfate. The formation of Acr, Cro, and HNE-derived 1,N(2)-propanodeoxyguanosine adducts (Acr-, Cro-, and HNE-dG) in the incubation mixture was determined by reversed-phase HPLC analysis. The results showed that Acr and Cro adducts are primarily derived from omega-3 PUFAs, although Acr adducts are also formed, to a lesser extent, from oxidized AA and LA. HNE-dG adducts were detected exclusively in incubations with AA. The kinetics of the formation of these adducts was determined during incubations for 2 weeks and 5 days. The rate of Acr adduct formation was about 5-10-fold that of Cro adducts, depending on the type of PUFAs, and the rate of formation of HNE adducts from AA was also considerably slower than that of Acr adducts. Unlike other cyclic adducts, the formation of Acr adducts was independent of types of PUFAs, but its yield was proportional to the number of double bonds in the fatty acid. Only one of the isomeric Acr adducts was detected, and its stereoselective formation is consistent with that observed previously in vivo. Two previously unknown cyclic adducts, one derived from pentenal and the other from heptenal, were also detected as products from omega-3 and omega-6 fatty acids, respectively. This study demonstrated the specificity for the formation of the cyclic adducts of Acr, Cro, and HNE and other related enals by oxidation of omega-3 and omega-6 PUFAs. These results may be important for the understanding of the specific roles of different types of fatty acids in tumorigenesis.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=14637245&query_hl=2&itool=pubmed_docsum
1: Mutat Res. 2003 Oct 29;531(1-2):25-36. Related Articles, Links
Click here to read
Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from omega-3 and omega-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation.
Chung FL, Pan J, Choudhury S, Roy R, Hu W, Tang MS.
Division of Carcinogenesis and Molecular Epidemiology, Institute for Cancer Prevention, American Health Foundation Cancer Center, Valhalla, NY 10595, USA. fchung@ifcp.us
The cyclic 1,N(2)-propanodeoxyguanosine adducts, derived from alpha,beta-unsaturated aldehydes or enals, including acrolein (Acr), crotonaldehyde (Cro), and trans-4-hydroxy-2-nonenal (HNE), have been detected as endogenous DNA lesions in rodent and human tissues. Collective evidence has indicated that the oxidative metabolism of polyunsaturated fatty acids (PUFAs) is an important pathway for endogenous formation of these adducts. In a recent study, we examined the specific role of different types of fatty acids, omega-3 and omega-6 PUFAs, in the formation of cyclic adducts of Acr, Cro, and HNE. Our studies showed that the incubation of deoxyguanosine 5'-monophosphate with omega-3 or omega-6 fatty acids under oxidative conditions in the presence of ferrous sulfate yielded different amounts of Acr, Cro, and HNE adducts, depending on the types of fatty acids. We observed that Acr- and Cro-dG adducts are primarily formed from omega-3, and the adducts derived from longer chain enals, such as HNE, were detected exclusively from omega-6 fatty acids. Acr adducts are also formed from omega-6 fatty acids, but to a lesser extent; the yields of Acr adducts are proportional to the number of double bonds present in the PUFAs. Two previously unknown cyclic adducts, one from pentenal and the other from heptenal, were detected as products from omega-3 and omega-6 fatty acids, respectively. Because omega-6 PUFAs are known to be involved in the promotion of tumorigenesis, we investigated the role of HNE adducts in p53 gene mutation by mapping the HNE binding to the human p53 gene with UvrABC nuclease and determined the formation of HNE-dG adducts in the gene. The results showed that HNE-dG adducts are preferentially formed in a sequence-specific manner at the third base of codon 249 in the p53 gene, a mutational hotspot in human cancers. The DNA repair study using plasmid DNA containing HNE-dG adducts as a substrate in HeLa cell extracts showed that HNE adducts are readily repaired, and that nucleotide excision repair appears to be a major pathway involved. Together, results of these studies provide a better understanding of the involvement of different PUFAs in DNA damage and their possible roles in tumorigenesis.
Publication Types:
* Review
PMID: 14637245 [PubMed - indexed for MEDLINE]
Mary Anne in TX
07-10-2006, 06:42 AM
http://en.wikipedia.org/wiki/Omega-6_fatty_acid
This made it simple to me. I followed the other links on the page and found more good information to help me understand (at least these people's opinion) the importance of 6 to3. I'm still reading and I'm beginning to understand. I'm getting why my husband's health changed and the doctors thought he'd been on statins when he had just eaten and supplemented right. If he can do it, I can too. Thanks to all who keep making me learn!
ma
marymary
07-10-2006, 09:12 AM
I just received my copy of "Cure" magazine, Summer issue Volume 5, Number 2 2006.
On page 14 there is an article entitled "The Blame Game, Moving past myriad rationales for cancer guilt"
Here is an excerpt from the article:
"Labels lead to guilt, which can be a huge burden for newly diagnosed patients because it lurks around almost every turn. We feel guilt about causing our cancer, about having our families go through it, about not being able to do what we did before, if only for a short time. Then there are the financial burdens, and the list goes on. Particular guilt comes with behaviors linked to cancer: smoking, sun overexposure, a common sexually transmitted disease and obesity.
It's not unusual to try and find an answer to why cancer occurs, says Kymberley Bennett, PhD, assistant professor of psychology at Indiana State University in Terre Haute. "With any stressor, and cancer is a big stressor, we try to figure out why it happened to us," she says. "Ultimately, we want to try to identify something that we can, in turn, control."
And stressing about the cause of cancer can lead to additional stress, says Dr. Bennett, who recently led a study of 115 women newly diagnosed with breast cancer that showed that those who blamed themselves for their cancer showed higher levels of distress than those who didn't. The findings also suggested that self-blame negatively affected a patient's ability to psychologically adjust throughout the year following diagnosis."
I think the danger here is that of blaming the victim. The unpalatable truth is, no one knows what causes cancer. Period.
R.B. may be correct in his(?) assertions that Omega 3's and 6's play some sort of a role in cancer development/treatment. The fact is, however, that despite all of our very best efforts many of us here on this forum will die untimely deaths and that is not our fault. I can't help but bristle whenever I catch a nasty whif of blame.
Yes, R.B., I am taking Fish Oil supplements. I will probably die from breast cancer anyway.
I admire your dedication to research, however, perhaps on your wife's behalf? Unless I am mistaken, and you a a female. Clearly you are a warrior, and every country needs its warriors, whatever your sex may be.
Mary
RhondaH
07-10-2006, 10:23 AM
a wealth of information comes from this source and I for one am PISSED off as to the negativity that comes out on the board (we have lost a lot of good members...Gina, ALMOST lost AL and many others...due to people not just voicing their opinion and offering constructive criticism, but adding unnecessary comments) not to mention that there ARE male breast cancer survivors on the board. I belive that cancer has MANY causes (ie, smoking, poor diet, genetics, environment, lack of exercise, etc.) and while some of us may have gotten it because of 1 cause, others may have gotten it for another (or MANY causes). I choose to do EVERYTHING I can to not get it again (surgery, drugs, diet, exercise, yoga, prayer) and do offer myself 1 cheat day a week so as to not feel deprived. Mary, you go ahead and die of cancer (since that's what you choose to believe), but I and all the OTHER survivors choose to LIVE, some WITH cancer and others WITHOUT. Understand that there are SEVERAL people on the board who offer helpful information that have not had breast cancer, BUT they provide valuable information for those that do. I'm done.
Rhonda
Thank you for your response.
Blame.
I apologise if my posts allow interpretation as blame. This is not in any way my intention. In life we are where we are - changing the past is not an option.
Control.
It is widely accepted that diet can influence health.
IF improved diet gives people something they have some small sense of control over it seems to me providing it is not obsessive that any sense of control must be good news.
If it achieve really positive benefit so much the better.
Implication of fats in cancer.
I am certain fats are implicated in the risk of some cancers and a wide number of other inflammatory based diseases, a number of issues of the nervous system including depression, as well as the immune system and general health. This is based on extensive reading of trials and the works of others. I would challenge anybody with the time to read what I have seen to come to a different conclusion
Gender.
Thanks for the compliment but definatively male, and always so.
Reasons for posting
Various including previous contact with BC sufferer, time on my hands, a need to be kept mentally occupied, a sense that the issue of fats is one that needs airing and the answers found, the implications are too enormous to ignore, and once you have glimpsed them they are not easily put back in the box. Answering questions make one check things, prompts new directions of thought, and gives one a sense of being of a little use.
Causes of cancer.
Human nature and the human dynamic. There is no "profit" (in the widest sense job opportunities, praise, conferences, funding etc.) in finding cancer causes, except where so obvious that they may involve the companies in a law suit. There have been suggestions that trans fats may be problematic for human consumption and yet the level of research on trans fats is moderate. For example a search on PubMed for trans fats and herceptin produces about 1700 for both but trans fats are consumed by probably billions and if as suggested they have negative health impacts the health / life cost will be truly huge huge in global terms. But there is not "profit" in researching / restricting trans fats and the situation will not change except by government intervention, public outcry, or sufficient potential medical downsides to justify the rsik of lawyers involving themselves in a group action. It is suggested they have no nutritional advantage so why are we conducting an experiment on global health?
I am not complaining about the amount of research on herceptin which is clearly making a huge difference to many women. I merely making the point that research and new products is "sexier" than prevention at very many levels - and the reality is we to give equal attention to both side of the problem cause and treatment. How that is to be achieved is another issue.
RB
marymary
07-10-2006, 02:33 PM
Of course, Rhonda, none of us on this board have chosen or ever would have chosen breast cancer. My friend Katie, who died two weeks back, never chose to have this horrible disease. I am not trying to be negative, but I did find the article in Cure magazine to be thought provoking.
Personally speaking, from the day I was diagnosed I asked myself "Why has this disease happened to me?". Further I wondered "and why did I get the worst variety (Her2Neu) of the worst?" I think it's probably the number one question we all ask ourselves. There's even a group called "Why Me?".
Like so many other sufferers, I would try just about anything to get a survival advantage. I am currently taking Herceptin, A/I's, have had radiation of my body and my brain. I even sought the help of a faith healer. Much to my husband's chagrin I am eating broccoli and salads like a rabbit and do take fish oil. But I can't believe that this is my fault. Or your fault. Or Katie's fault. Faults, I think, are character defects and not diseases.
This is a wonderful site and I have gained much support and inspiration here. For me the struggle and the challenge of breast cancer is not just physical, although it certainly is that. Today I am struggling with pain and this is a brand new thing for me. The bigger struggle is psychological, feeling like I have any control at all in a situation where there is none. Trying to move past anger that this has happened to me at all. Trying to feel like cancer is not my fault, that it is not something I have mistakenly brought on myself by some unknown means. Struggling to feel valuable to my family, my friends and society, that I still have value even though my body may be under assault. That I am inherently valuable, not only for the services that I provide but just by being me. I imagine that these struggles are not isolated to me alone, but are common to everyone who comes to the board. They are the tie that binds.
Mary
Mary mary
A powerful comment. We are all "frail" flawed and human it is part of our condition.
At the risk of being repetitive I note that many posts say I take threes or fish oil etc as part of their personal program, but few make reference to balancing the sixes.
Please excuse the "shout" but I wonder if I am managing to convey the other half of the omega 3/EPA DHA message which is
PLEASE BALANCE THE SIXES AND THREES.
Please do excuse me if you have already more than got that part of the message too.
Fish oil together with flaxseed or oil (personal preference see flax seed debate) according to reports is really beneficial at lots of levels, BUT the one that is at the root of the INFLAMMATORY PATHWAYS, and IN VAST excess in the average diet is OMEGA SIX family which includes the key player AA Arachidonic acid. Omega three six ratios in the US are reported as in some cases up to 1:50. The often suggested best average is 1:1. The pathways to make the longer chain omega threes are reported to go astray around one 1:7.
So for most it is necessary to look at your omega six intake, cut right down or out on vegetable, nut and seed oils except those exceptions that are high in three, moderate nut intake, and beware of processed food. (Me too - this is where this quest started when I realised how skewed my own intake was)
Thanks for your post. It sounds like you have been through a great deal.
RB
"There have been a number of clinical trials assessing the benefits of dietary supplementation with fish oils in several inflammatory and autoimmune diseases in humans, including rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriasis, lupus erythematosus, multiple sclerosis and migraine headaches. Many of the placebo-controlled trials of fish oil in chronic inflammatory diseases reveal significant benefit, including decreased disease activity and a lowered use of anti-inflammatory drugs."
By the same author as the initial posts.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=12480795&query_hl=4&itool=pubmed_docsum
1: J Am Coll Nutr. 2002 Dec;21(6):495-505. Related Articles, Links
Click here to read
Omega-3 fatty acids in inflammation and autoimmune diseases.
Simopoulos AP.
The Center for Genetics, Nutrition and Health, Washington, DC 20009, USA. cgnh@bellatlantic.net
Among the fatty acids, it is the omega-3 polyunsaturated fatty acids (PUFA) which possess the most potent immunomodulatory activities, and among the omega-3 PUFA, those from fish oil-eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)--are more biologically potent than alpha-linolenic acid (ALA). Some of the effects of omega-3 PUFA are brought about by modulation of the amount and types of eicosanoids made, and other effects are elicited by eicosanoid-independent mechanisms, including actions upon intracellular signaling pathways, transcription factor activity and gene expression. Animal experiments and clinical intervention studies indicate that omega-3 fatty acids have anti-inflammatory properties and, therefore, might be useful in the management of inflammatory and autoimmune diseases. Coronary heart disease, major depression, aging and cancer are characterized by an increased level of interleukin 1 (IL-1), a proinflammatory cytokine. Similarly, arthritis, Crohn's disease, ulcerative colitis and lupus erythematosis are autoimmune diseases characterized by a high level of IL-1 and the proinflammatory leukotriene LTB(4) produced by omega-6 fatty acids. There have been a number of clinical trials assessing the benefits of dietary supplementation with fish oils in several inflammatory and autoimmune diseases in humans, including rheumatoid arthritis, Crohn's disease, ulcerative colitis, psoriasis, lupus erythematosus, multiple sclerosis and migraine headaches. Many of the placebo-controlled trials of fish oil in chronic inflammatory diseases reveal significant benefit, including decreased disease activity and a lowered use of anti-inflammatory drugs.
Publication Types:
* Review
PMID: 12480795 [PubMed - indexed for MEDLINE]
This fits in with other trials but good to see it in writing.
No mention of looking at omega six intake and effect of reductions which could possibly going to produce significant effect as well.
Some trials please
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=12720588&query_hl=31&itool=pubmed_DocSum
1: Br J Nutr. 2003 May;89(5):679-89.Click here to read Links
Comparison of the effects of linseed oil and different doses of fish oil on mononuclear cell function in healthy human subjects.
* Wallace FA,
* Miles EA,
* Calder PC.
Institute of Human Nutrition, School of Medicine, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK.
Studies on animal and human subjects have shown that greatly increasing the amount of linseed (also known as flaxseed) oil (rich in the n-3 polyunsaturated fatty acid (PUFA) alpha-linolenic acid (ALNA)) or fish oil (FO; rich in the long-chain n-3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) in the diet can decrease a number of markers of immune function. The immunological effects of more modest doses of n-3 PUFA in human subjects are unclear, dose-response relationships between n-3 PUFA supply and immune function have not been established and whether ALNA has the same effects as its long-chain derivatives is not known. Therefore, the objective of the present study was to determine the effect of enriching the diet with different doses of FO or with a modest dose of ALNA on a range of functional responses of human monocytes and lymphocytes. In a randomised, placebo-controlled, double-blind, parallel study, forty healthy males aged 18-39 years were randomised to receive placebo or 3.5 g ALNA/d or 0.44, 0.94 or 1.9 g (EPA+DHA)/d in capsules for 12 weeks. The EPA:DHA ratio in the FO used was 1.0:2.5. ALNA supplementation increased the proportion of EPA but not DHA in plasma phospholipids. FO supplementation decreased the proportions of linoleic acid and arachidonic acid and increased the proportions of EPA and DHA in plasma phospholipids. The interventions did not alter circulating mononuclear cell subsets or the production of tumour necrosis factor-alpha, interleukin (IL) 1beta, IL-2, IL-4, IL-10 or interferon-gamma by stimulated mononuclear cells. There was little effect of the interventions on lymphocyte proliferation. The two higher doses of FO resulted in a significant decrease in IL-6 production by stimulated mononuclear cells. It is concluded that, with the exception of IL-6 production, a modest increase in intake of either ALNA or EPA+DHA does not influence the functional activity of mononuclear cells. The threshold of EPA+DHA intake that results in decreased IL-6 production is between 0.44 and 0.94 g/d.
PMID: 12720588 [PubMed - indexed for MEDLINE]
"DHA feeding increased its concentration from 2.3 to 7.4 wt% in the PBMNC total lipids, and decreased arachidonic acid concentration from 19.8 to 10.7 wt%. It also lowered prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) production, in response to lipopolysaccharide, by 60-75%. Natural killer cell activity and in vitro secretion of interleukin-1beta and tumor necrosis factor alpha were significantly reduced by DHA feeding."
PGE2 is a percusor of aromatase which is a percusor of oestrogens.
So as a preventative in terms of oestrogen restriction DHA at higher doses may be a useful dietary additive. See previous post as to DHA fish oil dosages. Low dosages were reported as not showing the same effects.
Again omega six intake / reduction not examined to determine impact.
Please see posts on balancing omega threes and sixes.
Please do talk to youe medical advisor about significant dietary changes.
You can always think about printing the trials to take i to save you trying to explain. Any feed back positive or negative is most welcome.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=10443964&dopt=Abstract
1: Lipids. 1999 Apr;34(4):317-24. Related Articles, Links
Docosahexaenoic acid ingestion inhibits natural killer cell activity and production of inflammatory mediators in young healthy men.
Kelley DS, Taylor PC, Nelson GJ, Schmidt PC, Ferretti A, Erickson KL, Yu R, Chandra RK, Mackey BE.
USDA, ARS, Western Human Nutrition Research Center, Presidio of San Francisco, California 94129, USA. Dkelley@whnrc.usda.gov
The purpose of this study was to examine the effects of feeding docosahexaenoic acid (DHA) as triacylglycerol on the fatty acid composition, eicosanoid production, and select activities of human peripheral blood mononuclear cells (PBMNC). A 120-d study with 11 healthy men was conducted at the Metabolic Research Unit of Western Human Nutrition Reach Center. Four subjects (control group) were fed the stabilization diet throughout the study; the remaining seven subjects were fed the basal diet for the first 30 d, followed by 6 g DHA/d for the next 90 d. DHA replaced an equivalent amount of linoleic acid; the two diets were comparable in their total fat and all other nutrients. Both diets were supplemented with 20 mg D alpha-tocopherol acetate per day. PBMNC fatty acid composition and eicosanoid production were examined on day 30 and 113; immune cell functions were tested on day 22, 30, 78, 85, 106, and 113. DHA feeding increased its concentration from 2.3 to 7.4 wt% in the PBMNC total lipids, and decreased arachidonic acid concentration from 19.8 to 10.7 wt%. It also lowered prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) production, in response to lipopolysaccharide, by 60-75%. Natural killer cell activity and in vitro secretion of interleukin-1beta and tumor necrosis factor alpha were significantly reduced by DHA feeding. These parameters remained unchanged in the subjects fed the control diet. B-cell functions as reported here and T-cell functions that we reported previously were not altered by DHA feeding. Our results show that inhibitory effects of DHA on immune cell functions varied with the cell type, and that the inhibitory effects are not mediated through increased production of PGE2 and LTB4.
Publication Types:
* Clinical Trial
PMID: 10443964 [PubMed - indexed for MEDLINE]
This is a link which sort of explains what a lippolysacceride is in this complex.
Something to get the prostaglandin out of bed (the membrane) and off to work (immune defence). If somebody can could confirm this it would be helpful.
http://en.wikipedia.org/wiki/Lipopolysaccharide
Mice were fed a high omega six diet 43 % energy from corn oil (high omega six source).
Estrogen receptors up SIX fold.
And equally mind boggoling the potential fro offspring to carry a greater risk level. I have seen this suggested elsewhere.
(ER is not the same as HER which relates to growth factors - it took me a while to work that one out - please tell me if I am wrong!)
"In adult female mice, a 6-fold increase in the number of ER binding sites and 2-fold increase in PKC activity were found in the mammary glands of the high-fat mice when compared with the low-fat mice."
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=9485017
1: Cancer Res. 1998 Feb 15;58(4):654-60. Links
Consumption of a high-fat diet alters estrogen receptor content, protein kinase C activity, and mammary gland morphology in virgin and pregnant mice and female offspring.
* Hilakivi-Clarke L,
* Stoica A,
* Raygada M,
* Martin MB.
Lombardi Cancer Center, Department of Psychiatry, Georgetown University, Washington, DC 20007, USA.
Previous studies have shown that a diet high in polyunsaturated fatty acids increases mammary tumor incidence in adult and pregnant mice and rats and in the female offspring. The present study investigated whether a high-fat diet alters the number of estrogen receptor (ER) binding sites and protein kinase C (PKC) activity in the mammary gland of these animals. In the female offspring, the effects of maternal exposure to a high-fat diet during pregnancy on development of the mammary epithelial tree were studied also. BALB/c mice were kept on a diet containing either 43% (high-fat) or 16% (low-fat) calories from corn oil, which consists mostly of n-6 polyunsaturated fatty acids, for 1 month. In adult female mice, a 6-fold increase in the number of ER binding sites and 2-fold increase in PKC activity were found in the mammary glands of the high-fat mice when compared with the low-fat mice. In pregnant mice, a high-fat diet increased ER binding sites by 61% and PKC activity by 51%. In contrast to adult and pregnant mice, females exposed to a high-fat diet only in utero through their pregnant mother exhibited a significantly reduced number of mammary ER binding sites by age 45 days (78% decrease) and a reduction in PKC activity by ages 30 and 100 days (44 and 20% decrease, respectively). The mammary epithelial tree of the high-fat offspring contained more terminal end buds and was less differentiated than that of the low-fat offspring. These findings show that consumption of a high-fat diet increases ER and PKC in the adult and pregnant mouse mammary gland, perhaps contributing to the fat-induced promotion of mammary tumorigenesis. In contrast, reduced ER and PKC following a high-fat exposure in utero may be associated with increased susceptibility to carcinogenesis, possibly due to an increased number of terminal end buds that are the sites of neoplastic transformation in the mammary gland.
PMID: 9485017 [PubMed - indexed for MEDLINE]
Unregistered
07-14-2006, 04:49 AM
i live in greece. unfortunately the hospitals here in greece are full of cancer patients, especially in crete.
my mother has metastatic breast cancer, since she was a child she followed a very healthy nutrition but unfortunately this did'nt helped to prevent the disease.
The truth is that -at the moment- she never had symptoms of the disease. she feels very good, full of energy, she does a lot of things every day.
from this point of view, maybe this could be a sign that greek diet helps cancer patients to have a good qol and live with dignity.
take care
lorenzo
Thank you for your post.
I am glad your mother has a good qol.
I was sorry to hear of the suggestion of high numbers of cases in Crete. I would be positive to know of corners that had managed to avoid the increase that are being seen in numbers.
The articles do refer to the pre 1960 diet, and I guess was based on then (1960) statistics.
The introduction in dietary changes, vegetable oils, vegetable oils in processed foods etc may have changed the comparative cancer ratio bringin them more in line with other western countries since then.
It is not something I have specifically looked at.
Also sadly there are always going to be those for whom diet may offer better qol but have some sort of predisposition, exposure to other environmental factors etc.
Thank you agin for your post.
I hope your mother continues to enjoy a good qol. grape vines, Tavernas feta, juicy fresh peaches, local honey, feta basil and tomatoes come to mind but that was some years ago.
RB
RobinP
07-14-2006, 02:33 PM
RB thanks so much for the omega three balancing dietary posts which are prudent for overall healthy living and to help prevent many disease conditions. I think it has made me more conscious of what I, my kids and husband eats which is a good thing. Afterall, we are what we eat to a certain degree, and also as the above abstracts suggests we are what mother ate while we were in utero as well. Of course, I agree that genetics and environment also plays into the equation and defines our weakness, strengths and our suspectibility to disease.
I have see trial that suggest negative impacts for trans fats including blocking the pathways to make long chain fats which could compromise immune function, exacerbate related conditions, and as previously posted potentially impact on risks of cancer etc.
Margerines come in different "shapes" and sizes with different levels of polyunsaturates contents and thrans fats etc.
But you may like to try this with your brand, and some butter as a contol.
The author has a way with words.
RB
http://www.healthy-communications.com/butterormargerine.html
Subject Butter or Parkay?
Date Sat, 18 Mar 2006
Margarine was originally manufactured to fatten turkeys. When it killed the
turkeys, the people who had put all the money into the research wanted a
payback so they put their heads together to figure out what to do with this
product to get their money back. It was a white substance with no food
appeal so they added the yellow coloring and sold it to people to use in
place of butter. How do you like it? They have come out with some clever
new flavorings.
DO YOU KNOW... the difference between margarine and butter?
Read on to the end...gets very interesting!
Both have the same amount of calories.
Butter is slightly higher in saturated fats at 8 grams compared to 5 grams.
Eating margarine can increase heart disease in women by 53% over eating
the same amount of butter, according to a recent Harvard Medical Study.
Eating butter increases the absorption of many other nutrients in other
foods.
Butter has many nutritional benefits where margarine has a few only because
they are added!
Butter tastes much better than margarine and it can enhance the flavors of
other foods.
Butter has been around for centuries where margarine has been around for
less than 100 years.
And now, for Margarine. Very high in trans fatty acids.
Triple risk of coronary heart disease.
Increases total cholesterol and LDL (this is the bad cholesterol) and
lowers HDL cholesterol, (the good cholesterol)
Increases the risk of cancers up to five fold.
Lowers quality of breast milk.
Decreases immune response.
Decreases insulin response.
And here's the most disturbing fact.... HERE IS THE PART THAT IS VERY
INTERESTING!
Margarine is but ONE MOLECULE away from being PLASTIC..
This fact alone was enough to have me avoiding margarine for life and
anything else that is hydrogenated (this means hydrogen is added, changing
the molecular structure of the substance).
You can try this yourself
Purchase a tub of margarine and leave it in your garage or shaded area.
Within a couple of days you will note a couple of things
* no flies, not even those pesky fruit flies will go near it (that should
tell you something)
* it does not rot or smell differently because it has no nutritional value
nothing will grow on it. Even those teeny weeny microorganisms will not a
find a home to grow.
Why? Because it is nearly plastic. Would you melt your Tupperware and
spread that on your toast?
Share This With Your Friends.....(If you want to "butter them up")
RhondaH
07-15-2006, 04:11 AM
IF I "splurge" on my diet, I would rather use the REAL thing (i.e. butter, sugar) instead of the margarine, splenda, etc. as it seems that all the "stuff" they put in the food to lower the calories and/or fat, we have YET to know what it will do to our bodies and while YES, it may be helping us lose weight, do we REALLY know what it is doing to our bodies that's why everything is "real". It just seems like all the low fat, artificially sweetened food (with fewer) calories MAY be doing us more harm than good. Well, I have to go now as I'm off to the market to pick up my 40lbs of organic blueberries (sounds like a lot, BUT I use them as well as other berries...already froze 25lbs of strawberries...in Diana Dyers phytochemical shake that I have every day) AND I'm splurging and making a blueberry cobbler...mmm. Take care and God bless.
Rhonda
See also previous post re DHA reducing bone loss and here a 2006 trial as well
"Bone marrow from LF-CO animals appeared to be more resistant to araC treatment than either MF group. Thus, DHA, fed as DHASCO, has advantages over low or moderate n-6 diets and chow as it is has both hypolipidemic- and bone marrow-enhancing properties in weanling Fischer 344 rats. This suggests that DHA supplementation may be useful in adjuvant chemotherapy."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=9076666
1: Lipids. 1997 Mar;32(3):293-302. Links
Incorporation of long-chain n-3 fatty acids in tissues and enhanced bone marrow cellularity with docosahexaenoic acid feeding in post-weanling Fischer 344 rats.
* Atkinson TG,
* Barker HJ,
* Meckling-Gill KA.
Department of Human Biology and Nutritional Sciences, University of Guelph, Ontario, Canada.
We wanted to examine the effects of an oil rich in docosahexaenoic acid (DHA), without eicosapentaenoic acid, on the composition of membrane phospholipid in a variety of tissues. Our in vitro studies had previously shown that DHA could modify glucose and nucleoside transport in cells in culture and also increase selectivity of the nucleoside drug, arabinosylcytosine (araC) toward tumor cells. Here we wanted to examine what effect DHA supplementation would have in the whole animal in terms of the chemosensitivity of normal bone marrow, the dose-limiting tissue during chemotherapy, to araC. The purpose was to determine whether fatty acid supplementation might be useful as an adjuvant to chemotherapy. We fed diets containing 5% (w/w) low fat-corn oil (LF-CO group), 10% moderate fat-safflower oil (MF-SO group), or 10% DHASCO (MF-DHA group) to weanling Fischer 344 rats for 8-9 wk. Feed intake and growth were not different between the different diets. Similarly, treatment of animals with the chemotherapeutic drug araC did not differentially affect growth, feed intake, or tissue fatty acid composition for the different diet groups. Fatty acid compositions of bone marrow, liver, red blood cells, plasma phospholipid and triglyceride, as well as skeletal and cardiac muscle, were substantially different between the dietary groups. The DHASCO oil contained 46% DHA (22:6n-3) and resulted in profound incorporation of DHA in all tissues examined. The most dramatic response was seen in skeletal muscle of MF-DHA fed animals where DHA represented 46% of membrane phospholipid fatty acids. This is likely to have consequences to muscle function. Although DHASCO contains a similar level of saturated fatty acids (42%), few differences in saturates were noted between the various dietary groups for most of the tissues examined. Both LF-CO and MF-SO diets were hypercholesterolemic, and the LF-CO was also hypertriglyceridemic compared to the chow-fed animals. Animals fed the MF-DHA diet had the lowest triglyceride levels of any of the treatment groups and cholesterol levels comparable to chow-fed animals. MF-DHA had substantially higher numbers of colony-forming units-granulocyte macrophage (CFU-GM) as reflected in a twofold higher bone marrow cellularity than either chow or LF-CO animals, suggesting expansion of the bone marrow compartment with DHA feeding. Although higher than LF-SO, the number of CFU-GM in MF-SO animals was not significantly higher than animals fed chow. Bone marrow from LF-CO animals appeared to be more resistant to araC treatment than either MF group. Thus, DHA, fed as DHASCO, has advantages over low or moderate n-6 diets and chow as it is has both hypolipidemic- and bone marrow-enhancing properties in weanling Fischer 344 rats. This suggests that DHA supplementation may be useful in adjuvant chemotherapy.
PMID: 9076666 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16102959
1: J Nutr Biochem. 2006 Apr;17(4):282-9. Epub 2005 Jun 21.Click here to read Links
Dietary ratio of n-6/n-3 PUFAs and docosahexaenoic acid: actions on bone mineral and serum biomarkers in ovariectomized rats.
