It is hard to sort out the inflammatory effects of short/long-chain omega-6 and omega-3 fatty acids. Vegetable antioxidants make the picture even worse. The absolute, as well as relative amounts, of the various types of fatty acids make a difference. It also now appears that oxidation prior and during digestion may be important to the impact of polyunsaturated fatty acids (PUFAs). The source (perhaps even the meal composition) of the PUFAs was as important as omega-3 versus omega-6, for common, short chain PUFAs.In some studies, omega-3 PUFAs, such as the short-chain alpha linolenic acid (ALA) common in flax seed or the long-chain fish oil FUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), reduced cancer in human and mice. Earlier work in cell cultures showed that all of PUFAs suppressed the growth of cancer cells.
A large French study (reference below) began in 1993. Approximately 100,000 women between the ages of 40 and 65 volunteered to provide dietary and breast malignancy information and ca. 75,000 qualified for the study (the French component of EPIC, European Investigation of Cancer and Nutrition) . The dietary data provided information on the fatty acid composition of meals and revealed who was eating vegetable antioxidants and vitamins.
Major findings:
- Neither omega-6 nor omega-3 fatty acids were related directly to breast cancer risk.
- Long chain omega-3 fatty acids (EPA and DHA) reduced breast cancer in the group of women with the highest consumption of omega-6 PUFAs.
- High LA or ALA consumption in the form of vegetable oils or vegetables reduced cancer incidence.
- High LA or ALA consumption in the form of processed foods or nuts was associated with a higher incidence of breast cancer.
- Longer chain PUFAs were not associated with increased risk, regardless of source.
What does this mean?
- The source of the PUFA is of paramount importance. This study may apply more specifically to cancers and less to other inflammation-based degenerative diseases. The general anti-inflammatory diet may need refinement. I would suggest the following additions:
- Retain the preference for the more omega-3 friendly olive oil or perhaps flax oil versus the omega-6 rich vegetable oils (corn, soy, safflower), but focus on freshness and do not heat these oils.
- The data seem to be in favor of saturated fats for cooking. That means a shift to coconut oil.
- Vegetable antioxidants may be most important in the gut during digestion. Do these antioxidants even enter the blood stream? Certainly some alkaloids get to the brain, but much of the impact of the less mobile, large molecules may be restricted to the gut.
- An extension of this discussion may be to encourage eating more leafy vegetables with meat. That may be the paleo-diet connection.
Thiébaut AC, Chajès V, Gerber M, Boutron-Ruault MC, Joulin V, Lenoir G, Berrino F, Riboli E, Bénichou J, Clavel-Chapelon F. 2009. Dietary intakes of omega-6 and omega-3 polyunsaturated fatty acids and the risk of breast cancer. Int J Cancer. Feb 15;124(4):924-31.
17 comments:
The cancer/omega-3 connection certainly is complicated. I just found the following study:-
Omega-3 PUFA: Good or bad for prostate cancer?
Any thoughts on what's going on here?
P.S. Mum was discharged from hospital into a nursing home last Friday to allow her to rebuild her strength and mental faculties so that she can eventually return to her home. Today, she got out of her chair, walked 12 feet to the door of her room and then back to her chair. It was hard work for her, though.
Prostate enlargement and prostate cancer may be related to a type of autoimmune disease or infection that produces a chronic local infection that may transition into cancer. This might be equivalent to the predisposition of other tissues, e.g. gut, thyroid, that produce problems when inflamed. Omega-3s would make sense to decrease inflammation, but the organs contributing to seminal fluid may have altered omega-3 metabolism, because of the net export of DHA in the fluid. (That is why women exposed continuously to seminal fluid have fewer miscarriages, and longer gestation.) The omega-3 metabolism in the prostate may be similar to the brain, which doesn't convert short ALA to EPA or DHA. Aspirin should be helpful.
I haven't been able to read the full meta-analysis, but there's something rather important missing from the abstract.... any mention of Linoleic Acid intake or status.
In a typical Western diet, A-LNA is accompanied by over ten times as much LA. Therefore, looking at A-LNA intake or status alone is meaningless.
The above "study" gave me a strong feeling of deja vu and after a little rummaging, I found THIS.
I will not be giving up my powdered linseed & protein shakes and salmon!
I accept your criticism of the article -- it was rather unpleasant reading -- and your final conclusion to eat unprocessed PUFAs. My point of emphasis in using this article was the pairing of PUFAs with plant antioxidants during digestion.
The website that you provided in your last comment explored the pitfalls of PUFA processing -- exposing naked PUFAs to oxygen in the presence of a source of energy, e.g. heat or light, results in reactive oxidation products. What is left out is the most important oxidation environment, the stomach.
