Question about Quercetin-Rosemary, BBS, Tender, anyone?

Carol--I highly doubt he is talking of Curcumen.  Research is pretty positive with that one although investigational.

Yes, I'm familiar with Zyflamend and New Chapter is an excellant company,  I took it to help with

the musculoskeletal Femara issues.  It helped but I had to discontinue it because it disagreed with my stomach---but I have stomach issues anyhow.  Thought it was very good.  --Love Green curry---Save me some! 

By the way Rosemary ---Add Folate to that list--

I posted this under Confusion at the vitamin counter but it bears repeating-

Cover story is Confused about Vitamins-Too Little or Too Much- focusing on  Folic , Selenium, and Vitamin D

From what I've gleaned it says if you take a multi with 400 mcg of folic acid---don't eat any cereal,
energy bar or other food that contains 400mcg in the serving you eat.

Joel Mason, director of vitamins and Carcinogenisis Laboratory at the Jean Mayer USDA Human Nutrition Research Center of Aging at Tufts University in Boston says--Colorectal Cancers rose soon after companies started adding folic acid to foods but that still has yet to be proved.

Seems that they have compelling data that getting adequatefolic acid protects against certain cancers but an abundant quantity may accelerate carcinogenisis.

Here is the deal--The Ovarian Cancer Screening trial found a 19% higher risk of BC in postmenopausal women
who were taking at least 400mcg from supplements.

But, in Sweden another study showed a lower risk of BC in women who took the most Folic Acid 380 to 400mcg a day.
But here is the big difference why this is misleading.
Flour is not fortified in Sweden where they are getting much less folic acid. 
So getting more is still much less than we get from our diets!

The thought is that "maybe folic acid only enhances the growth of tumors when you exceed the threshold."

This has left experts unsure of the wisdom of adding folic acid to flour, "especially when some advocates of reducing birth defects want it raised" when colorectal, prostate and breast cancer increase as we age.
We could be harboring precancerous lesions and folic acid may fuel their growth.

And since we are getting all this additional involuntary folic acid we may be benefiting some and harming others.

Also, the article talked about the follow-up of a three year trial that had given a placebo or 1000mcg of folic acid to 1000 people who already had a precancerous polyp (adenoma) removed from their colon or rectum.
"we saw an increased risk of advanced adenomas in people who got folic acid," says co-author John Baron,
a professor of medicine at Dartmouth School of medicine.  And more Folic Acid Takers (10%)than placebo (4%) had at least 3 new adenomas and more folic acid takers (11%) than placebo (6%) were diagnosed with cancer outside the colon or rectum.
 

Seems like more than enough reason for us post menopausal gals to get this into our diet---
Thanks BBS, Carol C, Rosemary, and Marilyn ---I had not a clue about CLA being investigated for reducing BC.  Thanks for bringing attention to this supplement.  Still think diet is the way to go for me right now.
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From the California Breast Cancer research program

Reduced Breast Cancer Metastasis by Conjugated Linoleic Acid

University of California, Davis    
Investigator(s): Kent  Erickson , Ph.D. -
Award Type: Innovative Awards > ITaMoCAs
Award Cycle: 1998 (Cycle IV)     Grant #: 4CB-0157     Award Amount: $199,627

Research Priorities
Innovative Treatment Modalities > New drug design: creative science


Initial Award Abstract (1998)
The overall goal of this project is to determine how a specific type of dietary fat can reduce and potentially prevent the spread of breast cancer to other parts of the body, the process of metastasis. Despite advances in surgery and development of additional therapies for the treatment of tumors in the breast, most deaths are caused by the spread of the tumor. Since less than 10% of women have tumors that have completely spread to distant organs when their cancer is first detected, if agents were discovered to block metastasis, great advances could be made in prevention of the most devastating part of the disease.

