Daniel Steinberg was a renowned cardiologist and lipid researcher (Masterjohn, 2009). He is credited with convincing Merck to bring a statin drug (lovastatin) to market, despite concerns about statin toxicity.

“Merck was among the first companies to develop a statin program, but was on the verge of shutting it down based on rumors that statins caused cancer in dogs. Along with Mike Brown, Joe Goldstein, and a number of prominent clinicians, Dan convinced Merck to continue the program, leading to the introduction of the first clinical statin capable of significant reductions of cholesterol levels in humans.” (Glass, 2015)

Brown and Goldstein won the Nobel Prize for discovering the LDL receptor, which was thought to play a crucial role in cardiovascular disease (CVD), since at the time it was thought that LDL was driving CVD.

However, their attempts to figure out how were fruitless. The first step in the atherosclerosis that can lead to CVD is the creation of “foam cells”, macrophages (a type of white blood cell) that are stuffed full of LDL and the cholesterol and fats that LDL transport throughout the body. However, incubating macrophages with LDL did not result in the macrophages converting into foam cells, and the fact that humans without LDL receptors still got CVD, sometimes at very young ages, indicated that the LDL receptor was not the key player (Goldstein, 1979).

Brown and Goldstein showed that a “modification” of LDL was necessary to make macrophages start the necessary process of internalizing ‘excess’ LDL. But they couldn’t determine what the modification was in the body, just that the modification they used, which is not found in the body, worked.

In 1991 Steinberg wrote,

“It was Goldstein and Brown who first proposed that modification of LDL was a prerequisite for macrophage uptake (3).” (Witztum, 1991)

Footnote 3 was (Goldstein, 1979).

The Culprit

In 2007, upon publication of his magnum opus description of how statins became the preeminent treatment for CVD, Steinberg explained the genesis of the research showing the “pathogenesis” (the origin of the disease) of CVD:

“Then Hessler and collaborators in Cleveland demonstrated that the changes induced in LDL by incubation with endothelial cells were due to free radical modification (78). Steinbrecher et al. in La Jolla independently came to the same conclusion with regard to the mechanism by which endothelial cells converted LDL into a ligand for macrophage receptors (79).” (Steinberg, 2007)

Steinberg, as senior author of the 1984 Steinbrecher paper, had published “Modification of Low Density Lipoprotein by Endothelial Cells Involves Lipid Peroxidation and Degradation of Low Density Lipoprotein Phospholipids” (Steinbrecher, 1984).

The “lipid” being “peroxidized” was linoleic acid, the chief polyunsaturated fat in seed oils. In addition to the fact that the only lipid they used in this experiment was linoleic acid, the TBARS test that they used strongly reacts to peroxidized linoleic acid (Ohkawa, 1978).

“The extent of lipid peroxidation was directly assessed using the thiobarbituric acid assay and, as shown in Figs. 1 and 2, the generation of thiobarbituric acid-reactive material paralleled the macrophage uptake of LDL. (Steinbrecher, 1984)

Moreover, the antioxidants they used, especially vit. E, are well known to protect linoleic acid against peroxidation. The “modified” LDL became known as “oxidized” LDL (oxLDL), as it was clear to all that this was the mechanism by which LDL went from a non-atherogenic, “native” state, to the atherogenic, pathological state. In discussing a follow-up paper of Steinberg’s (Brown and Goldstein wrote:

“The search for a physiological ligand for the scavenger receptor bore fruit when Steinberg and co-workers discovered that oxidized LDL competes for the binding of acetyl-LDL and delivers sufficient cholesterol to produce a foam cell (reviewed in ref. 5).” (Brown, 1990)

Ref. 5 is “Beyond Cholesterol. Modifications of Low-Density Lipoprotein That Increase Its Atherogenicity”, (Steinberg, 1991), a review of his team’s work up until that point, published in the New England Journal of Medicine, a premier medical journal.

“All these changes, however, depend on a common initiating step—the peroxidation of polyunsaturated fatty acids in the LDL lipids.” (Steinberg, 1989)

The predominant polyunsaturated fatty acid (PUFA) in LDL is linoleic acid, from seed oils. (Spiteller, 1998)

Steinberg and the researchers he worked with, especially Joseph Witztum, went on to do a number of other experiments looking at the peroxidation of linoleic acid and the effect of that peroxidation on LDL and its role in atherosclerosis. They showed that replacing linoleic acid with oleic acid, which is not susceptible to peroxidation, prevented the oxidation of LDL. In a latter review paper (Witztum, 1991), they describe these experiments.

“The importance of the fatty acid composition was impressively demonstrated by our recent studies of rabbits fed a diet high in linoleic acid (18:2) or in oleic acid (18:1) for a period of 10 wk. LDL isolated from the animals on oleic acid-rich diet were greatly enriched in oleate and low in linoleate. This LDL was remarkably resistant to oxidative modification, measured either by direct parameters of lipid peroxidation (i.e., TBARS and conjugated dienes) or by the indirect criterion of uptake by macrophages (53)….

“In a recent study, human volunteers were fed a similar oleic acid-rich diet. When their LDL was tested for susceptibility to oxidative modification, it was reduced albeit to a lesser degree than that noted in the rabbit studies (54). These studies demonstrate the feasibility of dietary modification of LDL fatty acid content in order to reduce its susceptibility to modification.” (Witztum, 1991)

Concluding that the root cause is that, “there is a vast excess of polyunsaturated fatty acids in LDL, in relationship to the content of natural, endogenous antioxidants.” (Witztum, 1991)

Ref. 53 above is, “Low Density Lipoprotein Rich in Oleic Acid Is Protected Against Oxidative Modification: Implications for Dietary Prevention of Atherosclerosis.” (Parthasarathy, 1990), another paper in which Steinberg is senior author.

In this paper, they fed rabbits, a long-standing model of atherosclerosis, either a high-linoleic or high-oleic sunflower oil (Trisun 80, non-GMO). Steinberg observed, “Yet diets in which polyunsaturated fatty acids are substituted for saturated fatty acids are considered to be beneficial in that they lower plasma cholesterol levels (14).” Ref. 14 is referring to the National Diet-Heart Study (NDHS).

