Thursday, March 14, 2019

Response to Gary Taubes on Omega-6 Fats (Seed Oils) and Obesity

I was a guest on their sixth episode: [2]

Where we discussed omega-6 fats (n-6) from seed oils, and their impact on health and fitness.

Shawn posed a question to Taubes about processed vegetable oils (seed oils), as a follow-up of sorts to our discussion.

This is actually the second time that a question from me about one of my favorite topics made it into a podcast interview w/ Taubes, the first was in 2011, detailed in this post. [3]

"Taubes answers about the way I expected him to.  Thoughtfully, but wheat and linoleic acid have not been focuses of his research."

This time (eight years later) he has thought about it some more, and asks some reasonable questions and makes some reasonable objections. I respect the fact that this has not been his focus, and he's quite forthright about his lack of knowledge on the topic. Which is fine, no one can be an expert on everything, and that's why the back-and-forth the internet allows for is such a great thing.
(I'm manually transcribing this, so any errors in what Taubes or the others say will be mine, unfortunately.)

SB, starting at time 43:46: "There has been some recent interest, outside of sugar, in things like processed vegetable oils. And there's a lot of people pointing to that as a competing hypothesis for some of our health issues. What is your, sort of, thoughts on the fact that, you know, we didn't have processed vegetable oils in the diet since the late 1800s, essentially, in any significant quantity since maybe Proctor & Gamble lobbied the American Heart Association to include Crisco in the diet in the 1920s. What are your thoughts on that particular substance as far as, ah, being a potential driver for some of these health issues?
GT: "I can give you a firm 'I don't know'."

Fair enough. Taubes is a careful thinker, and he likes to stick to the facts.

But he has some more thoughts.

GT: "Um, and I was thinking about this [in] my latest book. And I know, you know, my friends, some of my friends believe that — people that I respect, and their intelligence I respect, uh, believe that processed vegetable oils are playing a major role. They could be.
"My feeling is, you can see the effects of sugar and refined grains in populations that didn't have processed vegetable oils. You know, uh, South Pacific Islanders uh, Native Americans pre 1940s...
"There was a large observation prior to the 1960s that obesity and diabetes and heart disease and hypertension could be attributed to processed grains and sugars. Its effect... If you think of it like a, uh, criminal case... [skip elaboration here] ...Some of them predate the spread of processed vegetable oils to those populations, but they don't predate the appearance of sugar and white flour, particularly sugar. Then I think sugar is always at the scene of the crime and vegetable oils aren't."
"...Soy oil worries me. But soy oil is processed soy and soy fats and we had the Japanese consuming soy well before they had elevating rates of obesity and diabetes. So there's ways I see that that hypothesis can be refuted in a way that the sugar hypothesis can't." 
So my general feeling is that if we could find a population that didn't eat sugar, but did eat Crisco, we could see what the effects of Crisco are.  And disassociate them from sugar. And we can find populations that ate sugar but didn't eat Crisco and we see obesity and diabetes in those populations. 
"So the fundamental problem to me, and this is the argument I make in my book, is you add sugar to any diet, you're going to have problems — you know, obesity, diabetes, metabolic syndrome. Vegetable oils on top of that might make it worse....
"The other thing that worries me about the vegetable oil hypothesis, and I've said this to my friends, is..." 

He goes on to discuss a paper he co-wrote with Walter Willett, Ron Krauss, and Nita Forouhi, on the epidemiology of "Dietary fat and cardiometabolic health: evidence, controversies, and consensus for guidance" [4], and Willett's work on other observational studies Willett bases his advocacy of seed oils on.

"...If the vegetable oils were bad for them, I would expect to see some sign of it, in those studies. Um, and I don't. And that doesn't mean that the hypothesis is wrong, but it would seem that somehow... It could be that these people would be much healthier still, if they were eating butter, lard instead of rapeseed oil. And so all we see there is that they're a little bit healthier, and not a lot healthier. And that's the kind of problem with those trials. Who knows...." 
"I don't know what to make of that hypothesis. I feel bad that I don't pay it enough attention."

Taubes has a few other thoughts, and he and Shawn discuss it a little further, but that seems to be the meat of his thoughts.

So that's a few points I would like to discuss.

When you evaluate a hypothesis, the most important thing to do is evaluate ALL the evidence available. You can't skip the things that don't agree with your hypothesis. You either have to explain them in light of the hypothesis, or modify or discard the hypothesis.