Conjugated linoleic acid is a component found in some sources of dietary fat. It has been also found to be a potent chemoprotective agent against breast cancer in experimental animals. Although some dietary fats, such as those from plant oils, increased breast cancer while others, such as those from fish oils, reduced breast cancer growth, large changes in the amounts of dietary fat were necessary to achieve those alterations. In contrast, very low dietary concentrations of conjugated linoleic acid can significantly alter experimental breast cancer. Consequently, small alterations in dietary fat consumption, either through natural sources or as a supplement, has a great potential for reducing or preventing tumor metastasis.

In this project, we propose to investigate how conjugated linoleic acid reduces breast cancer by focusing on how it can alter metastasis. This step was selected because preliminary studies indicate that it may be altered by dietary fat. We believe this change may be due to reduction of prostaglandin E2, a fat-based mediator which has been shown to influence metastasis.

From this work, we hope to determine how dietary conjugated linoleic acid functions to reduce or prevent the spread of breast cancer. Although conjugated linoleic acid has not been tested in humans, these experiments in mice should provide a basis for future human studies to reduce the mortality of women diagnosed with the disease.
 
 

Final Report (2001)
The overall goal of this research project is to determine how a specific fatty acid can reduce and potentially prevent the spread of breast cancer. Conjugated linoleic acid (CLA), a fatty acid found in some sources of dietary fat, has been found to be a potent anticancer agent against breast tumors in mice. In this year 2 grant period, we focused our experiments to test whether synthetic conjugated linoleic acid, in very low dietary concentrations (as low as 0.1% in the diet), could reduce mouse breast tumor growth and spread in a mouse model which displays many of the characteristics of human tumors. In addition, we assessed the effect of dietary CLA on the potential expression of proteins that could make tumors less aggressive or more aggressive.

The results of our first set of experiments showed that dietary CLA significantly decreased not only the number of tumor cells that spread to other parts of the body but the degree to which they formed new tumors. Moreover, when mice were fed CLA, it took longer for tumors to establish at their primary site compared to mice that were fed diets containing no CLA. Those results were observed when the level of CLA in the diet was as low as 0.1%. Greater reductions in breast cancer metastasis were observed with 0.5% and 1.0% dietary CLA. The effects were observed in mice that were fed diets that contained relatively high levels of total fat and relatively high levels of the fatty acid linoleic acid, which is known to promote metastasis in this tumor model.

In our second set of studies, we observed that CLA had a modest effect of reducing the potential expression of certain types of proteins known as proteases which could increase the aggressiveness of tumor cells, and slightly increased the expression of other proteins, antiproteases, that could reduce the aggressiveness of tumor cells.

Our future direction involves determining the mechanism by which CLA reduces breast cancer in mice. Knowing the mechanism(s) will allow us to first, select appropriate biomarkers for CLA and breast cancer, necessary for a human trial; and second, design treatment modalities that could potentially reduce or even prevent breast cancer. In addition, the use of CLA as a possible adjuvant therapy would not be costly and would be more widely available since it is found in the diet.

Although CLA has not yet been tested in humans for the reduction or prevention of breast cancer, the results of these experiments should provide a basis for future human studies and thus, reduce mortality of women diagnosed with the disease.
 
 

Invasion of Metastasis. In: D. Herber, G.L., Blackburn and V.L. Go (Eds.), Nutritional Oncology, Academic Press, New York p. 29-40, 1998
    Periodical:     Index Medicus:
      Authors: Erickson, K.L. and N.E. Hubbard
      Yr:     Vol:     Nbr:     Abs:     Pg:

Involvment of AP-2 in PGE2-enhanced macrophage VEGF production. FASEB Journal 13:A361, 1999.
    Periodical:     Index Medicus:
      Authors: Mukutmoni-Norris, M. and K.L. Erickson
      Yr:     Vol:     Nbr:     Abs:     Pg:
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this is from eating wild
What is CLA?