“It was a truly heroic undertaking in which food manufacturers provided specially processed foods in which the saturated fat content was manipulated. Participants ordered their fat-containing foods from a central depot and were given dietary instructions.” Steinberg, 2007)

Saturated fat was replaced with polyunsaturated fat. It was the birth of ultra-processed foods, and the stealth replacement of fats provided a model the government pursued for decades across the entire food industry (Rowe, 2011).

But this is the key sentence from (Parthasarathy, 1990):

“In fact, dietary intervention studies have shown that such diets appear to reduce the risk of clinical coronary heart disease (15), presumably by decreasing plasma LDL levels. However, it is quite possible that the LDL in such patients is more readily oxidized and is therefore more atherogenic but that the decrease in LDL concentration more than compensates for any such increased susceptibility of LDL to oxidative modification. In other words, a polyunsaturated fatty acid-rich diet may have two opposing effects but with an overall balance that is favorable-i.e., antiatherogenic.” (Parthasarathy, 1990)

Ref. 15 is to (Dayton, 1969), aka The LA Veterans Study. Here’s how those authors describe their own study:

“…we consider our own trial, with or without the support of other published data, to have fallen short of providing a definitive and final answer concerning dietary prevention of heart disease.” (Dayton, 1969)

So citing this study as compelling only works if the only criteria you use is lowering cholesterol and heart disease outcomes, but not total mortality. That’s a bad idea.

(Interestingly, the problem in (Dayton, 1969) was increased cancer mortality in humans on the high seed oil diet. Steinberg convinced Merck to ignore the concern of cancer in dogs to bring lovastatin to market. I think it’s a bad idea for cardiologists to focus only on cardiovascular disease and ignore the rest of the body.)

That aside, the idea that lower LDL cholesterol might be beneficial even in the face of a higher Ω-6 PUFA intake isn’t of itself a crazy idea. I’ve often said that if you won’t fix your diet by removing seed oils, a statin is probably not a bad idea. There is evidence that statins do reduce CVD in a high-Ω-6 diet—see every single statin trial done—even if it’s probably by a lot less than the ~20% the industry-sponsored trials showed. Statins do have pleiotropic effects (effects other than the intended one, in this case the lowering of cholesterol production) specifically they seem to be antioxidants (Zhang, 2024), which directly effects the actual pathway of CVD disease initiation and progression, as Steinberg showed.

So I think it’s fair to say that Steinberg & Co. demonstrated the actual mechanism of CVD initiation and progression. It’s the peroxidation (rancidity) of Ω-6 fats in the body. This is such a core notion of modern cardiology that current reviews of pathogenesis like (Borén, 2020) cite (Steinberg, 1989), and place the oxidation of LDL at the start of the atherosclerotic alteration of LDL.

Lyon Diet-Heart Study

At this point I should mention the most successful diet-heart trial of all time. In 1994, in the midst of Steinberg & Co.’s research into seed oils and CVD a French cardiologist, Michel de Lorgeril, published “Mediterranean Alpha-Linolenic Acid-Rich Diet in Secondary Prevention of Coronary Heart Disease.”

This study was designed to mimic a Cretan diet, in light of Steinberg’s research (Reaven, 1993) on the role of linoleic acid in CVD, to produce a better outcome than a study like the NDHS and its successor. It succeeded.

This study attacked CVD in secondary prevention (people who have already had a heart attack, the most high-risk cases) with a two-pronged approach against Ω-6 fats in heart disease. It was a multi-intervention approach, like many other studies, but in my opinion, and based on Steinberg’s research, the two significant prongs are the decrease in linoleic acid, and the increase in alpha-linolenic acid.

“The experimental group consumed significantly less lipids, saturated fat, cholesterol, and linoleic acid but more oleic and alpha-linolenic acids confirmed by measurements in plasma.” (de Lorgeril, 1994)

(I discussed why reducing fats is not meaningful in this post, if you are interested.)

For the benefit of Ω-6 linoleic acid reduction, see Steinberg’s research, and others to be discussed below. Alpha-linolenic acid is a plant-based, 18-carbon Ω-3 fat that converts into EPA (eicosapentaenoic acid, an animal-based long-chain Ω-3 fat). EPA is currently marketed by cardiologists as Vascepa, a synthetic—and thus more profitable—version of EPA for CVD risk reduction (Chance, 2019).

(EPA replaces the long-chain Ω-6 fat arachidonic acid (AA) in cell and LDL membranes, and this is thought to be why it offers benefits in CVD. There’s less AA than linoleic acid, but it can be a problem (Spiteller, 1998))

Compared to the trials which increased Ω-6 fats, but didn’t include Ω-3 fats, and saw an increase in CVD, de Lorgeril’s study saw a 70% decrease in mortality.

(It was excluded from (Ramdsen, 2016a) because it, “Did not substitute LA-rich oil in place of SFA”.)

This was also better than the trials that increased both Ω-3 and Ω-6 fats, like the LA Veterans Trial (Ramsden, 2016a, Appendix A, CHD=CVD).

The American Heart Association saw fit to revise their recommendations after (de Lorgeril, 1994) was published, and recommended a ‘Mediterranean’ diet with alpha-linolenic acid. They failed to emphasize the reduction in linoleic acid.

“AHA Science Advisory: Lyon Diet Heart Study. Benefits of a Mediterranean-style, National Cholesterol Education Program/American Heart Association Step I Dietary Pattern on Cardiovascular Disease.” (Kris-Etherton, 2001)

I hope she got a nice bonus for squaring that circle.

This is a problematic recommendation because we know that high linoleic acid impairs the conversion of alpha-linolenic acid to EPA.

“We showed that reducing [linoleic acid]-rich oils and incorporating [alpha-linolenic acid]-rich plant sources (flaxseed oil and walnuts) in recipes achieved an n-6/n-3 ratio potentially conducive to improved health outcomes and is sufficient to meet the EPA needs of individuals adhering to a vegetarian or meatless diet.” (Wein, 2010)

Steinberg on the Studies

He discusses a number of the diet-heart trials, calling the NDHS “heroic”, as above, but trashes the Minnesota Coronary Survey (MCS, also referred to as the Minnesota Coronary Experiment—MCE).