Cells lining the stomach don't just secrete HCl, but rather, they manipulate ferro/ferrichlorides that are reduced in parietal cells by hydroxylamine to yield HCl, nitrous oxide and reduced iron complex.
Robertson DS. 2005. The chemical reactions in the human stomach and the relationship to metabolic disorders..Med Hypotheses.64(6):1127-31.
The chemistry of the stomach is rather daunting, but my point is that thrusting unprotected PUFAs into the oxidizing environment of the stomach might be expected to produce carcinogens. It is safer to make the passage in the form of PUFAs bound to crude plant material, i.e. powdered linseed/flaxseed.
The cryptic, contradictory quality of the biomed research on PUFAs may be due in part to the tempermental chemistry of PUFAs in meal mixtures passing through the stomach. Depending on how you compose each forkfull of food, your meal may be an anti-inflammatory cureall or a toxic potion.
I just found your blog through Chris at Conditioning Research and am very excited!
You mention replacing cooking the oils we use for cooking from PUFAs to saturated oils and mentioned coconut oil.
I came across a couple of studies and wondered if you could take a look at them:
(this first link is the most important. it discusses the use of mcts and concommitant increase in liver fibrosis with a progression of NAFLD to NASH.)
http://www.medscape.com/viewprogram/4837_pnt
http://www.cababstractsplus.org/abstracts/Abstract.aspx?AcNo=19891413441
http://www.answers.com/topic/medium-chain-triglycerides
*****
I have NAFLD and worry about what percent of fat to have in my diet and specifically what kind of fat to eat.
I have replaced most PUFA presence in the diet with SFAs and MUFAs. I currently get about 4-5% of a 70% fat diet from PUFAs.
You can see what kind of diet I've had at www.todayiate.blogspot.com
This is where I track my daily food with pictures, nutritional analysis and weight.
I really appreciate your opinion!
Pooti,
This is a little out of my comfort zone molecularly speaking, but I am looking into it. I will add a comment if I figure it out.
Thanks for looking in.
Pooti,
Fatty liver seems to be a common stepping stone to metabolic syndrome and type II diabetes. As such, it is a symptom of chronic inflammation. The fat build up probably has nothing to do with dietary fat, except for the omega-6/-3 impact on inflammation. Otherwise, you would see statins being pushed as cures. Statins would probably have some impact, but I would hesitate to promote their use.
I would suggest checking your vitamin D levels and my next interest would be methionine/cycteine/B12/folic acid. Those are all involved in fat metabolism, as well as oxidative stress, e.g. methionine deficiency produces fatty liver.
The bottom line is to follow the basic anti-inflammatory diet recommendations and shift over to an active life style. Increasing muscle mass and decreasing body fat are helpful.
That depletes my wisdom on the specific subject of NAFLD. If I get some more coherent thoughts, I will write an article. If I missed some points, please ask more questions.
I hope that this helps. Thanks for stopping by.
Art
HI Dr. Art. thanks for answering. Sorry to be inarticulate in my question! I'm wondering if perhaps the study is flawed in some way? I'm wondering if the study is really showing a relationship between liver fibrosis and the consumption of MCTs and coconut oil. The reason? It occurs to me that one way to increase sat fat in the diet and decrease PUFA/MUFA is to eat coconut oil or supplement with mcts. But, the risk of progressing NAFLD to NASH worries me.
Do you think this study is legit?
I am also going to start taking Vit E and will start a B supplement. Do you have a particular brand of B vit and amount that you recommend? I'm having the Vit D retested soon but in the meantime am taking 5800iu/day.
Thanks so much!
Pooti,
I think that the studies are silly. They show that inflammation is the fundamental cause of liver damage and that high carbs are a typical source of the problem leading to inflammatory cytokine production and obesity.
Decreasing calorie intake (especially carbs -- Nigel, above, has authoritative suggestions on his blog) to initiate significant weight loss will provide a quick stop to inflammation.
Alterations in lipids, based on my observations, will change the rate of complications in the presence of continuing inflammation, but it doesn't get at the source of the problem, which is dietary-based inflammation, supported by inflammatory obesity with inadequate muscle-mass building exercise.
I don't know enough about the intricacies of liver fat metabolism in individual cases to provide a prescription for fatty acids that might alter the course of the disease. It is just more straightforward to attack the cause = multiple sources of inflammation.
I think that Nigel has some recommendations on B vitamin amounts. I don't worry about brands.
The major problem is usually high blood sugar caused by too much starch at one time. Too much means two slices of bread in a sandwich, or two buns on a burger or a whole ripe banana or a plate of pasta or a whole potato. It may make sense to be inefficient chewing food with a high starch content to spread out the glucose release over more time. In general, small meals are better and avoid starch/sugar (high fructose corn syrup is the worst.)