The Basics. CLA is a newly discovered good fat called "conjugated linoleic acid" that may be a potent cancer fighter. In animal studies, very small amounts of CLA have blocked all three stages of cancer: 1) initiation, 2) promotion, and 3) metastasis. Most anti-cancer agents block only one of these stages. What's more, CLA has slowed the growth of an unusually wide variety of tumors, including cancers of the skin, breast, prostate, and colon.(1)

Human CLA research is in its infancy, but a few studies have suggested that CLA may have similar benefits in people. A recent survey determined that women with the most CLA in their diets had a 60 percent reduction in the risk of breast cancer. (2)

Where do you get CLA? Many people take a synthetic version that is widely promoted as a diet aid and muscle builder. New research shows that the type of CLA in the pills may have some potentially serious side effects, including promoting insulin resistance, raising glucose levels, and reducing HDL (good) cholesterol .(3)

Few people realize that CLA is also found in nature, and this natural form does not have any known negative side effects. The most abundant source of natural CLA is the meat and dairy products of grassfed animals. Research conducted since 1999 shows that grazing animals have from 3-5 times more CLA than animals fattened on grain in a feedlot. Simply switching from grainfed to grassfed products can greatly increase your intake of CLA. (4)

Learn more about the health benefits of products from pasture-raised animals.

Beyond the Basics. On the molecular level, CLA resembles another type of fat called "linoleic acid" or LA. (Both CLA and LA have 18 carbon atoms and two double bonds holding the chain together. The main difference is in the placement of those bonds.) However, CLA and LA appear to have opposite effects on the human body. For example, LA promotes tumor growth but CLA blocks it.

There are 28 possible types (isomers) of CLA, each one with a slightly different arrangement of chemical bonds. The type most commonly found in meat and dairy products has double bonds between the 9th and 11th carbon atoms and is referred to as "cis 9, trans-11 CLA" or "rumenic acid."

1. Ip, C., J. A. Scimeca, et al. (1994). "Conjugated linoleic acid. A powerful anticarcinogen from animal fat sources." Cancer 74(3 Suppl): 1050-4.

Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid, which is found preferentially in dairy products and meat. Preliminary studies indicate that CLA is a powerful anticarcinogen in the rat mammary tumor model with an effective range of 0.1-1% in the diet. This protective effect of CLA is noted even when exposure is limited to the time of weaning to carcinogen administration. The timing of this treatment corresponds to maturation of the mammary gland to the adult stage, suggesting that CLA may have a direct effect in reducing the cancer risk of the target organ. Of the vast number of naturally occurring substances that have been demonstrated to have anticarcinogenic activity in experimental models, all but a handful of them are of plant origin. Conjugated linoleic acid is unique because it is present in food from animal sources, and its anticancer efficacy is expressed at concentrations close to human consumption levels.

2. Aro, A., S. Mannisto, I. Salminen, M. L. Ovaskainen, V. Kataja, and M. Uusitupa. "Inverse Association between Dietary and Serum Conjugated Linoleic Acid and Risk of Breast Cancer in Postmenopausal Women." s 38, no. 2 (2000): 151-7.)

3. Riserus, U., P. Arner, et al. (2002). "Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome." Diabetes Care 25(9): 1516-21.

