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David Brown on the Demise of Saturated Fat Phobia and the Hazard of Omega-6

Humanity is in a world of hurt, and increasingly so as the modern foods and beverages of commerce proliferate about the globe. And while there's growing concern about added sugars, refined grain products, and sugar-sweetened beverages, few are aware that the food supply would be far less toxic if its omega-6 content were drastically reduced. Fewer still are familiar enough with omega-6 research to appreciate the magnitude of the public health disaster wrought by the anti-saturated fat campaign.

I've been a long-time watch dog of the public health sector's anti-saturated fat rhetoric. Before the Internet, I clipped thousands of articles about cholesterol, saturated fat, and sugar out of newspapers and magazines. Actually, from 1977 to about 2005, when I gained access to the Internet, I accumulated only three articles about sugar. That's because up until 2004 there was hardly any money available for sugar research. That's all changed. What hasn't changed is that there is still little interest in the omega-6 hazard. Over that same period I collected zero articles on omega-6. And if I were still relying on the print media, I likely would still be unaware of the scope of the damage wrought by the introduction of omega-6 seed oils into the food supply.

Fortunately, for me at least, there's the Internet and Evelyn Tribole. She used to blog regularly at Omega-6 Research News and Commentary. It was fortunate for me because it was her blog that introduced me to Bill Lands and his research. That man literally saved my life. For up until November of 2009 I routinely ate a peanut butter sandwich for lunch daily during the work week. When I heard Dr. Lands say, "Did you know that peanuts contain 4,000 milligrams of omega-6 in each 28 gram, one ounce serving of peanuts, and one milligram of omega-3?", I realized my mistake. Since giving up peanut butter I have regained considerable strength and stamina. In addition, gingivitis is no longer a problem.

Beginning in early 2010, I established a Google Alert for "Omega-6, Lenoleic Acid." This has allowed me to track omega-6 research. The most recent item of interest is this British Medical Journal Article.

Conclusions. Advice to substitute polyunsaturated fats for saturated fats is a key component of worldwide dietary guidelines for coronary heart disease risk reduction. However, clinical benefits of the most abundant polyunsaturated fatty acid, omega 6 linoleic acid, have not been established. In this cohort, substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit. These findings could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats.

This particular research has stirred things up a bit eliciting this response from the American Heart Association:

The British Medical Journal study is interesting, but not conclusive. It is offset by a large body of scientific evidence that continues to show cardiovascular benefits associated with eating mono- and poly-unsaturated fat, rich in Omega-6 linoleic acids, in place of saturated fats,” said Penny Kris-Etherton, Ph.D., R.D., American Heart Association spokesperson and distinguished professor of nutrition at Pennsylvania State University.

The American Heart Association continues to recommend limiting saturated fats to less than seven percent of total calories consumed and supports eating between five to ten percent of total calories from Omega-6 PUFAs, within the context of an overall healthy dietary pattern that emphasizes fruit, vegetables, high-fiber whole grains, low-fat dairy products, lean meat, poultry and fish,” Kris-Etherton said.

Note: Dr. Kris-Etherton was a member of the 2005 Dietary Guidelines Advisory Committee.

Normally, any negative findings related to omega-6 research go unreported. This time it's different. Even the food industry is paying attention. The article is also getting coverage by the Medical News establishment, The Boston Globe, and Forbes. Here are a few more headlines:

If nothing else, there's a good bit of intrigue in the case: The case of the missing data.

Scientists don't always report everything they discover. Sometimes loose bits of data can be packed up in a box with a bunch of old books and research papers and left in a garage in Sydney, Australia. And that means intriguing, puzzling findings that didn't make sense back in the day, can slowly retreat into scientific oblivion, about to be lost to humankind for all eternity.

Except that, in this case, the phone rang and a determined scientist from Bethesda, Md. having managed to track down one of the last surviving members of a research team, asked Boonseng Leelarthaepin if he knew what happened to the dataset from the Sydney Diet Heart Study that wrapped up in 1973. Luckily Leelarthaepin is a packrat and he knew where to look. [...]

