Low-Fat Diets Disappoint for Cancer and Heart Disease (women ages 50 to 79

[RedEarth]

SEATTLE, Feb. 7 - Low-fat diets failed to reduce the risk of breast and colon cancer and also fell short for cardiovascular disease, according to a large controlled intervention trial.


Despite the long-held hope that a diet low in fat and high in fruits and grains could reduce the risk of these ailments, no benefit was found, according to results from the Women's Health Initiative Randomized Controlled Dietary Modification Trial.


The empty-glass findings-at least for now-- were reported in three separate studies in the Feb. 8 issue of the Journal of the American Medical Association.


The large primary prevention trial conducted at 40 U.S. clinical centers from 1993 to 2005 enlisted 48,835 postmenopausal women ages 50 to 79 years.

http://www.medpagetoday.com/PrimaryCare/DietNutrition/tb/2636

[HysteryDiagnosis]

1. Lowfat can also minimize the intake of the healthy fats.... and that

is just criminal. Heart disease begins in childhood, the arteries of vietnam soldiers showed advanced atherosclerosis and arteriosclerosis, they started this study late in life.... too late to reverse decades of the effects of the SAD diet. (Standard American Diet).




Would you believe 48 cyllinders??

[ayeshahaqqiqa]

2. Selenium

the latest studies involving this mineral hold hopes that a proper amount of selenium in the diet can inhibit cancer cell growth and also help fend off viruses. I volunteer for a health non-profit, and this is the message in the latest newsletter. It's been sent to the foundation president for editing, or I'd have a copy where I could cite the sources for this-just skimmed the article today as I put the newsletter together.

[Wordie]

5. I read something recently about Vitamin D that said much the same.

...but see my post below. (Sorry if I'm a bit cynical on this issue.)

[RedOnce]

10. Yes, Selenium...

J Nutr. 2006 Jan;136(1):172-6.

Low Serum Selenium and Total Carotenoids Predict Mortality among Older Women Living in the Community: The Women's Health and Aging Studies.

Ray AL, Semba RD, Walston J, Ferrucci L, Cappola AR, Ricks MO, Xue QL, Fried LP.

The Johns Hopkins Medical Institutions, Baltimore, MD; Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, PA.

Selenium and the carotenoids play an important role in antioxidant defenses and in the redox regulation involved in inflammation. We tested the hypothesis that low selenium and carotenoids predict mortality in older women living in the community. Women who were enrolled in the Women's Health and Aging Studies I and II in Baltimore, MD (n = 632; 70-79 y old) had serum selenium and carotenoids measured at baseline and were followed for mortality over 60 mo. Median (minimum, maximum) serum selenium and carotenoids were 1.53 (0.73, 2.51) mumol/L and 1.67 (0.13, 9.10) mumol/L; 14.1% of the women died. The 5 major causes of death were heart disease (32.6%), cancer (18.0%), stroke (9.0%), infection (6.7%), and chronic obstructive pulmonary disease (5.6%). Adjusting for age, education, smoking, BMI, poor appetite, and chronic diseases, higher serum selenium and higher serum total carotenoids (HR 0.77, 95% CI 0.64-0.84/1 SD increase in log(e) total carotenoids; P = 0.009) were associated with a lower risk of mortality. Women living in the community who have higher serum selenium and carotenoids are at a lower risk of death.

PMID: 16365078

[Wordie]

3. I've often wondered about some of the sorts of studies that claim

to find such links as the Seattle study couldn't find. It seems to me that they may confuse correlation with causation. In other words, the people in the earlier studies who have X or Y diet and get A,B,or C amount or type of exercise may just have been healthier in the first place. Maybe the truth of the matter is that people who are healthy just like to eat well and exercise, but that doing so for the average or unhealthy person really changes little.

I probably didn't state that very well...

(Disclaimer: not medical advice.)

[ayeshahaqqiqa]

7. What was interesting in the selenium study

was that at least one part of it was to study the rates of cancer and other diseases in different geographical areas in the world. Like I said, I don't have the article with me now, but as I recall it said that in areas where selenium is plentiful in the soil, the rates of certain specific illnesses was less than in other areas where selenium was deficient. I find this type of "geographical study" to be fascinating, especially if it is done along with other types of studies.

[mike_c]

4. low-CALORIE diet and moderate exercise are still...

...the best life-style choices, IMO, along with eating a balanced array of real foods to comprise that diet. There isn't any magic prescription-- the same things that contribute to peak health at 20 do so at 65, too-- it's just that our ability to withstand the damage from deviating from good habits declines as we accumulate wear and tear throughout life.

I think the simple truth is that we are just not well evolved for living beyond 50 years old or so-- degenerative decline is inevitable for most of us, and the margin of forgiveness becomes thinner and thinner.

[HysteryDiagnosis]

6. I said, reduction of the already low levels of healthy fats included

in the SAD diet is criminal, if you can understand this, you can understand the role of fish oil and healthy fats in preventing disease and promoting a higher level of health.