OBJECTIVE: Conjugated linoleic acid (CLA) is a group of dietary fatty acids with antiobesity and antidiabetic effects in some animals. The trans10cis12 (t10c12) CLA isomer seems to cause these effects, including improved insulin sensitivity. Whether such isomer-specific effects occur in humans is unknown. The aim of this study was to investigate whether t10c12 CLA or a commercial CLA mixture could improve insulin sensitivity, lipid metabolism, or body composition in obese men with signs of the metabolic syndrome. RESEARCH DESIGN AND METHODS: In a randomized, double-blind controlled trial, abdominally obese men (n = 60) were treated with 3.4 g/day CLA (isomer mixture), purified t10c12 CLA, or placebo. Euglycemic-hyperinsulinemic clamp, serum hormones, lipids, and anthropometry were assessed before and after 12 weeks of treatment. RESULTS: Baseline metabolic status was similar between groups. Unexpectedly, t10c12 CLA increased insulin resistance (19%; P < 0.01) and glycemia (4%; P < 0.001) and reduced HDL cholesterol (-4%; P < 0.01) compared with placebo, whereas body fat, sagittal abdominal diameter, and weight decreased versus baseline, but the difference was not significantly different from placebo. The CLA mixture did not change glucose metabolism, body composition, or weight compared with placebo but lowered HDL cholesterol (-2%; P < 0.05). CONCLUSIONS: These results reveal important isomer-specific metabolic actions of CLA in abdominally obese humans. A CLA-induced insulin resistance has previously been described only in lipodystrophic mice. Considering the use of CLA-supplements among obese individuals, it is important to clarify the clinical consequences of these results, but they also provide physiological insights into the role of specific dietary fatty acids as modulators of insulin resistance in humans.

4. Dhiman, T. R., G. R. Anand, et al. (1999). "Conjugated linoleic acid content of milk from cows fed different diets." J Dairy Sci 82(10): 2146-56.

Conjugated linoleic acid in milk was determined from cows fed different diets. In Experiment 1, cows were fed either normal or high oil corn and corn silage. Conjugated linoleic acid was 3.8 and 3.9 mg/g of milk fatty acids in normal and high oil treatments, respectively. In Experiment 2, cows consumed one-third, two-thirds, or their entire feed from a permanent pasture. Alfalfa hay and concentrates supplied the balance of feed for the one-third and two-third pasture treatments. Conjugated linoleic acid was 8.9, 14.3, and 22.1 mg/g of milk fatty acids in the one-third, two-third, and all pasture treatments, respectively. Cows grazing pasture and receiving no supplemental feed had 500% more conjugated linoleic acid in milk fat than cows fed typical dairy diets.
--------------------------

and this from the journal of nutrition

Nutrition and Cancer
Conjugated Linoleic Acid Blocks Estrogen Signaling in Human Breast Cancer Cells1
Prasong Tanmahasamut*,2, Jingbo Liu*,2, Lawrence B. Hendry{dagger} and Neil Sidell*,3

* Division of Research, Department of Gynecology and Obstetrics, Emory University School of Medicine, Atlanta, GA 30322; and {dagger} Accelerated Pharmaceuticals, Augusta, GA 30903

3To whom correspondence should be addressed. E-mail: Nsidell@emory.edu.

Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid found in dairy products and meat from ruminants, has been widely shown to possess anticarcinogenic activity against breast cancer both in vitro and in animal models. However, little information is available concerning the mechanisms of the antitumor effects of these compounds. In this study, we investigated whether CLA has direct antiestrogenic activity in estrogen receptor positive (ER+) breast cancer cells. Treatment of the ER+ cell line, MCF-7, with 5 purified CLA isomers as well as "mixed" CLA showed a dose-dependent growth inhibition with the 9cis,11cis and 9cis,11trans being the most and least potent isomers, respectively. In assessing effects on a number of variables that play obligatory roles in the estrogen signaling pathway, we determined that CLA treatment downregulated ER{alpha} expression at both mRNA and protein levels and decreased binding activity of nuclear protein to a canonical estrogen response element (EREv). Using a reporter gene construct (EREv-tk-Luc) that was transiently transfected into MCF-7 cells, we also demonstrated inhibition of promoter activity by CLA that was directly mediated by blockage of activity through the ERE. The results indicated that the order of potency of the CLA isomers for inhibiting activation of EREv was similar to that demonstrated for their antiproliferative activity on MCF-7 cells. Taken together, these findings demonstrate that CLA compounds possess potent antiestrogenic properties that may at least partly account for their antitumor activity on breast cancer cells.

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