"The recovery actually took a substantial amount of time because it was in a format that wasn't readable by today's standards," Dr. Ramsden told me. He's a researcher with the U.S. National Institutes of Health, and he knew there was some potentially important information on that magnetic tape.

Dr. Ramsden tracked down some old equipment, recruited some experts, and after much technical handwringing, and format configuring, the data, that had originally been stored on punch cards, was translated into modern computer language so that it could be reanalyzed and interpreted. And what Dr. Ramsden found in that data made headlines this week.

It was a second look at an old clinical trial, first published in the 1970s, that had set out to measure the dietary effects of saturated versus unsaturated fat. It was assumed that if blood cholesterol could be lowered by reducing saturated fat in the diet, lives would be saved. But in this study, the subjects who switched to unsaturated fat had a higher risk of death.

"That was really unexpected," Leelarthaepin told me on the phone from Sydney. Because unsaturated fat can lower cholesterol, "in theory, survival would be better," he said. "But it was the other way around."

Back then, Leelarthaepin was a research assistant on the study and, at the same time, he was collecting data for his own PhD on a different aspect of the research. I asked him what they were saying to each other in the lab when they were faced with a puzzling increase in mortality. "We had no idea" he said. "We thought there must be some other factor influencing that." They adjusted the data, factoring in other risk factors like smoking, and still the observation held up. There seemed to be an increased risk of death from simply eating more vegetable oil.

I'd recommend reading the rest of it. It's a veritable whodunit.

While this bit of research may signal a change, I'm not holding my breath. As Ray Medina noted in his Revisiting The Sydney Diet Heart Study blog post, "The US edible oils manufacturing industry includes about 200 companies with combined annual revenue of about $55 billion. Major companies include Archer Daniels Midland, Bunge, Cargill Foods, and CHS. The industry is highly concentrated: the eight largest companies account for about 80 percent of industry revenue." With this kind of financial clout, it may take an act of congress to reverse the anti-saturated fat campaign and out the omega-6 hazard. I'm working on that. Anyone else care to write to congressmen and senators and their policy advisors?

David Brown is an independent, lay researcher who focusses on anti-saturated fat reporting by writing to to reporters and researchers alike, alerting them to research they might not be aware of with respect to saturated fats, as well as the potential hazards of omega-6 fats.

Comments

  1. I can’t seem to find the article right now (I think it was on Global News), but it came out a few weeks ago. The article had a title that caught my attention, something like “Omega 3s increase risk of heart disease.”

    Anyway finally what I gathered from reading the article was that if you eat a lot of omega 6s, omega 3s won’t “balance it out” because you will just be swimming in polyunsaturated fatty acids. You have to NOT eat a lot of omega 6s, and balance THAT out with omega 3s. I looked around the “paleosphere” to see if anyone had talked about, but I only found Robb Wolf who adressed it quickly while answering a question in a podcast. He had the same interpretation as me, but it still makes me wonder…

    Also, what is up with omega 9s!? We never hear talk about that!

    • Lyna, I believe this is the article you are referring to: http://life.nationalpost.com/2013/01/23/excessive-omega-fatty-acids-may-make-heart-health-worse-not-better-b-c-researchers/ The researcher is Sanjoy Ghosh. We’ll want to keep an eye on Ghosh because he is beginning to stir things up by asking the right questions. The article said, “This is not the first time that Ghosh has produced findings that turned popular notions about nutrition and health on their head. As a graduate student Ghosh discovered by accident that so-called “heart healthy” oils rich in Omega-6 polyunsaturated fatty acids inflicted damage to the hearts of rats and neo-natal pigs. The result was so shocking that Ghosh was turned down for publication by all the major scientific journals.”