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“Clearly, the Minnesota Coronary Survey cannot be regarded as a meaningful test of the lipid hypothesis. Yet it is often included in meta-analyses and often appears on lists of studies allegedly disproving the lipid hypothesis.” (Steinberg, 2007)

This is doubly-odd, as the MCS was a follow-on from the NDHS.

“In addition, a study of a group of hospitalized patients is being conducted by Dr. I. D. Frantz, Jr., of the University of Minnesota.” (Page, 1964)

As Frantz explained, describing the MCS:

“Two diets were served. The control diet involved little departure from the institutional diet served before the trial. The treatment diet represented a compromise between the B and C diets of the National Diet-Heart Study, with target values of 45% of calories from fat, a polyunsaturated/ saturated fat (P/S) ratio of 2.5, and less than 150 mg of cholesterol daily.” (Frantz, 1989)

Of course one can conduct a higher-quality study in a hospital, where more variables can be controlled, than in people living at home, as in the rest of the NDHS.

(Page, 1964) was written by Irvine Page, who initiated and designed the NDHS and thus the MCS.

“Page and the members of his committee were pioneers, sufficiently persuaded by the evidence available to invest a significant piece of their time and energy in a quest for the definitive clinical trial. They were by no means evangelical. In his Editorial [(Page, 1964)], Page put it this way, “No one knows whether a free-living, healthy population will continue with the changes in eating habits we suggest. Nor do we know whether, if their blood cholesterol levels are moderately reduced, heart attacks will decrease. At least we will try to find out.” (Steinberg, 2007)

Moreover:

“This book might never have been written if Irvine H. Page had not suggested it to me almost 20 years ago. He wrote me a note shortly before his death in 1991, saying in essence that it was my duty “to write the history – so that people will remember the uphill battle it was to gain acceptance of the lipid hypothesis.” Page was one of the first cardiologists to recognize the plausibility of the hypothesis and to champion efforts to prove it at the clinical level (11;12). (Steinberg, 2007)

Ultimately the problem is that the MCS does disprove the lipid hypothesis.

“This finding that greater lowering of serum cholesterol was associated with a higher rather than a lower risk of death in the MCE does not provide support for the traditional diet-heart hypothesis.” (Ramsden, 2016a)

Steinberg discusses the Finnish Mental Hospitals Survey (FMHS) and Oslo Diet-Heart (ODHS) approvingly, however, although he misrepresents the rigorousness of the designs. Most modern meta-analyses of this topic exclude both.

“…excluding Oslo Diet Heart 1966 as it increased both omega-3 and omega-6 fats and included a multivitamin in the intervention group (so was multifactorial), and Finnish Mental Hosp 1972 as it was a cluster-randomised trial, with only two clusters (and used a cross-over approach inappropriate for outcomes that develop over time such as CVD). Both trials we excluded reported statistically significant reductions in their primary outcomes.” (Hooper, 2018)

Steinberg’s Conclusion

So there’s ‘good’ evidence for statins—I wince, see (Vancheri, 2016)—and really good evidence for seed oils. How does Steinberg proceed?

In (Steinberg, 2007), “The Cholesterol Wars: The Skeptics vs the Preponderance of Evidence” he fails to mention:

• Linoleic acid

• Oleic acid

• Mediterranean diet

• de Lorgeril

He discusses oxLDL a bit, but mentions his and Witztum’s research peripherally, never making the connection between linoleic acid and oxLDL. He discusses the utility of antioxidants, never mentioning what oxidation they are supposed to prevent, and certainly never mentioning reducing linoleic acid to reduce CVD risk.

This is odd.

Where did he write this book?

“My eternal gratitude goes to my good friend and long-time collaborator, Joseph L. Witztum, who provided me with space and support for this post-Emeritus undertaking. Some of the themes in the book may have been drawn from his songbook. We sang them together for many years.” (Steinberg, 2007)

Some of the verses have been discarded, however.

He discusses oxLDL in the context of creating a vaccination for it using an antibody— Steinberg held a patent on such an antibody.

Ultimately Steinberg does what Page and the American Heart Association have done: bury the evidence. No doubt Page suspected this history would adhere to the party line, despite Steinberg’s research findings.

Page was president of the AHA in 1956-7, when they started promoting the consumption of seed oils for heart disease (Newport, 2024).

At the very least one can say that Page and the other cardiologists and scientists involved in this project should have been clear that the project failed: they did not prove that consuming more seed oils would have any beneficial effect on heart disease rates.

The intervention in the MCS was 13% linoleic acid. The AHA now says, sotto voce”

“The AHA has been cautious about recommending marked increases in polyunsaturates; the consequences of prolonged ingestion of large quantities of these fats are not known. To be on the safe side, the AHA has not recommended very high intakes of polyunsaturated fats for the general population. While some replacement of saturated fats by polyunsaturates seems safe, it may be prudent not to exceed 10% of total calories….”

“Finally, it should be emphasized again that the AHA does not recommend high-polyunsaturated fat diets similar to those used in the above clinical trials for the general public.” (Grundy, 1982)

The Dietary Guidelines goes further:

“…High intakes of linoleic acid create a pro-oxidant state that may predispose to several chronic diseases, such as CHD [CVD] and cancer. Therefore, an AMDR [Acceptable Macronutrient Distribution Ranges] of 5 to 10 percent of energy is suggested for linoleic acid.” (Institute of Medicine, 2005)

The problem, as Ramdsen explains:

“The MCE intervention provided ≈13%E (%E) as LA. According to NHANES, more than 13 million American adults currently consume ≥13%E as LA.” (Ramsden, 2016b)

The correct quantity is likely closer to 2%E. Note the the control diet in the MCS, with a slightly lower mortality rate, was 4.7%.

Steinberg’s research took this a step farther, however. He showed that the primary fat in seed oils drives heart disease. What’s known as the “oxidative modification hypothesis” is now the dominant paradigm in cardiology, if one is intellectually honest.