So Taubes raises the following points, to summarize:

  1. Timeline of introduction of seed oils
    (statements that data pre 1960s or 1940s indicate absence of seed oils)
  2. Seed oils aren't always present, sugar is.a. Native Americans pre 1940s
    b. South Pacific Islanders
  3. Soy, soybean oil, and Japan.
  4. Crisco vs. seed oils
  5. China, Japan, and sugar intake.
  6. Seed oils and cardiovascular disease

(N.B. I use the term seed oils to differentiate between high n-6 oils produced from seeds such as soy, peanut, rape, grape, etc., and oils produced from fruits such as olive, palm, and avocado. Since the n-6 content seems to be the harmful element, this is an important distinction. Coconut and palm seed are two seed oils that are low in n-6 fats.)

1. Timeline of introduction of seed oils

Cottonseed oil was invented in 1768, and first patented in 1799. The first cottonseed oil mill opened in 1829. [1.1] 

"The U.S. recognized the progress of the cottonseed industry and began to include cottonseed oil mills in the annual U.S. census in 1860."

Detoxification of cottonseed oil (which is acutely toxic in the native form) allowed human consumption to begin.

"The early refined cottonseed oil was light in flavor and slightly yellow, which was perfect for the dilution of expensive olive oil. The adulteration was undetectable, but eventually led to tariffs on the outgoing U.S. cottonseed oil and all exports to Italy were discontinued."

By the 1880s cottonseed oil had become such a common element in the American diet that: [1.2]

"...dairy interests in twenty-six states met in New York City, in 1886, to urge Congress to intervene in behalf of their fight on oleomargarine."

Oleomargarine was made from beef fat or cottonseed oil, and had become so common that:

"To these interests it seemed that American oleomargarine was suddenly and rapidly capturing their butter market, having already displaced "one-fifth of the purest product of the dairy""

And the ingredients in oleomargarine become quite clear in considering the voting:

"The eleven cotton states cast 66 of the 101 votes against the measure in the House and 18 of the 24 negative votes in the Senate."

Oleomargarine and adulterated olive oil (still a problem today) weren't the only ways in which processed vegetable oils had made it into the American diet: [1.1]

"By the late 1880s, the domestic demand for cottonseed oil increased when the price of lard became high. Initially, meat packers secretly were adding cottonseed oil to lard. This process was discovered when a slaughter and meatpacking company, Armour and Co., realized that they had been receiving deliveries of more lard than the existing hog population could have produced. The adulterations of lard lead to a Congressional investigation, which resulted in the mandatory use of the term “lard compound.”

From [1.2]:

"Compound lard was estimated, in 1888, to constitute about half of the total of 600,- 000,000 pounds of lard produced in the country and about forty per cent of the 320,000,000 pounds exported; and this compound consisted of mixtures of pure lard, beef stearine, and cottonseed oil, with the oil estimated at forty per cent."

"Among the sample of American lards mentioned in the tables there appears to be only one which is genuine... Generally the manufacturers in the United States make no pretence of exporting pure lard. The chief adulterant found is cotton seed oil..."

It's notable that the leading diet used by researchers to induce obesity and metabolic syndrome in laboratory animals is a high-n-6, lard-based diet, Research Diet's D12492 [1.4], [1.5].

(N.B. The n-6 in lard is what seems to be the problem, so if you can find lard that isn't compound or from pigs fed lots of grain and seed oils, it shouldn't be a problem. Since everyone asks this question next...)

2.a Seed oils aren't always present, sugar is; Native Americans pre 1940s

So it's quite clear that seed oils were a part of the American diet long before the studies quoted by Taubes in Good Calories, Bad Calories [2.1] were undertaken.

"Studies of the Sioux of the South Dakota Crow Creek Reservation in the 1920s, Arizona Apaches in the late 1950s, North Carolina Cherokees in the early 1960s, and Oklahoma tribes in the 1970s all reported levels of obesity comparable to that in the United States today, but in populations living in extreme poverty."

Taubes mentions what they ate: 

"The staple of the Sioux diet on the reservation was “grease bread,” fried in fat and made from white flour..."

And mentions earlier that they ate almost no butter. They used lard: [2.2]

"All of these tribes have attempted to maintain their native pattern whenever possible, but increasingly have depended on items purchased at stores and trading posts. The demand for sugar, coffee, tea, flour, and lard is noted for all of these groups in modern times." 

As we've already seen, lard had been comprised of a large amount of cottonseed oil for quite some time. The diet of the Native American on a reservation, starch, sugar, and n-6-rich lard, strongly resembles the obesity-inducing D12492 diet.