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16005051&query_hl=1&itool=pubmed_docsum
Centre de Recherches Biologiques, Chemin de Montifault, 18800 Baugy, France.

The relationship between high fish consumption and low mortality following coronary heart disease (CHD) and low incidence of breast cancer was first mentioned 3 decades ago. The fishes of interest are rich in omega-3 long-chain polyunsaturated fatty acids (omega-3 LC-PUFAs), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which could be the active nutrients. The current consensus about cardioprotection is that omega-3 LC-PUFAs would mainly exert antiarrhythmic effects. One of the proposed mechanisms is that circulating non-esterified LC-PUFAs partition into cardiac cells membrane phospholipids and exert a direct effect on ionic channels and/or modify intracellular calcium homeostasis. In another hypothesis, changes in the metabolism of phosphoinositides would be involved and lead to the differential activation of PKC isoforms. As compared to the mechanisms proposed for the cardioprotective effects of omega-3 LC-PUFAs, less is known about the molecular mechanisms involved in breast cancers prevention. Some proposed mechanisms such as the modulation of phosphoinositides metabolism and/or modulation of intracellular calcium homeostasis, are common to both pathologies. Other hypotheses involve the alteration of the cellular redox status induced by highly peroxidizable polyunsaturated fatty acids (FA), or the modulation of gene expression, both phenomena being tightly linked to apoptosis. In this review, we report and compare some proposed mechanisms for the involvement of omega-3 LC-PUFAs in both cardiac and breast cancer protection. Deliberately, we chose to discuss only the mechanisms, which are less described in other reviews such as ionic channels in cancer, calcium homeostasis, PKC activation or matrix metalloproteinases in both cancer and cardiac models. The leitmotiv along this review is that cardio- and cancero-protective effects use common pathways. Comparison of the cellular effects might therefore help to highlight the "protective" pathways.

PMID: 16005051

Then there are these.....

1: Wu WH, Lu SC, Wang TF, Jou HJ, Wang TA. Related Articles, Links
Abstract Effects of docosahexaenoic acid supplementation on blood lipids, estrogen metabolism, and in vivo oxidative stress in postmenopausal vegetarian women.
Eur J Clin Nutr. 2005 Nov 9;
PMID: 16278686

2: Tuoya, Baba N, Shimoishi Y, Murata Y, Tada M, Koseki M, Takahata K. Related Articles, Links
Abstract Apoptosis induction by dohevanil, a DHA substitutive analog of capsaicin, in MCF-7 cells.
Life Sci. 2005 Oct 27;
PMID: 16260002

3: Stillwell W, Shaikh SR, Zerouga M, Siddiqui R, Wassall SR. Related Articles, Links
Abstract Docosahexaenoic acid affects cell signaling by altering lipid rafts.
Reprod Nutr Dev. 2005 Sep-Oct;45(5):559-79. Review.
PMID: 16188208

4: Siddiqui RA, Zerouga M, Wu M, Castillo A, Harvey K, Zaloga GP, Stillwell W. Related Articles, Links
Abstract Anticancer properties of propofol-docosahexaenoate and propofol-eicosapentaenoate on breast cancer cells.
Breast Cancer Res. 2005;7(5):R645-54. Epub 2005 Jun 7.
PMID: 16168109

5: Maheo K, Vibet S, Steghens JP, Dartigeas C, Lehman M, Bougnoux P, Gore J. Related Articles, Links
Free Full Text Differential sensitization of cancer cells to doxorubicin by DHA: a role for lipoperoxidation.
Free Radic Biol Med. 2005 Sep 15;39(6):742-51.
PMID: 16109304

6: Jude S, Roger S, Martel E, Besson P, Richard S, Bougnoux P, Champeroux P, Le Guennec JY. Related Articles, Links
Abstract Dietary long-chain omega-3 fatty acids of marine origin: a comparison of their protective effects on coronary heart disease and breast cancers.
Prog Biophys Mol Biol. 2006 Jan-Apr;90(1-3):299-325. Epub 2005 Jun 15.
PMID: 16005051

7: Schley PD, Jijon HB, Robinson LE, Field CJ. Related Articles, Links
Free Full Text Mechanisms of omega-3 fatty acid-induced growth inhibition in MDA-MB-231 human breast cancer cells.
Breast Cancer Res Treat. 2005 Jul;92(2):187-95.
PMID: 15986129

8: Duncan RE, El-Sohemy A, Archer MC. Related Articles, Links
Abstract Regulation of HMG-CoA reductase in MCF-7 cells by genistein, EPA, and DHA, alone and in combination with mevastatin.
Cancer Lett. 2005 Jun 28;224(2):221-8. Epub 2004 Dec 16.
PMID: 15914273

9: Menendez JA, Lupu R, Colomer R. Related Articles, Links
Abstract Exogenous supplementation with omega-3 polyunsaturated fatty acid docosahexaenoic acid (DHA; 22:6n-3) synergistically enhances taxane cytotoxicity and downregulates Her-2/neu (c-erbB-2) oncogene expression in human breast cancer cells.
Eur J Cancer Prev. 2005 Jun;14(3):263-70.
PMID: 15901996