“The oxidative modification hypothesis was strongly supported by a number of lines of evidence, both in vitro and in vivo. No attempt will be made here to review this large body of evidence. The interested reader is referred to several comprehensive reviews (86-90).” (Steinberg, 2007)

Steinberg’s research makes clear that his process starts with the consumption of excess linoleic acid. He takes a victory lap for his research while hiding the core finding.

If we want to avoid the disease, and not just “treat” it, we must address the root cause.

Thanks to for his review of Steinberg’s 2007 book, and for educating me early on on the topic of oxidized LDL and CVD.

“…One would get the idea from reading The Cholesterol Wars that there is actually good science showing that we should reduce our intake of butter and use vegetable oil instead! And nothing could be further from the truth.” (Masterjohn, 2009)

References

Borén, Jan, M. John Chapman, Ronald M. Krauss, et al. 2020. “Low-Density Lipoproteins Cause Atherosclerotic Cardiovascular Disease: Pathophysiological, Genetic, and Therapeutic Insights: A Consensus Statement from the European Atherosclerosis Society Consensus Panel.” European Heart Journal 41 (24): 2313–30. https://doi.org/10.1093/eurheartj/ehz962.

Brown, Michael S., and Joseph L. Goldstein. 1990. “Scavenging for Receptors.” Nature 343 (6258): 508–9. https://doi.org/10.1038/343508a0.

Chance, Blair. 2019. “FDA Approves Omega-3 Fish-Oil Medication Vascepa to Reduce Risk of Death in People with High Cholesterol.” News. ABC News, December 16. https://abcnews.go.com/Health/fda-approves-omega-fish-oil-medication-vascepa-reduce/story?id=67748996.

Dayton, Seymour, Morton Lee Pearce, Sam Hashimoto, Wilfrid J. Dixon, and Uwamie Tomiyasu. 1969. “A Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing Complications of Atherosclerosis.” Circulation 40 (1s2): II–1. https://doi.org/10.1161/01.CIR.40.1S2.II-1.

Glass, Christopher K., and Joseph L. Witztum. 2015. “Daniel Steinberg, 1922–2015.” Proceedings of the National Academy of Sciences of the United States of America 112 (32): 9791. https://doi.org/10.1073/pnas.1512413112.

Goldstein, Joseph L., Y. K. Ho, Sandip K. Basu, and Michael S. Brown. 1979. “Binding Site on Macrophages That Mediates Uptake and Degradation of Acetylated Low Density Lipoprotein, Producing Massive Cholesterol Deposition.” Proceedings of the National Academy of Sciences of the United States of America 76 (1): 333–37. https://doi.org/10.1073/pnas.76.1.3.

Grundy, Scott M., David Bilheimer, Henry Blackburn, et al. 1982. “Rationale of the Diet-Heart Statement of the American Heart Association. Report of the AHA Nutrition Committee.” Arteriosclerosis: An Official Journal of the American Heart Association, Inc. 2 (2): 177–91.

Hooper, Lee, Lena Al‐Khudairy, Asmaa S. Abdelhamid, et al. 2018. “Omega‐6 Fats for the Primary and Secondary Prevention of Cardiovascular Disease.” Cochrane Database of Systematic Reviews, no. 7. https://doi.org/10.1002/14651858.CD011094.pub3.

Institute of Medicine. 2005. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. National Academy of Sciences. https://doi.org/10.17226/10490.

Kris-Etherton, Penny M., Robert H. Eckel, Barbara V. Howard, Steve C. St Jeor, and Terry L. Bazzarre. 2001. “AHA Science Advisory: Lyon Diet Heart Study. Benefits of a Mediterranean-Style, National Cholesterol Education Program/American Heart Association Step I Dietary Pattern on Cardiovascular Disease.” Circulation 103 (13): 1823–25. https://doi.org/10.1161/01.CIR.103.13.1823.

Masterjohn, Christopher. 2009. “Cholesterol Wars by Daniel Steinberg.” Blog. The Weston A. Price Foundation, March 27. https://www.westonaprice.org/book-reviews/the-cholesterol-wars-by-daniel-steinberg/.

Newport, Mary T., and Fabian M. Dayrit. 2024. “The Lipid–Heart Hypothesis and the Keys Equation Defined the Dietary Guidelines but Ignored the Impact of Trans-Fat and High Linoleic Acid Consumption.” Nutrients 16 (10): 10. https://doi.org/10.3390/nu16101447.

Ohkawa, H., N. Ohishi, and K. Yagi. 1978. “Reaction of Linoleic Acid Hydroperoxide with Thiobarbituric Acid.” Journal of Lipid Research 19 (8): 1053–57. https://doi.org/10.1016/S0022-2275(20)40690-X.

Page, Irvine H. 1964. “Editorial: The National Diet-Heart Study.” Circulation 29 (1): 4–5. https://doi.org/10.1161/01.CIR.29.1.4.

Parthasarathy, S., J. C. Khoo, E. Miller, J. Barnett, J. L. Witztum, and D. Steinberg. 1990. “Low Density Lipoprotein Rich in Oleic Acid Is Protected Against Oxidative Modification: Implications for Dietary Prevention of Atherosclerosis.” Proceedings of the National Academy of Sciences 87 (10): 3894–98. https://doi.org/10.1073/pnas.87.10.3894.

Ramsden, Christopher E., Daisy Zamora, Sharon Majchrzak-Hong, et al. 2016a. “Re-Evaluation of the Traditional Diet-Heart Hypothesis: Analysis of Recovered Data from Minnesota Coronary Experiment (1968-73).” Research. BMJ 353 (April). https://doi.org/10.1136/bmj.i1246.

Ramsden, Christopher E., Daisy Zamora, Sharon F. Majchrzak-Hong, et al. 2016b. “Re: Re-Evaluation of the Traditional Diet-Heart Hypothesis: Analysis of Recovered Data from Minnesota Coronary Experiment (1968-73).” BMJ 2016 (353): i1246. https://doi.org/10.1136/bmj.i1246.