GT: "Weston Price tells that story, in Nutrition and Physical Degeneration..." [1, time 30:51]

I agree that Price's book [2.3] is a reliable source for diets in the period written. What does Price record about the diet of the Native Americans?

"A study was made of an Indian reservation in New York State for comparison and for making an estimate of typical modern American Indian life with regard to dental caries and nutrition. For this study a band of 450 in the Tuscarora Reservation northeast of Niagara Falls was visited... In both reservations they were using commercial vegetable fats, jams and marmalades, sweetened goods, syrups and confections very liberally."

Price goes a bit further, identifying what he calls "displacing foods adopted from our modern civilization", on which he blames the malnutrition he sees. His list: "These include chiefly white flour, sugar, polished rice, vegetable fats and canned goods".

2.b Seed oils aren't always present, sugar is; South Pacific Islanders

Sadly, Price doesn't make this easy on me. 

"...the imported foods of white flour, sugar, sugar products, syrup, polished rice, and the like..."

I certainly expect "the like" includes the vegetable fats (seed oils) Price mentions elsewhere, but it's not clear. One can certainly infer that the South Pacific would have been the recipient of cottonseed oil, which was a big export crop even by WWI, but it's rather difficult to find details. 

Australian Imports from America, 1903-1907. [2.4]

We do know that Australia imported a fair bit of US lard and cottonseed oil in the early 1900s, [2.4] and it's fair to assume it was present on the trading ships price describes as bringing wheat, sugar, "and the like" to the rest of South Pacific. 

Given the wide variation of circumstances in the area, but also the continuing lack of obesity in those societies like the the Kitavans that eat a lot of carbohydrate but little seed oils, [2.5] it's difficult to come to a conclusion here without being more specific.

Seed oils are certainly consumed throughout the region currently, and we do know that coconut oil, the traditional fat of the region, is protective against obesity in animal models and in humans that base their diet on it, while n-6 fats induce it. [2.6]

3. Soy, soybean oil, and Japan

Soy was indeed a traditional Japanese and Chinese food, but it was in the form of fermented soy products like tofu, natto, or soy sauce. The oil was not produced or consumed in any large quantity that I can identify, instead rapeseed oil was a traditional cooking and lighting oil. [3.1] One presumes the Japanese weren't consuming large amounts of rape oil as the oil is toxic in large amounts, due to its erucic acid content (canola oil is rape oil bred to be erucic-free). [3.2] One of the more compelling papers advocating the dangers of seed oils in the human diet in fact comes from Japan, and notes the correlation of obesity and ill health with the increased consumption of n-6 seed oils. [3.3]

Obesity is rare in Japan still, although it has increased as sugar consumption has remained stable and seed oil consumption has increased. [3.1]

"...Japan’s dietary habits have seen dramatic changes in the postwar decades. Meat consumption increased roughly nine-fold between 1955 and 2005 and consumption of [seed] oil rose about five-fold over those five decades, he pointed out."

4. Crisco vs. seed oils

Crisco was originally a hydrogenated (hydrogen added to "saturate" the fat with hydrogen) cottonseed oil. The evidence used to ban synthetic trans fats like those in Crisco was largely epidemiological in nature, and much of it was in fact produced by Walter Willett. [4.1] Fred Kummerow, an experimentalist, campaigned against trans fats for decades, and is generally credited (including by Willett) with leading the science.

World Nutrition published, in celebration of Kummerow's 100th birthday, an essay by him titled "My Diet". [4.2] Willett wrote part of the introduction. Here are Kummerow's thoughts on seed oils, and Willett's pro-seed-oil epidemiology:

"We all need to limit consumption of foods cooked in over-heated and over-used oils, keep omega 6/ omega 3 ratios in balance... 
"Reducing saturated fats and increasing polyunsaturated fats will increase the level of omega 6 fatty acids, creating an unhealthy imbalance in omega 6/omega 3 ratios."

It turns out that there is only one study comparing the effects of trans fats and seed oils directly. [4.3]

"In addition, the influence of the type of fat consumed on health has been debated for years and vegetable oil is recommended over animal fats for the reduction of cardiovascular disease and oxidative stress, which has resulted in an increased intake of omega-6 fatty acids, especially linoleic acid (LA)...
"We conclude that [high n-6] lard-based high-fat diets accentuate the increase in weight gain and the development of obesity and insulin resistance more than hydrogenated vegetable-shortening diets."

As one waggish blogger observed: [4.4]

"Question: If you are in a position of power over innocent folks who are trying to eat healthy food, which fat would you ban? 
"Answer: The wrong one!"

