Turmeric is useful for all inflammatory disorders and for autoimmune conditions.

[Unregistered]

More on tumeric

For me it interesting that it is effective against inflamatory disorders.

I wonder if there is any communality in involvment (if opposing effect) in body mechanisms with omega six a percusor of inflamatory body responses



RB

http://www.azcentral.com/health/wellness/articles/0207qaweil0207.html

ABSTRACTs

In the M.D. Anderson study, researchers injected mice with breast cancer cells from a woman whose disease had spread to her lungs. The cells began to grow in the mice and then were surgically removed. The mice then were divided into four groups: one got no treatment, one got curcumin, one got the cancer drug Taxol and the fourth group got curcumin plus Taxol. Cancer spread to the lungs among half the mice in the curcumin-only group and 22 percent of those in the curcumin/Taxol group. The other groups fared far worse: among the mice that received Taxol alone, 75 percent developed lung tumors; and the cancer spread to the lungs among 95 percent of the mice that were given no treatment.................


Turmeric is useful for all inflammatory disorders and for autoimmune conditions. It also may have a role in the prevention and treatment of Alzheimer's disease. (Elderly villagers in India appear to have the lowest rate of Alzheimer's in the world, perhaps due to the fact that Indians eat turmeric with almost every meal. Some animal studies have shown that curcumin blocked the formation and accumulation of the plaque that characterizes Alzheimer's.)

Overall, turmeric appears to have significant anti-inflammatory and cancer-protective effects. These seem most evident at doses well below pharmaceutical strength, which suggests that it would be wise to consume more foods spiced with turmeric.

[TriciaK]

My chiropractor put me on a supplement called "KappArest" from Biotics Research Corporation that contains a 1,150 mg proprietory blend of herbs, starting with curcumin or tumeric. I take 3 a day, and have noticed a decrease in pain. Hopefully it is doing good for cancer control, too. The chiropractor coaches a rugby team and he says this supplement is invaluable for muscle or joint pain. He was very interested when I told him about the cancer connection. My husband, who has rhuematoid arthritis, says it helps him, too.

[AlaskaAngel]

I use it myself daily and for whatever value it has I am NED, but have not actively tried to get my husband to use it... but he has some severe joint problems... Thanks for the suggestion. I will see if I can get the Meat Monster in the house to at least put something good ON the meat...

A.A.

[Unregistered]

I take a level table spoon of "haldi" very day just for general health. As a spice it is very reasonable and may for those on budgets be a cheaper source. I have not checked out realtive concentration to tablets etc.

Interestingly I first came across it in a sports nutrition magazine for joint health, and took it following a knee injury.

Omega three is also good for joint health.

RB

[Unregistered]

More on cox 2 and PPARs and lipid intake - why my guess is that lipid intake in a fundamental factor in many areas of health including BC vascular and cardiac.

My recollection is that omega three primarily is related to PPAR alpa, and omega six to ppar gama, which would tie in with PPAR alpha preventing cox 2, iinflamatory factors etc.

I will post the trial when I refind it. I would again stress this mine is strictly amateur viewpont. I am just desparately trying to convince readers that balancing omega threes and sixes is something that readers should actively consider for themselves.

RB



http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=10431661&dopt=Abstract


Peroxisome proliferator-activated receptor-alpha activators regulate genes governing lipoprotein metabolism, vascular inflammation and atherosclerosis.

Fruchart JC, Duriez P, Staels B.

Department of Atherosclerosis, INSERM U325, Pasteur Institute, University of Lille II, France. Jean-Charles.Fruchart@pasteur-lille.fr

The peroxisome proliferator-activated receptors (PPARs) [alpha, delta (beta) and gamma] form a subfamily of the nuclear receptor gene family. All PPARs are, albeit to different extents, activated by fatty acids and derivatives; PPAR-alpha binds the hypolipidemic fibrates whereas antidiabetic glitazones are ligands for PPAR-gamma. PPAR-alpha activation mediates pleiotropic effects such as stimulation of lipid oxidation, alteration in lipoprotein metabolism and inhibition of vascular inflammation. PPAR-alpha activators increase hepatic uptake and the esterification of free fatty acids by stimulating the fatty acid transport protein and acyl-CoA synthetase expression. In skeletal muscle and heart, PPAR-alpha increases mitochondrial free fatty acid uptake and the resulting free fatty acid oxidation through stimulating the muscle-type carnitine palmitoyltransferase-I. The effect of fibrates on the metabolism of triglyceride-rich lipoproteins is due to a PPAR-alpha dependent stimulation of lipoprotein lipase and an inhibition of apolipoprotein C-III expressions, whereas the increase in plasma HDL cholesterol depends on an overexpression of apolipoprotein A-I and apolipoprotein A-II. PPARs are also expressed in atherosclerotic lesions. PPAR-alpha is present in endothelial and smooth muscle cells, monocytes and monocyte-derived macrophages. It inhibits inducible nitric oxide synthase in macrophages and prevents the IL-1-induced expression of IL-6 and cyclooxygenase-2, as well as thrombin-induced endothelin-1 expression, as a result of a negative transcriptional regulation of the nuclear factor-kappa B and activator protein-1 signalling pathways. PPAR activation also induces apoptosis in human monocyte-derived macrophages most likely through inhibition of nuclear factor-kappa B activity. Therefore, the pleiotropic effects of PPAR-alpha activators on the plasma lipid profile and vascular wall inflammation certainly participate in the inhibition of atherosclerosis development observed in angiographically documented intervention trials with fibrates.

