The traditional diet of Greece and cancer.

[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.

[R.B.]

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

[R.B.]

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/en...RVAbstractPlus

[R.B.]

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/en...ubmed_RVDocSum

[R.B.]

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.

[R.B.]

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/0...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.

[R.B.]

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]

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

[R.B.]

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...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

[R.B.]

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]

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 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 and Make AOL Your

[R.B.]

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.

[R.B.]

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/en..._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."

[R.B.]

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/1...ubmed_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.

[R.B.]

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/1...ubmed_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

[R.B.]

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/1...ubmed_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.

[R.B.]

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/1...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.

[R.B.]

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.or...ull/11/10/3828

[R.B.]

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.

[R.B.]

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