5. China, Japan, and sugar and seed oil intake.

So it turns out we do have a couple of places where sugar consumption is low, and seed oil consumption is relatively high. They're China and India. Both have among the lowest sugar consumptions in the world. [5.1]

Per-capita sugar consumption [5.1]

China's is 1/10th of America's, and Japan's is about half. So if sugar causes obesity, why is China, and not Japan, having an obesity epidemic? Why is India having an obesity and diabetes epidemic? Japan remains the skinniest industrial nation on Earth, while children in China are at American levels of obesity.

I find it implausible that reducing America's sugar consumption by 90% should be expected to do nothing for obesity. That's what we would need to do to match China. Would it really have no effect?

I doubt Taubes would make that argument.

The sugar hypothesis offers no explanation for this discrepancy that I'm aware of, but the seed oil hypothesis does.

Seed oil consumption has been going up across Asia: [5.2]

Seed oil consumption [5.2]

It turns out that in animal models, omega-3 fats protect against the obesity-inducing effects of the n-6 fats in seed oils.

This would certainly explain the skinny Japanese, as they have one of the highest consumptions of omega-3 [n-3] rich fish in the world.

I want to stress that I'm no fan of high sugar consumption, and consider it to be quite obviously unhealthy. I personally have been on a low-sugar diet for ~30 years, but if we're going to solve a problem we need to understand the root cause correctly.

6. Seed oils and cardiovascular disease

There is indeed epidemiological research showing that seed oils are supposed to reduce cardiovascular disease, as Taubes mentions, and signed his name to in this paper [4]. However it's not nearly as clear as Willett makes it seem to be. A large Cochrane Collaboration meta-analysis in 2018 found: [6.1]

"This is the most extensive systematic assessment of effects of omega‐6 fats on cardiovascular health, mortality, lipids and adiposity to date, using previously unpublished data. We found no evidence that increasing omega‐6 fats reduces cardiovascular outcomes other than MI, where 53 people may need to increase omega‐6 fat intake to prevent 1 person from experiencing MI. Although benefits of omega‐6 fats remain to be proven, increasing omega‐6 fats may be of benefit in people at high risk of MI. Increased omega‐6 fats reduce serum total cholesterol but not other blood fat fractions or adiposity."

That and the two related papers together weigh in at ~850 pages, so let's not discuss in depth here. We'll just observe that the epidemiological evidence is astonishingly weak.

MI with differing n-6 diets [6.2]
There is epidemiological and mechanistic evidence indicating that a low-seed-oil diet may be protective against CVD, however.

Despite the 850 pages Cochrane produced, they managed to not discuss the most successful study ever in reducing CVD, specifically looking at lowering n-6 and increasing n-3 to protect against MI in those that have already had one, the Lyon Diet Heart Study. [6.2] This was the most successful heart-disease prevention trial in history, and resulted in the still-continuing popularity of the Mediterranean diet. It's rather difficult to reconcile the advice to eat more n-6 for their cardioprotective effects with the results of this study.

N-6 (18:2) and n-3 (18:3) intervention in Lyon [6.2]

The three living populations with undetectable rates of CVD, the Kitavans, [6.3] Tsimane, [6.4] and Tukisenta [6.6], all do not consume processed seed oils. The Japanese and Koreans, back when they consumed low levels of seed oils [5.2] also had near-zero rates of CVD. [6.7]

There's also clear mechanistic evidence going back to the 1980s showing that the important part of the progression of CVD is oxidized n-6 fats consumed via the diet. [6.8]


Gary Taubes has important questions about the hypothesis that excess linoleic acid from consumption of seed oils is a major causal factor in CVD and other modern chronic diseases.

I hope that I've addressed his questions and concerns here in a manner that makes it clear that this is a hypothesis worthy of serious consideration.

There are many topics that I did not elaborate on in this post, such as the interactions between different types of fats, low-fat diets, and carbohydrate consumption. Some of those topics are addressed elsewhere on this blog or on my twitter feed, for the curious.

[1] Baker, Shawn, and Zach Bitter. “Human Performance Outliers Podcast: Episode 6: Tucker Goodrich.” Podcast. Human Performance Outliers Podcast, April 28, 2019.

[2] Baker, Shawn, and Zach Bitter. “Human Performance Outliers Podcast: Episode 76: Gary Taubes.” Podcast. Human Performance Outliers Podcast, March 1, 2019.