* Watkins BA,
* Li Y,
* Seifert MF.
Center for Enhancing Foods to Protect Health, Lipid Chemistry and Molecular Biology Laboratory, Purdue University, West Lafayette, IN 47907-2009, USA. baw@purdue.edu
Hypoestrogenic states escalate bone loss in animals and humans. This study evaluated the effects of the amount and ratio of dietary n-6 and n-3 polyunsaturated fatty acids (PUFAs) on bone mineral in 3-month-old sexually mature ovariectomized (OVX) Sprague-Dawley rats. For 12 weeks, the rats were fed either a high-PUFA (HP) or a low-PUFA (LP) diet with a ratio of n-6/n-3 PUFAs of 5:1 (HP5 and LP5) or 10:1 (HP10 and LP10). All diets (modified AIN-93G) provided 110.4 g/kg of fat from safflower oil and/or high-oleate safflower oil blended with n-3 PUFAs (DHASCO oil) as a source of docosahexaenoic acid (DHA). Fatty acid analyses confirmed that the dietary ratio of 5:1 significantly elevated the amount of DHA in the periosteum, marrow and cortical and trabecular bones of the femur. Dual-energy X-ray absorptiometry measurements for femur and tibia bone mineral content (BMC) and bone mineral density showed that the DHA-rich diets (HP5 and LP5) resulted in a significantly lower bone loss among the OVX rats at 12 weeks. Rats fed the LP diets displayed the lowest overall serum concentrations of the bone resorption biomarkers pyridinoline (Pyd) and deoxypyridinoline, whereas the bone formation marker osteocalcin was lowest in the HP groups. Regardless of the dietary PUFA content, DHA in the 5:1 diets (HP5 and LP5) preserved rat femur BMC in the absence of estrogen. This study indicates that the dietary ratio of n-6/n-3 PUFAs (LP5 and HP5) and bone tissue concentration of total long-chain n-3 PUFAs (DHA) minimize femur bone loss as evidenced by a higher BMC in OVX rats. These findings show that dietary DHA lowers the ratio of 18:2n-6 (linoleic acid)/n-3 in bone compartments and that this ratio in tissue correlates with reduced Pyd but higher bone alkaline phosphatase activity and BMC values that favor bone conservation in OVX rats.
PMID: 16102959 [PubMed - indexed for MEDLINE]
"Taken together, these results indicate that {omega}-3 PUFA regulate COX-2-mediated invasion in brain-metastatic melanoma."
http://www.jlr.org/cgi/content/abstract/46/6/1278
Role of {omega}-3 polyunsaturated fatty acids on cyclooxygenase-2 metabolism in brain-metastatic melanoma
Yvonne Denkins1, Doty Kempf, Melissa Ferniz, Shilpa Nileshwar and Dario Marchetti
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803
Published, JLR Papers in Press, March 16, 2005. DOI 10.1194/jlr.M400474-JLR200
1 To whom correspondence should be addressed. e-mail: ydenkins@vetmed.lsu.edu
Cyclooxygenase-2 (COX-2) is important in the progression of epithelial tumors. Evidence indicates that {omega}-6 PUFAs such as arachidonic acid (AA) promote the growth of tumor cells; however, {omega}-3 fatty acids [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] inhibit tumor cell proliferation. We investigated the effects of {omega}-3 PUFA on the expression and function of COX-2 in 70W, a human melanoma cell line that metastasizes to the brain in nude mice. We show that 1) tumor necrosis factor-{alpha} upregulates the expression of both COX-2 mRNA and prostaglandin E2 (PGE2) production, and 2) {omega}-3 and {omega}-6 PUFA regulate COX-2 mRNA expression and PGE2 production. AA increased COX-2 mRNA expression and prostaglandin production in {omega}-6-stimulated 70W cells. Conversely, COX-2 mRNA expression decreased in cells incubated with EPA or DHA. AA increased MatrigelTM invasion 2.4-fold, whereas EPA or DHA did not. Additionally, PGE2 increased in vitro invasion 2.5-fold, whereas exposure to PGE3 significantly decreased invasion. Our results demonstrate that incubation of 70W cells with either AA or PGE2 increased invasiveness, whereas incubation with EPA or DHA downregulated both COX-2 mRNA and protein expression, with a subsequent decrease in MatrigelTM invasion.
Taken together, these results indicate that {omega}-3 PUFA regulate COX-2-mediated invasion in brain-metastatic melanoma.
For those of you who may have read the "very thought provoking" http://www.her2support.org/vbulletin/showthread.php?t=23104&highlight=provoking post on the man who claimed to have significantly impacted on lung cancer by balancing the omega threes and sixes here is some more evidence that would support such a possibility.
RB
http://carcin.oxfordjournals.org/cgi/content/abstract/26/4/779
Decreased n-6/n-3 fatty acid ratio reduces the invasive potential of human lung cancer cells by downregulation of cell adhesion/invasion-related genes
Shu-Hua Xia, Jingdong Wang and Jing X. Kang*
Departments of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA
* To whom correspondence should be addressed. Tel: +1 617 726 8509; Fax: +1 617 726 6144; Email: kang.jing@mgh.harvard.edu
Recent studies have shown opposing effects of n-6 and n-3 fatty acids on the development of cancer and suggest a role for the ratio of n-6 to n-3 fatty acids in the control of cancer. However, whether an alteration in the n-6/n-3 fatty acid ratio of cancer cells affects their invasive potential has not been well investigated. We recently developed a genetic approach to modify the n-6/n-3 ratio by expression of the Caenorhabditis elegans fat-1 gene encoding an n-3 desaturase that converts n-6 to n-3 fatty acids in mammalian cells. The objective of this study was to examine the effect of alteration in the n-6/n-3 fatty acid ratio on the invasive potential of human lung cancer A549 cells. Adenovirus-mediated gene transfer of the n-3 desaturase resulted in a marked reduction of the n-6/n-3 fatty acid ratio, particularly the ratio of arachidonic acid to eicosapentaenic acid. Cell adhesion assay showed that the cells expressing fat-1 gene had a delayed adhesion and retarded colonization. Matrigel assay for invasion potential indicated a 2-fold reduction of cell migration in the fat-1 transgenic cells when compared with the control cells. An increased apoptosis was also observed in the fat-1 transgenic cells. Microarray and quantitative polymerase chain reaction revealed a downregulation of several adhesion/invasion-related genes (MMP-1, integrin-{alpha}2 and nm23-H4) in the fat-1 transgenic cells. These results demonstrate that a decreased n-6/n-3 fatty acid ratio reduces the invasion potential of human lung cancer cells by probably downregulating the cell adhesion/invasion-related molecules, suggesting a role for the ratio of n-6 to n-3 fatty acids in the prevention and treatment of cancer.
Fats in milk will obviously depend on feed as cows like us are what they eat.
So I suppose you need to know what your organics cows ate but a Uk trial suggests organic milk has a better fat profile.
High levels of vegetable seed in feed are likely to produce high six contents.
Interestingly swiss cows from alpine pastures seem to have high omega three content.
RB
http://www.dairy-science.org/cgi/content/abstract/89/6/1938
Comparing the Fatty Acid Composition of Organic and Conventional Milk
K. A. Ellis*,1, G. Innocent*, D. Grove-White{dagger}, P. Cripps{dagger}, W. G. McLean{ddagger}, C. V. Howard§ and M. Mihm#
* Division of Animal Production and Public Health, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow, G61 1QH, UK
{dagger} Division of Livestock Health and Welfare, University of Liverpool, Faculty of Veterinary Medicine, Leahurst, Neston, CH64 7TE, UK
{ddagger} Department of Pharmacology & Therapeutics School of Biomedical Sciences, Sherrington Buildings, Ashton Street, Liverpool, Merseyside, L69 3GE, UK
§ Centre for Molecular Biosciences, University of Ulster, Cromore Road, Coleraine, Co. Londonderry, BT52 1SA, UK
# Division of Cell Sciences, Institute of Comparative Medicine, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow, G61 1QH, UK
1 Corresponding author: k.ellis@vet.gla.ac.uk
During a 12-mo longitudinal study, bulk-tank milk was collected each month from organic (n = 17) and conventional (n = 19) dairy farms in the United Kingdom. All milk samples were analyzed for fatty acid (FA) content, with the farming system type, herd production level, and nutritional factors affecting the FA composition investigated by use of mixed model analyses. Models were constructed for saturated fatty acids, the ratio of polyunsaturated fatty acids (PUFA) to monounsaturated fatty acids, total n-3 FA, total n-6 FA, conjugated linoleic acid, and vaccenic acid. The ratio of n-6:n-3 FA in both organic and conventional milk was also compared. Organic milk had a higher proportion of PUFA to monounsaturated fatty acids and of n-3 FA than conventional milk, and contained a consistently lower n-6:n-3 FA ratio (which is considered beneficial) compared with conventional milk. There was no difference between organic and conventional milk with respect to the proportion of conjugated linoleic acid or vaccenic acid. A number of factors other than farming system were identified which affected milk FA content including month of year, herd average milk yield, breed type, use of a total mixed ration, and access to fresh grazing. Thus, organic dairy farms in the United Kingdom produce milk with a higher PUFA content, particularly n-3 FA, throughout the year. However, knowledge of the effects of season, access to fresh grazing, or use of specific silage types could be used by producers to enhance the content of beneficial FA in milk.
Key Words: organic farming • fatty acid • n-3 fatty acid • conjugated linoleic acid
http://circ.ahajournals.org/cgi/content/abstract/109/1/103
Basic Science Reports
High {omega}-3 Fatty Acid Content in Alpine Cheese
The Basis for an Alpine Paradox
Christa B. Hauswirth, MD; Martin R.L. Scheeder, Dr sg agr; Jürg H. Beer, MD
From the Department of Medicine, Kantonsspital Baden, and the Federal Institute of Technology, Zürich, Switzerland.
Correspondence to J.H. Beer, MD, Department of Medicine, Kantonsspital Baden, 5404 Baden, Switzerland. E-mail hansjuerg.beer@ksb.ch
Received June 17, 2003; revision received August 21, 2003; accepted August 22, 2003.
Background— {alpha}-Linolenic acid (ALA) may protect from cardiovascular disease. Because fresh alpine grass contains high amounts of ALA, we hypothesized that the levels of {omega}-3 fatty acids would concentrate to nutritional relevance in the cheese of milk from cows with alpine grass feeding compared with cheese from silage and concentrate feeding; the newly available cheese produced from cows fed with linseed supplementation should contain even higher ALA concentrations.
Methods and Results— Forty different cheeses were analyzed by gas chromatography for their fatty acid profile: (1) 12 from well-defined alpine regions around Gstaad, Switzerland; (2) 7 commercially available English cheddar cheeses; (3) 6 cheeses from cows fed with linseed supplementation; (4) 7 industrial-type Emmentals; and (5) 8 alpine cheeses with partial silage feeding. The alpine cheese contained 4 times more linolenic acid (C18:3{omega}-3) compared with cheddar, more total {omega}-3 fatty acids, and showed a significantly lower n-6:{omega}-3 ratio. Conjugated linoleic acid (C18:2 c9/t11) was 3-fold higher, whereas the amount of palmitic acid was 20% lower. The Emmental reached 40% of the ALA content compared with alpine cheese, and surprisingly, cheese from linseed-supplemented cows contained only 49% of that of the alpine cheese (P<0.001 for each trait in the 5 cheese groups).
Conclusions— Cheese made of milk from cows grazed on alpine pastures had a more favorable fatty acid profile than all other cheese types. Alpine cheese may be a relevant source of ALA and other cardioprotective fatty acids.
Key Words: nutrition • fatty acids • coronary disease • diet • death, sudden
ABSTRACT
"The omega-3 fatty acids continue to accumulate research that suggests that they may prevent a variety of diverse chronic diseases and potentially some acute clinical scenarios. In the first part of this article, the potential for these compounds to prevent certain cardiovascular conditions are discussed. In the second part, the potential for an impact in arthritis, numerous areas of cancer research, depression, maternal and child health, neurologic diseases, osteoporosis, and other medical disciplines are also briefly covered. "
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15885582&query_hl=80&itool=pubmed_docsum
1: Urol Oncol. 2005 Jan-Feb;23(1):36-48.Click here to read Links
An introduction to dietary/supplemental omega-3 fatty acids for general health and prevention: part II.
* Moyad MA.
Phil F. Jenkins Director of Complementary & Alternative Medicine, Department of Urology, University of Michigan Medical Center, Ann Arbor, 48109-0330, USA. moyad@umich.edu
The correction of a subtle nutritional deficiency that may reduce the risk of a future chronic disease is indeed a challenge. However, some specific examples in the past, such as the addition of folic acid to prevent neural tube defects and calcium and vitamin D to prevent osteoporosis, should provide some encouragement that some conditions can be prevented with the appropriate addition of a deficient compound. One of the most intriguing current and future impacts on public health may come from a higher intake of omega-3 fatty acids, such as alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). The omega-3 fatty acids continue to accumulate research that suggests that they may prevent a variety of diverse chronic diseases and potentially some acute clinical scenarios. In the first part of this article, the potential for these compounds to prevent certain cardiovascular conditions are discussed. In the second part, the potential for an impact in arthritis, numerous areas of cancer research, depression, maternal and child health, neurologic diseases, osteoporosis, and other medical disciplines are also briefly covered. The future appears bright for these agents, but specifically which conditions, who qualifies, testing, frequency, adequate sources, future trials, and numerous other questions need to be addressed and answered before the potential impact can catch up to the recent hype.
PMID: 15885582 [PubMed - indexed for MEDLINE]
Blocking delta destaurase 5 will inhibit the formation of Archnidonic acid the omega six raw material for the eisosanoid pathways.
It may aslo push the omega six to DGLA conversion via the series one pathway which is reported as producing less inflamatory agents that the series two pathways.
This presumably acounts for its reported anti inflamatory properties.
But does it also block the 5 pathway for omegas threes long chain fabrication in the body (DHA and EPA)? (AMENDMENT I have just found a trial which suggests it does not which makes it a really interesting dietary adjunct) [Trial see below)
Also if excess omega six souces is a factor in inflamtion in a persons body the consequences in blocking the elongation pathways. The body has been supplied with the omega six and has to do something with it - burn it in exercise or for energy - store it in fat - and if there is too much of it in the circulation trials suggest things start going wrong with inapproriate oxidation leading heart conditions.
All of which might lead on to the conclusion that the easiest long term option is not getting to much in the first place.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=1291640
1: J Nutr Sci Vitaminol (Tokyo). 1992 Aug;38(4):353-63. Links
Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid metabolism in primary cultured rat hepatocytes.
* Fujiyama-Fujiwara Y,
* Umeda R,
* Igarashi O.
Institute of Environmental Science for Human Life, Ochanomizu University, Tokyo, Japan.
Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid (PUFA) were studied in rat primary cultured hepatocytes. When sesamin was added to culture medium containing 20:4 (n-3), rat hepatocytes after 24 h of incubation produced 20:5 (n-3) from 20:4 (n-3), whereas when incubated with 20:3 (n-6), the metabolite by delta 5-desaturation did not accumulate, and consequently, the ratio of 20:3 (n-6)/20:4 (n-6) increased with the amount of sesamin added. Curcumin was more effective than sesamin in this respect. Both sesamin and curcumin interfered with chain elongation of PUFAs. An addition of 18:3 (n-6) or 18:4 (n-3) increased the cellular concentrations of 20:3 (n-6) or 20:4 (n-3), respectively, but the simultaneous addition of sesamin or curcumin inhibited the chain elongation of C18 acids (the fatty acids with 18 carbons) into corresponding C20 and C18 acids. Similarly, the elongation from C20 of n-3 and n-6 families to C22 was also inhibited with sesamin and curcumin. These results suggested that: 1) sesamin and curcumin inhibited delta 5-desaturation of n-6 fatty acid, but not n-3 fatty acid in rat hepatocytes; 2) curcumin was more effective than sesamin; 3) chain elongation was also inhibited by sesamin and curcumin.
PMID: 1291640 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=9610840
1: Prostaglandins Leukot Essent Fatty Acids. 1998 Mar;58(3):185-91. Links
Dietary alpha-linolenic acid increases TNF-alpha, and decreases IL-6, IL-10 in response to LPS: effects of sesamin on the delta-5 desaturation of omega6 and omega3 fatty acids in mice.
* Chavali SR,
* Zhong WW,
* Forse RA.
Department of Surgery, Harvard Institute of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Sesamin (a non-fat portion of sesame seed oil) inhibits delta-5 desaturase activity resulting in an accumulation of dihomo-gamma-linolenic acid (DGLA) which can displace arachidonic acid (AA) and decrease the formation of pro-inflammatory mediators. We investigated the effects of consumption of diets containing 0.25wt% sesamin and 15 wt% safflower oil (SO) (providing 12% of the added fat as linoleic acid) or a 15 wt% 2:1 mixture of linseed oil and SO (LOSO) (providing 6% alpha-linolenic acid and 6% linoleic acid) for 3 weeks on the liver membrane fatty acid composition and on the production of prostaglandin (PG) E2, TNF-alpha, IL-6 and IL10 in mice. Consumption of sesamin-supplemented SO and LOSO diets resulted in a significant increase in the levels of 20:3omega6 (DGLA), suggesting that sesamin inhibited delta-5 desaturation of omega6 fatty acids. In animals fed LOSO diets, the levels of alpha-linolenic acid, eicosapentaenoic acid (EPA) and of docosahexaenoic acid (DHA) were elevated with a concomitant decrease of arachidonic acid (AA) in the liver membrane phospholipids. Further, in animals fed LOSO diets with or without sesamin, an increase in the circulating levels of TNF-alpha was associated with a concomitant decrease in PGE2. Despite a lack of differences in the levels of AA, the PGE2 levels were significantly lower in mice fed sesamin-supplemented SO compared to those fed SO alone. Thus, these data suggest that irrespective of the availability of a specific fatty acid as a substrate, through regulating the PGE2 synthesis, the production of TNF-alpha could be modulated.
PMID: 9610840 [PubMed - indexed for MEDLINE]
1: Neuro Endocrinol Lett. 2005 Dec;26(6):745-51. Links
In chronic fatigue syndrome, the decreased levels of omega-3 poly-unsaturated fatty acids are related to lowered serum zinc and defects in T cell activation.
* Maes M,
* Mihaylova I,
* Leunis JC.
M-Care4U Outpatient Clinics, and the Clinical Research Center for Mental Health, Antwerp, Belgium.
There is now evidence that major depression is accompanied by decreased levels of omega3 poly-unsaturated fatty acids (PUFA), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). There is a strong comorbidity between major depression and chronic fatigue syndrome (CFS). The present study has been carried out in order to examine PUFA levels in CFS. In twenty-two CFS patients and 12 normal controls we measured serum PUFA levels using gas chromatography and mass spectrometry. We found that CFS was accompanied by increased levels of omega6 PUFAs, i.e. linoleic acid and arachidonic acid (AA), and mono-unsaturated fatty acids (MUFAs), i.e. oleic acid. The EPA/AA and total omega3/omega6 ratios were significantly lower in CFS patients than in normal controls. The omega3/omega6 ratio was significantly and negatively correlated to the severity of illness and some items of the FibroFatigue scale, i.e. aches and pain, fatigue and failing memory. The severity of illness was significantly and positively correlated to linoleic and arachidonic acid, oleic acid, omega9 fatty acids and one of the saturated fatty acids, i.e. palmitic acid. In CFS subjects, we found significant positive correlations between the omega3/omega6 ratio and lowered serum zinc levels and the lowered mitogen-stimulated CD69 expression on CD3+, CD3+ CD4+, and CD3+ CD8+ T cells, which indicate defects in early T cell activation. The results of this study show that a decreased availability of omega3 PUFAs plays a role in the pathophysiology of CFS and is related to the immune pathophysiology of CFS. The results suggest that patients with CFS should respond favourably to treatment with--amongst other things--omega3 PUFAs, such as EPA and DHA.
PMID: 16380690 [PubMed - indexed for MEDLINE]
If you are debating the best way to get your fish omega threes and sixes the articles below would provide arguments for fish oil or wild fish however humble, and thats without looking at other issues.
I must admit the figures made my draw drop.
The conversion rate from wild fish as food to farmed fish is apparently about 4 or 5 to 1.
A high price to fill our shelves with particular fish types?
I am not against farming fish to preserve wild stocks but where is the environmental "value" balance.
RB
Antarctic Krill: a case study on the ecosystem implications of fishing
http://72.14.221.104/search?q=cache:YeERi6C7rhIJ:www.lighthouse-foundation.org/fileadmin/LHF/PDF/Antarctic-krill-LF_EN.pdf+plankton+krill+omega+three+fats+analysis&hl=en&gl=uk&ct=clnk&cd=9&lr=lang_en&client=firefox-a
ABSTRACT
The fish farming industry already uses up
around 75% of the world’s fish oil and
around 40% of the world’s fish meal. By
2010, these figures might go up to 90% and
56% respectively, according to predictions
by the International Fish Meal and Fish Oil
Manufacturers Association (IFOMA). FAO
has indicated that by 2010, farmed salmon and trout alone could consume 620,000 tonnes
of fish oil (Staniford 2002). With demand exceeding supply and rising prices, fish oil has
been labelled “the new blue gold” (Staniford 2001).
http://72.14.221.104/search?q=cache:ZPb9mDl9g8AJ:www.esa.org/science/Issues/FileEnglish/issue8.pdf+fish+farming+conversion+rates+fish+oil&hl=en&gl=uk&ct=clnk&cd=2&lr=lang_en&client=firefox-a
ABSTRACT
"Number 8
Winter 2001
Effects of Aquaculture on World Fish Supplies
SUMMARY
Global production of farmed fish, shrimp, clams, and oysters more than doubled in weight and value during the
1990s while landings of wild-caught fish remained level. Many people look to this growth in aquaculture to relieve
pressure on ocean fish stocks, most of which are now fished at or beyond capacity, and to allow wild populations to
recover. Production of farmed fish and shellfish does increase world fish supplies. Yet by using increasing amounts of wild-
caught fish to feed farmed shrimp and salmon, and even to fortify the feed of herbivorous fish such as carp, some sectors
of the aquaculture industry are actually increasing the pressure on ocean fish populations.
The available scientific evidence indicates that some types of aquaculture are on a destructive path that poses a
threat not only to wild fish stocks but also to the industry’s own long-term potential. One of the most disturbing trends is
the rapid expansion and intensification of shrimp and salmon farming and culture of other high-value carnivorous marine
fish such as cod, seabass, and tuna. Production of a single kilogram of these species typically uses two to five kilograms
of wild-caught fish processed into fish meal and fish oil for feed.
Besides this direct impact on wild fish stocks, some aquaculture as currently practiced degrades the marine
environment and diminishes the ecological life support services it provides to fish, marine mammals, and seabirds, as well
as humans. These impacts include
• Destruction of hundreds of thousands of hectares of mangrove forests and coastal wetlands for construction
of aquaculture facilities
• Use of wild-caught rather than hatchery-reared finfish or shellfish fry to stock captive operations, a practice
that often leads to a high rate of discarded bycatch of other species
• Heavy fishing pressure on small ocean fish such as anchovies for use as fish meal, which can deplete food for
wild fish such as cod, as well as seals and seabirds
• Transport of fish diseases into new waters and escapes of non-native fish that may hybridize or compete with
native wild fish
As aquaculture production continues to expand and intensify, both its reliance and its impact on ocean fisheries are
likely to increase. The balance between farmed and wild-caught fish, as well as the total supply of fish available for human
consumption, will depend on future trends in aquaculture practices. If the goal of aquaculture is to produce more fish for
consumers than can be produced naturally, then it will become increasingly counterproductive to farm carnivores that must
be fed large amounts of wild-caught fish that form the foundation of the ocean food chain. Indeed, non-carnivorous
species such as marine mollusks and carps account for most of the current net gain in world fish supplies from aquaculture.
Without clear recognition of its dependence on natural ecosystems, the aquaculture industry is unlikely to develop
to its full potential or continue to supplement ocean fisheries. We recommend the adoption of four priority goals for
aquaculture:
• Encourage farming of species lower on the food web – that is, fish with herbivorous or omnivorous diets or
filter feeders such as oysters
• Improve feed management and efficiency in industrial aquaculture systems and develop substitutes for fish-
derived feed ingredients
• Develop integrated fish farming systems that use multiple species to reduce costs and wastes while increasing
productivity
• Promote environmentally sound aquaculture practices and resource management
Governments have a key role to play in developing regulations to protect coastal ecosystems and in reexamining
subsidies to unsustainable marine fisheries. Development agencies are strategically placed to help in developing and
implementing sustainable production practices and in financing otherwise economically and socially unattainable reforms in
developing countries. If public and private interests act jointly to reduce the environmental costs generated by fish farm-
ing, present unsustainable trends can be reversed and aquaculture can make an increasingly positive contribution to global
fish supplies..............."
Cover (clockwise from top): shrimp ponds in Honduras (courtesy CODDEFFAGOLF); basket of milkfish (J. Primavera); harvesting catfish in
Mississippi (K. Hammond, courtesy USDA).
Having done some more searches on the subject of fish farming there is contoversy about the "conversion" rate.
Here is another link to an article on conversion which contains three figues and one from the industry to balance things.
RB
http://www.davidsuzuki.org/Oceans/Fish_Farming/Salmon/Net_Loss.asp
Net loss of wild fish to produce farmed salmon
A total of 2.7 to 3.5 tonnes of wild fish are used to make 1 tonne of farmed salmon
ABSTRACT
"Since a salmon farm in BC currently uses between 1.3 and 1.7 tonnes of dry feed (ie: FCR of 1.3 to 1.7) to make one tonne of farmed salmon, then the total amount of wild fish used to make one tonne salmon is between 2.7 and 3.5 tonnes (ie: the FCR multiplied by 2.08). It should be noted that in practice, BC salmon farms do not often reach the lower FCR of 1.3 which is achievable only when feed is used very efficiently on the farm. Rather than taking pressure off ocean resources then, salmon farming is currently adding greatly to that pressure..........................Much more research needs to be done and it is unclear when, or if the day will come when farmed salmon will be vegetarian. In the meantime, the stress on the ocean ecosystem will increase as salmon aquaculture expands globally. The consumption of 6.2 tonnes of wild fish for each tonne of salmon produced not only means less food for humans, but also for the many ocean species that rely on these fish as part of their food chain. Currently, the continued expansion of salmon farming is not sustainable.."
http://www.wfga.net/issues.asp?id=37
The Environmental Impact Of Salmon Farms
Please also see prior posts on COX inhibitors and DHA.
This is prostate but there seems to be some communality of mechanisms in many cancers.
RB
1: Int J Cancer. 2006 Apr 27; [Epub ahead of print]Click here to read Links
Docosahexaenoic acid in combination with celecoxib modulates HSP70 and p53 proteins in prostate cancer cells.
* Narayanan NK,
* Narayanan BA,
* Bosland M,
* Condon MS,
* Nargi D.
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, NY.
The role of cyclooxygenase-2 (COX-2) and the mechanism by which it influences the development and behavior of prostate cancer is unclear. Selective COX-2 inhibitors may be effective against prostate cancer via COX-2-independent mechanisms. But administration of high doses of COX-2 inhibitors over longer period of time may not be devoid of side effects. There is increasing interest in using COX-2 inhibitors in combination with other chemopreventive agents to overcome the issue of toxicity. However, the molecular mechanisms underlying their combined actions are not well understood. Therefore, the present study was designed to determine the effects of low doses of docosahexaenoic acid (DHA) in combination with celecoxib on the molecular targets at the proteins level in rat prostate cancer cells. Two-dimensional gel electrophoresis, in combination with mass spectrometry analysis, was used for protein identification. Western blot analysis confirmed the proteins identified. Paraffin-embedded tissue sections from the rat prostate tumor were used to detect base level expression of heat shock protein 70 (HSP70) and p53. The rate of cancer cell growth was inhibited more effectively (p < 0.01) by DHA in combination with celecoxib at lower doses (2.5 muM each). A total number of twelve proteins were differentially expressed by the combined action of DHA and celecoxib at low doses. It was interesting to note that these agents activated both HSP70 and p53 proteins. Activation of HSP70 by the combined actions of DHA and celecoxib in the presence of wild-type p53 reveals a unique COX-2 independent mode of action against prostate cancer. (c) 2006 Wiley-Liss, Inc.
PMID: 16646082 [PubMed - as supplied by publisher]
More links between repoduction and prostaglandins. " Although the mechanism by which prostaglandins modulate these changes remains unclear, much evidence suggests that prostaglandins and their receptors and downstream signalling pathways are involved in angiogenesis and in alterations in cell adhesion, morphology, motility, invasion and metastases. "
Whilst omega threes and GLA both produce separte series of prosaglandins series 1 and series 3 the limited materila I have read links 1 and 3 to moderating roles in cell maturation etc, and series 2 which are derived from omega six and AA are the drivers.
More questions
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15380812
1: Trends Endocrinol Metab. 2004 Oct;15(8):398-404.Click here to read Links
Prostaglandin receptor signalling and function in human endometrial pathology.
* Jabbour HN,
* Sales KJ.
MRC Human Reproductive Sciences Unit, Centre for Reproductive Biology, The University of Edinburgh Academic Centre, 49 Little France Crescent, Edinburgh EH16 4SB, Scotland, UK. h.jabbour@hrsu.mrc.ac.uk
Prostaglandins are bioactive lipids that exert an autocrine or paracrine function by binding to specific G-protein-coupled receptors (GPCRs) to activate intracellular signalling and gene transcription. Prostaglandins are key regulators of reproductive processes, including ovulation, implantation and menstruation. Prostaglandins have been ascertained to have a role in various pathological changes of the reproductive tract including menorrhagia, dysmenorrhea, endometriosis and cancer. Although the mechanism by which prostaglandins modulate these changes remains unclear, much evidence suggests that prostaglandins and their receptors and downstream signalling pathways are involved in angiogenesis and in alterations in cell adhesion, morphology, motility, invasion and metastases. The potential role of prostaglandin receptors in pathological changes of the endometrium has significance for the future development of therapeutic interventions.
PMID: 15380812 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16310177
Fishing for prostanoids: deciphering the developmental functions of cyclooxygenase-derived prostaglandins.
* Cha YI,
* Solnica-Krezel L,
* DuBois RN.
Department of Medicine and Cancer Biology, Cell and Developmental Biology, Vanderbilt University Medical Center and Vanderbilt Ingram-Cancer Center, Nashville, TN 37232-2279, USA.