Reaven, P., S. Parthasarathy, B. J. Grasse, E. Miller, D. Steinberg, and J. L. Witztum. 1993. “Effects of Oleate-Rich and Linoleate-Rich Diets on the Susceptibility of Low Density Lipoprotein to Oxidative Modification in Mildly Hypercholesterolemic Subjects.” Journal of Clinical Investigation 91 (2): 668–76.

Rowe, Sylvia, Nick Alexander, Nelson Almeida, et al. 2011. “Food Science Challenge: Translating the Dietary Guidelines for Americans to Bring About Real Behavior Change.” Journal of Food Science 76 (1): R29–37. https://doi.org/10.1111/j.1750-3841.2010.01973.x.

Spiteller, Gerhard. 1998. “Linoleic Acid Peroxidation—the Dominant Lipid Peroxidation Process in Low Density Lipoprotein—and Its Relationship to Chronic Diseases.” Chemistry and Physics of Lipids 95 (2): 105–62. https://doi.org/10.1016/S0009-3084(98)00091-7.

Steinberg, D., S. Parthasarathy, T. E. Carew, J. C. Khoo, and J. L. Witztum. 1989. “Beyond Cholesterol. Modifications of Low-Density Lipoprotein That Increase Its Atherogenicity.” The New England Journal of Medicine 320 (14): 915–24. https://doi.org/10.1056/NEJM198904063201407.

Steinberg, Daniel. 2007. The Cholesterol Wars: The Skeptics vs the Preponderance of Evidence. Academic Press. https://amzn.to/3OX6YZn.

Steinbrecher, U. P., S. Parthasarathy, D. S. Leake, J. L. Witztum, and D. Steinberg. 1984. “Modification of Low Density Lipoprotein by Endothelial Cells Involves Lipid Peroxidation and Degradation of Low Density Lipoprotein Phospholipids.” Proceedings of the National Academy of Sciences of the United States of America 81 (12): 3883–87. https://doi.org/10.1073/pnas.81.12.3883.

Vancheri, Federico, Lars Backlund, Lars-Erik Strender, Brian Godman, and Björn Wettermark. 2016. “Time Trends in Statin Utilisation and Coronary Mortality in Western European Countries.” Cardiovascular Medicine. BMJ Open 6 (3): e010500. https://doi.org/10.1136/bmjopen-2015-010500.

Wien, Michelle, Sujatha Rajaram, Keiji Oda, and Joan Sabaté. 2010. “Decreasing the Linoleic Acid to α-Linolenic Acid Diet Ratio Increases Eicosapentaenoic Acid in Erythrocytes in Adults.” Lipids 45 (8): 683–92. https://doi.org/10.1007/s11745-010-3430-3.

Witztum, J. L., and D. Steinberg. 1991. “Role of Oxidized Low Density Lipoprotein in Atherogenesis.” Journal of Clinical Investigation 88 (6): 1785–92. https://doi.org/10.1172/JCI115499.

Zhang, Yaoxia, Yuanyuan Qu, Ruiping Cai, et al. 2024. “Atorvastatin Ameliorates Diabetic Nephropathy Through Inhibiting Oxidative Stress and Ferroptosis Signaling.” European Journal of Pharmacology 976 (August): 176699. https://doi.org/10.1016/j.ejphar.2024.176699.

Introduction

For starters, I am not a carnivore. I mostly eat beef, fish, full-fat dairy, and fruit, with some vegetables.

I also have some starch, and some sugar. Ice cream is a health food.

I avoid wheat, seed oils, seeds, and seed-fed animals, like chicken or pork. I prefer grass-fed beef to seed-fed beef, but won’t avoid the latter.

So off I went to a meditation retreat, and the only menu available was a vegetarian diet. They offered a gluten-free vegetarian diet to comply with dietary restrictions like mine, so I signed up. While I’ve not been diagnosed officially as celiac, depending on what country I’m in, I could be. So a gluten-free diet for me a an absolute requirement.

I don’t think a vegetarian diet is as healthy as an omnivorous diet containing healthy meats (I’ll include fish in my definition of meat), but it’s not going to kill you in 10+ days! But I was certainly curious, and a little apprehensive, to see what effect it would have on me.

Food on Offer

For breakfast, they typically had oatmeal—not gluten free, more on this later—often some other starch, like quinoa, or something else. They had stewed prunes everyday, definitely more about that later! They also had fresh fruit; oranges, apples, and/or bananas. They offered yogurt everyday.

For beverages they had coffee or decaf, a variety of caffeinated or not teas, and whole milk.

They also had soy and rice “milk”. They offered sugar and hot honey. Hot honey is delicious!

Breakfast was served from 6:30am to 7:15. As we couldn’t talk to each other, this was plenty of time.

For lunch they typically had some other starch. White and/or brown rice, pasta, or some Indian-style starch meal with rice and other things, and Indian spices. Since this was a bilingual Hindi/English course, they focused on Indian spices and dishes. Luckily, I love Indian food. They also had a salad bar, with mixed greens, minced beets and carrots, chick peas, and grated cheese. They had two different salad dressings. They also had either yogurt or sour cream; on one day they had a burritos, and for that day sour cream replaced the yogurt. They usually also had the same selection of fresh fruit as at breakfast.

They offered whole-wheat bread and rice cakes; and a selection of toppings, peanut butter, strawberry jam (yes, you could have lived on peanut butter and jelly sandwiches each day, once my favorite food!), tahini, sunflower seeds, flax seeds, and some other stuff I never ate and don’t recall. Salt, pepper, and a variety of other spices of an Indian flavor for this course. Gluten-free soy-sauce (tamari), a couple types of hot sauce, balsamic vinegar.

Lunch was served from 11:00am to 11:45.

They didn’t offer dinner (see the related post above), just the same fruits and tea or coffee. On a bunch of different days they had some special beverage on offer. On Vipassana Day they celebrated with hot mulled apple cider, which was delicious. On several days they had a yummy ginger tea made by the kitchen, and they always had a selection of teas available, with whole milk or the other faux “milks”.

Tea-time was 5:00pm to 5:45.

I was usually out of the dining hall in 30 minutes or less, including cleaning my dishes.

Snacks were not available, and you were not allowed to take food or bring food in to keep in your room. So what you got in the dining hall was it for the day.