[3] Goodrich, Tucker. “Gary Taubes Interviewed By Jimmy Moore.” Blog. Yelling Stop (blog), January 31, 2011.

[4] Forouhi, Nita G., Ronald M. Krauss, Gary Taubes, and Walter Willett. “Dietary Fat and Cardiometabolic Health: Evidence, Controversies, and Consensus for Guidance.” BMJ 361 (June 13, 2018): k2139.

[1.1] Jennings, Barbara. “Dr. Otto’s Amazing Oil.” Pennsylvania Center for the Book, September 21, 2010.

[1.2] Nixon, Herman Clarence. “The Cleavage within the Farmers’ Alliance Movement.” The Mississippi Valley Historical Review 15, no. 1 (1928): 22–33.

[1.3] Sessional Papers of the Dominion of Canada. Vol. 1. 23 vols. Dominion of Canada, 1890.

[1.4] “D12492 Formula - OpenSource Diets - Search Formulas - Research Diets, Inc.” D12492. Accessed March 5, 2019.

[1.5] Masterjohn, Christopher. “This Just In: The Infamous Lard-Based High-Fat Rodent Diet Is Twice as High in PUFA as Previously Reported.” Blog. Chris Masterjohn, PhD, November 19, 2011.

[2.1] Taubes, Gary. Good Calories, Bad Calories. Penguin RandomHouse, 2008.

[2.2] Moore, William, Marjorie Silverberg, and Merrill Read. “Nutrition, Growth and Development of North American Indian Children.” National Institute of Child Health and Human Development, 1972.

[2.3] Price, Weston. “Nutrition and Physical Degeneration.” A Project Gutenberg of Australia eBook, 1938.

[2.4] Statistics, Australia Commonwealth Bureau of Census and, and Sir George Handley Knibbs. Trade and Customs and Excise Revenue of the Commonwealth of Australia, 1907.

[2.5] Lindeberg, Staffan, Peter Nilsson-Ehle, and Bengt Vessby. “Lipoprotein Composition and Serum Cholesterol Ester Fatty Acids in Nonwesternized Melanesians.” Lipids 31, no. 2 (February 1, 1996): 153–58.

[2.6] Deol, P., J. R. Evans, J. Dhahbi, K. Chellappa, D. S. Han, S. Spindler, and F. M. Sladek. “Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver.” PloS One 10, no. 7 (2015): e0132672–e0132672.

[3.1] Nagata, Kazuaki. “Japan Needs Imports to Keep Itself Fed.” The Japan Times Online, February 26, 2008.

[3.2] Maheshwari, P. N., D. W. Stanley, and J. I. Gray. “Detoxification of Rapeseed Products.” Journal of Food Protection 44, no. 6 (June 1, 1981): 459–70.

[3.3] Okuyama, Harumi, Tetsuyuki Kobayashi, and Shiro Watanabe. “Dietary Fatty Acids — The n-6n-3 Balance and Chronic Elderly Diseases. Excess Linoleic Acid and Relative n-3 Deficiency Syndrome Seen in Japan.” Progress in Lipid Research 35, no. 4 (December 1, 1996): 409–57.

[4.1] “Shining the Spotlight on Trans Fats.” The Nutrition Source, September 18, 2012.

[4.2] Kummerow, Fred. “My Diet.” World Nutrition, February 2015.

[4.3] Kubant, R, A N Poon, D Sánchez-Hernández, A F Domenichiello, P S P Huot, E Pannia, C E Cho, S Hunschede, R P Bazinet, and G H Anderson. “A Comparison of Effects of Lard and Hydrogenated Vegetable Shortening on the Development of High-Fat Diet-Induced Obesity in Rats.” Nutrition & Diabetes 5, no. 12 (December 2015): e188.

[4.4] Dobromylskyj, Petro. “Trans Fats vs Linoleic Acid.” Blog. Hyperlipid (blog), March 4, 2017.

[5.1] Ferdman, Roberto. “Where People around the World Eat the Most Sugar and Fat - The Washington Post,” February 5, 2015.

[5.2] Hiraga, Midori. “Increase of Vegetable Oil Consumption Under Food Regimes: A Preceding Example of Japan to Be Compared with Rapid Increase of Vegetable Oil Availability in Asian Countries Especially in China (Oral Presentation at the 4th Annual LCIRAH Conference, 2014 London).” presented at the 4th Annual LCIRAH Conference, 2014 London, London, Great Britain, 2014.