Publication Types:

* Review


PMID: 10431661 [PubMed - indexed for MEDLINE]

[Becky]

Perhaps some of us just don't respond to your messages - like me. But I agree wholeheartedly with you on balancing the Omega 3 with Omega 6. I feel that this is one pathway to try to block in order to not only prevent a recurrence but also (very importantly) to prevent a new primary. There are a few pathways that interest me - Cox 2 (were the 6/3 balance comes in). I also take a full strength aspirin a day for this as well - I have to be careful as I take fish oil and cod liver oil (which also thin the blood but....). I also feel strongly about glycemic index and the insulin (IG) pathways so I exercise (walk and run - sometimes an exercise tape but mostly aerobic exercise) and watch what I eat (besides 6/3 ratio). No fruit alone, grains, veggies - I will occassionally use butter but oil wise - only extra virgin olive and canola (if I need an oil that can take more heat).

I also take extra D to downregulate cyclin D1 and hopefully more fully activate the FAS receptors and some maitake to activate Pten if I happen to have it and it is in an inactive state.

I really do appreciate your contributions to this website.

Sincerely

Becky

[Unregistered]

As usual the more I read the more complex it all gets.

I dont pretend to understand much of this, I just get occasional hints of a maybe outline in the mist.

This abstract relates Cox 2 arachidonic acid which are both involved in the omega six eicosanoid pathway, PPAR gamma, and fat storage metabolism which in a sense is a key function of the breast.

It also links in insulin.

My point is that the make up of fat intake potentially has the ability to influence the bodies operation at a very fundamental level, and in areas that are reported to be relevant to breast cancer.

I am afraid you will have to draw your own inferences - this is strictly amateur interest.

RB


http://mend.endojournals.org/cgi/content/full/16/11/2628

ABSTRACT

THE PEROXISOME PROLIFERATOR-activated receptors (PPARs, NR1C1, NR1C2, NR1C3; Ref. 1) are members of the nuclear receptor superfamily. They function as heterodimers with the receptor of 9-cis-retinoic acid (RXR, NR2B; Ref. 1), and bind to specific peroxisome proliferator response elements (PPREs) to regulate transcription of their target genes. Three different PPAR genes have been characterized, which give rise to four distinct proteins ({alpha}, ß/{delta}, {gamma}1, and {gamma}2). Although the PPARs were first cloned as orphan members of the nuclear receptor gene family, rapid progress has been made in their functional analysis. This research contributed to a better understanding of the importance of fatty acids as hormones and has established the PPARs as molecular targets for the development of drugs to treat human diseases (2).

PPAR{gamma} is expressed predominantly in adipose tissue, where it is known to play a critical role in adipocyte differentiation and fat deposition (3, 4). It can be activated by arachidonic acid-metabolites generated by the cyclooxygenase and lipooxygenase pathways (5, 6, 7) and by fatty acid-derived components released from oxidized low density lipoproteins (8). The antidiabetic thiazolidinediones (TZDs), currently used as insulin sensitizers, are the best synthetic PPAR{gamma} ligands in terms of specificity and affinity, although the mechanism by which activation of PPAR{gamma} leads to an improvement of insulin action is still debated (3, 4, 9). Moreover, deletion of one allele of PPAR{gamma} was recently shown to protect mice from high fat diet (HFD)-induced adipocyte hypertrophy and insulin resistance, underlying the complexity of the role of PPAR{gamma} in insulin sensitivity (10).

The most extensively studied therapeutic utility for PPAR{gamma} has been in the treatment of type 2 diabetes. ......

[Unregistered]

As usual the more I read the more complex it all gets.

I dont pretend to understand much of this, I just get occasional hints of a maybe outline in the mist.

This abstract relates Cox 2 arachidonic acid which are both involved in the omega six eicosanoid pathway, PPAR gamma, and fat storage metabolism which in a sense is a key function of the breast.

It also links in insulin.

My point is that the make up of fat intake potentially has the ability to influence the bodies operation at a very fundamental level, and in areas that are reported to be relevant to breast cancer.

I am afraid you will have to draw your own inferences - this is strictly amateur interest.

RB


http://mend.endojournals.org/cgi/content/full/16/11/2628

ABSTRACT

THE PEROXISOME PROLIFERATOR-activated receptors (PPARs, NR1C1, NR1C2, NR1C3; Ref. 1) are members of the nuclear receptor superfamily. They function as heterodimers with the receptor of 9-cis-retinoic acid (RXR, NR2B; Ref. 1), and bind to specific peroxisome proliferator response elements (PPREs) to regulate transcription of their target genes. Three different PPAR genes have been characterized, which give rise to four distinct proteins ({alpha}, ß/{delta}, {gamma}1, and {gamma}2). Although the PPARs were first cloned as orphan members of the nuclear receptor gene family, rapid progress has been made in their functional analysis. This research contributed to a better understanding of the importance of fatty acids as hormones and has established the PPARs as molecular targets for the development of drugs to treat human diseases (2).