Calories

I was a little worried about not being able to get enough calories for the first couple of days. This was never an issue in practice. There were no servers, so you could take as much as you liked, or go back for seconds, which was encouraged. I usually only eat two meals a day, so while I ate the fruit at tea time for the first couple of days because of a fear of not getting enough food, after that I usually skipped the afternoon fruit for the rest of the course.

The First Day

They had a light dinner for the first evening before the first full day. They had a soup, and something starchy, as well as the salad bar. I sighed and put the salad dressing (which was delicious) on my salad, along with greens, beets, carrots, chick peas, and cheese. I figured I was going to be pretty unhappy with all the seed oils by the end of the course, and wondered what it would do to my gut.

As their accommodation for people with special dietary requirements they labeled foods that contained wheat, soy, or dairy. This was done manually, and this was a problem immediately at breakfast. The oatmeal was labeled as gluten-free, so I had some oatmeal, which I used to eat regularly.

Oats do not contain gluten, but are typically processed in facilities that also process wheat, so are usually cross-contaminated with wheat. I learned this by buying a fancy oatmeal back when I was fixing my diet starting in 2010, and having a bad reaction to it. I called the manufacturer, and they explained that while they didn’t include wheat in the recipe (not on the label), that I should expect it to be contaminated with wheat. One can get gluten-free oatmeal, but it doesn’t taste as good, darnit. I stopped eating oatmeal years ago.

This oatmeal was delicious, which should have clued me in…

I forget what we had for lunch, so I guess it wasn’t memorable. The kitchen is staffed by volunteers, except for a paid, part-time kitchen director; so I think it took them a couple days to hit their stride. The food improved steadily.

Gluten-Free?

The next morning I couldn’t figure out what to eat, and met Jomi. He knew what was in most of the food, and when I questioned him on one item he went and got the package to let me read the ingredients.

Then he warned me not to eat the oatmeal, that it was not gluten-free. He didn’t introduce himself as such, but I learned afterward that he was the kitchen director.

Drat, the oatmeal was what I had had for breakfast the morning before, and that explained why I was wiped out and falling asleep during the meditation sessions for the rest of the day, and the dietary distress I started experiencing immediately after.

Luckily I didn’t have any neurological effects, other than the sleepiness, but in the past I’ve suffered from blindness, auras (I get a migraine without pain from gluten exposure, and loss of the ability to speak (expressive aphasia), and on one memorable occasion, face blindness (prosopagnosia). Every time this has happened the effect has passed after several hours, but the first time I had aphasia I wound up in a stroke ward for four days. They thought I had had a minor stroke.

Face blindness means you can’t recognize people’s faces. Usually when I have a serious reaction to a gluten exposure I’ll go watch TV or something for a while, until it passes, since I can’t talk to anyone. In this case I was watching the Supergirl TV show that used to be on. It’s pretty obvious which character is Supergirl, due to the suit, but I couldn’t recognize her face at all, or any other other actors.

Now you understand why a gluten-free diet is my number-one concern. The effects have always passed, but I worry about the time when they don’t. It clearly can’t be good to be doing that sort of damage to my brain.

In hindsight I really should have introduced myself to the kitchen staff immediately, and not relied upon the hand-labeling. Jomi took great care of me from that point onwards, in a couple of cases making me gluten-free pasta when the lunch entree was not gluten-free, and making a delicious quinoa, mushroom and spice breakfast that lasted me for days 2 and 3. He went out of his way, and whenever I had a question he was quick to answer. I had no more issues, and the effects of the gluten exposure passed after a couple of days.

Most days there was white rice, however, and this became a staple, as I had anticipated it would.

I don’t like having to eat a gluten-free diet, and it’s a pain because of the inconvenience for me as well as the staff, but as they had advertised that they offered a gluten-free diet, I expected them to deliver. I wouldn’t have been able to attend at all otherwise.

Satiety

So folks claim that the problem with a high-carb diet is ‘hypoglycemia’, where your blood sugar rises and then falls, triggering cravings for more carbs (Berlin, 1994; Wyatt, 2021).

“After glucose intake, seven patients had symptoms (palpitations, headache, tremor, generalized sweating, hunger, dizziness, sweating of the palms, flush, nausea, and fatigue), whereas in the control group, one subject reported flush and another palpitations, tremor, and hunger.” (Berlin, 1994)

As you can see from those studies, it’s not exactly hypoglycemia, but it’s a real effect seemingly related to insulin resistance. I used to get this prior to fixing my diet; I would actually get the shakes and everything.

Not this time. I was full every time I left the dining hall, had no signs of anything like being “hangry”, and woke up ready for breakfast but perfectly fine with waiting the two hours until the dining hall served it.

So satiety, for me, was fine.

Weight

I wasn’t really planning on writing a post about this, so I didn’t measure my weight before going. Judging by my belt and mirror, I lost some weight during the course, but nothing to be alarmed about.

I don’t have any idea about what anyone else ate in their own lives, but I did note that while there were a few overweight individuals, only one was actually obese. He was Indian. On the men’s side, it was a pretty uniformly healthy-weight group of people. A few of the Indians ate special diets, and one had some type of sensor/pump on his triceps, which I presume was for diabetes. I didn’t speak to the gentleman, so never found out what that was for.

Fats

So I anticipated having to eat a lot of seed oils during this course. I never asked about this aspect, as I don’t think eating seed oils for ten days would have any effect on me beyond intestinal distress, which can occur for me after just one meal containing seed oils.

So I shrugged and anticipated an unpleasant experience in that regard, and thought that I wouldn’t be taking the OmegaQuant test that my friend has been bugging me to take, as I would get loaded up with Ω-6 fats.

But often when I go to a restaurant, I will ask for some sour cream and some vinegar, and make my own salad dressing with salt and pepper. It’s delicious, and perfectly satisfactory from a fatty-acid standpoint.

So I decided to take a look at the yogurt. I was expecting some horrible zero-fat yogurt, but much to my surprise and delight it was not only whole-milk, but grass-fed!

So this became my staple. Happy day!

I suspect I may have gotten a better Omega Balance during this course than I normally do.