Prostaglandin G/H synthases (PGHS), commonly referred to as cyclooxygenases (COX-1 and COX-2), catalyze a key step in the synthesis of biologically active prostaglandins (PGs), the conversion of arachidonic acid (AA) into prostaglandin H(2) (PGH(2)). PGs have important functions in a variety of physiologic and pathologic settings, including inflammation, cardiovascular homeostasis, reproduction, and carcinogenesis. However, an evaluation of prostaglandin function in early development has been difficult due to the maternal contribution of prostaglandins from the uterus. The emergence of zebrafish as a model system has begun to provide some insights into the roles of this signaling cascade during vertebrate development. In zebrafish, COX-1 derived prostaglandins are required for two distinct stages of development, namely during gastrulation and segmentation. During gastrulation, PGE(2) signaling promotes cell motility, without altering the cell shape or directional migration of gastrulating cells. During segmentation, COX-1 signaling is also required for posterior mesoderm development, including the formation of vascular tube structures, angiogenesis of intersomitic vessels, and pronephros morphogenesis. We propose that deciphering the role for prostaglandin signaling in zebrafish development could yield insight and ultimately address the mechanistic details underlying various disease processes that result from perturbation of this pathway.
PMID: 16310177 [PubMed - indexed for MEDLINE]
A different cancer but same general direction of importance of omega three six balance.
I am scratching my head over aspects of the diagram but will work on it.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16566819&query_hl=51&itool=pubmed_docsum
1: J Carcinog. 2006 Mar 27;5:9.Click here to read Click here to read Links
The yin and yang of 15-lipoxygenase-1 and delta-desaturases: Dietary omega-6 linoleic acid metabolic pathway in prostate.
* Kelavkar U,
* Lin Y,
* Landsittel D,
* Chandran U,
* Dhir R.
Department of Urology and University of Pittsburgh Cancer Institute, 5200 Center Ave,, SHMC-Suite G-37, Pittsburgh, PA, 15232, USA. kelavkarup@upmc.edu.
ABSTRACT : One of the major components in high-fat diets (Western diet) is the omega (omega, n)-6 polyunsaturated fatty acid (PUFA) called linoleic acid (LA). Linoleic acid is the precursor for arachidonic acid (AA). These fatty acids are metabolized to an array of eicosanoids and prostaglandins depending upon the enzymes in the pathway. Aberrant expression of the catabolic enzymes such as cyclooxygenases (COX-1 and/or -2) or lipoxygenases (5-LO, 12-LO, 15-LO-1, and 15-LO-2) that convert PUFA either AA and/or LA to bioactive lipid metabolites appear to significantly contribute to the development of PCa. However, PUFA and its cellular interactions in PCa are poorly understood. We therefore examined the mRNA levels of key enzymes involved in the LA and AA pathways in 18 human donor (normal) prostates compared to 60 prostate tumors using the Affymetrix U95Av2 chips. This comparative (normal donor versus prostate cancer) study showed that: 1) the level of 15-LO-1 expression (the key enzyme in the LA pathway) is low (P < 0.001), whereas the levels of delta-5 desaturase (P < 0.001, the key enzyme in the AA pathway), delta-6 desaturase (P = 0.001), elongase (P = 0.16) and 15-lipoxygenase-2 (15-LO-2, P = 0.74) are higher in donor (normal) prostates, and 2) Contrary to the observation in the normal tissues, significantly high levels of only 15-LO-1; whereas low levels of delta-6 desaturase, elongase, delta-5 desaturase and 15-LO-2 respectively, were observed in PCa tissues. Although the cyclooxygenase (COX)-1 and COX-2 mRNA levels were high in PCa, no significant differences were observed when compared in donor tissues. Our study underscores the importance of promising dietary intervention agents such as the omega-3 fatty acids as substrate competitors of LA/AA, aimed primarily at high 15-LO-1 and COX-2 as the molecular targets in PCa initiation and/or progression.
PMID: 16566819 [PubMed - in process]
More of the same.
RB
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16611404
1: Neoplasia. 2006 Feb;8(2):112-24.Click here to read Links
Prostate Tumor Growth and Recurrence Can Be Modulated by the omega-6:omega-3 Ratio in Diet: Athymic Mouse Xenograft Model Simulating Radical Prostatectomy.
* Kelavkar UP,
* Hutzley J,
* Dhir R,
* Kim P,
* Allen KG,
* McHugh K.
Department of Urology and Cancer Institute, University of Pittsburgh, Pittsburgh, PA, USA, Email: kelavkarup@upmc.edu.
Evidence indicates that a diet rich in omega (omega)-6 polyunsaturated fatty acids (PUFAs) [e.g., linoleic acid (LA)] increases prostate cancer (PCa) risk, whereas a diet rich in omega-3 decreases risk. Precisely how these PUFAs affect disease development remains unclear. So we examined the roles that PUFAs play in PCa, and we determined if increased omega-3 consumption can impede tumor growth. We previously demonstrated an increased expression of an omega-6 LA-metabolizing enzyme, 15-lipoxygenase-1 (15-LO-1, ALOX15), in prostate tumor tissue compared with normal adjacent prostate tissue, and that elevated 15-LO-1 activity in PCa cells has a protumorigenic effect. A PCa cell line, Los Angeles Prostate Cancer-4 (LAPC-4), expresses prostate-specific antigen (PSA) as well an active 15-LO-1 enzyme. Therefore, to study whether or not the protumorigenic role of 15-LO-1 and dietary omega-6 LA can be modulated by altering omega-3 levels through diet, we surgically removed tumors caused by LAPC-4 cells (mouse model to simulate radical prostatectomy). Mice were then randomly divided into three different diet groups-namely, high omega-6 LA, high omega-3 stearidonic acid (SDA), and no fat-and examined the effects of omega-6 and omega-3 fatty acids in diet on LAPC-4 tumor recurrence by monitoring for PSA. Mice in these diet groups were monitored for food consumption, body weight, and serum PSA indicative of the presence of LAPC-4 cells. Fatty acid methyl esters from erythrocyte membranes were examined for omega-6 and omega-3 levels to reflect long-term dietary intake. Our results provide evidence that prostate tumors can be modulated by the manipulation of omega-6:omega-3 ratios through diet and that the omega-3 fatty acid SDA [precursor of eicosapentaenoic acid (EPA)] promotes apoptosis and decreases proliferation in cancer cells, causing decreased PSA doubling time, compared to omega-6 LA fatty acid, likely by competing with the enzymes of LA and AA pathways, namely, 15-LO-1 and cyclooxygenases (COXs). Thus, EPA and DHA (major components of fish oil) could potentially be promising dietary intervention agents in PCa prevention aimed at 15-LO-1 and COX-2 as molecular targets. These observations also provide clues as to its mechanisms of action.
PMID: 16611404 [PubMed - in process]
"Modulation of cancer development with low n-6/n-3 ratio diets containing specific dietary FA could be a promising tool in cancer intervention in the liver."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15691018&query_hl=23&itool=pubmed_DocSum1: Lipids. 2004 Oct;39(10):963-76. Links
Dietary modulation of fatty acid profiles and oxidative status of rat hepatocyte nodules: effect of different n-6/n-3 fatty acid ratios.
* Abel S,
* De Kock M,
* Smuts CM,
* de Villiers C,
* Swanevelder S,
* Gelderblom WC.
Medical Research Council, Tygerberg, South Africa. stefan.abel@mrc.ac.za
Male Fischer rats were fed the AIN 76A diet containing varying n-6/n-3 FA ratios using sunflower oil (SFO), soybean oil (SOY), and SFO supplemented with EPA-50 and GLA-80 (GLA) as fat sources. Hepatocyte nodules, induced using diethylnitrosamine followed by 2-acetylaminofluorene/partial hepatectomy promotion, were harvested, with surrounding and respective dietary control tissues, 3 mon after partial hepatectomy. The altered growth pattern of hepatocyte nodules in rats fed SFO is associated with a distinct lipid pattern entailing an increased concentration of PE, resulting in increased levels of 20:4n-6. In addition, there is an accumulation of 18:1 n-9 and 18:2n-6 and a decrease in the end products of the n-3 metabolic pathway in PC, suggesting a dysfunctional delta-6-desaturase enzyme. The hepatocyte nodules of the SFO-fed rats exhibited a significantly reduced lipid peroxidation level that was associated with an increase in the glutathione (GSH) concentration. The low n-6/n-3 FA ratio diets significantly decreased 20:4n-6 in PC and PE phospholipid fractions with a concomitant increase in 20:5n-3, 22:5n-3, and 22:6n-3. The resultant changes in the 20:4/20:5 FA ratio and the 20:3n-6 FA level in the case of the GLA diet suggest a reduction of prostaglandin synthesis of the 2-series. The GLA diet also counteracted the increased level of 20:4n-6 in PE by equalizing the nodule/surrounding ratio. The low n-6/n-3 ratio diets significantly increased lipid peroxidation levels in hepatocyte nodules, mimicking the level in the surrounding and control tissue while GSH was decreased. An increase in n-3 FA levels and oxidative status resulted in a reduction in the number of glutathione-S-transferase positive foci in the liver of the GLA-fed rats. Modulation of cancer development with low n-6/n-3 ratio diets containing specific dietary FA could be a promising tool in cancer intervention in the liver.
PMID: 15691018 [PubMed - indexed for MEDLINE]
Interesting RB
http://grande.nal.usda.gov/ibids/index.php
Impact of fish oil and melatonin on cachexia in patients with advanced gastrointestinal cancer: a randomized pilot study.
Author: Persson,-C; Glimelius,-B; Ronnelid,-J; Nygren,-P
Citation: Nutrition. 2005 Feb; 21(2): 170-8
Abstract: OBJECTIVE: The effect of fish oil (FO), melatonin (MLT), or their combination and dietary advice on cachexia and biochemistry variables reflecting cachexia were investigated in patients with advanced gastrointestinal cancer. METHODS: Twenty-four patients not amenable to standard anticancer treatment and with documented weight loss and/or decreased serum albumin were included. They were randomized to 30 mL/d of FO, which provided 4.9 g of eicosapentaenoic acid and 3.2 g of docosahexanoic acid, or 18 mg/d of MLT for 4 wk. During the next 4 wk, all patients had FO and MLT. Serum or plasma was analyzed for tumor necrosis factor-alpha, interleukin-1beta, soluble interleukin-2 receptor, interleukin-6, and interleukin-8 and the fatty acids eicosapentaenoic acid, docosahexanoic acid, arachidonic acid, and linoleic acid. RESULTS: Serum levels of eicosapentaenoic acid and docosahexanoic acid increased as expected with FO. No major changes in biochemical variables and cytokines were observed with any intervention. In the FO group, 5 of 13 patients (38%) showed weight stabilization or gain compared with 3 of 11 patients (27%) in the MLT group. After combining interventions, approximately 63% of patients showed such responses. CONCLUSIONS: FO, MLT, or their combination did not induce major biochemical changes indicative of a strong anticachectic effect. Nonetheless, the interventions used may have produced a weight-stabilizing effect.
Where n6 - n3 is high genes have been shon in trials to be regulated by a factor of 10. Genes regulated include HER2.
RB
"n-3 polyunsaturated fatty acids, usually provided as fish oil, modulate expression of a number of genes with such broad functions as DNA binding, transcriptional regulation, transport, cell adhesion, cell proliferation, and membrane localization. These effects, in turn, may significantly modify cell function, development and/or maturation."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15075705&query_hl=3&itool=pubmed_docsum
1: Curr Opin Clin Nutr Metab Care. 2004 Mar;7(2):151-6.Click here to read Links
Polyunsaturated fatty acids and gene expression.
* Lapillonne A,
* Clarke SD,
* Heird WC.
USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030-2600, USA.
PURPOSE OF REVIEW: This review focuses on the effect(s) of n-3 polyunsaturated fatty acids on gene transcription as determined by data generated using cDNA microarrays. Introduced within the past decade, this methodology allows detection of the expression of thousands of genes simultaneously and, hence, is a potentially powerful tool for studying the regulation of physiological mechanisms that are triggered or inhibited by nutrients. RECENT FINDINGS: Recent data generated with cDNA microarrays not only confirm the effects of n-3 polyunsaturated fatty acids on regulation of lipolytic and lipogenic gene expression as determined by more traditional methods but also emphasize the tissue specificity of this regulation. cDNA microarray experiments also have expanded our understanding of the role of n-3 polyunsaturated fatty acids in regulation of expression of genes involved in many other pathways. These include: oxidative stress response and antioxidant capacity; cell proliferation; cell growth and apoptosis; cell signaling and cell transduction. SUMMARY: The cDNA microarray studies published to date show clearly that n-3 polyunsaturated fatty acids, usually provided as fish oil, modulate expression of a number of genes with such broad functions as DNA binding, transcriptional regulation, transport, cell adhesion, cell proliferation, and membrane localization. These effects, in turn, may significantly modify cell function, development and/or maturation.
PMID: 15075705 [PubMed - indexed for MEDLINE]
Generally beyond me and I do not have the time to delve but does this help explain why omega three has synergistic effects with some chemos etc.
At simplest level in colon cancer was shown to "In view of the central role of oncogenic Ras in the development of colon cancer, the finding that n-3 and n-6 PUFA differentially modulate Ras activation may partly explain why dietary fish oil protects against colon cancer development."
As far as this site goes just another hint that balancing the omega threes and sixes and having regard to omega three intake is worth consideration.
RB
http://ajpcell.physiology.org/cgi/content/full/280/5/C1066
ABSTRACT
Ras proteins are critical regulators of cell function, including growth, differentiation, and apoptosis, with membrane localization of the protein being a prerequisite for malignant transformation. We have recently demonstrated that feeding fish oil, compared with corn oil, decreases colonic Ras membrane localization and reduces tumor formation in rats injected with a colon carcinogen. Because the biological activity of Ras is regulated by posttranslational lipid attachment and its interaction with stimulatory lipids, we investigated whether docosahexaenoic acid (DHA), found in fish oil, compared with linoleic acid (LA), found in corn oil, alters Ras posttranslational processing, activation, and effector protein function in young adult mouse colon cells overexpressing H-ras (YAMC-ras). We show here that the major n-3 polyunsaturated fatty acid (PUFA) constituent of fish oil, DHA, compared with LA (an n-6 PUFA), reduces Ras localization to the plasma membrane without affecting posttranslational lipidation and lowers GTP binding and downstream p42/44ERK-dependent signaling. In view of the central role of oncogenic Ras in the development of colon cancer, the finding that n-3 and n-6 PUFA differentially modulate Ras activation may partly explain why dietary fish oil protects against colon cancer development.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16854453&query_hl=11&itool=pubmed_docsum
Roles of the RAF/MEK/ERK and PI3K/PTEN/AKT pathways in malignant transformation and drug resistance.
* McCubrey JA,
* Steelman LS,
* Abrams SL,
* Lee JT,
* Chang F,
* Bertrand FE,
* Navolanic PM,
* Terrian DM,
* Franklin RA,
* D'Assoro AB,
* Salisbury JL,
* Mazzarino MC,
* Stivala F,
* Libra M.
Department of Microbiology & Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA; Leo Jenkins Cancer Center, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
The Ras/Raf/MEK/ERK and PI3K/PTEN/AKT signaling cascades play critical roles in the transmission of signals from growth factor receptors to regulate gene expression and prevent apoptosis. Components of these pathways are mutated or aberrantly expressed in human cancer (e.g., Ras, B-Raf, PI3K, PTEN, Akt). Also, mutations occur at genes encoding upstream receptors (e.g., EGFR and Flt-3) and chimeric chromosomal translocations (e.g., BCR-ABL) which transmit their signals through these cascades. These pathways interact with each other to regulate growth and in some cases tumorigenesis. For example, in some cells, PTEN mutation may contribute to suppression of the Raf/MEK/ERK cascade due to the ability of elevated activated Akt levels to phosphorylate and inactivate Raf-1. We have investigated the genetic structures and functional roles of these two signaling pathways in the malignant transformation and drug resistance of hematopoietic, breast and prostate cancer cells. Although both of these pathways are commonly thought to have anti-apoptotic and drug resistance effects on cells, they display different cell-lineage-specific effects. Induced Raf expression can abrogate the cytokine dependence of certain hematopoietic cell lines (FDC-P1 and TF-1), a trait associated with tumorigenesis. In contrast, expression of activated PI3K or Akt does not abrogate the cytokine dependence of these hematopoietic cell lines, but does have positive effects on cell survival. However, activated PI3K and Akt can synergize with activated Raf to abrogate the cytokine dependence of another hematopoietic cell line (FL5.12) which is not transformed by activated Raf expression by itself. Activated Raf and Akt also confer a drug-resistant phenotype to these cells. Raf is more associated with proliferation and the prevention of apoptosis while Akt is more associated with the long-term clonogenicity. In breast cancer cells, activated Raf conferred resistance to the chemotherapeutic drugs doxorubicin and paclitaxel. Raf induced the expression of the drug pump Mdr-1 (a.k.a., Pgp) and the Bcl-2 anti-apoptotic protein. Raf did not appear to induce drug resistance by altering p53/p21(Cip-1) expression, whose expression is often linked to regulation of cell cycle progression and drug resistance. Deregulation of the PI3K/PTEN/Akt pathway was associated with resistance to doxorubicin and 4-hydroxyl tamoxifen, a chemotherapeutic drug and estrogen receptor antagonist used in breast cancer therapy. In contrast to the drug-resistant breast cancer cells obtained after overexpression of activated Raf, cells expressing activated Akt displayed altered (decreased) levels of p53/p21(Cip-1). Deregulated expression of the central phosphatase in the PI3K/PTEN/Akt pathway led to breast cancer drug resistance. Introduction of mutated forms of PTEN, which lacked lipid phosphatase activity, increased the resistance of the MCF-7 cells to doxorubicin, suggesting that these lipid phosphatase deficient PTEN mutants acted as dominant negative mutants to suppress wild-type PTEN activity. Finally, the PI3K/PTEN/Akt pathway appears to be more prominently involved in prostate cancer drug resistance than the Raf/MEK/ERK pathway. Some advanced prostate cancer cells express elevated levels of activated Akt which may suppress Raf activation. Introduction of activated forms of Akt increased the drug resistance of advanced prostate cancer cells. In contrast, introduction of activated forms of Raf did not increase the drug resistance of the prostate cancer cells. In contrast to the results observed in hematopoietic cells, Raf may normally promote differentiation in prostate cells which is suppressed in advanced prostate cancer due to increased expression of activated Akt arising from PTEN mutation. Thus in advanced prostate cancer it may be advantageous to induce Raf expression to promote differentiation, while in hematopoietic cancers it may be beneficial to inhibit Raf/MEK/ERK-induced proliferation. These signaling and anti-apoptotic pathways can have different effects on growth, prevention of apoptosis and induction of drug resistance in cells of various lineages which may be due to the expression of lineage-specific factors.
PMID: 16854453 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16885352&query_hl=11&itool=pubmed_docsum
1: Cancer Res. 2006 Aug 1;66(15):7540-7547.Click here to read Links
p38{gamma} Mitogen-Activated Protein Kinase Integrates Signaling Crosstalk between Ras and Estrogen Receptor to Increase Breast Cancer Invasion.
* Qi X,
* Tang J,
* Loesch M,
* Pohl N,
* Alkan S,
* Chen G.
Departments of Radiation Oncology, Pharmacology and Experimental Therapeutics, and Pathology and Program in Molecular Biology, Loyola University Chicago, Maywood, Illinois and Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin.
Ras is believed to stimulate invasion and growth by different effector pathways, and yet, the existence of such effectors under physiologic conditions has not been shown. Estrogen receptor (ER), on the other hand, is both anti-invasive and proliferative in human breast cancer, with mechanisms for these paradoxical actions remaining largely unknown. Our previous work showed an essential role of p38gamma mitogen-activated protein kinase in Ras transformation in rat intestinal epithelial cells, and here, we show that p38gamma integrates invasive antagonism between Ras and ER to increase human breast cancer invasion without affecting their proliferative activity. Ras positively regulates p38gamma expression, and p38gamma in turn mediates Ras nonmitogenic signaling to increase invasion. Expression of the Ras/p38gamma axis, however, is trans-suppressed by ER that inhibits invasion and stimulates growth also by distinct mechanisms. Analysis of ER and its cytoplasmic localized mutant reveals that ER additionally binds to p38gamma protein, leading to its specific down-regulation in the nuclear compartment. A p38gamma-antagonistic activity of ER was further shown in a panel of breast cancer cell lines and was shown independent of estrogens by both ER depletion and ER expression. These results revealed that both Ras and ER use distinct pathways to regulate breast cancer growth and invasion, and that p38gamma specifically integrates their antagonistic activity to stimulate cell invasion. Selective targeting of p38gamma-dependent invasion pathways may be a novel strategy to control breast cancer progression. (Cancer Res 2006; 66(15): 7540-7).
PMID: 16885352 [PubMed - as supplied by publisher]
This was interesting in that it confirms in rats that the breast does manifacture long chain fats eg DHA and not just accumulate them.
AND linoleic acid. the omega six mother fat in excess in the diet inhibits that ability.
WHICH ties in with what is being observed in general trends in mothers production of long chain fats in breast milk.
It links to BC in that one could postulate that the same characterisitics might be seen carried into proliferating cells....
RB
http://www.jlr.org/cgi/content/abstract/47/3/553
Synthesis of long-chain polyunsaturated fatty acids in lactating mammary gland
: role of {Delta}5 and {Delta}6 desaturases, SREBP-1, PPAR{alpha}, and PGC-1
Maricela Rodriguez-Cruz*,{dagger}, Armando R. Tovar§, Berenice Palacios-González§, Martha del Prado* and Nimbe Torres1,§
* Unidad de Investigación Médica en Nutrición, Coordinación de Investigación en Salud, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico City, DF 06720 Mexico
{dagger} Posgrado en Ciéncias Biológicas, Facultad de Medicina, UNAM, Mexico City, DF 04510, Mexico
§ Departamento de Fisiolog*a de la Nutrición, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, DF 14000 Mexico
Published, JLR Papers in Press, December 6, 2005.
1 To whom correspondence should be addressed. e-mail: nimbet@quetzal.innsz.mx
The purpose of this work was to study whether rat lactating mammary gland can synthesize PUFAs through the expression of {Delta}5 and {Delta}6 desaturases ({Delta}5D and {Delta}6D), whether these enzymes are regulated by the transcription factors sterol-regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator-activated receptor {alpha} (PPAR{alpha}) and the coactivator peroxisome proliferator-activated receptor {gamma} coactivator 1ß (PGC-1ß), and whether these desaturases are regulated by the lipid concentration in the diet. The results showed that on day 12 of lactation, ~35% of the linoleic acid in the diet, which is the precursor of PUFAs, is transferred to the mammary gland. There was expression of {Delta}5D and {Delta}6D in mammary gland, and it was regulated by the corn oil content in the diet. The higher the corn oil content in the diet, the lower the expression of both desaturases. Induction of {Delta}5D and {Delta}6D was associated positively with similar changes in SREBP-1 and PGC-1ß. Expression of PPAR{alpha} was barely detected and was not affected by the corn oil content in the diet, whereas PGC-1ß expression increased as the corn oil in the diet increased. These results indicate that the lactating mammary gland has the capacity to synthesize PUFAs and can be regulated by the lipid content in the diet.
Supplementary key words sterol-regulatory element binding protein 1 • peroxisome proliferator-activated receptor {alpha} • peroxisome proliferator-activated receptor {gamma} coactivator 1
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16798867&query_hl=3&itool=pubmed_docsum
1: J Dent Res. 2006 Jul;85(7):648-52.Click here to read Links
Omega-3 Fatty Acid effect on alveolar bone loss in rats.
* Kesavalu L,
* Vasudevan B,
* Raghu B,
* Browning E,
* Dawson D,
* Novak JM,
* Correll MC,
* Steffen MJ,
* Bhattacharya A,
* Fernandes G,
* Ebersole JL.
Center for Oral Health Research, College of Dentistry, 159 HSRB, University of Kentucky, Lexington, KY 40536-0305, USA; and.
Gingival inflammation and alveolar bone resorption are hallmarks of adult periodontitis, elicited in response to oral micro-organisms such as Porphyromonas gingivalis. We hypothesized that omega (omega)-3 fatty acids (FA) dietary supplementation would modulate inflammatory reactions leading to periodontal disease in infected rats. Rats were fed fish oil (omega-3 FA) or corn oil (n-6 FA) diets for 22 weeks and were infected with P. gingivalis. Rats on the omega-3 FA diet exhibited elevated serum levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), documenting diet-induced changes. PCR analyses demonstrated that rats were orally colonized by P. gingivalis; increased IgG antibody levels substantiated this infection. P. gingivalis-infected rats treated with omega-3 FA had significantly less alveolar bone resorption. These results demonstrated the effectiveness of an omega-3 FA-supplemented diet in modulating alveolar bone resorption following P. gingivalis infection, and supported that omega-3 FA may be a useful adjunct in the treatment of periodontal disease. Abbreviations: PUFA, polyunsaturated fatty acid; EPA, eicosapentanoic acid; DHA, docosahexanoic acid; and PCR, polymerase chain-reaction.
PMID: 16798867 [PubMed - in process]
This is a useful and thought provoking article on those looking at their hormone levels in relation to BC..
"Recent prospective studies have provided strong evidence that the risk of developing breast cancer in postmenopausal women is increased by high serum levels of testosterone and estradiol, low levels of sex hormone-binding globulin, and, hence, high circulating levels of free steroid sex hormones (1, 2, 3, 4, 5, 6, 7) . Evidence is accumulating that Western dietary habits contribute this high-risk hormonal profile, but the efficacy of changes in diet in reducing the availability of sex hormones has not been sufficiently investigated."
The trial looks at the impact of some dietary changes on hormone levels.
RB
http://cebp.aacrjournals.org/cgi/content/full/10/1/25
(FULL ARTICLE LINK)
Reducing Bioavailable Sex Hormones through a Comprehensive Change in Diet: the Diet and Androgens (DIANA) Randomized Trial1
Franco Berrino2, Cristina Bellati, Giorgio Secreto, Edgarda Camerini, Valeria Pala, Salvatore Panico, Giovanni Allegro and Rudolf Kaaks
Unit of Epidemiology (F. B., C. B.,V. P.), Unit of Nuclear Medicine (G. S.), Unit of Laboratory Medicine (E. C.), Istituto Nazionale Tumori, 20133 Milan, Italy; Department of Clinical and Experimental Medicine, Federico II University, 80131 Naples, Italy (S. P.); Association Le Cinque Stagioni, 10018 Ivrea, Italy (G. A.); and Nutrition and Cancer Unit, International Agency for Research on Cancer, 69372 Lyon, France (R. K.)
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
High serum levels of testosterone and estradiol, the bioavailability of which may be increased by Western dietary habits, seem to be important risk factors for postmenopausal breast cancer. We hypothesized that an ad libitum diet low in animal fat and refined carbohydrates and rich in low-glycemic-index foods, monounsaturated and n-3 polyunsaturated fatty acids, and phytoestrogens, might favorably modify the hormonal profile of postmenopausal women. One hundred and four postmenopausal women selected from 312 healthy volunteers on the basis of high serum testosterone levels were randomized to dietary intervention or control. The intervention included intensive dietary counseling and specially prepared group meals twice a week over 4.5 months. Changes in serum levels of testosterone, estradiol, and sex hormone-binding globulin were the main outcome measures. In the intervention group, sex hormone-binding globulin increased significantly (from 36.0 to 45.1 nmol/liter) compared with the control group (25 versus 4%,; P < 0.0001) and serum testosterone decreased (from 0.41 to 0.33 ng/ml; -20 versus -7% in control group; P = 0.0038). Serum estradiol also decreased, but the change was not significant. The dietary intervention group also significantly decreased body weight (4.06 kg versus 0.54 kg in the control group), waist:hip ratio, total cholesterol, fasting glucose level, and area under insulin curve after oral glucose tolerance test. A radical modification in diet designed to reduce insulin resistance and also involving increased phytoestrogen intake decreases the bioavailability of serum sex hormones in hyperandrogenic postmenopausal women. Additional studies are needed to determine whether such effects can reduce the risk of developing breast cancer.......................MORE
Please excuse me pushing this thread back up for any who may be new to the Forum.
There is also the "cancer Diet" thread for those looking for diet ideas.
RB
1771 views for both the Greek Diet, and Cancer Diet when I visited just now.
I wonder what the chances of that are.
RB
chrisy
09-16-2006, 04:13 PM
Pretty good, since each of these "timeless topics" have a great sponsor bumping them up to keep them visible. Thanks!
p.s. I visited both, too...just trying to keep my "Breast cancer diet/Greek diet" balance correct. I know you would approve!
RobinP
09-17-2006, 06:54 AM
What about other diet measures beside omega 3 fats. I use olive oil to bind the her2 receptor, use genistein ( yes I know it's contraversial as a phytoestrogen) for the Her1(yes I know by testing I am her1+), use quercetin natural products for the her 3 (again I am her3+ too), green tea as a general antioxidant, vitamin A products and oatmeal to bind the estrogen receptor, tumeric also to prevent spread and seeding of her2. Finally, I use vit. D and calcium for bone health but it may also play a role in preventing some cancers too, especially colon.
Just a reminder for new members that diet can impact on your cancer risk profile.
Diet does change the way you express your genes, a bit like you can change the tonal nature of your music using a graphic equaliser on your stereo.
I accept it is difficult.
I am sorry to keep labouring it but talking with women giving their time to collect for a support group reminded my how many evidently are not convinced, almost to the point of being hostile to suggestions diet is significant even (if not more so) after contracting BC.
It was saddly evident of possibly how few people are aware of the significant potential of diet to reduce rsik profiles, and the resistance to it as an idea among significnat numbers.
RB
Mary Anne in TX
10-01-2006, 06:26 AM
Thanks for keeping this "front and center"! Everytime I read the information (new and old) it reminds me how much better I feel when I pay close attention to what goes in my mouth!!!! And it gets me back on track!
ma
chrislmelb
10-01-2006, 08:28 PM
always good to read your thoughts and answers to others' questions.
Take care
Christine
RhondaH
10-02-2006, 09:01 AM
MIA for a while. Good to see you. Take care and God bless.
Rhonda
Rhonda, Christine, Mia, thanks for the comments. I'm touched.
Marbles Institute Associate (as in lost a few) is closer some might say. Nothing as gallant as MIA I'm afraid.
Thanks.
RB
julierene
10-03-2006, 10:56 AM
I guess one of my main concerns is that we don't know WHAT diet does to our gene expression. We are so on the edge of what diet can do. Look at the Beta Carotene study they did. That is one of the reasons I would caution anyone taking megadoses of anything that is supposedly "good" for you. There is such a thing as "too much of a good thing".
Good point
I wish they would fund trials. An animal trial on skeletal muscle did show high omega six increased HER2 expression. But I agree with you and again wish they would fund trials to sort out these basics.
We do know our ancestors did not have access to large quantities of cheap vegetable oils, trans fats etc. Or necessarily clean water, better all year round food availability, better housing and some fantastic medical advances.