10: Wu M, Harvey KA, Ruzmetov N, Welch ZR, Sech L, Jackson K, Stillwell W, Zaloga GP, Siddiqui RA. Related Articles, Links
Abstract Omega-3 polyunsaturated fatty acids attenuate breast cancer growth through activation of a neutral sphingomyelinase-mediated pathway.
Int J Cancer. 2005 Nov 10;117(3):340-8.
PMID: 15900589

11: Chiu LC, Wong EY, Ooi VE. Related Articles, Links
Abstract Docosahexaenoic acid from a cultured microalga inhibits cell growth and induces apoptosis by upregulating Bax/Bcl-2 ratio in human breast carcinoma MCF-7 cells.
Ann N Y Acad Sci. 2004 Dec;1030:361-8.
PMID: 15659818

12: Baumgartner M, Sturlan S, Roth E, Wessner B, Bachleitner-Hofmann T. Related Articles, Links
Abstract Enhancement of arsenic trioxide-mediated apoptosis using docosahexaenoic acid in arsenic trioxide-resistant solid tumor cells.
Int J Cancer. 2004 Nov 20;112(4):707-12.
PMID: 15382055

13: Heller AR, Rossel T, Gottschlich B, Tiebel O, Menschikowski M, Litz RJ, Zimmermann T, Koch T. Related Articles, Links
Abstract Omega-3 fatty acids improve liver and pancreas function in postoperative cancer patients.
Int J Cancer. 2004 Sep 10;111(4):611-6.
PMID: 15239141

14: Tsujita-Kyutoku M, Yuri T, Danbara N, Senzaki H, Kiyozuka Y, Uehara N, Takada H, Hada T, Miyazawa T, Ogawa Y, Tsubura A. Related Articles, Links
Free Full Text Conjugated docosahexaenoic acid suppresses KPL-1 human breast cancer cell growth in vitro and in vivo: potential mechanisms of action.
Breast Cancer Res. 2004;6(4):R291-9. Epub 2004 Apr 26.
PMID: 15217495

15: Simopoulos AP. Related Articles, Links
Abstract The traditional diet of Greece and cancer.
Eur J Cancer Prev. 2004 Jun;13(3):219-30. Review.
PMID: 15167223

16: Menendez JA, Ropero S, Mehmi I, Atlas E, Colomer R, Lupu R. Related Articles, Links
Free Full Text Overexpression and hyperactivity of breast cancer-associated fatty acid synthase (oncogenic antigen-519) is insensitive to normal arachidonic fatty acid-induced suppression in lipogenic tissues but it is selectively inhibited by tumoricidal alpha-linolenic and gamma-linolenic fatty acids: a novel mechanism by which dietary fat can alter mammary tumorigenesis.
Int J Oncol. 2004 Jun;24(6):1369-83.
PMID: 15138577

17: Rose DP, Rayburn J, Hatala MA, Connolly JM. Related Articles, Links
Abstract Effects of dietary fish oil on fatty acids and eicosanoids in metastasizing human breast cancer cells.
Nutr Cancer. 1994;22(2):131-41.
PMID: 14502842

[mike_c]

8. thanks for all the references, but did you mean to reply to me...

...or to the OP? Your tone suggests that you disagreed with me, but I don't think we have any disagreement, hence I wonder if you replied to me mistakenly. I said avoid overeating, eat good foods instead of manufactured junk, and exercise. :shrug:

[HysteryDiagnosis]

9. Everyone in general.... I want all to see that the American diet which

is notoriously low in healthy fats can spur on disease... no disagreements with you, sorry for posting in the wrong spot... :)

[RedOnce]

11. This makes sense to me.

[KurtNYC]

12. What I found interesting about their conclusion and the MSM

headline on the analysis was that the data from this study showed that women who ate 8% less fat (as a percentage of total calories) were 9% less likely to develop breast cancer. The study was designed to have a bigger difference between the groups but the low fat group ate more fat than they were supposed to. In fact, both groups increased their fat intake over the 8 years of the study. And there was a difference in cancer rates between the two but it wasn't a large enough difference to be statistically significant. So I think the best description of the study's results is that they are inconclusive; and NOT a conclusive indication that diet had no effect.

In the first year, the women on the low-fat diets reduced the percentage of fat in their diet to 24 percent of daily calories, and by the end of the study their diets had 29 percent of their calories as fat. In the first year, the women in the control group were eating 35 percent of their calories as fat, and by the end of the study their dietary fat content was 37 percent. The two groups consumed about the same number of calories.
...
Dr. Rossouw said he was still intrigued by the breast cancer data, even though it was not statistically significant. The women on low-fat diets had a 9 percent lower rate of breast cancer; the incidence was 42 per thousand per year in women in the low-fat diet group, compared with 45 per thousand per year in women consuming their regular diet.

http://www.nytimes.com/2006/02/08/health/08fat.html?pagewanted=2