Good luck. Let me know how it is working.
Art
Thanks Dr. Ayers. I do already follow a low carb diet (< or = to 20g of non-netted veggie carbs per day). My history is complicated...Thanks for your help and for your opinion on the study!
For me there is a mass of evidence that Omega 6 increases and Omega 3 reduces the risk of BC.
This is a thread I post to on the subject with reference to a large number of papers on the topic.
http://her2support.org/vbulletin/showthread.php?t=24410
R.B.
The link between cancer and inflammation is obvious through NFkB, so it naturally follows that a high omega-6 to 3 ratio is going to be pro-cancerous.
Thank you for your heroic work in raising awareness to the dangers of vegetable oils (excluding olive oil.)
We still have to remember that omega-6 oils are essential for normal function, e.g. the gut, but in the current agribusiness-dominated economy, it is important to shout down the purported benefits of polyunsaturated vegetable oils.
Art
How is it that consumption of ALA and LA in the form of eating nuts was associated with increased risk but this risk was not found with consumption of vegetable oils which are certainly rich in both ALA and LA? I am totally confused. As a woman who wants to minimize breast cancer risk -- I've eaten a dairy free - grain free -- low carb paleo style diet. Meat/veggies/small amounts of fruit/lots of almonds/hazelnuts/ and cheats of very dark chocolate 85% or cocoa nibs/powder. Recently I passed kidney stones so high oxalate greens and nuts (I'd been eating 8oz of almonds or hazelnuts a day as snack -- I am quite thin -- plus lots of leafy greens -- chard, spinach, broccoli, bok choy etc to make up for lack of calcium in diet plus chocolate are off the menu for the time being. I had also been eating large amounts of curry spice and turmeric plus daily sardines with bones. I unwittingly became a walking oxalate machine. What to do now? Since dropping the nuts (I replaced with low oxalate pumpkin seeds to keep calories up) but have dropped 5 pounds and am now way too thin.
Anonymous,
There have been discussions at Peter's Hyperlipid blog about anecdotal increased incidence of kidney stones sometime after people embark on a low carb/paleo diet.
http://high-fat-nutrition.blogspot.com/2009/10/there-have-been-comments-from-two.html
One theory, which sounds entirely plausible to me, that non-symptomatic kidney calcifications (perhaps huge stones) were there all along (esp with a SAD diet), but started to dissolve when the LC/paleo diet commenced. Eventually the stones dissolve enough to start passing into the ureters, thereby causing pain and symptoms.
Hope you feel better soon.
Anna
Anonymous,
I agree with Anna and think that you may have loosened up old stones.
I think that nuts, as is true of seeds and seed oils, are high in omega-6 oils. I think that the problem with the nuts comes when they are roasted and the polyunsaturated oils are oxidized. They may be safer raw.
You seem to be short on calories and the obvious source is saturated fats from animal sources. You eat meat. What do you do with the fat? Animal fat should be a safer source of calories than nuts.
I hope that the stones pass uneventfully. Thanks for the comments/questions.
i was curious on how to speed up elimination of excess pufas omega 6s from the body and came across this information
Exp Clin Endocrinol Diabetes 1996;104 Suppl 4:41-5 Iodolactones and iodoaldehydes--mediators of iodine in thyroid autoregulation.Dugrillon A Central Clinical Laboratory, University of Heidelberg, Germany. “Within the last decades multiple iodolipid-classes have been identified in thyroid tissue. For a long time they have been supposed to be involved in thyroid autoregulation, but for the time being no specific compounds could be isolated. A new approach was stimulated by the finding that thyroid cells were able to iodinate polyunsaturated fatty acids to form iodolactones and by the identification of alpha-iodohexadecanal (alpha-IHDA) as the major compound of an iodolipid fraction.”
i wonder how this works. will increasing iodine intake and keeping fat intake low work well for the short term?
Thanks Dr ayers
Having found myself in somewhat of the same Oxalate boat as Anonymous at 11:16 am, I'd be grateful to know if you have any experience with the probiotic VSL#3, Dr. Ayers. According to their website, "each dose contains 450 billion live lactic acid bacteria per packet in defined ratios of lyophilized Bifidobacterium breve, Bifidobacterium longum, Bifidobacterium infantis, Lactobacillus acidophilus, Lactobacillus plantarum, Lactobacillus paracasei, Lactobacillus bulgaricus, Streptococcus thermophilus." This product is recommended at several Low-Oxalate groups, along with using Calcium citrate to chelate oxalates and heal the gut. Would be most grateful for your thoughts, if you have the time.
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