      Omega-9s are monounsaturated oils which seem to be benign. The body makes some omega-9s from stearic acid, an 18 carbon chain saturated fatty acid. Interestingly, the edible oils industry has quietly increased the omega-9 content of soybean, Canola, and sunflower oils through selective breeding. Here’s an article I wrote for FoodAndBeveragePeople that furnishes the details: http://www.foodandbeveragepeople.com/cm/news/saturated_fats

    • Yes, that was the article! Thank you for the reply :)

  2. Brock in HK says:

    I love how people get all spun up about “words” rather than understanding the definition of the words and using that to build understanding. “Omega 6″ or “Omega 3″ become a brand and sound fancy and healthy. “Saturated fat” sounds sluggish, like a wet sponge, and is therefore bad. Those terms are specific scientific descriptions of the composition and shape of the molecule, and don’t describe what they do in the human body in any way.

  3. Baby Girl says:

    Richard I was reading about Naked Vegan Chef’s in the Daily Mail and it made me think of you so I thought I’d wander over here and see what is up with you these days.

  4. Sweddy 22 says:

    An interesting response on the BMJ’s website, underneath the actual article. It is funny how a few facts can cause such a stir… during my dietetic internship we delved into Evelyn Tribole’s Intuitive Eating concept, which was great. However this campaing vs. Omega 6 is a little overly progressive in my opinion. The response is as follows :::: Sorry for the length :::::::

    No reasons for changing present recommendations to replace dietary SAFA by PUFA for cardiovascular protection22 February 2013Gerard Hornstra PhD,
    Professor of Experimental Nutrition (Rtd), Maastricht University,
    Maastricht, The Netherlands
    and
    Connie Diekman MEd, RD, FADA,
    Director of University Nutrition, Washington University in St Louis,
    Academy of Nutrition and Dietetics Past President

    on behalf of the International Expert Movement on Health Significance of Fat Quality of the Diet, a working group under the auspices of the International Union of Nutritional Sciences

    Dear Sir,
    We congratulate Christopher Ramsden and colleagues on an elegant piece of ‘scientific archeology’, in which they recalculated and re-evaluated the results of the 40-year-old Sydney Diet Heart Study (SDHS) 1 and concluded that ‘substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease’ 2.

    In fact, their findings confirm the original SDHS results, that excess consumption of linoleic acid (LA) to replace saturated fatty acids (SAFA) in the diet of male coronary heart disease patients was associated with reduced survival after 2-7 years of follow-up. Unfortunately, the participants were not blinded to the treatment, because the intervention group received special instructions, oils, and margarines to increase their polyunsaturated fatty acid (PUFA) intake and to reduce SAFA consumption, whereas the control group did not receive a similar treatment with control products. In addition, the trial was confounded by multiple changes within both groups, not only in diet (see below) but also in lifestyle (e.g. sharp decrease in cigarette smoking, considerable reductions in caloric in take, body weight, and alcohol consumption, and substantial increase in physical exercise). These lifestyle changes commenced after the cardiovascular event, continued during the trial, and could not be corrected for.

    In the original SDHS paper 1, the authors clearly stated that, based on multivariate analyses, ‘none of the dietary factors were significantly related to survival’. In contrast, Ramsden and colleagues, who applied different statistics, held the high linoleic acid intake fully responsible for the negative outcome observed. Results of Ramsden’s diet recalculations differed only slightly from the original dietary composition data, which is quite an achievement, since post hoc diet calculations are acknowledged to be extremely difficult and can be rather inaccurate 3. Because of these relatively small dietary discrepancies, the different statistical methods applied must have been crucial to the dissimilarity between both outcomes.

    Ramsden’s approach inevitably needed to violate the golden rule of Good Clinical Practice, that any study evaluation plan needs to be part of the study design and should, therefore, precede study execution. However, Ramsden and colleagues should have explained why they decided to use different statistics. Moreover, it would have been illustrative and more convincing if the reason(s) for the different outcomes had been described, and if results had been presented of cross-validation studies (evaluation of original data with present statistics, and assessment of recalculated data with original statistics).