What Did I Eat?

So after discovering the yogurt, for breakfast I would have yogurt with fruit including those stewed prunes, typically an apple or maybe an apple and a banana diced into the yogurt, with a dash of strawberry jam. Delicious.

For lunch I would have whatever gluten-free starch dish was on offer, sometimes rice, sometimes some mystery dish with an Indian name, and of course the gluten-free part of the burrito dish the day that was served. A fair bit of beans, I suppose, as this was pretty much the only protein on offer. I would have some of the vegetables, maybe a taste of the Indian spicy pickles (preserved in some seed oil, blech, but very tasty). I would also have a salad, prepared as above with a yogurt or sour-cream based dressing I created myself, and another dash of jam. A couple of days I added a dash of tahini.

I was not suffering at all. I was quite pleased, in fact. It was much better than I had been expecting.

Intermittent fasting

From the beginning of breakfast to 11:30am when I usually left the lunch hall to go for a walk is five hours. That’s a 19-hour fast on most days, except when I decided to have an apple or a banana at tea. That was effortless. Of course it helps that they kept us pretty busy, especially in the evenings, but I never thought about the fact that there were no snacks available.

The Downside

On my normal meat-and-dairy-based diet I typically have a bowel movement once a day.

Since I had my sigmoid colon resection (they remove that section of the colon) 18 years ago, a first-thing-in-the-morning poop has been a routine.

I had a colleague who also had a sigmoid colon resection for colon cancer, and he reported the same effect. The surgeon never mentioned this effect of removing the sigmoid.

Aside from when you’re camping in the woods—imagine frenzied hole-digging first thing in the morning in a primitive campsite, and you’ll get the idea—this is quite convenient, you get it out of the way and you have the rest of the day free.

Well, that was over.

The high carb and fiber load (for me) left me gassy and a bit bloated. Three, four, or even five BMs a day became the norm. Basically, every time I went to the dining hall and sent a new meal down, I had to proceed to the bathroom to make room for it. Maybe this is partly because of my missing sigmoid colon, “The primary job of the sigmoid is to act as a holding chamber for fecal matter until it can be moved out of your body.” But regardless, I felt like a tube of toothpaste constantly being stuffed full of more toothpaste. Not fun. I was really looking forward to getting home and being able to go back to my regular diet.

And I noticed that the intestinal noise in the meditation hall seemed to increase pretty steadily during the course of the course, culminating in the burping fiasco (the poor victim was an Indian guy) mentioned in the previous post.

A few days after getting back I suffered from a bout of constipation. I never get constipation, and I can’t but think that there’s a connection.

Stewed prunes are a famous remedy for constipation. They were served every morning. That and the large can in the dining hall of something with a hand-written label, “Colon cleanser”, makes me think I’m not the only one who had bowel problems with the vegetarian diet.

Conclusion

So it was an interesting experiment, and one that went a lot better than I was expecting, thanks to the grass-fed, whole milk yogurt.

If you subscribe to the notion of ahimsa (see the related post) this is how I would recommend you construct your diet: generally in the traditional Indian manner. Starch, fruit, beans, vegetables, and healthy dairy fats, but no seed oils. Intermittent fasting to force your body to burn stored fat throughout the rest of the day. I felt just fine on this diet, with the exception noted above.

But I definitely won’t be making this my staple diet at home. Farting all night and sitting on the toilet multiple times a day is not something I want to make part of my life.

Goenkaji, the founder of this school, was a big advocate for intermittent fasting, as he constructed the diet schedule, and for vegetarianism. It doesn’t seem to be enough to keep one slim.

But I doubt he avoided the vegetable oils…

References

Berlin, I., A. Grimaldi, C. Landault, F. Cesselin, and A. J. Puech. 1994. “Suspected Postprandial Hypoglycemia Is Associated with Beta-Adrenergic Hypersensitivity and Emotional Distress.” The Journal of Clinical Endocrinology & Metabolism 79 (5): 1428–33. https://doi.org/10.1210/jcem.79.5.7962339.

Wyatt, Patrick, Sarah E. Berry, Graham Finlayson, et al. 2021. “Postprandial Glycaemic Dips Predict Appetite and Energy Intake in Healthy Individuals.” Nature Metabolism, April 12, 1–7. https://doi.org/10.1038/s42255-021-00383-x.

My daughter Grace is engaged to a Japanese fellow, Yuto (who speaks English, thank Heavens for me!), and she recently recommended to me that I attend a Vipassana meditation course.

Yuto had done this course when he was backpacking in India, and thought it was terrific, and that I would benefit from doing it also.

My daughter is one of the smartest people I know, her IQ is 20 points higher than mine, and I very much respect her opinion, both of Yuto and, thus, of Yuto’s opinions. And obviously he’s asked my daughter to marry him, so he must be a smart guy.

So I did a little research. It didn’t seem to be a cult (my obvious first concern) and the program is basically non-religious. I’m a Catholic, and know a fair bit about Hinduism, and am not interested in converting, although I have great respect for the Hindus and their religion.

My daughter thought I should fly to India and take the course there, to get the full experience. That seemed a bit impractical to me right at the moment.

But I discovered that the oldest Vipassana (vi-PA-sha-na) center outside of India is two hours away from me. That seemed reasonable, and as it happens, they had a course coming up in a window that would work well for me.

So I applied. It was a Hindi-language oriented course (addressing part of my daughter’s desire for the full experience!), so I went on the waitlist until they got enough Indians to fill up that requirement. Then I got accepted.

The Course

“Vipassana means ‘to see things as they really are’.”

It’s also translated as “insight”. So the goal of the course is to increase your insight into yourself, and thus allow you to see things as they really are. It’s derived from Buddhism, they claim it’s the only direct line of descent from Buddha’s actual teachings. I don’t know if that’s actually correct or not, but it doesn’t really matter.

The course is ten days long. This is the biggest negative: you really have to set aside a solid block of time to do the course. And it’s actually longer than ten days, as you travel to the center. One guy, an American, flew in from India to attend, which all the Indians thought was very funny. The course is ten solid days, but it’s really twelve days of your time. It’s starts at 7pm on the first day, you then have ten solid days of training, and it ends at 7am on the 12th day, after which you travel away.