RB
kat in the delta
10-09-2006, 08:35 PM
All I know is that Cancer seems to GROW in an ACIDIC BODY. WE need to find out ALL the foods that NEUTRALIZE the acid to make our bodies MORE ALKALINE. You would not believe Which foods they are--example apples and oranges...Who will make the list ? gotta get off --kat in the delta
kat in the delta
10-09-2006, 08:39 PM
1. Eat food to make our bodies more alkaline.
2. get rid of the magnetic chaos around us
3. Detox our bodies--colon, liver,,,,,etc
4. Learn to deal or get rid of stress
Really all of these can make our bodies acidic which we want to REVERSE-kat in the delta
rsvp what do YOU ALL think ??????????
This is an abstract from an article I saved.
I will try and find the link to it and post it.
Thank you for bringing it up as a subject.
This seems to sum it up plus carbonated drinks, and I wonder about vitamin C unbuffered when used as a preservative etc. I also cannot recall the situation re orange juice etc, which in addition in high quantities is a source of fruit sugars which in excess - all healthy things in moderation. I have started significantly diluting all purchased fruit juices.
"fish, meat, poultry, eggs, shellfish, cheese, milk, and cereal grains are net acid producing, whereas fresh fruit, vegetables, tubers, roots, and nuts are net base producing. Legumes yield near-zero mean acid values. Salt is net acid producing because of the chloride ion."
“fish, meat, poultry, eggs, shellfish, cheese, milk, and cereal grains are net acid producing, whereas fresh fruit, vegetables, tubers, roots, and nuts are net base producing. Legumes yield near-zero mean acid values. Salt is net acid producing because of the chloride ion. …As a result, healthy adults consuming the standard US diet sustain a chronic, low-grade pathogenic metabolic acidosis that worsens with age as kidney function declines. Virtually all preagricultural diets were net base yielding because of the absence of cereals and energy-dense, nutrient-poor foods—foods that were introduced during the Neolithic and Industrial Eras and that displaced base-yielding fruit and vegetables ”
I hope this helps a little.
RB
Mary Anne in TX
10-10-2006, 06:17 PM
I did a google search of alkaline & acid foods and found some charts that were really good, but on some items them differed! It really did help though! I'll keep reading them to find the ones that most often agree!
Watching what I eat has helped me so much these past 10 months!
Mary Anne.
If you find some particularly interesting ones could you post the links.
Many thanks
RB
Mary Anne in TX
10-11-2006, 05:51 AM
http://www.thewolfeclinic.com/acidalkfoods.html
Here is one chart that is easy to read and fairly complete.
http://www.liferesearchuniversal.com/acid.html
Here is one other that is easy to use.
Now, I just have to do it!
mary anne
kat in the delta
10-11-2006, 08:59 AM
Thanks for looking us the info on foods--WE all need foods that Neutralize the acid in our bodies because cancer and most diseases love to live in an acidic body. I found that you can replace reg.salt with Sea Salt which is more alkaline(NONacid).
What about MILK----
Cancer craves SUGAR--so refined sugar should be a NO-NO for all of us. I guess someone or all of Us can make a list of Acid forming foods and a list of Foods that neutalize acid
--Any volunteers ??? I cannot stay on net long now......
Which are good site ?? from the Mayo Clinic, or MDAnderson, or Memorial Sloan Kettering Cancer Center or some dietician page or nutrition page.....Let me know what you all find out and we can all help each other ....................kat in the delta
kat in the delta
10-11-2006, 09:20 AM
Mary Ann, Those sites you found were both excellant..& don't forget to drink Water--(mineral,spring,purified ??? )&..what other foods are missing? gotta run now...thanks for info for all...kat in the delta
keep looking if you can.......
Also look at what would prevent Magnetic interference with our bodies....We all may need to buy a bracelet or such......
I know that microwaves are NOT good,,,,and Cell Phones.....what else ???
And we need to detox. our bodies of toxins--colon -liver and more.....
To eliminate STRESS is a hard one for me.......really need to run now, but could go on .....kat.
Mary Anne in TX
10-11-2006, 02:18 PM
http://www.essense-of-life.com/info/foodchart.htm
Ok, here is a chart that points out the unknown foods that I referred to earlier.
Good charts!
mary anne
Mary Anne
Thank you for those great links - exellent additions to this thread.
Sugar has the potential to create problems at all sorts of levels, poor digestion, upsetting of the fat metabolism, empty calories....
Sugar sucrose which breaks down into glucose and fructose from memory. It is a huge subject on its own.
It is clear from papers that consumption of refined sugars, particularly above a minimum can potentially have significant negative effects in the body.
Some are suggesting it is in general terms possibly a bigger factor in IBS than gluten etc. It certainly makes thought provoking reading. Good digestion is essential to health. And yes I could do better too.
Here is one link by way of example.
http://www.bashaar.org.il/files/101022005111814.pdf
RB
kat in the delta
10-15-2006, 10:42 AM
Help me Robbie,
So is olive oil good or NOT good for you..Can you tell me some common foods and oils that ARE GOOD for you...Then, tell me those that are NOT as good for you
I would appreciate your help.........this has been alot for me to absorb as I just started from the top of this thread...thanks,
KAT
Well done for making the effort to try and understand this huge subject.
It is as usual complicated, but I will try and deal with the basics.
Olive oil is a complex mix of a lot of fats and chemicals.
This link gives an idea as to the mix of fats it contains. http://www.nutritiondata.com/facts-C00001-01c208D.html
18:1 is likely to be mainly oleic, 18:2 linoleic (omega six) 18:3 linolenic (omega three). So in olive oil you are getting a mix of fats, and mainly mono saturates (1 double bond eg 18:1 - 18 the number of carbons - 1 the number of double bonds.)
Mono saturates are better to cook with as they oxidise less, but add what you need for taste etc at end,
But if you use a lot it is important to rember 10% - 15% of a virgin oil and up to 50% of a processed oil is omega six.
There are also other chemicals in olive oil that are reported to have a benificial effect.
http://www.her2support.org/vbulletin/showthread.php?t=21918&highlight=olive+oil
So in general terms,
- moderation - less is probably more in general terms
- be very aware to add in the omega six it contains in working out approx your three six intake.
- use only quality virgin oils
- remember the body can make omega nines but it is complex and your body may appreciate a helping hand with provision of a little
Every body is different and will metabolise fats differently. If it is a choice becuase you do not tolerate fat or some other reason I would put fish oil first, and include a little olive oil now and then.
This thread may help too
http://www.her2support.org/vbulletin/showthread.php?t=25565&highlight=olive+oil
And this one.
http://www.her2support.org/vbulletin/showthread.php?t=25565&highlight=olive+oil
In general diet terms on diet - there are lots of books many of which cover more or less the same ground. Here are some thoughts but best check out some book at the library if you get time.
- as wide a variety as possible (a green food supplement is a way of getting some things you would not usually include in your diet Green Frog as a make is quite good)
- Green things and lots of them, frozen if fresh is not available spinach, broccoli etc. highly coloured fruit and veg, some dried seaweed.
- Some nuts mixed as much as will fit on your palm.
- Some pulses if your digestion will tolerate them
- Whole grain but in strict moderation and better pre germinated as reportedly easier to digest.
- a little occasional grass fed meat, farm raised chicken, offal etc if you are not vegitarian - corn fed animals have higher level of omega six
- fish including oily - small quick growing are less likely to be polluted sardines, mackerel - but again variety - all fish is good but wild is better.
- a variety of herbs and spices, ginger, curcumin, .....
- cut out vegetable oils except a little flaxseed (do not cook), maybe canola, perillia etc but you must watch the six content and strictly in moderation
- some fish oil to bring your intake of DHA up to about 2 grams a day.
Avoid "processed food" as in manifiactures prepreapred etc as far as is practicable - just because they usually contain vegetable oils etc. or at least read the label first, and regretabl they end up sadly going back on the shelf most times.
Sugar, sugar subsitutes, high salt levels, are very definate avoids.
So between sugars and vegetable oils most processed food is out.
Rhonda's "Cancer Diet" posted on this site is thought provoking.
Some suggest dairy and some say no. For those that tolerate it maybe a tiny bit of butter, maybe yogourt, maybe goats cheese, but small quantities.
You will find your taste changes and previous treats like crisps etc strangely end up tasting less desireable.
Getting ones digestion sorted out is key, which may mean no sugar, avoiding grains which can be difficult to digest for some, (Breaking the Vicious Cycle Elaine Gotterschall - is an interesting book on digestion - but may not be ideal receipies in respect of balancing omega threes and sixes, (high omega six in almonds) and I would have concern about too much honey....) for a bit etc.
Etc.
Do talk to your doctor about significant dietary change.
I hope the above helps. I am afraid beyond the basics you will have to find what suits you.
RB
Just to put the thread back on the current map for any that may not have seen it.
Diet can and does alter the way you express your genes including BRAC and HER2.
Rhonda breast cancer diet thread in another useful nutritional thread.
RB
julierene
12-03-2006, 12:53 AM
I used to read my pH and only once in the first 2 years of reading my monthly pH did I have anything past normal. I had normal pH even when my cancer came back... and just to disprove the pregnancy test theory - I got a negative pregnancy test too... I honestly don't know who comes up with this stuff. But these two tests were a waste of my money. Is there anyone who can show that the pH strips or the pregnancy tests actually WORKED for them?
StephN
12-03-2006, 02:13 PM
Another interesting topic. We had a thread going on acid/alkaline when Lyn was here contributing months back. I am sure a search here will turn it up.
I have no experience with those test strips myself, but DO try to stay to the less acid side in my diet. It can be very surprising what foods you think are acid that really do not fall into that category.
Start a new thread with this subject, OK?
P.S. Looks like your tests are coming out negative for active disease - YAY!
heblaj01
12-03-2006, 05:21 PM
I have no personal opinion on the validity of the acid/alkaline theory but here is a contrary position by an MD:
http://www.quackwatch.org/01QuackeryRelatedTopics/DSH/coral2.html
Acid/Alkaline Theory of Disease Is Nonsense
I also read somewhere in the distant past that the theory of the acidic environment as enhancing cancer progression was based on the wrong assessment of the cause & effect in the fact that cancer cells release lactic acid ( not the acid causing cancer).
Just bringing this thread back in case of interest to those new to the site, or with a new interest in diet etc.
The links do emphasise the importance of diet, and even if a tiny bit of use to anyone contribution makes me feel better.
RB
Heart Sutra
12-27-2006, 05:24 PM
Hi,
Thought I would look up The Lyon Study, since it was quoted as reducing coronary disease, and cancer mortality.
Alas, I could find no reference to cancer within the study.
Maybe I found the wrong one? Seems like all roads point back to this one study, and it was designed to rate coronary disease recurrance.
The study had flaws. Mainly lack of control of its "control" group, and exceedingly small sample. 300+ each of experimental and control individuals. The diet of either group was assessed once. Less than a third of the control, and less than half of the experimental group, provided dietary data at the final meeting.
The conclusion is that the role of diet is uncertain regarding this particular study of recurrant coronary events(!) Encouraging results were had, but the study was flawed enough to make it no more than interesting...far from conclusive. Again, nothing at all about cancer.
So, maybe I found the wrong study. There was another one based in France by the same name, but it was also a study of coronary illness, and no mention is made of cancer.
There does seem to be quite an interest in diet and cancer links.
There must be more carefully conducted studies somewhere of this topic.
Whenever a study is quoted, it's good to review the source of the study. There are a lot of claims out there...
Thank you for your comment. All debate is good. I have not looked at the Lyon study in detail
http://www.americanheart.org/presenter.jhtml?identifier=4655
but there is a huge amount of evidence that diet has potential impact on risk factors for disease. At the most basic levels diet influences gene expression which is a fundamental mechanism in regulating body function.
If you get time you mike like to look at some of the links provided which in turn open out into a plethora of further trials. If you search on NCBI and dietary factors of interesrt and cancer you will find a huge number of trials.
Here is a view from the Mayo Clinic
http://www.mayoclinic.com/health/fish-oil/NS_patient-fishoil
"There is evidence from multiple large-scale population (epidemiologic) studies and randomized controlled trials that intake of recommended amounts of DHA and EPA in the form of dietary fish or fish oil supplements lowers triglycerides, reduces the risk of death, heart attack, dangerous abnormal heart rhythms, and strokes in people with known cardiovascular disease, slows the buildup of atherosclerotic plaques ("hardening of the arteries"), and lowers blood pressure slightly. However, high doses may have harmful effects, such as an increased risk of bleeding. Although similar benefits are proposed for alpha-linolenic acid, scientific evidence is less compelling, and beneficial effects may be less pronounced."
RB
Just to bring this forward again as diet is a topic at the moment.
RB
julierene
01-09-2007, 08:47 PM
I'm not sure why this was brought back up with the last post. It seems to be an argument for NOT taking the Omega-3's. All it seems to say is that it helps with the heart - NOT HELPFUL FOR THOSE OF US WHO ARE GOING TO DIE FROM CANCER FIRST! And that increased doses (which could very well be that of the widely sold dosage on the shelf) cause harmful effects. This is exactly why I think it's dangerous to be playing around with all the supplements. There is no telling if the cocktail of supplements many women take is harmful OR helpful.
This whole idea of balancing Omega 3 and 6 is great... but I have never once seen evidence to tell us how to do it on a daily basis with our diet - naturally. I'm a natural freak... and fish oil capsules gave me burping I couldn't deal with, fowl urine, and terrible gas... So I have looked for answers on the topic and never seen anything. Most on this site seem to push the capsules, which my system just can't tolerate.
I am definetly not on the fence with most of the women here about taking supplements - especially high doses... A good multi vitamin should be sufficient with a well balanced diet. I think something most people should do is - listen to their bodies. If high doses of this and that cause ulcers... don't take them! If it makes them feel better and is considered safe - have at it. I just don't think dietary factors play as much of a role as we would like them to. The virus thread was much more alarming to me - and probably holds a lot more weight to what we all seem to run from. Our own DNA and the constant effect viruses have on our own genetic makeup.
Why did I bring up the coronary issue
Because a previous post suggested omega three had no impact on coronary health. A positive impact on coronary health is one of the area that does seem to be accepted by a growing number of the medical profession.
Re impact of omega three - it is complex. The eicosanoid pathway is fundamental to the bodies mechanisms, and omega three and six play a very big part in it. Omega three and six have been reported as impacting on a huge number of health issues.
Re repeating - I take oil and not capsules. I used ot have a problem with repeating with cod liver oils oils but do not have a problem with the seven seas extra strength or Vita Cost Carlsons lemon flavoured. I do not know if these oils are more refined. Omega three has been shown to reduce IBS which is a factor in poor digestion.
Food does alter gene expression, this includes BRAC and HER 2. the difference between a high omega six and balanced 3/6 has been shown to produce changes of gene expression by a factor of ten for some gene in rodents. There are a number of small trials suggesting that omega three intake does play a part in cancer risk reduction, but there is a lack of wider trials
This is a good starting point on the huge subject of fats.
http://www.benbest.com/health/essfat.html
Other supplements is a whole huge other issue on which I make no comment.
To balance the omega threes and sixes you have to look at your intake and fat content. This is a good link. It is a bore at first but it does not take long to get an idea as to what contains high levels of omega six.
http://www.nutritiondata.com/topics/fatty-acids
Otherwise it is more of the usual - avoid processed foods, sugar, trans fats,....lots of variety - lots of green things - small quantity of nuts - as generally discussed in many healthy eating books.
It is not easy, there is much mixed information and my suggestion is to read round the topic and come to your own conclusions.
RB
heblaj01
01-10-2007, 10:53 PM
Julierene,
You appear to have difficulties in digesting fish oil pills. Setting aside an allergy to seafood, it is possible you need taking digestive enzymes at the same time as the oil pills, in particular the lipase enzyme.
Lipase & other digestive enzymes are also indicated for some people with poor bile &/or pancreatic secretion or whose gallbladder has been resected or is not functioning because it is filled with stones. I am in this latter category & I take enzyme supplements with oil pills.
It is also preferable to take oil pills at the end of meals.
NOTE:
A simple check to find out if someone has problems in digesting fats is the color of stools: yellowish is indicative of poor digestion.
More indications fats are in the thick of things....
DEFINATELY WORTH STRUGGLING TO UNDERSTAND
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=17168666
ABSTRACT
"A recent discovery that dietary fatty acids can interact with the human genome by regulating the amount and/or activity of transcription factors has opened a whole new line of research aimed to molecularly corroborate the ant-cancer benefits of the olive oil-based Mediterranean diet and the underlying mechanisms. Our most recent findings reveal that oleic acid (OA; 18:1n-9), the main olive oil's monounsaturated fatty acid, can suppress the overexpression of HER2 (erbB-2), a well-characterized oncogene playing a key role in the etiology, invasive progression and metastasis in several human cancers."
and
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=17134970
ABSTRACT
"CONCLUSIONS: i) These findings reveal that the omega-3 PUFA ALA suppresses overexpression of HER2 oncogene at the transcriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab- based immunotherapy. ii) Our results molecularly support a recent randomized double-blind placebo-controlled clinical trial suggesting that ALA may be a potential dietary alternative or adjunct to currently used drugs in the management of HER2-positive breast carcinomas. iii) Considering our previous findings demonstrating the <<HER2 upregulatory actions>> of the omega-6 PUFA linolenic acid (LA; 18:2n-6) and the <<HER2 down-regulatory actions >> of the omega-3 PUFA docosahexaenoic acid (DHA; 22:6n-3) and of the omega-9 monounsaturated fatty acid oleic acid (OA; 18:1n-9), it is reasonable to suggest that a low omega-6/omega-3 PUFA ratio and elevated MUFA levels, the two prominent <<fat features>> of the <<Mediterranean diet>>, should be extremely efficient at blocking HER2 expression in breast cancer cells."
RB
Just bringing this back up the list for anybody who may not have seen it in case of interest.
RB
Just bringing this back for anybody new on the forum, and adding a link to some trials suggesting long chain omega three intake is linked with a reduction in the risk of BC.
Please do talk to your ad visors about significant dietary changes. Fish oil can cause blood thinning etc.
RB
http://www.her2support.org/vbulletin/showthread.php?p=118638#post118638
and some more
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=16823509
ABSTRACT
"Essential fatty acids have long been identified as possible oncogenic factors. Existing reports suggest omega-6 (omega-6) essential fatty acids (EFA) as pro-oncogenic and omega-3 (omega-3) EFA as anti-oncogenic factors. The omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), inhibit the growth of human breast cancer cells while the omega-6 fatty acids induces growth of these cells in animal models and cell lines."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15986129
ABSTRACT
"The omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), inhibit the growth of human breast cancer cells in animal models and cell lines, but the mechanism by which this occurs is not well understood."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=9816126
[RBs comment - this is an older trial in mice but does raise the issue of the role of omega sixes - which are essential to human health but many question have been raised as to the impact where omega three and six are significantly out of balance]
ABSTRACT
"We showed previously that a diet rich in linoleic acid (LA), an omega-6 fatty acid, stimulates the growth and metastasis of human breast cancer cells in athymic nude mice. In contrast, diets supplemented with eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), omega-3 fatty acids, exert suppressive effects."
kat in the delta
04-05-2007, 01:24 PM
Hi --I have been talking to a MD who is also a Nutritionist and and she informed me about a whole food not really an extra supplement but --for those of us who do NOT get enough: green veggies, fruit, or berries in our diets. This has LOTs of research and I know 5 MD's, and others who are NOW HEALTHIER because of it. Some of you may have heard about it..For those who haven't, go to this site and if possible somewhere there, mention you heard about it from Kathy in Mississippi. GO TO: www.juiceplusmed.com (http://www.juiceplusmed.com) Tell me what YOU think........kat in the MS delta
ps--you cannot buy it from a store--but if you'd like to order some please e-mail me: katcdale@yahoo.com ,and I will foward to DR. Kim. Thanks. kat in the delta
The best source is likely to be a very wide ranging diet of whole veg etc, but a practical level many of us do not achieve that so there is a school of thought that green supplements are useful to widen our diet etc.
There are lots
http://www.google.co.uk/search?client=firefox-a&rls=org.mozilla%3Aen-US%3Aofficial&channel=s&hl=en&q=green+foods&meta=&btnG=Google+Search
Green Frog is one of a number I have used.
http://www.vitacost.com/productResults.aspx?Ntk=products&ss=1&x=11&y=6&Ntt=green%20frog
The benefits of omega three are not restricted to potentially reducing the risk profile of BC. but are wide ranging including brain function.
Previous posts have included suggestions that cancerous brain cells have exhibited high levels of omega six.
Omega-3 fatty acids: evidence basis for treatment and future research in psychiatry.
Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17194275&query_hl=1&itool=pubmed_docsum
"The preponderance of epidemiologic and tissue compositional studies supports a protective effect of omega-3 EFA intake, particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in mood disorders."
RB
Please talk to your advisor about significant dietary change. Omega threes can cause blood thinning etc.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=12416257
Abstract
"We conclude that total n-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that LC n-3 PUFAs, derived from fish oils, may have a protective effect."
I have posted this result before but it is so striking I have included it again. It is based on comparing fat in breast tissue to whether or not lumps were invasive.
Women in the third with the highest levels of DHA had about 30% of the number of invasive results compared with the women in the third with the lowest levels of DHA.
Another trial suggests that the fat composition in the breast will change significantly in a few months with change in diet. Eg eat more omega three and less omega six and it will show up significantly in your breast tissue in a matter of months
As usual please discuss dietary changes with your advisors.
There are no definitive answers so I can only suggest you try and read round the subject a little too.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=11857389
ABSTRACT
Experimental studies have indicated that n-3 fatty acids, including alpha-linolenic acid (18:3 n-3) and long-chain n-3 polyunsaturated fatty acids inhibit mammary tumor growth and metastasis. Earlier epidemiological studies have given inconclusive results about a potential protective effect of dietary n-3 polyunsaturated fatty acids on breast cancer risk, possibly because of methodological issues inherent to nutritional epidemiology. To evaluate the hypothesis that n-3 fatty acids protect against breast cancer, we examined the fatty acid composition in adipose tissue from 241 patients with invasive, nonmetastatic breast carcinoma and from 88 patients with benign breast disease, in a case-control study in Tours, central France. Fatty acid composition in breast adipose tissue was used as a qualitative biomarker of past dietary intake of fatty acids. Biopsies of adipose tissue were obtained at the time of surgery. Individual fatty acids were measured as a percentage of total fatty acids, using capillary gas chromatography. Unconditional logistic regression modeling was used to obtain odds ratio estimates while adjusting for age, height, menopausal status and body mass index. We found inverse associations between breast cancer-risk and n-3 fatty acid levels in breast adipose tissue. Women in the highest tertile of alpha-linolenic acid (18:3 n-3) had an odds ratio of 0.39 (95% confidence intervals [CI] = 0.19-0.78) compared to women in the lowest tertile (trend p = 0.01). In a similar way, women in the highest tertile of docosahexaenoic acid (22:6 n-3) had an odds ratio of 0.31 (95% CI = 0.13-0.75) compared to women in the lowest tertile (trend p = 0.016). Women in the highest tertile of the long-chain n-3/total n-6 ratio had an odds ratio of 0.33 (95% confidence interval = 0.17-0.66) compared to women in the lowest tertile (trend p = 0.0002). In conclusion, our data based on fatty acids levels in breast adipose tissue suggest a protective effect of n-3 fatty acids on breast cancer risk and support the hypothesis that the balance between n-3 and n-6 fatty acids plays a role in breast cancer. Copyright 2001 Wiley-Liss, Inc.
PMID: 11857389 [PubMed - indexed for MEDLINE]
Here is a good review of omega 3 from MD anderson
http://www.mdanderson.org/departments/cimer/display.cfm?id=467db095-402c-491c-bca3175c121ad450&method=displayfull&pn=6eb86a59-ebd9-11d4-810100508b603a14
Thank you DNG.
It is indeed a very useful and informative resource - a recommended bookmark and skim / read.
RB
RobinP
04-20-2007, 10:08 AM
I just found this article to have sound physiological reasons for why diet and lifestyle MAY help to prevent breast cancer. I think that some of us, with some of the worse genes, would still get bc no matter what, then others may benifit from lifestyle changes. Personally, I think one of the biggest reasons for bc since the 1940s has been due to environmental estrogen drugs found in food and in human medication sources such as the pill, oxytocin, plastics, HRT for the older than 50 yr. old,etc. Still, that doesn't mean that a good diet may help to prevent or lessen the aggressieness of the bc.
Foods alter the way we express our genes (switch on and the number we switch on and where) and that includes Her2 BRAC1 etc.
Expression can be dramatically changed by diet.
The China Study a book by T Colin Campbell about $25US makes thought provoking reading.
In essence much still to know but for HER 2
Omega three - good
Omega nine - good
low Omega six - good
Clearly as usual it is not that simple but the summary below adds to the weight of evidence that strict moderation of fat intake, balancing the omega threes and sixes and quality of intake are well worth serious consideration.
As usual if undertaking significant dietary change please talk to your advisers.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=17134970
ABSTRACT
CONCLUSIONS: i) These findings reveal that the omega-3 PUFA ALA suppresses overexpression of HER2 oncogene at the transcriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab- based immunotherapy. ii) Our results molecularly support a recent randomized double-blind placebo-controlled clinical trial suggesting that ALA may be a potential dietary alternative or adjunct to currently used drugs in the management of HER2-positive breast carcinomas. iii) Considering our previous findings demonstrating the <<HER2 upregulatory actions>> of the omega-6 PUFA linolenic acid (LA; 18:2n-6) and the <<HER2 down-regulatory actions >> of the omega-3 PUFA docosahexaenoic acid (DHA; 22:6n-3) and of the omega-9 monounsaturated fatty acid oleic acid (OA; 18:1n-9), it is reasonable to suggest that a low omega-6/omega-3 PUFA ratio and elevated MUFA levels, the two prominent <<fat features>> of the <<Mediterranean diet>>, should be extremely efficient at blocking HER2 expression in breast cancer cells.
Becky
04-29-2007, 07:19 AM
Bringing this to the top for Nancy d
Just bring this back for anybody new who may not have seen it.
RB
Heart Sutra
05-08-2007, 01:31 PM
Diet has been pretty well established to be of such individual affect, that an all encompassing dietary solution working for all people is rather unlikely. Of course, eating pretzels and malt balls is probably less helpful than eating a more balanced diet...
R.B. just curious as to your diagnosis and history, I don't see one added to your profile.
Thank you for being here and for offering all of the information that you do.
Kevin and Sue
Heart Sutra
I have previously openly declared I am a male with an interest in the impact of omega six and omega three on a range of conditions, functions of the body etc. I am strictly amateur but do read widely. I am learning too. I do try and practice what I suggest, but could do better.
I had a relative who died of BC. I had a lump excised which was not likely to be BC but could have been and the experience was thought provoking.
RE your comment - "that an all encompassing dietary solution working for all people is rather unlikely"
Our bodies all function at a basic level in very similar ways. The food you eat alters the way you express your genes - the number of copies you switch on including HER2 and BRAC.
Trials on other issues such as cardiac health have shown in general terms people respond similarly to a low fat low protein "healthy" diet, (following general recommendations above).
Our modern diet breaks so many of the basic rules that we are not talking about fine tuning - this is about the basics. We have evolved / been designed to live in an environment with a range of diets, but those never included refined foods, high levels of sugars, salt, trans fats, vegetable oils. These push the body outside its design parameters. The consequence is a greatly increased of range of conditions.
There is a strong argument that better diet for those who eat high levels of refined food...... will reduce the risk for all [some more than others and on the average]
Of course once you have the basics sorted out one could consider fine tuning but the problem is it is very difficult to know exactly what does what. Given we were used to a much wider variety than we have now and plants are a veritable natural pharmacy (a mixture of positive and negative both of which the body can use - to support, or utilise in its armoury) variety seems a good strategy.
The China Study (about $20 US new)
http://www.thechinastudy.com/about.html
It is a very though provoking read. I have questions as to whether his conclusions would have changed in any way if he had looked at the omega three six issues. He touches on fish as a protein source but there is not much on it either way in his book. (eg Eskimos would be a fish exception to the no protein rule) The fat that goes with meat protein is clearly an issue and strict moderation likely sensible as a minimum.
I would also highly recommend Smart Fats M Schmidt (there is a newer version) which is also very thought provoking.
RB
Just bringing this back up for new readers and adding a cross link to try and keep key material in one thread.
http://www.her2support.org/vbulletin/showthread.php?t=28215
RB
A useful diet link to add to the thread (also posted in articles of interest but putting a copy here makes it easier to find for those starting out)
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=526387
Nutrition and cancer: A review of the evidence for an anti-cancer diet
Michael S Donaldsoncorresponding author1
1Director of Research, Hallelujah Acres Foundation, 13553 Vantage Hwy, Ellensburg, WA 98926, USA
t has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (α-carotene, β-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures. When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.
Just to bump this up for any new visitors.
RB
Just bumping back up for those that might not have seen the thread.
RB
Lauriesh
08-07-2007, 05:28 AM
Bump
Laurie
Just bringing it back up for new members in case of interest
hutchibk
08-19-2007, 11:25 AM
Thanks for the bumps, as I had lost track of this thread and it is a very important one! I want to switch my entire diet (at least home cooked diet) to the healthiest aspects of Med/Greek. I have always loved the food, the freshness, the oils, etc...
The first trial you have seen before I think the rest a new here.
Just in case you have lost sight of the omega threes and sixes
RB
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17134970&ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
"These findings reveal that the omega-3 PUFA ALA suppresses overexpression of HER2 oncogene at the transcriptional level, which, in turn, interacts synergistically with anti-HER2 trastuzumab- based immunotherapy. ii) Our results molecularly support a recent randomized double-blind placebo-controlled clinical trial suggesting that ALA may be a potential dietary alternative or adjunct to currently used drugs in the management of HER2-positive breast carcinomas. iii) Considering our previous findings demonstrating the HER2 upregulatory actions of the omega-6 PUFA linolenic acid (LA; 18:2n-6) and the HER2 down-regulatory actions of the omega-3 PUFA docosahexaenoic acid (DHA; 22:6n-3) and of the omega-9 monounsaturated fatty acid oleic acid (OA; 18:1n-9), it is reasonable to suggest that a low omega-6/omega-3 PUFA ratio and elevated MUFA levels, the two prominent fat features of the Mediterranean diet, should be extremely efficient at blocking HER2 expression in breast cancer cells."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17311938&ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
"our results indicate that (n-3) FA modify the lipid composition of membrane rafts and alter EGFR signaling in a way that decreases the growth of breast tumors."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17571951&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
"Use of canola oil instead of corn oil in the diet may be a reasonable means to increase consumption of n-3 fatty acids with potential significance for slowing growth of residual cancer cells in cancer survivors."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17354239&ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
"In conclusion, we showed that erythrocyte compositions of specific fatty acids derived from fish intake, as biomarkers, are associated with lower risk of breast cancer, but further studies are needed to investigate mechanisms linked to the etiology. (c) 2007 Wiley-Liss, Inc."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17342305&ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
"Since DHA influences the product of a major tumour suppressor gene, this finding may contribute to the observation that high-fish consumption reduces the risk of breast cancer."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17052999&ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
"Our results support the premise that DHA and genistein exert complementary actions whilst genistein is antagonistic to AA for controlling PGE(2) production as well as invasiveness of MDA-MB-231 cells in culture by modulating the level of NFkappaB expression."