[6.1] Hooper, Lee, Lena Al‐Khudairy, Asmaa S. Abdelhamid, Karen Rees, Julii S. Brainard, Tracey J. Brown, Sarah M. Ajabnoor, et al. “Omega‐6 Fats for the Primary and Secondary Prevention of Cardiovascular Disease.” Cochrane Database of Systematic Reviews, no. 7 (2018).

[6.2] Lorgeril, Michel de, Patricia Salen, Jack L. Martin, I. Monjaud, Jacques Delaye, and Nicole Mamelle. “Mediterranean Diet, Traditional Risk Factors, and the Rate of Cardiovascular Complications after Myocardial Infarction: Final Report of the Lyon Diet Heart Study.” Circulation 99, no. 6 (1999): 779–85.

[6.3] Lindeberg, S., P. Nilsson‐Ehle, A. Terént, B. Vessby, and B. Scherstén. “Cardiovascular Risk Factors in a Melanesian Population Apparently Free from Stroke and Ischaemic Heart Disease: The Kitava Study.” Journal of Internal Medicine 236, no. 3 (1994): 331–40.

[6.4] Kaplan, Hillard, Randall C Thompson, Benjamin C Trumble, L Samuel Wann, Adel H Allam, Bret Beheim, Bruno Frohlich, et al. “Coronary Atherosclerosis in Indigenous South American Tsimane: A Cross-Sectional Cohort Study.” The Lancet 389, no. 10080 (April 29, 2017): 1730–39.

[6.5] Sinnett, P. F., and H. M. Whyte. “Epidemiological Studies in a Total Highland Population, Tukisenta, New Guinea: Cardiovascular Disease and Relevant Clinical, Electrocardiographic, Radiological and Biochemical Findings.” Journal of Chronic Diseases 26, no. 5 (May 1, 1973): 265–90.

[6.6] Sinnett, P. F., and H. M. Whyte. “Epidemiological Studies in a Highland Population of New Guinea: Environment, Culture, and Health Status.” Human Ecology 1, no. 3 (March 1, 1973): 245–77.

[6.7] Lee, Kyu Taik, Richard Nail, Laurence A. Sherman, Michael Milano, Kyu Taik Lee, Carl Deden, Hideshge Imai, et al. “Geographic Pathology of Myocardial Infarction: Part I. Myocardial Infarction in Orientals and Whites in the United States; Part II. Myocardial Infarction in Orientals in Korea and Japan; Part III. Myocardial Infarction in Africans in Africa and Negroes and Whites in the United States; Part IV. Measurement of Amount of Coronary Arteriosclerosis in Africans, Koreans, Japanese and New Yorkers.” The American Journal of Cardiology 13, no. 1 (January 1, 1964): 30–40.

[6.8] Witztum, J L, and D Steinberg. “Role of Oxidized Low Density Lipoprotein in Atherogenesis.” Journal of Clinical Investigation 88, no. 6 (December 1, 1991): 1785–92.


  1. You might include sunflower in the seed oil list - starting N.b. ...

  2. It would be interesting to test Dr. Bill Lands work on Omega 3 vs 6 competition in humans' prostaglandin production and inflammation response, specifically with the Japanese having such a higher dietary shift to consuming more seed oils yet remaining skinny:

    Lands reported that the first 1% of Omega fat consumption wins, suggesting that if Omega 3 is "first in" it is deterministic of metabolic destiny, regardless however much Omega 6 is consumed after that dose.

    I'm just not clear about when the competition begins and ends for that first 1%... first meal of the day?

  3. Tucker, thanks very much for this.

    I tried very hard to understand the scientific rationale for transfers alleged pathogenicity: Kummerow's books and papers.

    The accumulation of the numerous and various trans fatty acids in cell membranes, and their appearance in breast milk are unlikely to be salutary. There may, however, be compensatory physiologic mechanisms to preserve normal membrane properties.

    What bothered me was the greater reactivity of the parent omega 6 fatty acids compared to the more hydrogenated trans fats. It seemed then, and does now, that we have jumped from the frying pan into the fire.

  4. I think both your theories and Gary Taubes's theories can coexist. I personally got fat drinking beer, then eating pizza, then ice cream, then going back to a very low fat diet (oats, pasta, brown rice and beans), getting depressed, and then drinking beer... It was a cycle, but one with low PUFAs. Meanwhile, you seem to be highly susceptible to PUFAs. And of course most American people today get a double whammy of PUFAs and high carb.

    I think if what you are doing is presenting arguments that your theory is a plausible one, I agree with that. If instead, you are trying to say that Taubes's theories are wrong and yours are correct, I think that's more difficult. You both could be correct, for instance.