PPAR{gamma} is expressed predominantly in adipose tissue, where it is known to play a critical role in adipocyte differentiation and fat deposition (3, 4). It can be activated by arachidonic acid-metabolites generated by the cyclooxygenase and lipooxygenase pathways (5, 6, 7) and by fatty acid-derived components released from oxidized low density lipoproteins (8). The antidiabetic thiazolidinediones (TZDs), currently used as insulin sensitizers, are the best synthetic PPAR{gamma} ligands in terms of specificity and affinity, although the mechanism by which activation of PPAR{gamma} leads to an improvement of insulin action is still debated (3, 4, 9). Moreover, deletion of one allele of PPAR{gamma} was recently shown to protect mice from high fat diet (HFD)-induced adipocyte hypertrophy and insulin resistance, underlying the complexity of the role of PPAR{gamma} in insulin sensitivity (10).

The most extensively studied therapeutic utility for PPAR{gamma} has been in the treatment of type 2 diabetes. ......

[Unregistered]

A related subject this time CLA (found in fats of grass fed ruminants) also suggested in trails to reduce the risks of cancer.

It is interesting that it too appears to act on PPAR gamma.

Sorry no link as I somehow lost my place!, - and it may take some time to refind it.

RB




1: Comp Biochem Physiol B Biochem Mol Biol. 2002 Nov;133(3):395-404. Related Articles, Links
Click here to read
Dietary conjugated linoleic acid reduces body fat mass and affects gene expression of proteins regulating energy metabolism in mice.

Takahashi Y, Kushiro M, Shinohara K, Ide T.

Division of Food Functionality, National Food Research Institute, 2-1-12 Kannondai, Tsukuba Science City, Ibaraki 305-8642, Japan.

ICR and C57BL/6J mice were fed experimental diets containing either a 2% fatty acid preparation rich in conjugated linoleic acid (CLA) or a preparation rich in linoleic acid and free of CLA for 21 days. CLA greatly decreased weights of white adipose tissue and interscapular brown adipose tissue in the two strains. CLA reduced mRNA levels of glucose transporter 4 (Glut 4) in white and brown adipose tissue of both strains. A CLA-dependent decrease in mRNA levels of peroxisome proliferator activated receptor (PPAR) gamma was seen in interscapular brown adipose tissue of both strains and in white adipose tissue of C57BL/6J but not ICR mice. Dietary CLA was found to cause a decrease in the mRNA levels of uncoupling protein (UCP) 1 in brown adipose tissue when the value was corrected for the expression of a house-keeping gene (beta-actin) in the two strains. Uncorrected values were, however, indistinguishable between the animals fed the CLA diet and CLA-free diet. UCP 3 expression in brown adipose tissue was much lower in mice fed the CLA diet than in those fed the control diet in both strains. In contrast, CLA greatly up-regulated the gene expression of UCP 2 in brown adipose tissue. Dietary CLA also increased UCP 2 mRNA level in skeletal muscle. It is apparent that dietary CLA decreases white and brown adipose tissue mass, accompanying changes in the gene expression of proteins regulating energy metabolism in white and brown adipose tissues, and skeletal muscle of mice. Copyright 2002 Elsevier Science Inc.

PMID: 12431407 [PubMed - indexed for MEDLINE]

[Unregistered]

For those that are interested in this research that leaves you with a head full of a cooked spaggetti of information....


Here is a trial that links omega threes to PPAR alpha, re my earlier suggestion that I thought I had read that primarily but not exclusively PPAR gamma was connected to omega six and PPAR alph to omega three - and in very general but not exclusive terms as it all appears a great deal more complex and interlinked PPAR gamma deals with storage and alpha with utilisation by skeletal muscle etc.

RB


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15497766&query_hl=22&itool=pubmed_DocSum

1: Nutr Rev. 2004 Sep;62(9):333-9. Related Articles, Links
Click here to read
Polyunsaturated fatty acid regulation of gene expression.

Sampath H, Ntambi JM.

Department of Nutritional Sciences, University of Wisconsin, Madison, WI 53706, USA.

Polyunsaturated fatty acids (PUFAs), specifically the n-3 series, have been implicated in the prevention of various human diseases, including obesity, diabetes, coronary heart disease and stroke, and inflammatory and neurologic diseases. PUFAs function mainly by altering membrane lipid composition, cellular metabolism, signal transduction, and regulation of gene expression. PUFAs regulate the expression of genes in various tissues, including the liver, heart, adipose tissue, and brain. The role of transcription factors such as SREBP1c and nuclear receptors such as PPAR-alpha, HNF-4alpha, and LXRalpha in mediating the nuclear effects of PUFAs are addressed.

Publication Types:

* Review


PMID: 15497766 [PubMed - indexed for MEDLINE]