Just bumping this up and adding a few bits I came across by accident whilst looking for something else.
RB
CoQ10.
Very small numbers and not much detail but thought provoking.
Views on CoQ10 vary amongst oncologists so please discuss any supplementation with your advisor.
I simply seek to inform options.
RB
1: Clin Biochem. 2000 Jun;33(4):279-84.Click here to read Links
Coenzyme Q10 concentrations and antioxidant status in tissues of breast cancer patients.
Portakal O, Ozkaya O, Erden Inal M, Bozan B, Koşan M, Sayek I.
Department of Biochemistry, The Medical School of Osmangazi University, Eskişehir, Turkey. portakal@ada.net.tr
OBJECTIVES: An increasing amount of experimental and epidemiological evidence implicates the involvement of oxygen derived radicals in the pathogenesis of cancer development. Oxygen derived radicals are able to cause damage to membranes, mitochondria, and macromolecules including proteins, lipids and DNA. Accumulation of DNA damages has been suggested to contribute to carcinogenesis. It would, therefore, be advantageous to pinpoint the effects of oxygen derived radicals in cancer development. DESIGN AND METHODS: In the present study, we investigated the relationship between oxidative stress and breast cancer development in tissue level. Breast cancer is the most common malignant disease in Western women. Twenty-one breast cancer patients, who underwent radical mastectomy and diagnosed with infiltrative ductal carcinoma, were used in the study. We determined coenzyme Q10 (Q) concentrations, antioxidant enzyme activities (mitochondrial and total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase), and malondialdehyde (MDA) levels in tumor and surrounding tumor-free tissues. RESULTS: Q concentrations in tumor tissues significantly decreased as compared to the surrounding normal tissues (p < 0.001). Higher MDA levels were observed in tumor tissues than noncancerous tissues (p < 0.001). The activities of MnSOD, total SOD, GSH-Px and catalase in tumor tissues significantly increased (p < 0.001) compared to the controls. CONCLUSIONS: These findings may support that reactive oxygen species increased in malignant cells, and may cause overexpression of antioxidant enzymes and the consumption of coenzyme Q10. Increased antioxidant enzyme activities may be related with the susceptibility of cells to carcinogenic agents and the response of tumor cells to the chemotherapeutic agents. Administration of coenzyme Q10 by nutrition may induce the protective effect of coenzyme Q10 on breast tissue.
PMID: 10936586 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=7612003&ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Progress on therapy of breast cancer with vitamin Q10 and the regression of metastases.
Lockwood K, Moesgaard S, Yamamoto T, Folkers K.
Pharma Nord, Vejle, Denmark.
Over 35 years, data and knowledge have internationally evolved from biochemical, biomedical and clinical research on vitamin Q10 (coenzyme Q10; CoQ10) and cancer, which led in 1993 to overt complete regression of the tumors in two cases of breast cancer. Continuing this research, three additional breast cancer patients also underwent a conventional protocol of therapy which included a daily oral dosage of 390 mg of vitamin Q10 (Bio-Quinone of Pharma Nord) during the complete trials over 3-5 years. The numerous metastases in the liver of a 44-year-old patient "disappeared," and no signs of metastases were found elsewhere. A 49-year-old patient, on a dosage of 390 mg of vitamin Q10, revealed no signs of tumor in the pleural cavity after six months, and her condition was excellent. A 75-year-old patient with carcinoma in one breast, after lumpectomy and 390 mg of CoQ10, showed no cancer in the tumor bed or metastases. Control blood levels of CoQ10 of 0.83-0.97 and of 0.62 micrograms/ml increased to 3.34-3.64 and to 3.77 micrograms/ml, respectively, on therapy with CoQ10 for patients A-MRH and EEL.
PMID: 7612003 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=7908519&ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
1: Biochem Biophys Res Commun. 1994 Mar 30;199(3):1504-8.Click here to read Links
Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10.
Lockwood K, Moesgaard S, Folkers K.
Pharma Nord, Vejle, Denmark.
Relationships of nutrition and vitamins to the genesis and prevention of cancer are increasingly evident. In a clinical protocol, 32 patients having -"high-risk"- breast cancer were treated with antioxidants, fatty acids, and 90 mg. of CoQ10. Six of the 32 patients showed partial tumor regression. In one of these 6 cases, the dosage of CoQ10 was increased to 390 mg. In one month, the tumor was no longer palpable and in another month, mammography confirmed the absence of tumor. Encouraged, another case having a verified breast tumor, after non-radical surgery and with verified residual tumor in the tumor bed was then treated with 300 mg. CoQ10. After 3 months, the patient was in excellent clinical condition and there was no residual tumor tissue. The bioenergetic activity of CoQ10, expressed as hematological or immunological activity, may be the dominant but not the sole molecular mechanism causing the regression of breast cancer.
PMID: 7908519 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=PubMed&Cmd=ShowDetailView&TermToSearch=9177262&ordinalpos=16&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
1: Biochem Biophys Res Commun. 1997 May 19;234(2):296-9.Click here to read Links
Activities of vitamin Q10 in animal models and a serious deficiency in patients with cancer.
Folkers K, Osterborg A, Nylander M, Morita M, Mellstedt H.
Institute for Biomedical Research, University of Texas at Austin, 78712, USA.
New data on blood levels of vitamin Q10 in 116 cancer patients reveal an incidence of 23.1% of patients (N=17) with breast cancer whose blood levels were below 0.5 microg/ml. The incidence of breast cancer cases with levels below 0.6 microg/ml was 38.5%. The incidence is higher (p<0.05) than that for a group of ordinary people. Patients (N=15) with myeloma showed a mean blood level of 0.67 +/- 0.17 microg/ml. The incidence of a vitamin Q10 blood level below 0.7 microg/ml for these 15 cases of myeloma was 53.3%, which is higher (p<0.05) than the 24.5% found for a group of ordinary people.
PMID: 9177262 [PubMed - indexed for MEDLINE]
Just bumping this thread up again.
This is a link I found recently which is by the renowned expert AP Simopoulos.
Only the first section is free. It is well worth reading. It really emphasises the need to balance the omega three and sixes.
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=showproducts&ProduktNr=229515&searchWhat=books&searchParm=toc
It is great to see this thread is slowly building up a significant number of hits. It would be interesting to know now many come from outside the board so hopefully bringing in new visitors.
Thank you for your interest.
R.B.
Balancing the omega 3s and 6s - why - an experts explanation.
William Lands in a hero in the lipids world and continues to press his cause.
Eicosanoids are chemicals made from the omega three and sixes families that are huegely influential in the body. The chemicals are unique to each fat. It is a complex subject but you do not need to know the detail to get the gist that balancing the omega threes and sixes is a good risk reduction policy as part of a dietary strategy.
As always please discuss dietary change with your doctor.
The video below is worth looking at if you have the time. (about 18 mins)
One senses from the video that William Lands is an inspirational character.
RB
http://videocast.nih.gov/ram/crii01c303202000.ram
Monday, March 20, 2000
Author/Sponsor: Bill Lands, Ph.D., Senior Advisor, NIAAA, NIH
Total Running Time: 00:18:45
Bandwidth: 146 Kbps
This is a work of the United States Government. No copyright exists on this material.
If you enjoyed that last video lecture you may enjoy this.
I only found it recently. It is fascinating for those who are interested.
Thank you Professor White for an excellent and fascinating lecture.
http://videocast.nih.gov/ram/crii01c303202000.ram
It is more technical but it does emphasise the power and importance of omega three and particularly the products of omega six. You don't need to understand it all just to understand how important they are in the body. Don't worry to much about the terminology they are just all omega six chemical products.
It is understandable.
n3 = omega three
n6 = omega six
Eicosanoids = omega three or six chemicals.
Arachidonic acid = child of omega six (long chain omega six equivalent to EPA)
It also gives an inkling as to how wondrous it all is and why it is necessary to give the body the raw material it needs as substitutes wont work the same way.
Note the slide at the end where for the pathway under consideration DHA is a more effective cox blocker than many drugs.
Other pathways in the same family connect into blood vessel growth and oestrogen levels, and hence the relevance to BC, and why it is now beginning to be suggested that Cox blockers may reduce the BC risk.
It is complicated.
So the message is as ever to reduce the risk profile of a number of conditions including BC balance your omega threes and sixes within reasonable limits and ensure a supply of long chain omega threes.
Please discuss dietary change with your medical advisor.
RB
Benefits of omega threes again.
This also looks at saturated fats and it appears some saturated fats are associated with a lower risk of BC but I have not seen the full report as it is pay for view.
RB
Apr 2007
Erythrocyte fatty acids and breast cancer risk: a case-control study in Shanghai, China.
Shannon J, King IB, Moshofsky R, Lampe JW, Gao DL, Ray RM, Thomas DB.
Center for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, Portland, OR,
Abstract
"CONCLUSION: Our results support a protective effect of n-3 fatty acids on breast cancer risk and provide additional evidence for the importance of evaluating the ratio of fatty acids when evaluating diet and breast cancer risk."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17413110&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus
This emphasises the difference between oils with differing omega three content.
Unfortunately no information is given on the omega six content of the oils used.
RB
Dietary canola oil suppressed growth of implanted MDA-MB 231 human breast tumors in nude mice.
Hardman WE.
The Department of Biochemistry and Microbiology, Marshall University School of Medicine, Huntington, West Virginia 25701, USA. hardmanw@marshall.edu
Abstract
"Use of canola oil instead of corn oil in the diet may be a reasonable means to increase consumption of n-3 fatty acids with potential significance for slowing growth of residual cancer cells in cancer survivors."
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17571951&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
EPA and DHA act as Cox 2 blockers.
Genistein acts as a Cox blocker.
Genistein acts synergistically with DHA.
AA the daughter omega six increased invasiveness as one would expect.
Genistein with omega threes uprates PPAR gamma which feature is in BC but I cannot remember how - or what relation this bears to omega six. So a ?? for the moment.
Genistein is an active ingredient in soy. There is much discussion if soy is good or bad.
So on balance more ticks for omega threes, crosses for omega six and a maybe for genestein via soy.
RB
Complementary actions of docosahexaenoic acid and genistein on COX-2, PGE2 and invasiveness in MDA-MB-231 breast cancer cells.
Horia E, Watkins BA.
Center for Enhancing Foods to Protect Health, Lipid Chemistry and Molecular Biology Laboratory, Purdue University, West Lafayette, IN 47907, USA.
Abstract
"The n-3 PUFA and genistein alone lowered PGE(2) concentration, and genistein in combination with AA reversed the high level of this prostanoid in cell cultures enriched with AA. The degree of cell invasiveness was reversed by genistein in cell cultures treated with AA and further reduced in those given DHA. The n-3 PUFA, in contrast to AA, reduced COX-2 and NFkappaB expression. Genistein combined with AA reversed the effects of AA alone on the expression of COX-2 and NFkappaB. All three fatty acids increased the expression of PPARgamma in the cells only when combined with genistein. Our results support the premise that DHA and genistein exert complementary actions whilst genistein is antagonistic to AA for controlling PGE(2) production as well as invasiveness of MDA-MB-231 cells in culture by modulating the level of NFkappaB expression."
AndiBB pointed me to this trial. Thanks
Omega threes from whole fish are more effectively incorporated than fish oil.
Whole food sources have to be the best starting point.
This has to be balanced with the pollution issues dealt with in earlier parts of this thread.
And the good news is the fish oil is taken up.
I wonder if it varies with how and with what the fish oil is taken?
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17269556&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
1: Lipids. 2006 Dec;41(12):1109-14.Links
Enhanced incorporation of n-3 fatty acids from fish compared with fish oils.
Elvevoll EO, Barstad H, Breimo ES, Brox J, Eilertsen KE, Lund T, Olsen JO, Osterud B.
Norwegian College of Fishery Science, Department of Marine Biotechnology, University of Tromsø, Norway. edel.elvevoll@nfh.uit.no
"In conclusion, fish consumption is more effective in increasing serum EPA and DHA than supplementing the diet with fish oil."
Lipid raft is a description of a gang of fats that work as a unit in the cell membrane.
More potential benefts for omega three 3 and that omega six in large quantities has a negative impact.
RB
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17311938&ordinalpos=233&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
1: J Nutr. 2007 Mar;137(3):548-53.Click here to read Links
Comment in:
J Nutr. 2007 Mar;137(3):545-7.
(n-3) PUFA alter raft lipid composition and decrease epidermal growth factor receptor levels in lipid rafts of human breast cancer cells.
Schley PD, Brindley DN, Field CJ.
Department of Agricultural, Food, and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2P5.
To determine the mechanism by which the (n-3) fatty acids (FA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) decrease proliferation and induce apoptosis in MDA-MB-231 human breast cancer cells, we examined the effects of EPA and DHA on the lipid composition of lipid rafts as well as epidermal growth factor receptor (EGFR) raft localization and phosphorylation. (n-3) FA (a combination of EPA and DHA) inhibited (P < 0.05) the growth of MDA-MB-231 cells by 48-62% in the presence and absence, respectively, of linoleic acid (LA). More EPA and DHA were incorporated into lipid rafts isolated from MDA-MB-231 cells after treatment with (n-3) FA compared with cells treated with LA (P < 0.05). EPA and DHA treatment decreased (P < 0.05) lipid raft sphingomyelin, cholesterol, and diacylglycerol content and, in the absence of LA, EPA and DHA increased (P < 0.05) raft ceramide levels. Furthermore, there was a marked decrease in EGFR levels in lipid rafts, accompanied by increases in the phosphorylation of both EGFR and p38 mitogen-activated protein kinase (MAPK), in EPA+DHA-treated cells (P < 0.05). As sustained activation of the EGFR and p38 MAPK has been associated with apoptosis in human breast cancer cells, our results indicate that (n-3) FA modify the lipid composition of membrane rafts and alter EGFR signaling in a way that decreases the growth of breast tumors.
PMID: 17311938 [PubMed - indexed for MEDLINE]
Another one for the omega three collection :)
: Nutr Cancer. 1995;24(2):151-60.Links
Fatty acid composition of breast adipose tissue in breast cancer patients and in patients with benign breast disease.
Zhu ZR, Agren J, Männistö S, Pietinen P, Eskelinen M, Syrjänen K, Uusitupa M.
Department of Clinical Nutrition, University of Kuopio, Finland.
Fatty acid composition of triglycerides (TGs) and phospholipids (PLs) in breast adipose tissue was analyzed in 73 female breast cancer patients and 55 patients with benign breast disease. No differences were observed in the dietary intake of the major fatty acids (i.e., palmitic, stearic, oleic, and linoleic acids) or in the proportion of TGs and PLs in breast adipose tissue between the two groups. In postmenopausal women, however, the dietary intake of eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) was significantly lower in the breast cancer patients than in patients with benign breast disease. Accordingly, the percentage of docosahexaenoic acid of PLs in breast adipose tissue was significantly lower in breast cancer patients than in patients with benign breast disease among postmenopausal women. The stage of the breast cancer did not contribute to the observed alterations of fatty acid composition of PLs. Consonant with the previous epidemiologic data, the present results suggest that intake of the long-chain n-3 fatty acids (mainly derived from fish) may have a protective effect against breast cancer, particularly in postmenopausal women.
PMID: 8584451 [PubMed - indexed for MEDLINE]
Poor mice. May their lot not be in vain.
Thought provoking I think it is fair to say.
RB
http://archives.foodsafetynetwork.ca/ffnet/2005/4-2005/ffnet_april_20.htm#story1
Mother's prenatal and lactational diet may protect daughters from breast cancer
April 20, 2005
American Association for Cancer Research
Anaheim, Calif. – Mothers who eat foods rich in omega-3 fatty acids during pregnancy and while nursing, and who continue to feed their babies such a diet after weaning, may reduce their daughters' risk of developing breast cancer later in life dramatically, according to research presented here today at the 96th Annual Meeting of the American Association for Cancer Research. Either maternal or post-weaning dietary consumption of this type of fat – that is, taking in omega-3 fatty acids through food or supplements at any point in life from conception to at least puberty – also could reduce the incidence rate for breast cancer in female offspring significantly.
Conversely, mothers' consumption of omega-6 fats commonly found in Western diets could increase their daughters' risk of breast cancer.
"Diet matters, Mom," said W. Elaine Hardman, Ph.D., an assistant professor in the Division of Functional Foods at the Pennington Biomedical Research Center, Louisiana State University, Baton Rouge. "Inadvertently, we may be setting up our daughters to develop breast cancer 50 years from now."
Both omega-6 and omega-3 fatty acids are essential for human health; however, particularly in the Western hemisphere, omega-6 fatty acids far exceed omega-3 fatty acids in the typical diet. Meat, eggs, poultry, cereals, breads, baked goods, most vegetable oils, and margarine are among dietary sources of omega-6 fatty acids.
Omega-3 fatty acids occur most commonly in fish – especially cold-water fish such as tuna, salmon and mackerel – as well as in canola and flaxseed oils, soybeans and nuts.
Hardman based her hypothesis on existing research showing that maternal diets containing high amounts of omega-6 fatty acids increase maternal estrogen levels; increased maternal estrogen, in turn, has been linked to an increased incidence of breast cancer among female offspring.
Meanwhile, many foods rich in omega-3 fatty acids are known to block the effects of estrogen and boost immunity.
Working with mice bred with a genetic predisposition to develop breast cancer, Hardman compared the incidence rates for the disease in offspring depending upon theirs and their mothers' relative consumption of diets either high in omega-6 fatty acids, or high in omega-3 fatty acids.
The genetic make-up of the female mice was such that all would develop hyperplasia; that is, to grow too many normal cells, in the mammary ducts, by three months of age. By six months, that hyperplasia would progress to mammary adenocarcinoma.
The mice were bred and the mothers were fed diets high in either omega-6 fatty acids or high in omega-3 fatty acids, both during the gestation period and while breast-feeding the female young. After the daughters were weaned, one group was placed on a high-omega-6 fatty acid diet, while the other was fed predominantly omega-3 fatty acids.
In Hardman's experiment, all the young exposed only to omega-6 fatty acids, in utero, in nursing and after weaning, showed mammary gland tumors by six months of age. Conversely, fewer than 60 percent of the female offspring who ate richly of high omega-3 fatty acids either maternally or post-weaning formed mammary tumors by the age of eight months. Those exposed to omega-3 fatty acids both maternally and after weaning had a tumor incidence rate of just 13 percent.
The beauty of the mouse model, Hardman explains, is the ability it gives researchers to collapse an entire life-span into a matter of months, instead of years. By using mice programmed genetically to develop tumors in the mammary glands eliminates the element of chance.
Harman has observed suppression of tumor growth with as little as two percent omega-3 fatty acids in the diet.
"A couple of servings a week may be enough," she said. "A quarter of a cup of walnuts constitutes one serving."
For pregnant women who are concerned about ingesting mercury in fish, Hardman recommends fish oil supplements, readily available in grocery, drug and health food stores. The fish oil in supplements is well purified.
I posted this in response to another post, but felt it was sufficiently important to post here too.
I reiterate this is a ? and no more. I have seen many trials that suggest benefits of canola. Everything is about balance and choice.
I went on a canola hunt based on a caveat I read by Mary G. Enig, PhD is an expert of international renown in the field of lipid biochemistry. "It's true that these oils provide omega-3 fatty acids but there are other things wrong with them. Hemp oil contains the active ingredients of marijuana and these cannabinoids can show up in the urine of people who consume hemp oil. Supposedly heart-healthy canola oil causes unfavorable changes in blood lipids, vitamin E deficiencies and heart lesions in test animals." http://www.westonaprice.org/bookreviews/smartfats.html
These trials were on the basis of canola as a sole source. I have not seen the full report.
I have seen many trials showing benefits with canola.
There is no explanation as to why.
I just have to leave you with with a ? I highlight the "supposedly" as it may be Mary Enig is doing the same thing.
1: Toxicology. 2000 May 5;146(2-3):197-208.Links
Dietary intake of rapeseed oil or soybean oil as the only fat nutrient in spontaneously hypertensive rats and Wistar Kyoto rats - blood pressure and pathophysiology.
Naito Y, Yoshida H, Nagata T, Tanaka A, Ono H, Ohara N.
Department of Pharmacology, Hatano Research Institute, Food and Drug Safety Center, Ochiai 729-5, Hadano, Kanagawa, Japan.
Spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats were fed a diet containing 10% rapeseed (canola) oil or soybean oil as dietary fat, and given drinking water containing 1% NaCl for 26 weeks. From the 10th week and later, systolic blood pressure in the canola oil group became higher than that in the soybean oil group in each strain. The 26-week feeding of canola oil increased plasma lipids and the neutrophil counts, and decreased the platelet counts. In the canola oil group the heart and kidney tended to become heavier with sporadically found histologic lesions. Acetylcholine- and nitroprusside-induced dilating responses of isolated aortic rings and norepinephrine- and veratridine-induced increases in vascular tone of isolated perfused mesenteric arteries were not different between the two groups in each strain. These results demonstrate that canola oil intake as the only dietary fat elevates blood pressure of the rat provided with drinking water containing 1% NaCl through mechanisms other than blunt dilating response of the blood vessel due to dysfunction of the endothelium or vascular smooth muscle, the augmented response to norepinephrine in the arteries and the increased amount of norepinephrine in the sympathetic nerve endings. The lesions in the heart and kidney in SHR may be related to a strain-specific peripheral vascular deterioration which was disclosed by the extremely high blood pressure in the canola oil group.
PMID: 10814852 [PubMed - indexed for MEDLINE]
Related Links
* Thirteen-week dietary intake of rapeseed oil or soybean oil as the only dietary fat in Wistar Kyoto rats-change in blood pressure. [Food Chem Toxicol. 2000]
* Rapeseed oil ingestion and exacerbation of hypertension-related conditions in stroke prone spontaneously hypertensive rats. [Toxicology. 2003]
* Increase in blood pressure with enhanced Na+, K+ -ATPase activity in stroke-prone spontaneously hypertensive rats after 4-weeks intake of rapeseed oil as the sole dietary fat. [Pharmacol Toxicol. 2000]
* Changes of blood pressure in spontaneously hypertensive rats dependent on the quantity and quality of fat intake. [Biomed Biochim Acta. 1985]
* Effects of long-term intake of edible oils on hypertension and myocardial and aortic remodelling in spontaneously hypertensive rats.
This is the result of a search on hempseed and canaboids. (See previous post)
I had previously seen suggestions that hempseed products could show up in drugs tests which had caused problems.
I have seen trials that suggest dietary benefit.
This site claims there are no adverse effects
http://www.sixwise.com/newsletters/06/11/29/hemp_seed_the_misaligned_misunderstood_food_that_i s_possibly_one_of_the_healthiest_on_the_planet.htm
As was suggested trials show some of the active ingredient in found in oils, foods etc.
What the implications are I do not know.
http://www.ncbi.nlm.nih.gov/sites/en...RVAbstractPlus
http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/sites/en...RVAbstractPlus
1: J Pharm Biomed Anal. 2005 Jan 4;36(5):939-46.Links
A rapid and simple procedure for the determination of cannabinoids in hemp food products by gas chromatography-mass spectrometry.
Pellegrini M, Marchei E, Pacifici R, Pichini S.
Drug Research and Control Department, Istituto Superiore di Sanitá, V.le Regina Elena 299, 00161 Rome, Italy. manuela.pellegrini@iss.it
A rapid and simple procedure using liquid-liquid extraction and subsequent gas chromatographic mass-spectrometric detection has been developed for determination of Delta9-tetrahydrocannabinol (THC), cannabidiol (CBD) and cannabinol (CBN) in different hemp foods. After addition of Delta8-tetrahydrocannabinol as internal standard, both solid and liquid specimens were extracted with two volumes of 2 ml of hexane/isopropanol (9:1): Chromatography was performed on a fused silica capillary column and analytes were determined in the selected-ion-monitoring (SIM) mode. The method was validated in the range 1-50 ng/ml liquid samples or 1-50 ng/g solid samples for THC and CBN, and 2-50 ng/ml or ng/g for CBD. Mean recoveries ranged between 78.8 and 90.2% for the different analytes in solid and liquid samples. The quantification limits were 1 ng/ml or ng/g for THC and CBN and 2 ng/ml or ng/g CBD. The method was applied to analysis of various hemp foods. THC content in different products varied 50-fold, whereas CBN and CBD were absent in some samples and achieved hundreds of ng/ml or ng/g in others. The concentration ratio (THC + CBN)/CBD was used to differentiate between the phenotypes of cannabis plants in different specimens. Products possibly originating from drug-type cannabis plants were found in the majority of analyzed specimens.
This is a complex but informative review on the impact of polyunsaturated fats chemotherapy and radiation.
DHA leads to higher levels of oxidation by the mitchondria.
Fish oil seems to assist a number of treatments.
It is very complicated, much is unknown, but this is a useful article that you could show to your advisers if the omega threes and sixes are of interest.
Dietary Polyunsaturated Fatty Acids; Impact on Cancer Chemotherapy and Radiation. K A Conklin
http://www.thorne.com/media/essential_fatty_acids.pdf
RB
Andrea Barnett Budin
10-09-2007, 05:47 PM
Hi RB! Is it true that olive oil when heated (and cooked with) eliminates its' beneficial qualities? I heard an *expert* on TV say that. Have been following that advice, not cooking with it and destroying its benefits, only adding it to salad/using at room temp.
ALSO: Just wanted to note -- here or somewhere -- that my nut onc (nutritionist/oncologist) has told me not to eat LARGE fish, like tuna. The larger they are -- the longer they've been around to ingest mercury in waters. So I stick w/smaller fish, as he has explained the issue.
Andi
Looking forward to your book, Omega man!
Andi
Olive Oil heating
I have just replied to this but it has not appeared. :(
When looking at heating it is not just the fats but other compounds too like phenols.
The benefits of virgin olive oil come from both effect of oleic acid on the metabolism and other compounds.
In Summary
The industry view
http://www.oliveoilsource.com/cooking_olive_oil.htm
I liked the idea for a butter VOO spread contained in the above.
A more specialist view
http://pubs.acs.org/cgi-bin/abstract.cgi/jafcau/2002/50/i21/abs/jf020506w.html
Yes some damage and it reduces some phenols. Extended high temp cooking will damage fat content too.
VOO phenols have been suggested to reduce cancer risk.
I found a trial that said in plain language that phenol content was reduced by cooking but cannot refind it.
So cold best or add at end of cooking. For cooking better than most of the alternatives.
RB
Hi AndiBB,
Thank you for your kind words.
Re Fish size and pollution.
This is one for Fauxgypsy maybe?
My impression from general reading is that general feeling is that pollutant levels increase as one goes up the food chain, and like you understand that bigger longer living fish are more polluted in general terms.
But I am sure there are other factors too such as where the fish lived, and their feeding habits.
I have looked but have not yet found do not recall reading any papers (as against general articles) that answer this question, but feel sure they must exist. More reading required.
It all has to be taken in context of general background pollution through multiple sources including cleaning products, lotions and potions, chemicals on furnishings and unused clothes, incineration etc.
I have read on several occasions (and it is counter intuitive) that absorption through the skin of hormones toxins etc is much higher than through digestion. Digestion provides filtering and chemical treatment processes which reduce toxins, hormones ingested etc. So we are probably doing pretty well on our own :) without any help from the fish who never asked to be polluted in the first place.
It must be kept in perspective. There are very valid issues on consumption and pollution of fish, and careful informed choices have to be made. It was not the fish who put the pollutants there. Fish (unfortunately for them) provide a food source with real dietary benefit that is not really found elsewhere. (It is arguably time we gave greater emphasis to algal culture technology).
RB
Andrea Barnett Budin
10-12-2007, 10:21 AM
Thanks, RB. Some posts I could totally grasp, in layman's terms, in how do I transpose this information to real life. It is great to learn something new every day.
I think, as I believe you suggested, I will add olive oil at the end of cooking a dish, not to tamper too much w/its delicate flavor and benefits. And yes, none of us wants to be found w/PCPs in our blood, yet, depending on where you live, it is being reported to be so, more, or less, across the board. As Dr. Mitchell Gaynor discusses in his website, we must look at the pollutants in our environment, food chain, and so on. www.drgaynor.com (http://www.drgaynor.com/) In his interesting article (if you skim down) -- THE NEW WAR ON CANCER. AGAINST ALL CAUSES.
Congratulations Al Gore! Nobel Peace Prize. Wow! And good luck again RB on your book. Has to be a dream come true for you. The fruition of much labor and knowledge... Surely many will benefit from your endeavors, as we all do here. Lucky we have you amongst us.
Andi
<HR style="MARGIN-TOP: 10px">See what's new at AOL.com (http://www.aol.com/?NCID=AOLCMP00300000001170) and Make AOL Your (http://www.aol.com/mksplash.adp?NCID=AOLCMP00300000001169)
Thank you for the kind thought and encouragement AndiBB.
This trial result is intriguing in that it suggests the body may increase COX2 in response to an omega 3 shortage.
COX2 is the substance COX blocking drugs target.
The probable consequences of this in a high omega six world would be that the conversion ability of omega six products to the inflammatory chemicals including PGE2 would be increased.
COX2 is the substance used by the omega sixes to make the omega six family of inflammatory chemicals.
So another straw in the breeze that it is a sensible risk reduction strategy to balance omega three and six intake (as well as reducing the risk of bipolar disorder).
http://www.nature.com/mp/journal/v12.../4001887a.html
Dietary n-3 PUFA deprivation alters expression of enzymes of the arachidonic and docosahexaenoic acid cascades in rat frontal cortex
J S Rao1, R N Ertley1, J C DeMar Jr1, S I Rapoport1, R P Bazinet1 and H-J Lee1
Abstract
The finding that n-3 PUFA deprivation increases cPLA2, sPLA2 and COX-2 is opposite to what has been reported after chronic administration of anti-manic agents to rats and suggests that n-3 PUFA deprivation may increase susceptibility to bipolar disorder.
Omega six in vegetable oils in your diet is converted to arachidonic acid `AA' a member of the omega six family.
AA is converted by COX2 to products that show a relationship to breast and other cancers. The amount of these COX products your body produces is a function of how much omega six you eat. These products include the sex hormones through the aromatase pathways.
Omega three competes for and blocks conversion of AA by COX.
So the amount of omega three and six in your diet can impact on the COX2 pathways, and downstream direct or indirect products, including hormones.
RB
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17721268&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
COX-2 expression in invasive breast cancer: correlation with prognostic parameters and outcome.
Nassar A, Radhakrishnan A, Cabrero IA, Cotsonis G, Cohen C.
Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. anassar@emory.edu
"COX-2 expression is also associated with increased angiogenesis, lymph node metastasis, and Her2-neu overexpression. ". . . "In conclusion, COX-2 correlates with poor prognostic markers in breast cancer (large tumor size and high tumor grade), but not with outcome.". . .
An interesting paper linking stress to fat intake to the immune and inflammatory system. (I will also post to Greek Diet Thread as an interesting omega three six item)
RB
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=10807964
In humans, serum polyunsaturated fatty acid levels predict the response of proinflammatory cytokines to psychologic stress.