    Inclusion of the present results in Ramsden’s earlier meta-analysis of linoleic acid-specific saturated fat replacements 4 strengthened the initial trend for a cardiovascular risk increase of an excessively high LA intake. The hazard ratio increased from about 1.1 to 1.3, but possibly because of the limited size of the SDHS (63 all cause mortality cases and just 7 additional deaths in the intervention as compared to the control group), it still did not reach significance.
    We doubt whether this inclusion is justified, however, because the SDHS, originally planned as a dietary replacement trial, turned out to be flawed by multifactorial changes, as mentioned above. In addition, certain interpretations of the re-evaluation results deserve some scrutiny. Thus, although the dietary intervention intended to be an LA-specific SAFA replacement, it also significantly reduced the consumption of monounsaturated fatty acids, the impact of which on cardiovascular risk is not clear as yet 5. In addition, the authors neither excluded, nor corrected for, the possibility that the SDHS intervention reduced the omega-3 PUFA intake as a result of replacing the habitual cooking oils. Further, a possible increase in the consumption of industrial trans fatty acids by the intervention group was not accounted for, whereas at that time high PUFA margarines contained significant amounts (as high as 15 – 20%) of these cardiovascular risk increasing fatty acids (P. Clifton, W. Shrapnel, http://www.smc.org.au/2013/02/round-up-dietary-fats-and-heart-disease-bm… , and P. Zock, personal communication). These unintentional further changes may have affected mortality in the intervention group independent from an assumed LA effect.

    Considering these issues, we believe that the conclusion of Ramsden and colleagues that their findings ‘could have important implications for worldwide dietary advice to substitute omega 6 linoleic acid, or polyunsaturated fats in general, for saturated fats’ is not justified. This conclusion is incompatible with Ramsden’s earlier 4 and present 2 meta-analyses and with the meta-analysis of Mozaffarian and colleagues 6, all demonstrating that replacing SAFA (and industrial trans) with PUFA (being a mix of 15-20 en% LA and some omega-3 PUFA) significantly reduces the risk of coronary heart disease.

    Nonetheless it would be unwise to ignore the present outcome of Ramsden’s recalculation study, since it adds to the growing concern about the safety of an unlimited increase in LA consumption. Other contributions to the emerging LA skepticism are the well-documented reduction of the omega-3 long-chain PUFA status by dietary LA 7 8, its possible effects on early human development 9, its controversial pro-inflammatory potential 10 11, and its alleged contributing role in the present obesity epidemic 12 13.

    Finally, Ramsden and colleagues correctly stated that any potential adverse effect of linoleic acid from 8.5 (not 6, as mentioned in their paper) to 15 %, as possibly observed in the SDHS cohort, does not necessarily apply to lower LA intakes. Since the maximum recommended LA intake for the prevention of cardiovascular disease is about 10 % 14, WHO recommendations maximize LA intake to 9 % 15, and LA intake in most countries is between 3 and 7 % 16, we believe that Ramsden’s recalculation study need not affect current LA intake recommendations. It also does not mitigate the beneficial effect of replacing dietary saturated for polyunsaturated fats to reduce cardiovascular risk.