Maes M, Christophe A, Bosmans E, Lin A, Neels H.
Department of Psychiatry and Neuropsychology, University of Maastricht, Maastricht, The Netherlands.
"Psychologic stress in humans induces the production of proinflammatory cytokines, such as interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6), and that of the negative immunoregulatory cytokine, IL-10. An imbalance of omega6 to omega3 polyunsaturated fatty acids (PUFAs) in the peripheral blood causes an overproduction of proinflammatory cytokines."
"An imbalance in the omega6 to omega3 PUFA ratio appears to predispose humans toward an exaggerated Th-1-like response and an increased production of monocytic cytokines, such as TNF-alpha, in response to psychologic stress. The results suggest that increased omega3 PUFA levels may attenuate the proinflammatory response to psychologic stress."
Please do judge the article by its title.
It is a fascinating article looking at the links between, the immune system, inflammation, depression and stress, and importance of the omega three six balance. It is well worth a skim.
The article is about women post birth but the chemical agents and markers of inflammation and stress and the immune system figure in cancers too.
Cogitative therapy as part of the basket should not be disregarded. But equally I am not suggesting in any way that cogitative therapy should be considered other than what it is - a factor among many.
"One could even argue that cognitive therapy is anti-inflammatory. Two recent studies have demonstrated that negative beliefs, such as hostility, can increase the levels of proinflammatory cytokines – especially IL-6 [74,75]. Cognitive therapy is a treatment for depression with known efficacy [76]. The primary goal of cognitive therapy is to reduce negative cognitions. Since negative cognitions increase inflammation, reducing their occurrence will have physical effects as well – primarily reducing inflammation."
RB
A new paradigm for depression in new mothers: the central role of inflammation and how breastfeeding and anti-inflammatory treatments protect maternal mental health
Kathleen Kendall-Tackettcorresponding author1
1Family Research Laboratory, 126 Horton Social Science Center, 20 College Road, University of New Hampshire, Durham, New Hampshire, 03824, USA
file:///C:/Documents%20and%20Settings/Robert%20Andrew%20Brown/My%20Documents/Word%20Documents/RAB/Breast%20Cancer/Depression/PND%20Inflammation%20Immune%20system.htm
"PNI research suggests two goals for the prevention and treatment of postpartum depression: reducing maternal stress and reducing inflammation. Breastfeeding and exercise reduce maternal stress and are protective of maternal mood. In addition, most current treatments for depression are anti-inflammatory. These include long-chain omega-3 fatty acids, cognitive therapy, St. John's wort, and conventional antidepressants."
Just bringing this thread back up for any who may not have seen it.
RB
Again found whilst looking for something else!
They used 10 grams of fish oil a day which produced profound changes in plasma fatty acids. It also produced significant changes in fats in breast tissue.
Here is the link to the full article which is interesting. It looks at the idea the omega six three imbalance in the west is a significant fact in higher rates of BC.
Based on this article with supplementation and appropriate diet you can make a significant change to the fat profile of breast tissue in three months.
RB
http://jnci.oxfordjournals.org/cgi/reprint/89/15/1123
http://jnci.oxfordjournals.org/cgi/content/abstract/89/15/1123
Dietary modulation of omega-3/omega-6 polyunsaturated fatty acid ratios in patients with breast cancer
D Bagga, S Capone, HJ Wang, D Heber, M Lill, L Chap and JA Glaspy
Department of Medicine, School of Medicine, University of California at Los Angeles, 90095-6956, USA.
"Twenty- five women with high-risk localized breast cancer were enrolled in a dietary intervention program that required them to eat a low-fat diet and take a daily fish oil supplement throughout a 3-month period. Breast and gluteal fat biopsy specimens were obtained from each woman before and after dietary intervention."
"CONCLUSION: Short-term dietary intervention can lead to statistically significant increases in omega-3/omega-6 polyunsaturated fatty acid ratios in plasma and breast adipose tissue. Breast adipose tissue changed more rapidly than gluteal adipose tissue in response to the dietary modification tested in this study. Therefore, gluteal adipose tissue may not be a useful surrogate to study the effect of diet on breast adipose tissue. "
Mary Jo
12-09-2007, 07:15 AM
As always R.B., thank you for all the information you share with us. I always had the mentality "everything in moderation" and if that meant more sugar and less calories somewhere else so be it. Through all your wonderful information you share I see how wrong my thinkng always was.
Keep the information coming. We appreciate all you share with us.
Blessings and Peace to you R.B.
Mary Jo
Andrea Barnett Budin
12-09-2007, 03:11 PM
http://www.whfoods.com/nutrientchart.php?id=84
What are omega 3 fatty acids? THIS TOPIC IS SO IMPORTANT TO ALL OF US -- WE MUST TRY TO *INGEST* AS MUCH AS WE CAN OF THIS INFORMATION. Thought it was worth printing for us to easily access...
You've probably been hearing about omega 3 fatty acids in recent years. The reason? A growing body of scientific research indicates that these healthy fats help prevent a wide range of medical problems, including cardiovascular disease, depression, asthma, and rheumatoid arthritis.
Unlike the saturated fats found in butter and lard, omega 3 fatty acids are polyunsaturated. In chemistry class, the terms "saturated" and "polyunsaturated" refer to the number of hydrogen atoms that are attached to the carbon chain of the fatty acid. In the kitchen, these terms take on a far more practical meaning.
Polyunsaturated fats, unlike saturated fats, are liquid at room temperature and remain liquid when refrigerated or frozen. Monounsaturated fats, found in olive oil, are liquid at room temperature, but harden when refrigerated. When eaten in appropriate amounts, each type of fat can contribute to health. However, the importance of omega 3 fatty acids in health promotion and disease prevention cannot be overstated.
The three most nutritionally important omega 3 fatty acids are alpha-linolenic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).
Alpha-linolenic acid is one of two fatty acids traditionally classified as "essential." The other fatty acid traditionally viewed as essential is an omega 6 fat called linoleic acid. These fatty acids have traditionally been classified as "essential" because the body is unable to manufacture them on its own and because they play a fundamental role in several physiological functions. As a result, we must be sure our diet contains sufficient amounts of both alpha-linolenic acid and linoleic acid.
DIETARY SOURCES of alpha-linolenic acid include flaxseeds (http://www.whfoods.com/genpage.php?tname=foodspice&dbid=81), walnuts, hemp seeds, soybeans and some dark green leafy vegetables. Linoleic acid is found in high concentrations in corn oil, safflower oil, sunflower oil, and canola oil. Most people consume a much higher amount of linoleic acid than alpha-linolenic acid, which has important health consequences.
The body converts alpha-linolenic acid into two important omega 3 fats, eicosapentaenoic acid (EPA) and docosahexanoic acid (DHA). These fats can also be derived directly from certain foods, most notably cold-water fish including salmon, tuna, halibut, and herring. In addition, certain types of algae contain DHA. EPA is believed to play a role in the prevention of cardiovascular disease, while DHA is the necessary for proper brain and nerve development. How it Functions
What are the functions of omega 3 fatty acids?
Every cell in our body is surrounded by a cell membrane composed mainly of fatty acids. The cell membrane allows the proper amounts of necessary nutrients to enter the cell, and ensures that waste products are quickly removed from the cell. To perform these functions optimally, however, the cell membrane must maintain its integrity and fluidity. Cells without a healthy membrane lose their ability to hold water and vital nutrients. They also lose their ability to communicate with other cells. Researchers believe that loss of cell to cell communication is one of the physiological events that leads to growth of cancerous tumors.
Because cell membranes are made up of fat, the integrity and fluidity of our cell membranes is determined in large part by the type of fat we eat. Remember that saturated fats are solid at room temperature, while omega 3 fats are liquid at room temperature. Researchers believe that diets containing large amounts of saturated or hydrogenated fats produce cell membranes that are hard and lack fluidity. On the other hand, diets rich in omega 3 fats produce cell membranes with a high degree of fluidity.
In addition, recent in vitro (test tube) evidence suggests when omega 3 fatty acids are incorporated into cell membranes they may help to protect against cancer, notably of the breast. They are suggested to promote breast cancer cell apoptosis via several mechanisms including: inhibiting a pro-inflammatory enzyme called cyclooxygenase 2 (COX 2), which promotes breast cancer; activating a type of receptor in cell membranes called peroxisome proliferator-activated receptor (PPAR)-ã, which can shut down proliferative activity in a variety of cells including breast cells; and, increasing the expression of BRCA1 and BRCA2, tumor suppressor genes that, when functioning normally, help repair damage to DNA, thus helping to prevent cancer development.
Animal and test tube studies published in the November 2005 issue of the International Journal of Cancer suggest yet another way in which the omega-3 fatty acids found in cold water fish-docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)-help protect against breast cancer development.
All dietary fatty acids are incorporated into cell membranes, and the type of fatty acids dictates how a cell responds and grows. Researchers found that omega-3 fatty acids affect cell growth by activating an enzyme called sphingomyelinase, which then generates the release of ceramide, a compound that induces the expression of the human tumor suppressor gene p21, which ultimately causes cancer cell death. In the animal experiments, mice were fed diets rich in either omega-3 (fish oil) or omega-6 (corn oil) fatty acids after which breast cancer cells were implanted. Three weeks later, tumor volume and weight was significantly lower in mice on the omega-3 rich diet. In the lab culture experiments, when cells were treated with DHA or EPA, sphingomyelinase activity increased by 30-40%, and breast cancer cell growth dropped 20-25%.
Omega 3 fats also play an important role in the production of powerful hormone-like substances called prostaglandins. Prostaglandins help regulate many important physiological functions including blood pressure, blood clotting, nerve transmission, the inflammatory and allergic responses, the functions of the kidneys and gastrointestinal tract, and the production of other hormones.
In essence, all prostaglandins perform essential physiological functions. However, depending on the type of fat in the diet, certain types of prostaglandins may be produced in large quantities, while others may not be produced at all. This can set up an imbalance throughout the body that can lead to disease.
For example, EPA and DHA serve as direct precursors for series 3 prostaglandins, which have been called "good" or "beneficial" because they reduce platelet aggregation, reduce inflammation and improve blood flow. The role of EPA and DHA in the prevention of cardiovascular disease can be explained in large part by the ability of these fats to increase the production of favorable prostaglandins.
The omega 6 fats serve as precursors for series 1 and series 2 prostaglandins. Like the series 3 prostaglandins produced from omega 3 fats, series 1 prostaglandins are believed to be beneficial. On the other hand, series 2 prostaglandins are usually considered to be "bad" or "unhealthy," since these prostaglandins promote an inflammatory response and increase platelet aggregation. As a result, it is important to ensure proper balance of omega 3 and omega 6 fats in the diet. EPA Directly Anti-Inflammatory... A recently identified lipid (fat) product our bodies make from EPA, called resolvins, helps explain how this omega-3 fat provides anti-inflammatory effects on our joints and improves blood flow.
Resolvins, which have been shown to reduce inflammation in animal studies, are made from EPA by our cellular enzymes, and work by inhibiting the production and regulating the migration of inflammatory cells and chemicals to sites of inflammation. Unlike anti-inflammatory drugs, such as aspirin, ibuprofen and the COX-2 inhibitors, the resolvins our bodies produce from EPA do not have negative side effects on our gastrointestinal or cardiovascular systems.
Deficiency Symptoms... What are deficiency symptoms for omega 3 fatty acids?
Recent statistics indicate that nearly 99% of people in the United States do not eat enough omega 3 fatty acids. However, the symptoms of omega 3 fatty acid deficiency are very vague, and can often be attributed to some other health conditions or nutrient deficiencies.
Consequently, few people (or their physicians, for that matter) realize that they are not consuming enough omega 3 fatty acids. The symptoms of omega 3 fatty acid deficiency include fatigue, dry and/or itchy skin, brittle hair and nails, constipation, frequent colds, depression, poor concentration, lack of physical endurance, and/or joint pain. Individuals who have disorders involving bleeding, who bruise very easily, or who are taking blood thinners should consult with a medical practitioner before taking supplemental omega 3 fatty acids.
Polyunsaturated oils, including the omega 3 fats, are extremely susceptible to damage from heat, light, and oxygen. When exposed to these elements for too long, the fatty acids in the oil become oxidized, a scientific term that simply means that the oil becomes rancid.
Rancidity not only alters the flavor and smell of the oil, but it also diminishes the nutritional value. More importantly, the oxidation of fatty acids produces free radicals, which are believed to play a role in the development of cancer and other degenerative diseases.
As a result, oils rich in polyunsaturated fatty acids should be stored in dark glass, tightly closed containers in the refrigerator or freezer. In addition, these oils should never be heated on the stove. So, instead of sautéing your vegetables in flaxseed or walnut oil, make a salad dressing using these oils.
To increase the activity of your desaturase enzymes, be sure that your diet includes a sufficient amount of vitamin B6 (http://www.whfoods.com/genpage.php?tname=nutrient&dbid=108), vitamin B3 (http://www.whfoods.com/genpage.php?tname=nutrient&dbid=83), vitamin C (http://www.whfoods.com/genpage.php?tname=nutrient&dbid=109), magnesium (http://www.whfoods.com/genpage.php?tname=nutrient&dbid=75) and zinc (http://www.whfoods.com/genpage.php?tname=nutrient&dbid=115). In addition, limit your intake of saturated fat and partially hydrogenated fat, as these fats are known to decrease the activity of delta-6 desaturase. Also, to be on the safe side, consider including a direct source of EPA and DHA if your diet, such as wild-caught salmon, halibut, or tuna.
Omega 3 fatty acids may play a role in the prevention and/or treatment of the following health conditions:
Alzheimer's disease
Asthma
Attention deficit hyperactivity disorder (ADHD)
Bipolar disorder
Cancer
Cardiovascular disease
Depression
Diabetes
Eczema
High blood pressure
Huntington's disease
Lupus
Migraine headaches
Multiple sclerosis
Obesity
Osteoarthritis
Osteoporosis
Psoriasis
Rheumatoid arthritis
Salmon, flax seeds and walnuts are excellent sources of omega 3 fatty acids. Very good sources of these healthy fats include scallops, cauliflower, cabbage, cloves and mustard seeds. Good sources of these fats include halibut, shrimp, cod, tuna, soybeans, tofu, kale, collard greens, and Brussels sprouts. What are current public health recommendations for omega 3 fatty acids?
In 2002, the Institute of Medicine at the National Academy of Sciences issued Adequate Intake (AI) levels for linolenic acid, the initial building block for all omega 3 fatty acids found in the body. For male teenagers and adult men, 1.6 grams per day were recommended, For female teenagers and adult women, the recommended amount was 1.1 grams per day. These guidelines do not seem as well-matched to the existing health research on omega 3 fatty acids as guidelines issued by the Workshop on the Essentiality of and Recommended Dietary Intakes (RDI) for Omega-6 and Omega-3 Fatty Acids in 1999 sponsored by the National Institutes of Health (NIH). This panel of experts recommended that people consume at least 2% of their total daily calories as omega-3 fats. To meet this recommendation, a person consuming 2000 calories per day should eat sufficient omega-3-rich foods to provide at least 4 grams of omega-3 fatty acids.
This goal can be easily met by adding just two foods to your diet: flaxseeds (http://www.whfoods.com/genpage.php?tname=foodspice&dbid=81) and wild-caught salmon. Two tablespoons of flaxseeds contain 3.5 grams of omega 3 fats, while a 4 ounce piece of salmon contains 1.5 grams of omega 3 fats.
Vegans and vegetarians relying on ALA as their only source of omega-3 fatty acids should increase their consumption of ALA-rich foods accordingly to ensure sufficient production its important derivatives, EPA and DHA.
Personally, though I try to eat right, according to the info above, and allowing for my IBS issue (since Taxotere and I met up) -- I rely on supplements to keep me at healthy peak. We must each do the best we can...Andi http://cdn-cf.aol.com/se/smi/0201e05fca/06
I am sorry this page seems to have stretched.
Does anybody know how to fix it. I have looked but cannot see anything that helps.
<img src="http://digilander.libero.it/le.faccine/faccinea/cartelli/statici/1072.gif" alt="Oops 2" />
Andrea Barnett Budin
12-10-2007, 01:57 PM
OH DEAR. I HOPE IT WASN'T MY LONGGGG POST THAT MESSED SOMETHING UP. SORRY. http://cdn-cf.aol.com/se/smi/0201e05fca/03 I HAVEN'T A CLUE WHAT TO DO, OR EVEN TO SEE WHAT IS WRONG...
RB, DID YOU TRY TO POST SOMETHING THAT ISN'T APPEARING?
Andi
Hi Andi BB
No I am sure it is nothing to do with you. It may be just the way it is displaying on my screen.
Thanks for your post which was interesting.
Hi Andi BB,
I posted this yesterday and it seems to have got lost or I made an error <img src="http://www.world-of-smilies.com/html/images/smilies/computer/attachment-190.gif" alt="Sleeping 8" /> more likely!
NO it is not you it happened before your post. Maybe it is only on my system. The pages are now too wide to fit on the screen.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17571951&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Dietary canola oil suppressed growth of implanted MDA-MB 231 human breast tumors in nude mice.
Hardman WE.
The Department of Biochemistry and Microbiology, Marshall University School of Medicine, Huntington, West Virginia 25701, USA. hardmanw@marshall.edu
More evidence that improving the omega three <img src="http://www.world-of-smilies.com/wos_engel/wos_engell4.gif" alt="Good vs Evil 2" />six ratio improves risk of holding cancer in check.
RB
Andrea Barnett Budin
12-23-2007, 12:18 PM
More great news about OMEGA 3 / 6 RATIO for breast cancer! Thanks for that RB. I'm working on it.
I did have to laugh when I read the study on nude mice. Immediate reaction -- aren't they all nude? LOL... So I googled, for further info.
A nude mouse (http://en.wikipedia.org/wiki/Mouse) is a genetic mutant (http://en.wikipedia.org/wiki/Mutant) that has a deteriorated or removed thymus (http://en.wikipedia.org/wiki/Thymus) gland, resulting in an inhibited immune system (http://en.wikipedia.org/wiki/Immune_system) due to a greatly reduced number of T cells (http://en.wikipedia.org/wiki/T_cells). The phenotype, or main outward appearance of the mouse is a lack of body hair, which gives it the "nude" nickname. The nude mouse is valuable to research because it can receive many different types of tissue and tumor grafts, as it mounts no rejection (http://en.wikipedia.org/wiki/Rejection) response. These xenografts (http://en.wikipedia.org/wiki/Xenografts) are commonly used in research to test new methods of imaging and treating tumors. The genetic basis of the nude mouse mutation is a disruption of the FOXN1 gene [1] (http://jaxmice.jax.org/info/bulletin/bulletin06.html)[2] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=OMIM&dopt=Detailed&tmpl=dispomimTemplate&list_uids=600838).
RB, love your recent discovery of moving doodads...
A bit of fun is good for the Soul. Thanks... Andi http://cdn-cf.aol.com/se/clip_art/peeps-emt/babes-kids/clips/clip-girl
<img src="http://img52.exs.cx/img52/852/mousecheese20gm.gif" alt="Mouse" />Poor little mice. Thanks for clarifying that Andi. May they not die in vain for us.
This is an excellent understandable informative article.
Please discuss dietary changes with your doctor. Fish oil may cause blood thinning and other effects which are an issues for some.
This article may be of interest to your doctor.
RB
http://arthritis-research.com/content/8/1/202
Fish oil: what the prescriber needs to know
Leslie G Cleland email, Michael J James email and Susanna M Proudman email
Rheumatology Unit, Royal Adelaide Hospital, North Terrace, Adelaide, Australia <img src="http://www.comicguide.net/images/smilies/biene.gif" alt="Bee 5" />
"The authors declare the following complementary interests. LGC and MJJ in particular have longstanding research interests in the health benefits of dietary ω3 fats. The Preventive Care Centre of the Royal Adelaide Hospital, under LGCs' direction, distributes fish oil for therapeutic use. SMP directs the Early Arthritis Clinic of the Royal Adelaide Hospital, in which therapeutic effects of fish oil are under evaluation."
"There is a general belief among doctors, in part grounded in experience, that patients with arthritis need nonsteroidal anti-inflammatory drugs (NSAIDs). Implicit in this view is that these patients require the symptomatic relief provided by inhibiting synthesis of nociceptive prostaglandin E2, a downstream product of the enzyme cyclo-oxygenase (COX), which is inhibited by NSAIDs. However, the concept of 'safe' NSAIDs has collapsed following a multiplicity of observations establishing increased risk for cardiovascular events associated with NSAID use, especially but not uniquely with the new COX-2-selective NSAIDs. This mandates greater parsimony in the use of these agents. Fish oils contain a natural inhibitor of COX, reduce reliance on NSAIDs, and reduce cardiovascular risk through multiple mechanisms. Fish oil thus warrants consideration as a component of therapy for arthritis, especially rheumatoid arthritis, in which its symptomatic benefits are well established. A major barrier to the therapeutic use of fish oil in inflammatory diseases is ignorance of its mechanism, range of beneficial effects, safety profile, availability of suitable products, effective dose, latency of effects and instructions for administration. This review provides an evidence-based resource for doctors and patients who may choose to prescribe or take fish oil."
"Safe limits of long chain n3 polyunsaturated fatty acid ingestion"
"A dose of 3 g/day EPA plus DHA has been assessed as safe for general consumption [40]. ....."[/SIZE][/SIZE][/SIZE]
Mary Jo
01-03-2008, 08:31 PM
Hello R.B.
Tonight I decided to go through this entire thread to read and try to absorb all the valuable information you provide for us here. And you kow what I realized when I finished - while my brain was swimming with information and my eyes are crossedhttp://www.her2support.org/vbulletin/images/icons/icon7.gif you are an AWESOME BLESSING to this board and what you provide for us is so awesome. Thank you for all this information.
I'm still trying to understand it all. I'm not sure I ever will. I've got it down to eating my grains - more veggies than fruit - taking my tablespoon of Nordic Natural's Cod Liver Oil w/D plus my separate D3 tablet each day - my calcium w/D, my magnesium, my folic acid and working on the rest. Still eat more sugar than I'd like - some days better than others - but working hard at it.
Reading through this thread re-motivated me and helped me understand a little bit more tonight.
Bascially just wanted to say thanks. From my heart to yours.
I wish there was a simple - eat this eat that - don't eat this and that. I suppose there is but it probably isn't as simple as I'd like it to be.
You really are the best R.B. So, thanks.
Mary Jo
nitewind
01-04-2008, 11:25 AM
Mary Jo, I'm with you, I wish there was just a simple list of "dos and don'ts". I've read this thread many, many times, I must be learning disabled because no matter how hard I try, I don't know what to do. Up until I finished my year of herceptin, my onc has told me to take nothing else, no supplements, no nothing. Now, I'm finished with treatment and I feel like I'm out here left dangling on my own. Should I be taking something? Should I not? I feel so lost, can someone maybe just start me out with something simple that I can start with? I would appreciate any help that I can get, it's all so confusing (of course, I've always confused easily). Please help
Susan
Mary Jo
01-04-2008, 12:43 PM
Susan,
Then I'm learning disabled as well http://her2support.org/vbulletin/images/icons/icon7.gif Glad I'm not alone. Haha!
Oh well, look at it this way....God made us "special" people as well.
Love & peace,
Mary Jo
PinkGirl
01-04-2008, 01:00 PM
Marejo and Nitewind,
I'll add my name to the list of the supplement-ally challenged.
Why can't someone just give us a basic list of what to take?
I don't like to put myself down so I'll add that, in spite of being supplement-ally challenged, I am good with hamsters and chocolate.
nitewind
01-04-2008, 01:04 PM
I'm very good with dogs and grandchildren!!
Hopefully, someone will slip in here and give us a hand.
Mary Jo
01-04-2008, 01:21 PM
Hahahahaha Pinkgirl......................................Oh I'm not putting myself down.....Just so happy I'm not alone on that "special or as some may call us "special needs" list!! Hehe!
Chocolate..............................I have my masters degree in chocolate. http://her2support.org/vbulletin/images/icons/icon7.gif
Mary Jo
Andrea Barnett Budin
01-04-2008, 04:10 PM
Mary Jo, Susan, Pinkie -- I too have a love/hate relationship w/this thread. It is brilliant and full of great information, but the words tend to blur as my eyes cross and I think, Why do I suddenly feel so stupid?
I have had the good fortune of being led to a wonderful oncologist who specializes in nutrition. His knowledge of supplements and the like is akin to the white bearded Andrew Weill, who we've all seen on television over the years. Weill is Harvard educated and I have found that his advice is much the same as my nut/onc. I google every suggestion Dr. Gaynor gives me and I educate myself. It is a job, but I will not simply take a pill b/c a doc, as much as I respect him and as brilliant as he is, tells me to do so.
Before bc I never took pills. I prided myself on that. Well, now I am at the opposite extreme, and I believe my supplement regimen has contributed to my survival as much as the surgeon's expertise and the chemo that eradicated the ca and the monoclonal antibody that is keeping me alive, w/mets at bay.
RB's understanding of the need for a balance of Omega 3s and 6s is astute and way above my head. But, in simple terms, rather than being balanced, the American diet is about 20 to 1 -- that's WAY TOO MUCH *OMEGA 6*. We need Omega 6 but not in such drastic amnts that we typically consume. So it is wise to familiarize yourself w/those foods and ingredients that are rich in Omega 3s, which are essential to good health and have a multitude of benefits, especially in fighting bc!!
To that end I posted #176 within this thread. Have you found it buried in this book of a thread? I think it might be helpful.
I also have a thread called GAINING CONTROL, w/reference to a sister thread. It is full of what I have learned since 1998 (when I met throughout my liver) from my nut/onc guru/healer. He has a unique frame of reference as a hematologist and an oncologist who specializes in nutritional supplements. I have been taking his suggested herbal supplements since '98, through chemo (Taxotere) to today (now in my 10th yr of taking Herceptin).
I began slowly. Taking a list of 10 and starting w/1. Waiting a few days to be sure I had no adverse reactions, then adding another. And so on. I goggled every one and took notes, so I knew exactly what I was ingesting and why. My GAINING CONTROL thread (which you can type into the SEARCH within the yellow bar at the top of page -- to get to) lists alphabetically every supplement I now have evolved to take, the dosage recommended by nut/onc and a brief explanation of why I take it). I will see this oncologist in April and my list will be updated. Some remain as staples (such an Co-Enzyme Q10 -- 150 X 2 a day) and others are replaced. OMEGA 3 and 6 are another standard I adhere to. I have increased the amnt I take, based on all the news I keep hearing on television about the benefits (in reports and on shows like the Today Show, interviewing experts in this field). We are now hearing much about our increased need for D3, in the 1000s. Even if we get exposed to sun daily, as we age our need increases, and the use of sunscreen blocks the benefits as they protect us. We must delve into this important area, to help us heal, keep our immune systems at peak levels to fight any invasion, protect our hearts, neutralize free radicals and reduce recurrence of cancer. NO SMALL MATTER, to be sure!
ALPHA LIPOIC ACID, GRAPESEED EXTRACT, GREEN TEA EXTRACT (or the real thing 3X a day), CARNITHANE, GLUTAMINE, LYSINE, NAC (N-Aceetyl Cysteine) and ZINC are all being touted by the experts lately I have noted, in addition to my own onc nut. My other oncs have not had a problem w/my taking these supplements
(since '98, including during, and especially because of, Taxotere chemo for 9 mnths and while taking Herceptin to date). One of my oncs asked, You're still taking all this s**t?! I give a copy of my list of every pill I take, including my prescribed meds to all my docs.
MAGNESIUM is important (200 mg for those w/problems w/diarrhea, 400 for those w/normal bowels, more if you have constipation issues). Studies are recently showing that certain chemo patients aren't properly absorbing this important nutrient. So that must be evaluated and addressed.
SELENIUM is essential to include.
Traditional docs haven't had a half day's worth of education on nutrition in their entire medical training and education. So they commonly resist what they do not know. Many think supplements and vitamins are a waste of money and effort. Personally, with IBS issues, I cannot eat many fruits, dairy products and such, so supplements are especially important to add to my diet safely, w/o repurcussions.
I hope this information is intelligible and helpful to you. I wish us all GOOD HEALTH! Many disciplines must go in to achieving that. RB does his best to keep us well informed. Hopefully others can chime in, in plain English, so we all may take advantage of this seemingly overwhelming flood of facts and data.
Andi http://cdn-cf.aol.com/se/smi/0201e05fca/06
Thanks Marejo your thoughts are really appreciated.
I wish I could give you all the answers you seek. If the answers were absolutely known we would all be doing it already!
The point of this thread is simply to try and demonstrate the HUGE importance of balancing the Omega 3s and 6s, and getting a supply of long chain Omega 3 as found in fish oil and oily fish primarily. (And not everybody agrees about that, which is why I simply truly and present the information so you can make up your own mind)
As to dosages there is a lack of consensus. Several suggest between 2 and 3 grams of EPA + DHA a day, but it ranges from 200mg.
Regrettably the same arguments rage over supplements.
Needless to say I would not be going on about omega 3s and 6s if I did not think it was a worthwhile thing to do.
Mary Jo
01-04-2008, 06:00 PM
Hi R.B. ~ Now that I understand wherein you are saying it's all something we would all be doing if we knew what exactly to do. I guess the long and short of it is ........... do your best. Eat healthy.....exercise..........get D3 into our bodies..............fish oil and as the saying goes............everything in moderation. Nothing this complicated could ever be easy and if the answers all were to be found in this area I guess more would be known. But still I say thanks to you. Although I am confused by much of what you bring to us, I also have learned much. Also I know your goal is to educate us so we can make the right choices for ourselves. That must come from a heart that is big......a heart that is kind..........and just a downright generous soul.http://her2support.org/vbulletin/images/icons/icon7.gif
And to you Andi.......................the whole time I was reading your post I'm thinking to myself...................."why is Andi calling the onc. she respects so much a "nut?".........." Hahahahahahahahaha! Honestly, I thought you were calling him a "nut" and as I got closer to the bottom of your post it hit me "nut = nutrionist!" Hahahahahahaha! See, I wasn't kidding when I said I was a "special needs" case. LOL!
Thanks everyone. Happy eating and happy supplement taking BUT please throw a bit of chocolate in their for good measure. Afterall, life is short ~ so live a little.http://her2support.org/vbulletin/images/icons/icon12.gif
Hugs,
Mary Jo
Andrea Barnett Budin
01-04-2008, 06:49 PM
Oh, I KNOW MARY JO. I USED TO CALL HIM MY NUTR/ONCOL (boring, huh?)and then a friend from Australia emailed me about my nut/onc. She has quite the wit! We agreed that that was likely what many of his peers see him as. We had a good laugh too! So, now my guru has become my nut onc. In tribute to my astute and humorous friend and Sister Warrior/Survivor.
And he's such a good Soul, I'm sure he'd take it well. He's all into meditation and guided imagery, while dispensing his chemo and supplement lists. Very Zen. BE well. BE happy. And BE... With loving energy...
Andi http://cdn-cf.aol.com/se/clip_art/gstres/thghts/smile
A bit technical but on the same theme that more omega three <img src="http://www.world-of-smilies.com/wos_engel/wos_engell4.gif" alt="Good vs Evil 2" /> and less omega six reduces proliferation and induces cell death between 48-62% in the lab on a particular line of breast cancer cells MDA-MB-231 [A Her2 connected cell line].
LA = linoleic acid an Omega Six
"(a combination of EPA and DHA) inhibited (P < 0.05) the growth of MDA-MB-231 cells by 48-62% in the presence and absence, respectively, of linoleic acid (LA)."
"our results indicate that (n-3) FA modify the lipid composition of membrane rafts and alter EGFR signaling in a way that decreases the growth of breast tumors."
http://www.ncbi.nlm.nih.gov/pubmed/17311938?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
J Nutr. 2007 Mar;137(3):548-53.Click here to read Links
Comment in:
J Nutr. 2007 Mar;137(3):545-7.
(n-3) PUFA alter raft lipid composition and decrease epidermal growth factor receptor levels in lipid rafts of human breast cancer cells.
Schley PD, Brindley DN, Field CJ.
Department of Agricultural, Food, and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2P5.
Low Omega 3 <img src="http://www.world-of-smilies.com/wos_engel/wos_engell4.gif" alt="Good vs Evil 2" /> plus high Omega six = higher risk of BC
Abstract
"However, among subjects who consumed low levels of marine n-3 fatty acids (lowest quartile of intake), a statistically significant increase in risk was observed in individuals belonging to the highest vs the lowest quartile of n-6 fatty acid consumption (RR=1.87, 95% CI=1.06-3.27); the corresponding RR for advanced breast cancer was 2.45 (95% CI=1.20-4.97, P for trend=0.01). To our knowledge, these are the first prospective findings linking the intake of marine n-3 fatty acids to breast cancer protection."
http://www.ncbi.nlm.nih.gov/pubmed/14583770?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Br J Cancer. 2003 Nov 3;89(9):1686-92.Click here to read Links
Opposing effects of dietary n-3 and n-6 fatty acids on mammary carcinogenesis: The Singapore Chinese Health Study.
Gago-Dominguez M, Yuan JM, Sun CL, Lee HP, Yu MC.
USC/Norris Comprehensive Cancer Center, Keck School of Medicine of the University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA 90089-9181, USA. mgago@usc.edu
Flaxseed
In mice but an interesting trial on flaxseed.
Abstract
"In conclusion, FS [Flaxseed] inhibited MCF-7 tumor growth in a dose-dependent manner and enhanced the inhibitory effect of TAM due to the modulation of ER and growth factor signal transduction pathways."
http://www.ncbi.nlm.nih.gov/pubmed/17720953?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Flaxseed alone or in combination with tamoxifen inhibits MCF-7 breast tumor growth in ovariectomized athymic mice with high circulating levels of estrogen.
Chen J, Power KA, Mann J, Cheng A, Thompson LU.
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, 150 College Street, Toronto, ON, Canada M5S 3E2.
Flaxseed
Another interesting trial again with mice.
RB
"Our previous short-term study has shown that 10% flaxseed (FS) inhibits the growth of human estrogen dependent estrogen receptor positive breast tumors (MCF-7) xenografts in ovariectomized (OVX) athymic mice and enhances the tumor inhibitory effect of tamoxifen (TAM)."...
"In conclusion, after long-term treatment, FS did not stimulate tumor growth and combined with TAM, regressed tumor size in part due to downregulation of the expression of estrogen-related gene products and signal transduction pathways."
http://www.ncbi.nlm.nih.gov/pubmed/17640162?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlus
Dietary flaxseed interaction with tamoxifen induced tumor regression in athymic mice with MCF-7 xenografts by downregulating the expression of estrogen related gene products and signal transduction pathways.
Chen J, Power KA, Mann J, Cheng A, Thompson LU.
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
"Essential fatty acids have long been identified as possible oncogenic factors. Existing reports suggest omega-6 (omega-6) essential fatty acids (EFA) as pro-oncogenic and omega-3 (omega-3) EFA as anti-oncogenic factors. The omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), inhibit the growth of human breast cancer cells <img src="http://www.world-of-smilies.com/wos_engel/wos_engell4.gif" alt="Good vs Evil 2" /> while the omega-6 fatty acids induces growth of these cells in animal models and cell lines."
http://www.ncbi.nlm.nih.gov/pubmed/16823509?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Differential effects of omega-3 and omega-6 Fatty acids on gene expression in breast cancer cells.
Hammamieh R, Chakraborty N, Miller SA, Waddy E, Barmada M, Das R, Peel SA, Day AA, Jett M.
Division of Pathology, Walter Reed Army Institute of Research, 503 Robert Grant Road, Silver Spring, MD 20910, USA.
Just bringing this back in case anybody has not seen it and is interested.
RB
PinkGirl
03-03-2008, 04:29 PM
R.B.
Do you know if there have been any other studies
like the one in Toronto - regarding flax seed and er+
cancer? It is sort of the opposite of what we've been
told in the past. I asked my onc. about it and she
hadn't heard about the Princess Margaret study.
I was taking flax seed and then stopped. This
study suggests that I should be taking it.
Have I already asked you this question?
HI Pink Girl there is some material here that you could show to your onc.
I do not recall the Princess Margaret study - Do you have a link?.
This is the result of an NCBI search on BC and flax seed and flaxseed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=breast%20cancer%20flax%20seed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=breast%20cancer%20flaxseed
These are previous posts on this site that are particulalry useful
http://her2support.org/vbulletin/showthread.php?t=21962&highlight=flax+seed+estrogen
http://her2support.org/vbulletin/showthread.php?t=24657&highlight=flax+seed+estrogen
http://www.her2support.org/vbulletin/showthread.php?t=21826&pp=20&highlight=flax
PinkGirl
03-04-2008, 05:17 PM
Thanks RB
I think the Princess Margaret study might be
the same one as the U of Toronto.
Thanks for the links.
fullofbeans
03-05-2008, 06:47 AM
humm just read most of this post thank you R.B. again for some clarification especially about the veg oil one. Very informative! I had been eating lots of veg and some fish and like StephN I started to wonder if I still needed fish oil supplement..well I guess I do and will get my dose today.
Also just a little point on bioaccumulation of toxic in fish oil. You are right saying that small fish (often) contains less. If they are larger indeed they have more time to accumulate toxic. However an important factor is what they eat: if they are carnivorous and eat other fishes then they bioaccumulate much more toxic (since they take on the one of the fishes they have just absorbed). Other fishes such as the anchovy that "filter" the water are much less toxic. Therefore large predatory fish are generally the most toxic one.
Hi Full of Beans,
Thank you for your thoughts on pollution of fish. I had not thought about the difference between carnivores and filter feeders. Just lower down the food chain and so less levels of concentration of pollutants I guess is the point.
I suppose it also depends how polluted the waters are where they fish come from.
Re continued Omega 3 intake. Omega three is not heavily stored in fat under 1% for many but Omega Six is 10-25% of body fat in the west so a constant supply of Omega three in general terms is needed.
The often mentioned book is nearly nearly nearly finished - again!!, it is having its final set at the moment. I have just split it down into three and four sentence pars from bigger pars which heavy readers liked but occasional readers blanched at. I had not thought to show it to occasional readers. It has grown to about 370 pages - size 17cm by 24.4cm - 30 chapters each split into a number of small sections each covering a topic - over 800 refs, and hopefully understandable.
Hi
Sorry some how I posted twice so I have deleted the contents of one.
RB
Andrea Barnett Budin
03-05-2008, 06:06 PM
Very exciting RB! I understand being into the 100th edit, and I am far away from publishing! As Oscar Wilde said, "I have spent most of the day putting in a comma, and the rest of the day taking it out"... (Not to even mention Flori's comma woes!) Best of luck on your book, RB!!
My oncological nutritionist has told me to stay away from larger fish as they contain more mercury, having had more time to absorb it, just as FOB says. So I've been staying away from tuna. Today a friend told me about TONGOL TUNA! It is smaller, wild caught (as opposed to farm raised which has toxins and ?hormones). Any one hear about this? It's in all the health food stores around here. Whole Foods, etc.
They swim in Thailand and do not swim w/the dolphins, thus not endangering them.
Andi
Intriguing !
" Considerable evidence suggests strongly that the n-3 polyunsaturated fatty acid (PUFA) content of adipose breast tissue is inversely associated with an increased risk of breast cancer."
More questions than answers but these two trials do underline fats play important roles in breast function, which given breasts function is to supply nutrients including fats, is unsurprising.
Long chain Omega 3s DHA and EPA may be fundamental to function breasts in pregnancy, and may have a part in explaining lower rates in women that have been pregnant based on trials in mice.
Also FAS an enzyme critical to making fats from scratch is often hyperactive and over expressed in some aggressive breast cancers, and may be driven in the line of cells examined by HER2. Why does the breast switch on its fat making enzymes in cancer and what has it got do do with HER2? Omega 3s may turn down FAS.
http://www.ncbi.nlm.nih.gov/pubmed/15138577?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVAbstractPlusDrugs1
"Activity and expression of fatty acid synthase (FAS), a critical enzyme in the de novo biosynthesis of fatty acids in mammals, is exquisitely sensitive to nutritional regulation of lipogenesis in liver or adipose tissue. Surprisingly, a number of studies have demonstrated hyperactivity and overexpression of FAS (oncogenic antigen-519) in a biologically aggressive subset of human breast carcinomas,"......"FAS overexpression in SK-Br3 breast cancer cells is driven by increases in HER-2/neu signaling,"......"GLA- and/or omega-3 PUFA-induced repression of tumor-associated FAS may represent a novel mechanism of PUFA-induced cytotoxicity clinically useful against breast carcinomas carrying overexpression of FAS enzyme;"
BUT if you don't eat it you don't have it as the body cannot make Omega 3s from other fats. The body just is not able to make Omega 3s. It can convert the mother fat found in vegetable sources to the long chain fats if the pathways are not blocked.
This trial below is essentially saying that if you could make your own Omega 3 your breasts would want to make more of it in pregnancy because that is what genetically altered mice that can make Omega 3s do.
And that Omega 3s have a big part to play in changing the status of fat producing cells in the breast.
The mouse referred to is a genetically altered mouse with genes from a worm that allows the mouse to convert Omega six to omega three (which we cannot do) and from vague memory even make its own Omega six which we also cannot do.
Activation of Stat5 and induction of a pregnancy-like mammary gland differentiation by eicosapentaenoic and docosapentaenoic omega-3 fatty acids.
Liu YE, Pu W, Wang J, Kang JX, Shi YE.
Feinstein Institute for Medical Research, Department of Radiation Oncology, Long Island Jewish Medical Center, The Albert Einstein College of Medicine, New Hyde Park, NY 11040, USA.
The protective effect of early pregnancy against breast cancer can be attributed to the transition from undifferentiated cells in the nulliparous to the differentiated mature cells during pregnancy. Considerable evidence suggests strongly that the n-3 polyunsaturated fatty acid (PUFA) content of adipose breast tissue is inversely associated with an increased risk of breast cancer. Here, we report that there was a decrease in the n-6/n-3 PUFA ratio and a significant increase in concentration of n-3 PUFA docosapentaenoic acid and eicosapentaenoic acid in the pregnant gland. The functional role of n-3 PUFAs on differentiation was supported by the studies in the fat-1 transgenic mouse, which converts endogenous n-6 to n-3 PUFAs. Alternation of the n-6/n-3 ratio in favor of n-3 PUFA, and particularly docosapentaenoic acid, in the mammary gland of fat-1 mouse resulted in development of lobulo-alveolar-like structure and milk protein beta-casein expression, mimicking the differentiated state of the pregnant gland. Docosapentaenoic acid and eicosapentaenoic acid activated the Jak2/Stat5 signaling pathway and induced a functional differentiation with production of beta-casein. Expression of brain type fatty acid binding protein brain type fatty acid binding protein in virgin transgenic mice also resulted in a reduced ratio of n-6/n-3 PUFA, a robust increase in docosapentaenoic acid accumulation, and mammary differentiation. These data indicate a role of mammary derived growth inhibitor related gene for preferential accumulation of n-3 docosapentaenoic acid and eicosapentaenoic acid in the differentiated gland during pregnancy. Thus, alternation of n-6/n-3 fatty acid compositional ratio in favor of n-3 PUFA, and particularly docosapentaenoic acid and eicosapentaenoic acid, is one of the underlying mechanisms of pregnancy-induced mammary differentiation.
Pink Girl - One of `those coincidences' I came across this doing a spur of the moment search on google on flax and HER2 - it was my first pick on the 1st page and had no mention of the Princess Margaret hospital in the title (see above post) !
"The results of this clinical trial are in agreement with previous clinical and preclinical studies showing antitumor effects of flaxseed in prostate cancer patients (53), carcinogen-treated rats (32), athymic mice with established ER-positive (33), or ER-negative breast cancers (34, 35), and tumor-bearing transgenic mice (54). The 5% or 10% flaxseed diet used in the animal studies is approximately equivalent to 25 to 30 g of flaxseed given to patients with breast or prostate cancer, depending on the amount of other foods consumed. Our results are also in line with epidemiologic studies showing that high levels of lignan intake (26), plasma or urinary excretion of mammalian lignans (23–25) or high levels of {alpha}-linolenic acid in adipose tissues (28) are associated with a reduced risk of breast cancer."
Dietary Flaxseed Alters Tumor Biological Markers in Postmenopausal Breast Cancer
Lilian U. Thompson1, Jian Min Chen1, Tong Li2, Kathrin Strasser-Weippl2 and Paul E. Goss3
Authors' Affiliations: 1 Department of Nutritional Sciences, 2 Princess Margaret Hospital, University of Toronto, Toronto, Ontario, Canada, and 3 Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, Massachusetts
http://clincancerres.aacrjournals.org/cgi/content/full/11/10/3828
fullofbeans
03-07-2008, 05:44 PM
R.B. I did not know that you were writing a book on fats well done!
Well in that case if you need more precise info on pollutant bioaccumulation let me know. The actual issue is rather more complicated for example it also depends on migratory pattern, temperature (impact on their growth), spawning frequency (for example salmon spawn once in their life time other fish spawn several time a year) ect.. If I were you and if you wanted to touch on this subject I may consider to simply have a list of fish and their concurrent analysis of pollutant. From an ecological point of view I would also put whether the stock was fished in a sustainable manner, let's look after our ocean if we want to continue eating wild fish in the future.
I hope it helps
fullofbeans
03-07-2008, 06:06 PM
Whilst I am here ok I recently purchased a new fish oil supplement:
and the nutrition info is that out of the 500mg capsule: EPA 240 and DHA is 160mg. My old one (cheaper) was 1000mg with 165 mg EPA and 110DHA.
Obviously the recently purchased one seems much better doesn't it? I still however wonder: what is the rest made of? for example the recently purchase omg3 supplement has 38% omega 3, but what is the rest then; bearing in mind that the ratio of equilibrium mentioned seems to be much higher than that.
Whilst I am at it what fish oil sup would you recommend and how many per day should you take if you have a reasonably healthy diet? Many thanks
PinkGirl
03-07-2008, 06:13 PM
Super Potent Flax Seed Muffins
The following is the recipe used in clinical research on flax seed and breast cancer. The recipe yields a week¹s supply of muffins (7 muffins). Each muffin provides 25 grams of flax seed.
5/8 cup all-purpose flour
3/4 cup ground flaxseed
3/8 cup brown sugar
1/2 tbsp baking powder
1/2 tsp nutmeg
1/2 tsp cinnamon
1 1/2 cups skim milk
Bake muffins at 350°F for 30 minutes.
Many Thanks Full of beans.
I would be fascinated.
There is a chapter on wider environmental source and supply issues including ocean sources and high demands / efficiency issues of fish farming - algal production, genetic manipulation of crops etc, but it is fairly general.
Maybe the next edition!
fullofbeans
03-08-2008, 05:59 AM
Pinkgirl
: 7 days supply..uh.. because it is for 7 muffins..uh..not in my neck of the wood!!! more like 2 days :-) if it is in my house..muffins enter at your own risks..
Also I may want to add that I would replace sugar with xylitol (it is natural wood sugar despite chemical sounding name) and milk with oat milk...
humm flax seeds I wonder how long do they last if they are kept in the freezer (once packet open),anyone?
Andrea Barnett Budin
03-08-2008, 01:58 PM
I am taking MEGA EFA 1480 (EPA 400) (DHA 400) X 3 a day. This per nutritional oncologist. You can hardly turn on the news w/o hearing someone touting OMEGA 3s these days! RB's new book will be hitting the shelves at a most opportune time.
Remind us please, RB -- of the title we should be looking for. I know not yet, but sooooonnnn...
I know Salmon is full of Omega 3s. Anyone know about Chilean Sea Bass? I had it last night for dinner. It was delicious!
Andi http://cdn-cf.aol.com/se/smi/2b000001e1/06
Hi Full of Beans
I cannot make specific recommendations as to amounts.
Recommendations vary from 300mg of DHA to about 1.5 grams of DHA (2.7 grams DHA plus EPA). Some trials look at higher amounts. Regular intake is essential as the body does not store much Omega 3.
A trial suggested western women's uptake of DHA dropped off at about 2grams of DHA a day.
My personal take is that most in the west will have relatively high fat stores of Omega Six, and Omega six lurks everywhere in the processed food chain, nuts are generally high in Omega 6, so aim for a balance in the recognition the reality will be lower.
The vegetable based mother fats of Omega 6 and 3 and the long chain 3s need considering separately. The vegetable fats are both essential to body function and are about balanced in greens. Omega six mother fat is stored in fat between 5-25% dependent on dietary intake. The mother Omega three is not heavily stored. So it is a question of taking a sensible view on your Omega 3:6 mother fat balance taking into account existing fat stores in determining your intake of mother fats eg flax oil, olive oil, 369 oils etc.
The long chain fats can be made by the body from the mother Omega 3 but lots of things stop conversion. The body deals with all the fats differently and uses them for different things. I personally aim for 1.5 grams a day plus of DHA so 3tps plus of a quality fish oil. This is the best I have found so far http://www.vitacost.com/Carlson-Norwegian-Cod-Liver-Oil-High-In-EPA-DHA
http://www.vitacost.com/Carlson-The-Very-Finest-Fish-Oil
A mix of fish oil and cod liver will reduce the risk of excess A or D as fish oil does not contain significant A and D, although Cod liver does. Check labels for contents.
It is complex there are no absolute answers.
Fish oil composition details can be found on Nutritiondata.com
http://www.nutritiondata.com/
Please talk to your doctor about dietary change as fish oil can cause blood thinning and have other effects in a small number of people.
Andi BB - the book has come back, I have read it again!, - I think I am going word blind, - and gone back for hopefully the last few little bits - so soon!
RB
fullofbeans
03-16-2008, 07:48 AM
Thank you very much for the further information much appreciated!
Just bringing the thread back up for people that may not have seen it.
This video link is a bit complex in part but once it get past the PPARs it gives a fascinating insight into the growing appreciation that body functions all interlink and the potential impact of food in diet - gene expression - nutrigenomics - the effect of food on genes.
You can also see that those in commercial research are beginning to recognise a potential blurring of lines between drugs and food agents and the complications that causes for them.
http://videocast.nih.gov/launch.asp?13776
Interesting trial in lung cancer where the immune system is failing. The trial suggest fish oil fish oil may benefit and act as COX2 blocker. Fish oil has been shown to have the ability to intervene in the COX2 pathways.
RB
Effects of eicosapentaenoic and docosahexaenoic n-3 fatty acids from fish oil and preferential Cox-2 inhibition on systemic syndromes in patients with advanced lung cancer.
Cerchietti LC, Navigante AH, Castro MA.
Translational Research Unit, Angel H Roffo Cancer Institute, Universidad de Buenos Aires, Buenos Aires, Argentina. lcerchie@aecom.yu.edu
"Under the common denomination of Systemic Immune-Metabolic Syndrome (SIMS), we grouped many symptoms that share a similar pathophysiologic background. SIMS is the result of the dysfunctional interaction of tumor cells, stroma cells, and the immune system, leading to the release of cytokines and other systemic mediators such as eicosanoids. SIMS includes systemic syndromes such as paraneoplastic hemopathies, hypercalcemia, coagulopathies, fatigue, weakness, cachexia, chronic nausea, anorexia, and early satiety among others.......Comparing both groups, patients receiving fish oil + celecoxib showed significantly lower C-RP levels (P = 0.005, t-test), higher muscle strength (P = 0.002, t-test) and body weight (P = 0.05, t-test) than patients receiving fish oil + placebo. The addition of celecoxib improved the control of the acute phase protein response, total body weight, and muscle strength. Additionally, the consistent nutritional support used in our patients could have helped to maximize the pharmacological effects of fish oil and/or celecoxib. This study shows that by modulating the eicosanoid metabolism using a combination of n-3 fatty acids and cyclooxygenase-2 inhibitor, some of the signs and symptoms associated with a SIMS could be ameliorated.
TSund
04-06-2008, 11:23 AM
Just in case someone's curious, we are taking "Omega Ultra Marine" (brand is Designs for Health) that go heavy on the Omega 3's. They have another product that has more of a balance between 3 and 6's, but after reading RB's comments, I figured we were getting 6's in the diet and needed to lean towards the Omega 3's. This one has 550 mg per softgel with 300 mg EPA and 200 mg. Fish oil is from anchovy and sardine.
Andrea Barnett Budin
04-06-2008, 12:12 PM
FYI -- I am taking OMEGA 3 EPA (800) w/ DHA (400) x 3 a day. I too feel I am getting Omega 6s naturally and need to boost my 3s. I get most of my supplements from Vitacost on the net.
Andi
Mechanisms by which DHA reduces colon cancer risk and inflammatory disorders of the intestine.
Good digestion is important to all.
This underlines again Omega 3 DHA is important in many ways in body function.
1: Chem Phys Lipids. 2008 Mar 4 [Epub ahead of print]Click here to read Links
Mechanisms by which docosahexaenoic acid and related fatty acids reduce colon cancer risk and inflammatory disorders of the intestine.
Chapkin RS, Seo J, McMurray DN, Lupton JR.
Center for Environmental and Rural Health, Texas A&M University, United States; Faculty of Nutrition, Texas A&M University, United States.
A growing body of epidemiological, clinical, and experimental evidence has underscored both the pharmacological potential and the nutritional value of dietary fish oil enriched in very long chain n-3 PUFAs such as docosahexaenoic acid (DHA, 22:6, n-3) and eicosapentaenoic acid (EPA, 20:5, n-3). The broad health benefits of very long chain n-3 PUFAs and the pleiotropic effects of dietary fish oil and DHA have been proposed to involve alterations in membrane structure and function, eicosanoid metabolism, gene expression and the formation of lipid peroxidation products, although a comprehensive understanding of the mechanisms of action has yet to be elucidated. ............. Ultimately, this may allow organ systems such as the colon to optimally decode, respond, and adapt to the vagaries of an ever-changing extracellular environment.
Anticancer properties of oxidation products of docosahexaenoic acid.
Siddiqui RA, Harvey K, Stillwell W.
1: Chem Phys Lipids. 2008 Feb 23 [Epub ahead of print]Click here to read Links
Methodist Research Institute, Clarian Health Partners, Indianapolis, IN, United States; Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States; Department of Biology, Indiana University-Purdue University, Indianapolis, IN, United States.
Docosahexaenoic acid (DHA) is the longest, most unsaturated, and hence, most oxidizable fatty acid commonly found in nature. The mechanisms behind DHA's many biological functions remain a subject of much debate. Here we review one important, but often unstudied, aspect of DHA function, namely, the potential role of its many oxidation products. We divide this review into camps, enzymatic and non-enzymatic oxidations, and report their effects primarily on induction of apoptosis in cancer cells. We conclude that the study of the effects of lipid peroxidation products on biochemical function will be a difficult but highly rewarding area for future studies.
Mgarr
04-12-2008, 08:22 AM
Hi All,
I am reclaiming my emotional & physical health slowly but surely!
And I promised I would let you know about my progress on the anti-inflammatory diet so here it is.
The first thing I noticed right off is that my usually dry scaly skin has improved. As I continued on the diet the joint swelling decreased and I am feeling better, I have not completely stopped taking Enbrel but have been able to push my dose back; instead of every 7 days I can spread(with the okay from my rheumatologist) it from 10-12 days without pain or swelling. It is a work in progress and my challenges have lied with feeding my family - as they are not as willing to eat some of my choices. Being away from home is challenging too, I wasn't as strict when we went to FL during Easter and there was a noticeable difference in how I felt.
Secondly, I have been on Lexapro for approx. a year I have decreased my dose from 10mg to 5mg with the hopes of eliminating it.
So glad for RB and all of you who keep this thread in the forefront & continue to inform and discuss the importance of dietary choices. I am confident the next health update will even be more encouraging.
Mar
Mary Jo
04-12-2008, 10:26 AM
Hi Mary,
Thanks for the encouraging update on yourself and the reminder to us all that taking care of ourselves is a good thing. Proper nutrition and exercise can make all the difference in how we feel and the quality of our lives.
Thanks .....
Mary Jo
Mgarr
Thanks for the feed back.
There are several trials suggesting the long chain Omega 3s may assist in reducing inflammation and Omega 6s increase it. There is also quite a boy of work on why. But trial are mixed, and maybe because trials are often only for short periods, use quite low doses, take no account of Omega 6 in the diet or body fat stores, do not account of possible dietary conversion blockers etc.
It is always interesting to hear peoples experience.
When you say anti inflammation diet can you tell us more?
Many thanks
R.B.
Mgarr
04-13-2008, 09:36 AM
R.B. I would be happy to share what I have been doing. I started this not only because of breast cancer but the inflammatory arthritis I was diagnosed with 6 months after the end of my treatment.
I read what I could digest on Omega 3/6 (I'm right brained so it takes me some time) anyway, continued researching and came across a book called Too Young to Feel Old by rheumatologist, Richard Blau. Much of the book reiterated what has been discussed on this thread.
There is a section with a "28 day super menu" that is high in Omega 3 & low in 6, the ratio is below 5. I already ate many of the foods but as I kept reading I realized I did not know how to attain the proper ratio of fats.
Every day I take Carlson fish oil, flax oil or flax meal. Cook w/ walnut oil. Alot of anti-inflammatory foods & spices they include, almonds & walnuts, seafoods, lean organic meats, brown rice (lots of that, I miss my potatoes or "baked jacket") ginger, tumeric, cinnamon, garlic, onions, variety of fruits & veggies that have anti inflammatory properties.
Mgarr
04-14-2008, 08:47 AM
Here is just a sample of what my daily menu looks like:
2 tbsp. Carlson (before breakfast & dinner)
V-8 juice & Omega Oatmeal whole grain oatmeal, dried cherries, cinnamon & flax meal
Ginger tuna salad on WW(flax oil, ginger, water chestnuts, sesame seeds)
carrots & celery
Chopped salad special dressing (garlic, flax oil & balsamic)
3 spice baked chicken breast
brown rice w/ turmeric
broccoli w/ garlic
Possible benefits <img src="http://i115.photobucket.com/albums/n292/pjmailings/smilies/cheerleader.gif" alt="Cheerleaders 2" />of DHA [Long chain Omega 3 found in fish oil] with several anti cancer drugs.
RB
Inserm E-0211, Nutrition, Croissance et Cancer; Université François-Rabelais, Tours, France.
Docosahexaenoic acid (DHA, a lipid of marine origin) has been found to enhance the activity of several anticancer drugs through an oxidative mechanism. To examine the relation between chemosensitization by DHA and tumor cells antioxidant status, we used two breast cancer cell lines: MDA-MB-231, in which DHA increases sensitivity to doxorubicin, and MCF-7, which does not respond to DHA. Under these conditions, reactive oxygen species (ROS) level increased on anthracycline treatment only in MDA-MB-231. This was concomitant with a decreased cytosolic glutathione peroxidase (GPx1) activity, a crucial enzyme for protection against hydrogen and lipid peroxides, while major antioxidant enzyme activities increased in both cell lines in response to ROS. GPx-decreased activity was accompanied by an accumulation of glutathione, the GPx cosubstrate, and resulted from a decreased amount of GPx protein. In rat mammary tumors, when a DHA dietary supplementation led to an increased tumor sensitivity to anthracyclines, GPx1 activity was similarly decreased. Furthermore, vitamin E abolished both DHA effects on chemotherapy efficacy enhancement and on GPx1 inhibition. Thus, loss of GPx response to an oxidative stress in transformed cells may account for the ability of peroxidizable targets such as DHA to enhance tumor sensitivity to ROS-generating anticancer drugs.
Free Radic Biol Med. 2008 Apr 1;44(7):1483-91. Epub 2008 Jan 26.
Sensitization by docosahexaenoic acid (DHA) of breast cancer cells to anthracyclines through loss of glutathione peroxidase (GPx1) response.
Vibet S, Goupille C, Bougnoux P, Steghens JP, Goré J, Mahéo K.
More on Long chain Omega 3 DHA protecting against osteoporosis.
RB
1: Exp Biol Med (Maywood). 2008 May;233(5):592-602. Epub 2008 Mar 28.Click here to read Links
Docosahexaenoic Acid and 17{beta}-Estradiol Co-Treatment Is More Effective Than 17{beta}-Estradiol Alone in Maintaining Bone Post-Ovariectomy.
Poulsen RC, Moughan PJ, Kruger MC.
Institute of Food, Nutrition and Human Health, Massey University, Private Bag 11-222, Palmerston North 4442, New Zealand. M.C.Kruger@massey.ac.nz.
ABSTRACT
Bone-protective effects of combined treatment with long chain polyunsaturated fatty acids (LCPUFAs) and estrogenic compounds following ovariectomy have previously been reported. Recent evidence suggests the n-3 LCPUFA docosahexaenoic acid (DHA, 22:6n-3) is particularly bone-protective. The aim of this study was to determine whether combined treatment with DHA and estrogenic compounds has a beneficial effect on bone mass in ovariectomized (OVX) rats. Rats were randomized into 9 groups and either ovariectomized (8 groups) or sham-operated (1 group). Using a 2x4 factorial design approach, OVX animals received either no estrogenic compound, genistein (20 mg/kg body weight/day), daidzein, (20 mg/kg body weight/day) or 17beta-estradiol (1 mug/day) with or without DHA (0.5 g/kg body weight/day) for 18 weeks. Bone mineral content (BMC), area (BA), and density (BMD), plasma osteocalcin and IL-6 concentrations, and red blood cell (RBC) fatty acid composition were measured. Femur BMC was significantly greater in animals treated with DHA or 17beta-estradiol than in ovariectomized controls. . . continues
1: Exp Biol Med (Maywood). 2008 Apr 11 [Epub ahead of print]Click here to read Links
The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cardiovascular Disease and Other Chronic Diseases.
Simopoulos AP.
The Center for Genetics, Nutrition and Health.