    References

    1. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket RB. Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Adv Exp Med Biol 1978;109:317-30.
    2. Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, et al. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ 2013;346:e8707.
    3. Nettleton JA, Koletzko B, Hornstra G. ISSFAL 2010 Dinner Debate: Healthy Fats for Healthy Hearts – Annotated Report of a Scientific Discussion. Ann Nutr Metab 2011;58(1):59-65.
    4. Ramsden CE, Hibbeln JR, Majchrzak SF, Davis JM. n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials. Br J Nutr 2010;104(11):1586-600.
    5. Jakobsen MU, O’Reilly EJ, Heitmann BL, Pereira MA, Balter K, Fraser GE, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009;89(5):1425-32.
    6. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med 2010;7(3):e1000252.
    7. Rump P, Hornstra G. The n-3 and n-6 polyunsaturated fatty acid composition of plasma phospholipids in pregnant women and their infants. relationship with maternal linoleic acid intake. Clin Chem Lab Med 2002;40(1):32-9.
    8. Liou YA, King DJ, Zibrik D, Innis SM. Decreasing linoleic acid with constant alpha-linolenic acid in dietary fats increases (n-3) eicosapentaenoic acid in plasma phospholipids in healthy men. J Nutr 2007;137(4):945-52.
    9. Hornstra G. Essential fatty acids in mothers and their neonates. Am J Clin Nutr 2000;71(5 Suppl):1262S-9S.
    10. Fritsche KL. Too much linoleic acid promotes inflammation-doesn’t it? Prostaglandins Leukot Essent Fatty Acids 2008;79(3-5):173-5.
    11. Bjermo H, Iggman D, Kullberg J, Dahlman I, Johansson L, Persson L, et al. Effects of n-6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial. Am J Clin Nutr 2012;95(5):1003-12.
    12. Ailhaud G, Massiera F, Weill P, Legrand P, Alessandri JM, Guesnet P. Temporal changes in dietary fats: role of n-6 polyunsaturated fatty acids in excessive adipose tissue development and relationship to obesity. Prog Lipid Res 2006;45(3):203-36.
    13. Moon RJ, Harvey NC, Robinson SM, Ntani G, Davies JH, Inskip HM, et al. Maternal Plasma Polyunsaturated Fatty Acid Status in Late Pregnancy Is Associated with Offspring Body Composition in Childhood. J Clin Endocrinol Metab 2013;98(1):299-307.
    14. Kris-Etherton PM, Innis S, Ammerican Dietetic A, Dietitians of C. Position of the American Dietetic Association and Dietitians of Canada: dietary fatty acids. J Am Diet Assoc 2007;107(9):1599-611.
    15. WHO/FAO. Diet, nutrition and the prevention of chronic diseases. World Health Organ Tech Rep Ser 2003;916:i-viii, 1-149, backcover.
    16. Elmadfa I, Kornsteiner M. Dietary fat intake–a global perspective. Ann Nutr Metab 2009;54 Suppl 1:8-14.

    Competing interests: “The International Expert Movement (IEM) is a group of experts committed to improving the fat quality of the diet of everyone. IEM’s activities are funded by an unrestricted educational grant from Unilever N.V. under the auspices of the International Union of Nutritional Sciences”. http://www.theiem.org

    • I think the sane thing to do it eat whatever real foods you like, using only the fats than come packaged in those foods themselves and in terms of added fat, fat that comes from real foods used in sensible amounts.

      I’d be surprised if replacing any of those real food fats with industrial machinery oil would _cause_ decrease in _all cause_ mortality, or any particular category of mortality. Extraordinary claims require extraordinary proof.

    • Regarding the omega-6 hazard, one wonders how extraordinary the scientific evidence needs to be to overturn the claim that omega-6s are healthy because they lower total cholesterol. Dr. Ramsden had good reason to suspect that omega-6s are not heart-protective prior to initiating latest research effort. Excerpt from an earlier research paper:

      “Controlled trials in which high-LA oils replaced TFA- and SFA-rich fats have shown conflicting results, despite thefact that LA was accompanied by large amounts of medium- and long-chain n-3 PUFAs. A single small trial testing the specific effects of LA without n-3 PUFAs found increased CHD risk. The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70%. Although
      this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction.”

      Google – “PDF Dietary Fat Quality and Coronary Disease Prevention” to access this paper which Dr. Ramsden co-authored with, among others, Loren Cordain.

  5. Ray Peat is the main source of info on what’s wrong with PUFAs:
    http://www.raypeat.com

  6. Stephers says:

    Does anyone know why Stephan Guyenet removed a bunch of his blog posts on the evils of Omega-6 PUFAs? A whole bunch of articles linking them to heart disease are now gone from his Whole Health Source site, such as

    “Excess Omega-6 Fat Damages Infants’ Livers”
    “The Diet-Heart Hypothesis: Oxidized LDL, Part II ”
    “The Coronary Heart Disease Epidemic: Possible Culprits Part II.”.

    There are other posts missing as well and they all seem to deal with PUFAs. Has he changed his mind about Omega-6′s?

    I was able to track down archived versions elsewhere on the web, fortunately.

  7. If you would like more information on the omega-6 hazard, Google – David Brown Omega-6

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