Abstract Several sources of information suggest that human beings evolved on a diet with a ratio of omega-6 to omega-3 essential fatty acids (EFA) of ~1 whereas in Western diets the ratio is 15/1 - 16.7/1. Western diets are deficient in omega-3 fatty acids, and have excessive amounts of omega-6 fatty acids compared with the diet on which human beings evolved and their genetic patterns were established. Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today's Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a lower omega-6/omega-3 ratio), exert suppressive effects. In the secondary prevention of cardiovascular disease, a ratio of 4/1 was associated with a 70% decrease in total mortality. A ratio of 2.5/1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4/1 with the same amount of omega-3 PUFA had no effect. The lower omega-6/omega-3 ratio in women with breast cancer was associated with decreased risk. A ratio of 2-3/1 suppressed inflammation in patients with rheumatoid arthritis, and a ratio of 5/1 had a beneficial effect on patients with asthma, whereas a ratio of 10/1 had adverse consequences. These studies indicate that the optimal ratio may vary with the disease under consideration. This is consistent with the fact that chronic diseases are multigenic and multifactorial. Therefore, it is quite possible that the therapeutic dose of omega-3 fatty acids will depend on the degree of severity of disease resulting from the genetic predisposition. A lower ratio of omega-6/omega-3 fatty acids is more desirable in reducing the risk of many of the chronic diseases of high prevalence in Western societies, as well as in the developing countries.
Hi all,
If you see "goodvevil 2" in the text it should be one of these.
http://www.world-of-smilies.com/wos_engel/wos_engell4.gif
You will find it on the Mozzilla free smileys section.
THIS ONE HAS DISAPPEARED TOO _ It was a smiley with good and evil represented on a see-saw. The fulcrum was a face that looked at good and evil as they rose and fell in turn. The balancing of goodness and badness is a very ancient human dilemma. I am not sure why somebody or some machine has seen fit to ban it.
Unfortunately a search will not refind each article and I do not have time at the moment to reread the posts to find where the images have disappeared and replace them.
RB
ElaineM
05-10-2008, 03:41 PM
Hi,
Thanks for all the nutrition info everyone. I believe what we put in our bodies has a big impact on our overall health and our ability to keep cancer under control. Drugs are important, but they can't do all the work.
Int J Cancer. 2007 Jul 15;121(2):377-85.Click here to read Links
Breast cancer risk and erythrocyte compositions of n-3 highly unsaturated fatty acids in Japanese.
Kuriki K, Hirose K, Wakai K, Matsuo K, Ito H, Suzuki T, Hiraki A, Saito T, Iwata H, Tatematsu M, Tajima K.
Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, Nagoya 464-8681, Japan. kkuriki@aichi-cc.jp
"Dietary intake of fish rich in n-3 highly unsaturated fatty acids (HUFAs), such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), has been proposed to decrease cancer risk. In contrast to results from laboratory studies, however, protective effects for breast cancer have proved equivocal in epidemiological studies. In the present case-control study, we examined associations between breast cancer risk and fatty acid compositions in erythrocyte membranes as biomarkers for those intakes. Dietary information and blood samples were collected from 103 incident breast cancer cases and 309 non-cancer controls (matched by age and season) and erythrocyte fatty acids were measured .....In conclusion, we showed that erythrocyte compositions of specific fatty acids derived from fish intake, as biomarkers, are associated with lower risk of breast cancer, but further studies are needed to investigate mechanisms linked to the etiology.
This is not a trial for BC but there may be common factors like a role for COX2 in supporting cancers, and the blocking of COX 2 inhibiting cancer development.
Here they are suggesting a role for Omega 3 in support of chemo.
There have been an number of other trials that suggest this may be an interesting idea for further trialling.
RB
1: Pancreas. 2008 May;36(4):353-62.Click here to read Links
Opposing effects of n-6 and n-3 polyunsaturated fatty acids on pancreatic cancer growth.
Funahashi H, Satake M, Hasan S, Sawai H, Newman RA, Reber HA, Hines OJ, Eibl G.
Hirshberg Laboratories for Pancreatic Cancer Research, Department of Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
OBJECTIVES: Epidemiologic studies suggest that fish oil, rich in n-3 polyunsaturated fatty acids (PUFA), possesses antitumor activity, whereas n-6 PUFAs may stimulate the development of cancers. The aim of this study was to evaluate the effects of n-6 and n-3 PUFAs on the growth of pancreatic cancer. METHODS: The n-6 PUFA arachidonic acid (AA) stimulated the growth of cyclooxygenase (COX) 2 positive human pancreatic cancer (PaCa) cells, which was mediated by COX-2 generated prostaglandin E2 (PGE2) binding to EP2 and EP4 receptors. In contrast, the n-3 PUFA eicosapentaenoic acid decreased the growth of COX-2-positive and COX-2-negative PaCa cells. The COX-2-dependent mechanism of eicosapentaenoic acid was mediated by binding of PGE3 to EP2 and EP4 receptors. Dietary intake of n-3 PUFAs decreased the growth of pancreatic cancers in a xenograft model, which was accompanied by a decrease of PGE2 and an increase of PGE3 in the tumors. CONCLUSIONS: Our studies provide evidence that n-3 PUFAs possess antitumor activities, whereas n-6 PUFAs stimulate pancreatic tumor growth. The opposite effects of n-3 and n-6 PUFAs are mediated by the formation of different prostaglandin species. n-3 PUFAs may prove beneficial as monotherapy or combination therapy with standard chemotherapeutic agents in pancreatic cancer patients.
Complicated and rather beyond me, but may suggest Omega 6 archidonic acid has an important role in early proliferation of cells in the BCs examined. The underline is mine.
Archidonic acid is made in the body from the mother Omega six linoleic acid, which is find in high levels in many vegetable oils (see rest of this thread)
RB
Arachidonic Acid-induced Ca2+ entry is involved in early steps of tumor angiogenesis.
Fiorio Pla A, Grange C, Antoniotti S, Tomatis C, Merlino A, Bussolati B, Munaron L.
Department of Animal and Human Biology, University of Torino, Via Accademia Albertina 13, 10123 Turin, Italy. alessandra.fiorio@unito.it.
http://www.ncbi.nlm.nih.gov/pubmed/18403634?ordinalpos=69&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Growth factor-induced intracellular calcium signals in endothelial cells regulate cytosolic and nuclear events involved in the angiogenic process. Among the intracellular messengers released after proangiogenic stimulation, arachidonic acid (AA) plays a key role and its effects are strictly related to calcium homeostasis and cell proliferation. Here, we studied AA-induced intracellular calcium signals in endothelial cells derived from human breast carcinomas (B-TEC). AA promotes B-TEC proliferation and organization of vessel-like structures in vitro. The effect is directly mediated by the fatty acid without a significant contribution of its metabolites. AA induces Ca(2+)(i) signals in the entire capillary-like structure during the early phases of tubulogenesis in vitro. No such responses are detectable in B-TECs organized in more structured tubules. In B-TECs growing in monolayer, AA induces two different signals: a Ca(2+)(i) increase due to Ca(2+) entry and an inhibition of store-dependent Ca(2+) entry induced by thapsigargin or ATP. An inhibitor of Ca(2+) entry and angiogenesis, carboxyamidotriazole, significantly and specifically decreases AA-induced B-TEC tubulogenesis, as well as AA-induced Ca(2+) signals in B-TECs. We conclude that (a) AA-activated Ca(2+) entry is associated with the progression through the early phases of angiogenesis, mainly involving proliferation and tubulogenesis, and it is down-regulated during the reorganization of tumor-derived endothelial cells in capillary-like structures; and (b) inhibition of AA-induced Ca(2+) entry may contribute to the antiangiogenic action of carboxyamidotriazole. (Mol Cancer Res 2008;6(4):535-45).
1: Clin Transl Oncol. 2006 Dec;8(12):868-83.Links
Are the olive oil and other dietary lipids related to cancer? Experimental evidence.
Escrich E, Solanas M, Moral R, Costa I, Grau L.
Department of Cell Biology. Physiology and Immunology. Physiology Unit. Faculty of Medicine. Universitat Autònoma de Barcelona. Bellaterra, Barcelona. Spain.
There is a wealth of evidence supporting the relationship between dietary lipids and cancer, particularly those of the breast, colon and rectum and prostate. The main support comes from the international correlational studies and, especially, from experimental ones. The evidence from human analytical studies is less consistent because of several conflicting findings, probably due to methodological issues. Experimentally, it has been clearly demonstrated that quantity and type of dietary lipids as well as the particular critical phases of the carcinogenesis in which they act, are the essential factors in this relationship. Thus, whereas high dietary intake of n-6 polyunsaturated fatty acids (PUFA), primarily LA, and saturated fat has tumor-enhancing effects, long chain n-3 PUFA, CLA and GLA have inhibitory effects. Monounsaturated fatty acids (MUFA), mainly OA, present in high quantities in olive oil, seem to be protective although some inconsistent results have been reported. Bioactive compounds of virgin olive oil may also account for the protective effect of this oil, which is the main source of fat in the Mediterranean diet. Experimental studies have also provided evidence of several putative mechanisms of action of dietary lipids on cancer. Lipids can influence the hormonal status, modify cell membranes structure and function, cell signalling transduction pathways and gene expression, and modulate the function of the immune system. Although further studies are needed to evaluate and verify these mechanisms in humans, based on the multiple ways dietary lipids can act, they may have an important influence on tumorigenesis.
PMID: 17169760 [PubMed - in process]
: Clin Chim Acta. 2006 Nov;373(1-2):1-8. Epub 2006 May 16.
Omega-3 fatty acid effects on biochemical indices following cancer surgery.
Stehr SN, Heller AR.
http://www.ncbi.nlm.nih.gov/pubmed/16796997?ordinalpos=14&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Department of Anesthesiology and Intensive Care Medicine, University Hospital Carl Gustav Carus, Fetscherstrasse 74, D-01309 Dresden, Germany.
Epidemiological studies have indicated that a high intake of saturated fat and/or animal fat increases the risk of colon and breast cancer. Laboratory and clinical investigations have shown a reduced risk of colon carcinogenesis after alimentation with omega-3 fatty acids, as found in fish oil. Mechanisms accounting for these anti-tumor effects are reduced levels of PGE(2) and inducible NO synthase as well as an increased lipid peroxidation, or translation inhibition with subsequent cell cycle arrest. Further, omega-3 eicosapentaenoic acid is capable of down-regulating the production and effect of a number of mediators of cachexia, such as IL-1, IL-6, TNF-alpha and proteolysis-inducing factor. In patients with advanced cancer, it is possible to increase energy and protein intake via an enteral or parenteral route, but this seems to have little impact on progressive weight loss. Fish oil administration improved patients' conditions in cancer cachexia and during radio- and chemotherapy. In patients undergoing tumor resection surgery we observed improvement of liver and pancreas biochemical indices when omega-3 fatty acids were administered. This paper is a review of recent developments in the field of nutrition in cancer patients with emphasis on the acute phase response following cancer surgery and the beneficial aspects of fish oil administration.
They have inserted genes into mice that allows them to make their own omega three.
The breasts of these mice make high levels of Omega 3.
Babies have a high need for Omega 3s.
Humans cannot make Omega 3 from scratch, but it would be reasonable to assume human breasts would make high levels of Omega 3s if they have the raw materials to do so. A possible consequences of a deficit of Omega 3 could be cellular misfunction.
http://www.ncbi.nlm.nih.gov/pubmed/16555469?ordinalpos=20&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum1: Lipids. 2006 Jan;41(1):35-9.Links
N-3 polyunsaturated fatty acids endogenously synthesized in fat-1 mice are enriched in the mammary gland.
Ma DW, Ngo V, Huot PS, Kang JX.
Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Canada. davidwl.ma@utoronto.ca
In this study, we determined the phospholipid FA composition in the mammary gland of the transgenic Fat-1 mouse. This is the first animal model developed that can endogenously synthesize n-3 PUFA. The synthesis of n-3 PUFA is achieved through the expression of the fat-1 transgene encoding for an n-3 desaturase from Caenorhabditis elegans, which utilizes n-6 PUFA as substrate. Wild-type and Fat-1 female mice were terminated at 7 wk of age and the fifth mammary gland was removed. Lipids were extracted and phospholipids were separated by TLC and converted to FAME for analysis by GC. There was no significant change in total saturated, monounsaturated, and PUFA composition. However, there was a significant increase in total n-3 PUFA and a corresponding decrease in n-6 PUFA. The major n-3 PUFA that were enriched included 20:5n-3 and 22:6n-3. The n-6 PUFA that were reduced included 20:4n-6, 22:4n-6, and 22:5n-6. Overall, these findings demonstrate that female Fat-i mice have elevated levels of n-3 PUFA in the mammary gland. Moreover, the n-3 desaturase products are the same n-3 PUFA found in fish oil, which have been shown to have chemoprotective properties against breast cancer. Therefore, this newly developed mouse model may be highly useful for investigating molecular and cellular mechanisms by which n-3 PUFA prevents and inhibits breast cancer growth.
PMID: 16555469 [PubMed - indexed for MEDLINE]
Becky
05-26-2008, 04:04 PM
Bumping up
From one of the leaders in the Omega 3 6 field
Omega 6 in excess increases inflammatory pressures.
Asia Pac J Clin Nutr. 2008;17 Suppl 1:131-4.Links
The omega-6/omega-3 fatty acid ratio, genetic variation, and cardiovascular disease.
Simopoulos AP.
The Center for Genetics, Nutrition and Health, 2001 S Street, NW, Suite 530, Washington, DC 20009 USA. cgnh@bellatlantic.net
A high omega-6/omega-3 ratio, as is found in today's Western diets, promotes the pathogenesis of many chronic diseases, including cardiovascular disease. Increased dietary intake of linoleic acid (LA) leads to oxidation of low-density lipoprotein (LDL), platelet aggregation, and interferes with the incorporation of essential fatty acids (EFA) in cell membrane phopholipids. Both omega-6 and omega-3 fatty acids influence gene expression. Omega-3 fatty acids have strong anti-inflammatory effects, suppress interleukin 1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF alpha) and interleukin-6 (IL-6), whereas omega-6 fatty acids tend to be pro-inflammatory. Because inflammation is at the base of many chronic diseases, including coronary heart disease, dietary intake of omega-3 fatty acids plays an important role in the manifestation of disease, particularly in persons with genetic variation, as for example in individuals with genetic variants at the 5-lipoxygenase (5-LO). Increased dietary arachidonic acid (AA) significantly enhances the apparent atherogenic effect of genotype, whereas increased dietary intake of omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) blunts this effect. The diet-gene interaction further suggests that dietary omega-6 fatty acids promote, whereas marine omega-3 fatty acids EPA and DHA inhibit leukotriene-mediated inflammation that leads to atherosclerosis in this subpopulation.
PMID: 18296320 [PubMed - in process]
This is about cardiac health and not BC. I post it because it is unusually unequivocal in its statements on the benefits of omega 3s.
It seems to me that anything that assists with cardiac health is good news; it would be nice if they looked to see if omega 3s helped reduce any cardiac implications of Herceptin.
http://www.ncbi.nlm.nih.gov/pubmed/18541600?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
Am J Clin Nutr. 2008 Jun;87(6):1991S-6S.
Fish and n-3 fatty acids for the prevention of fatal coronary heart disease and sudden cardiac death.
Mozaffarian D.
Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Department of Epidemiology and Nutrition, Harvard School of Public Health, Boston, MA, USA. dmozaffa@hsph.harvard.edu
Large observational studies, randomized clinical trials, and experimental studies have evaluated the effects of fish and n-3 fatty acid consumption on fatal coronary heart disease (CHD) and sudden cardiac death (SCD), clinically defined events that most often share the final common pathway of fatal ventricular arrhythmia. These different study designs, each having complementary strengths and limitations, provide strong concordant evidence that modest consumption of fish or fish oil (1-2 servings/wk of oily fish, or approximately 250 mg/d of EPA+DHA) substantially reduces the risk of CHD death and SCD. Pooled analysis of prospective cohort studies and randomized clinical trials demonstrates the magnitude and dose-response of this effect, with 36% lower risk of CHD death comparing 0 and 250 mg/d of EPA+DHA consumption (P < 0.001), but then little additional benefit with higher intakes. Reductions in risk are even larger in observational studies utilizing tissue biomarkers of n-3 fatty acids that more accurately measure dietary consumption. The concordance of findings from different studies also suggests that effects of fish or fish oil on CHD death and SCD do not vary depending on presence or absence of established CHD. The strength and consistency of the evidence, and the magnitude of this effect are each notable. Because more than one-half of all CHD deaths and two-thirds of SCD occur among individuals without recognized heart disease, modest consumption of fish or fish oil, together with smoking cessation and regular moderate physical activity, should be among the first-line treatments for prevention of CHD death and SCD.
TSund
06-12-2008, 06:22 AM
RB,
Thanks for this.
Do I remember you posting some helpful relationship between Omega 3's and Auto-Immune disease?
THX
TRS
Tsund - thanks for the thanks,
I do not recall doing so, but there may have been a post that was looking at inflammation that also considered auto immune conditions.
Here are two trials that suggest that fish oil / Omegas 3 may assist reduce the risk of auto immune conditions.
RB
http://www.jacn.org/cgi/content/full/21/6/495
Journal of the American College of Nutrition, Vol. 21, No. 6, 495-505 (2002)
Published by the American College of Nutrition
REVIEW
Omega-3 Fatty Acids in Inflammation and Autoimmune Diseases
Artemis P. Simopoulos, MD, FACN
The Center for Genetics, Nutrition and Health, Washington, D.C
Abstract
"There have been a number of clinical trials assessing the benefits of dietary supplementation with fish oils in several inflammatory and autoimmune diseases in humans, including rheumatoid arthritis, Crohn’s disease, ulcerative colitis, psoriasis, lupus erythematosus, multiple sclerosis and migraine headaches. Many of the placebo-controlled trials of fish oil in chronic inflammatory diseases reveal significant benefit, including decreased disease activity and a lowered use of anti-inflammatory drugs."
http://www.ncbi.nlm.nih.gov/pubmed/11802309
Isr Med Assoc J. 2002 Jan;4(1):34-8.Links
n-3 fatty acids and the immune system in autoimmunity.
Ergas D, Eilat E, Mendlovic S, Sthoeger ZM.
Department of Internal Medicine B, Kaplan Medical Center, Rehovot, Israel. ergaz@clalit.org.il
"Therefore, the use of n-3 fatty acids can be recommended to the general healthy population, not only to prevent atherosclerosis but possibly also to reduce the risk of autoimmunity."
(I re-copied this to this thread as it is significant I suspect)
It all interconnects - what happy coincidences - The post on MS by Bill, and Hopeful of an MMP9 all come together at the same moment in a search for an article on MMP9 omega six and gene expression.
Conclusion Omega 3 suppresses MMP-9 which is a marker of MS and BC
http://www.springerlink.com/content/963788775224p348/
"The treatment with both ω-3 PUFA and fish oil dose-dependently inhibited the LPS-induced production of MMP-9. Our results suggest that a low fat diet supplemented with ω-3 PUFA may become recommended for the well being of MS patients under therapy."
MMP9 has been on my list of interest. I do not know exactly what it is, but saw a trial a long time ago that I will dig out that suggested the omega 3 and 6 significantly change gene expression of MMP9. I have been wondering ever since about MMP 9.
This was posted in articles of interest
http://breastcancersource.com/breast...48_0_0_0.aspx?
2 June 2008
Urine biomarker test confirms breast cancer precursor lesions
MedWire News: Matrix metalloproteinases can be detected in the urine of women with atypical breast hyperplasia and could form the basis for an accurate and convenient test for invasive breast cancer risk, researchers claim.
"Once validated in larger studies, such a test could potentially provide a useful adjunct for breast cancer risk assessment," Marsha Moses (Harvard Medical School, Boston, Massachusetts, USA) and colleagues comment, adding: "The goal of identifying women at high risk of developing breast cancer and providing safe effective risk reduction to this group is compelling."
Matrix metalloproteinases are required for the "angiogenic switch" - an early and critical event in breast cancer growth and progression, Moses et al explain in the journal Cancer Epidemiology, Biomarkers and Prevention.
Matrix metalloproteinase 9 (MMP-9) and a disintegrin and metalloprotease 12 (ADAM 12) are two established serum biomarkers in breast cancer.
More evidence Omega 6 LA is implicated in BC.
And why COX blockers may have an impact as the block these pathways.
And more PGE2 may = more aromatase = more oestrogen products
More oestrogen would result in more conversion of LA to AA the raw material for this process be enhancing long chain fat conversion.
SO this could be a self fuelling tumour loop where Omega 6 is present in excess and there is no Omega 3 to moderate the process.
RB
http://www.springerlink.com/content/n547j2538p317388/
Xin-Hua Liu1, Jeanne M. Connolly1 and David P. Rose1 Contact Information
(1) Division of Nutrition and Endocrinology, American Health Foundation, Valhalla, New York, USA
(2) Division of Nutrition and Endocrinology, American Health Foundation, 10595 Valhalla, NY, USA
Received: 21 August 1995 Accepted: 27 October 1995
Diets rich in linoleic acid (LA) stimulate the metastasis of MDA-MB-435 human breast cancer cells from the mammary fat pads of nude mice. This omega-6 fatty acid is metabolized to various cyclo-oxygenase and lipoxygenase products, several of which have been previously associated with tumor cell invasion and metastasis. We now report that MDA-MB-435 cells secreted increased levels of prostaglandin E2 (PGE2),
Striking figures for COX blockers.
DHA is a cox blocker.
It is suggested COX blockers seek to moderate the downstream effect of excess Omega 6.
So balancing Omega 3s and 6s may assist in any COX blocking based strategy.
Please discuss dietary change with your doctor. The posts are only intended to inform debate.
Chemoprevention of Breast Cancer in Rats by Celecoxib, a Cyclooxygenase 2 InhibitorRandall E. Harris2, Galal A. Alshafie, Hussein Abou-Issa and Karen Seibert
School of Public Health [R. E. H., G. A. A., H. A-I.], Comprehensive Cancer Center [R. E. H., H. A-I.], and Department of Surgery [H. A-I.], The Ohio State University College of Medicine, Columbus, Ohio 43210, and Searle Monsanto Research and Development, St. Louis, Missouri 63137 [K. S
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been observed to reduce the relative risk of breast cancer. This prompted our investigation of the chemopreventive potential of celecoxib, a specific cyclooxygenase 2 blocker, against mammary carcinogenesis induced by 7,12-dimethyl-benz(a)anthracene in female Sprague Dawley rats. Treatment with celecoxib was examined and compared to treatment with the general NSAID, ibuprofen, and to a control group receiving only dimethylbenz(a)anthracene. Dietary administration of celecoxib (1500 ppm) produced striking reductions in the incidence, multiplicity, and volume of breast tumors relative to the control group (68%, 86%, and 81%, respectively; P < 0.001). Ibuprofen also produced significant effects, but of lesser magnitude (40%, 52%, and 57%, respectively; P < 0.001). These results help confirm the chemopreventive activity of NSAIDs against breast cancer and provide the first evidence that a cyclooxygenase 2 blocking agent, celecoxib, possesses strong chemopreventive activity against mammary carcinogenesis.
Cancer therapy for animals
http://www.huntsvillecompounding.com/vet%20cancer.pdf
Gigi Davidson, BSPh, RPh, FSVHP, DICVP
North Carolina State University College of Veterinary Medicine
Raleigh, North Carolina
"Matrix metalloproteinases (especially MMP-2 and MMP-9) are
enzymes that are secreted to degrade the ECM. Any new blood
vessels formed by angiogenesis can migrate only after the ECM is
degraded. MMP-2 and MMP-9 have long been associated with
tumor progression and metastasis.6-8 Although mechanisms of MMP
inhibition remain obscure, n-3 omega fatty acids have been shown
to be very effective MMP inhibitors,"
Very largely outside my reading but another mechanism by which Omega 3s may reduce the risk of BC.
RB
http://www.ncbi.nlm.nih.gov/pubmed/18413760?ordinalpos=160&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
1: Cancer Res. 2008 Apr 15;68(8):2912-9.Click here to read Links
Peroxisome proliferator-activated receptor gamma-mediated up-regulation of syndecan-1 by n-3 fatty acids promotes apoptosis of human breast cancer cells.
Sun H, Berquin IM, Owens RT, O'Flaherty JT, Edwards IJ.
Department of Pathology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
Diets enriched in n-3 polyunsaturated fatty acids (n-3 PUFA) may protect against breast cancer but biochemical mechanisms are unclear. Our studies showed that the n-3 fatty acid docosahexaenoic acid (DHA) up-regulated syndecan-1 (SDC-1) in human breast cancer cells, and we tested the hypothesis that DHA-mediated up-regulation of SDC-1 induces apoptosis. DHA was delivered to MCF-7 cells by n-3 PUFA-enriched low-density lipoproteins (LDL) or by albumin in the presence or absence of SDC-1 small interfering RNA. The n-3 PUFA induced apoptosis, which was blocked by SDC-1 silencing. We also confirmed that SDC-1 up-regulation and apoptosis promotion by n-3 PUFA was mediated by peroxisome proliferator-activated receptor gamma (PPAR gamma). Using a luciferase gene driven by either a PPAR response element or a DR-1 site present in the SDC-1 promoter, reporter activities were enhanced by n-3 LDL, DHA, and PPAR gamma agonist, whereas activity of a luciferase gene placed downstream of a mutant DR-1 site was unresponsive. Cotransfection with dominant-negative PPAR gamma DNA eliminated the increase in luciferase activity. These data provide strong evidence that SDC-1 is a molecular target of n-3 PUFA in human breast cancer cells through activation of PPAR gamma and that n-3 PUFA-induced apoptosis is mediated by SDC-1. This provides a novel mechanism for the chemopreventive effects of n-3 PUFA in breast cancer.
PMID: 18413760 [PubMed - indexed for MEDLINE]
WOW - you cannot argue with measured fats in breast tissue, - they do not have momentary memory lapses about what people ate, - they do not respond to very short term dietary changes - they simply and accurately reflect diet.
For me this is powerful evidence that Omega 6 and 3 have a role in the risk of breast cancer occurrence.
The bold and underline are mine.
RB
"We conclude that total n-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that LC n-3 PUFAs, derived from fish oils, may have a protective effect."
Nutr Cancer. 2002;42(2):180-5.
http://www.ncbi.nlm.nih.gov/pubmed/12416257?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=2&log$=relatedarticles&logdbfrom=pubmed
Long-chain n-3-to-n-6 polyunsaturated fatty acid ratios in breast adipose tissue from women with and without breast cancer.
Bagga D, Anders KH, Wang HJ, Glaspy JA.
Division of Hematology-Oncology, Department of Medicine, University of California, Los Angeles School of Medicine, Los Angeles, CA 90095, USA.
Animal studies suggest that dietary polyunsaturated fatty acids (PUFAs) of the n-6 class, found in corn and safflower oils, may be precursors of intermediates involved in the development of mammary tumors, whereas long-chain (LC) n-3 PUFAs, found in fish oil, can inhibit these effects. This case-control study was designed to examine the relationship between the PUFA composition of breast adipose tissue and the risk of breast cancer. Using fatty acid levels in breast adipose tissue as a biomarker of past qualitative dietary intake of fatty acids, we examined the hypothesis that breast cancer risk is negatively associated with specific LC n-3 PUFAs (eicosapentaenoic acid and docosahexaenoic acid) and positively associated with n-6 PUFAs (linoleic acid and arachidonic acid). Breast adipose tissue was collected from 73 breast cancer patients and 74 controls with macromastia. The fatty acid levels were determined by gas-liquid chromatography. A logistic regression model was used to obtain odds ratio estimates while adjusting for age. The age-adjusted n-6 PUFA (linoleic acid and arachidonic acid) content was significantly higher in cases than in controls (P = 0.02). There was a trend in the age-adjusted data suggesting that, at a given level of n-6 PUFA, LC n-3 PUFAs (eicosapentaenoic acid and docosahexaenoic acid) may have a protective effect (P = 0.06). A similar inverse relationship was observed with LC n-3-to-n-6 ratio when the data were adjusted for age (P = 0.09). We conclude that total n-6 PUFAs may be contributing to the high risk of breast cancer in the United States and that LC n-3 PUFAs, derived from fish oils, may have a protective effect.
There are a number of trials with chemo drugs suggesting synergies with long chain Omega 3.
It is something obviously to discuss with your medical adviser before altering your diet.
If you want to search for your particular chemo combinations try entering the drug and DHA or EPA or Omega 3 and see what comes up. You could always take the result along with you to show your advisors. http://www.ncbi.nlm.nih.gov/
Here they are suggesting Omega 3 may effect Her2. [ In an other trial it has been shown Omega 3 and 6 change Her2 gene expression by significant amounts in rat skeletal muscular tissue.]
Trials on other cancers suggest that DHA may increase rates of cell death. In healthy cells long chain omega 3s may be protective and some reports suggest an antioxidant effect - and DHA seems to have a part to play in defective cell kill off. It is very complicated and I only post these views through the thick mist so you understand that DHA is OK for healthy cells - dolphins would be in trouble otherwise (-: with all the fish they eat.
http://www.ncbi.nlm.nih.gov/pubmed/18602809?ordinalpos=4&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsP anel.Pubmed_RVDocSum
J Nutr Biochem. 2008 Jul 3. [Epub ahead of print]Click here to read Links
The potential for treatment with dietary long-chain polyunsaturated n-3 fatty acids during chemotherapy.
Biondo PD, Brindley DN, Sawyer MB, Field CJ.
Department of Agricultural, Food and Nutritional Science, University of Alberta, Edmonton, Alberta, Canada T6G 2P5.
Dietary intake of long-chain omega-3 (or n-3) polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) can affect numerous processes in the body, including cardiovascular, neurological and immune functions, as well as cancer. Studies on human cancer cell lines, animal models and preliminary trials with human subjects suggest that administration of EPA and DHA, found naturally in our diet in fatty fish, can alter toxicities and/or activity of many drugs used to treat cancer. Multiple mechanisms are proposed to explain how n-3 PUFA modulate the tumor cell response to chemotherapeutic drugs. n-3 PUFA are readily incorporated into cell membranes and lipid rafts, and their incorporation may affect membrane-associated signaling proteins such as Ras, Akt and Her-2/neu. Due to their high susceptibility to oxidation, it has also been proposed that n-3 PUFA may cause irreversible tumor cell damage through increased lipid peroxidation. n-3 PUFA may increase tumor cell susceptibility to apoptosis by altering expression or function of apoptotic proteins, or by modulating activity of survival-related transcription factors such as nuclear factor-kappaB. Some studies suggest n-3 PUFA may increase drug uptake or even enhance drug activation (e.g., in the case of some nucleoside analogue drugs). Further research is warranted to identify specific mechanisms by which n-3 PUFA increase chemotherapy efficacy and to determine the optimal cellular/membrane levels of n-3 PUFA required to promote these mechanisms, such that these fatty acids may be prescribed as adjuvants to chemotherapy.
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