They have a number of rules that you must agree to follow in order to participate in the course.

No Killing!

The first definitely got my attention, “No killing”. Well, it’s good to know there will be no killing! While this is not a religious course, or an attempt to get you to convert to either Hinduism or Buddhism (which is derived from Hinduism) it emphasizes a certain moral code, and part of this code is the idea of ahimsa, or doing no harm to any living being. Luckily I did the course from April 15th to the 26th, which is early spring in Massachusetts where the center is, and so there were no mosquitoes around. Yes, no killing doesn’t refer just to the other students, but to things like mosquitoes. I would definitely recommend taking the course when there are no biting insects around! I discussed with some of the other students helping spiders outside, which is something I typically do anyway, but I’m normally a big fan of killing mosquitoes. It’s one of the few intrusions of the Hindu religion into the course, more about that later.

No Talking!

More significantly, the course requires you adhere to what they call ‘Noble silence’. You must refrain from any communication with the other students, or with the staff except when you have a question or, say, an issue with the accommodations. This includes no physical contact, or even making eye contact with anyone else.

Additionally, no cell phones, no reading materials of any sort, and, to keep you focused, there is no artwork in the entire facility that I had access to.

I left my wallet and my cell phone locked in my car (no need for money) although for people who flew in they will hold your phone and your valuables for the duration of the course.

At the beginning and on and after the 10th day the noble silence is not in effect. So I was able to talk to a couple of the other students at the beginning, both of whom were attending their second course.

No Booze!

They also require you to refrain from taking any intoxicants. No smoking, no alcohol, and only prescription drugs prescribed by a physician are allowed. Having just quit caffeine to great effect, I was amused to see that they offered coffee and tea at meals. I had decaf with my meals.

No Sex!

One other rule is total segregation of the sexes, which from another rule of no sexual activity. The facility is divided into male and female sides, with separate sleeping and eating facilities. The only time you see the ladies is in the meditation hall, where they sit on their side and the men on theirs. Instructors are similarly segregated, all female for the women. So sorry, this is not an Indian sex cult at all. Some hippie retreat! Even husbands and wives are separated.

No Religion or Exercise

All religious practices are proscribed, as is any exercise routine other than light exercise. They just installed a trail system on the 100-acre property, and that was a Godsend. They said that prior to that people would walk in circles on the lawn during the breaks, so we were able to walk in circles through the woods. I was able to follow the trees leafing out, and to see the spring ephemerals bloom. It is my favorite time of the year in the New England woods, so that was quite a treat. I didn’t bring my running watch, so I couldn’t track my miles, but I got a lot in.

A Strict Schedule

During the course, you are awoken at 4am by a guy walking the hall with a small gong, although they also recommend you bring an alarm clock, as most of us now rely on our cell phones. You then start the morning two-hour meditation period, either in your room or in the hall. Breakfast follows at 6:30 am. You then follow a schedule of either private or group mediation, with a few breaks for food and for rest. The last group session ends at 9pm, with a 30-minute question session afterwards. I went directly to bed at 9pm each day, as I was exhausted.

One of the practices cults (like those we call medical schools) use to indoctrinate members is sleep deprivation. Despite my initial research, I was still a bit apprehensive that maybe they were a really good, subtle cult. So I was attentive to the various tactics that might be used. Between the seven hours of prescribed sleep each night, and the various rest and meal periods, you can certainly get enough sleep. I napped sometimes, or fell asleep during trying to meditate in my room, and the sound of alarm clocks going off at the end of the various in-room meditation periods was a regular one.

The main meditation periods are from 8:00 am to 9, from 2:30 pm to 3:30, and from 6 to 7. These are held in the meditation hall, or in the meditation cells with permission. One day I got it in my head that the 8:00 am session was supposed to start at 8:30, and so stayed in my room. The course manage was knocking on my door in a moment or two; so attendance is, if not mandatory, certainly encouraged.

Seating is all assigned, at meals in the dining hall, in the meditation hall, in the cells, and of course for your room. The assignments are all different, however, so you do get to mingle with the entire class and not get to know any of them (no talking!).

Vegetarian Meals

I’ll do a longer post about how this went, but in keeping with the principle of ahimsa, the food was all vegetarian, but not vegan. My wife was very worried that it would be a vegan cult, but there was plenty of dairy (milk, yogurt, and cheese; all full-fat, no skimmed) to go with the meals, in the Indian vegetarian tradition. The food was pretty good, and I had no complaints about that. They do provide for special diets, and as I’m gluten-free that was a requirement for my attendance. No carnivore, though!

They provide all food, and you’re not allowed to bring your own or keep food in your room. Another cult technique is food deprivation: but the dining hall was self-serve, all-you-can-eat, and you were encouraged to go back for seconds. Lack of food was not an issue.

Intermittent Fasting

They only served breakfast and lunch. They had an afternoon tea, but only provide fruit (apples, oranges, and bananas), no dinner. There were lots of jokes about this being a prison, even by the founder, who quipped, “But at least in prison you get dinner!”

“Old students”, those who have already completed a course, are encouraged to have nothing but tea at tea time, but this was not enforced. I usually only eat two meals a day anyway, so it was fine. Due to the change in diet, I was a little concerned about being able to get enough calories, but wound up skipping the fruit most days during tea time. More about this topic in another post, as I said above.

Sitting

Ouch. More on this later. Do practice sitting lotus-style (Indian-style) prior to going to one of these courses. Ideally you should be able to sit like this for an hour. It’s not a requirement, you can get a chair, but if you can do sit lotus-style for an hour it will definitely make things better.

I spent most sessions envying Alok, who sat in the front row—ramrod straight and unmoving through every session. He wouldn’t even get up for the breaks, as the rest of us staggered out into the hallway!

One young fellow, William, sat across from me at the meal hall. He had quickly moved to a seat in the mediation hall, as had a few of the older gentlemen; and I could see from his face that he was having a really hard time getting through this. He wasn’t the only one. But on Day 10 I learned why: he had a damaged back, and had had two back surgeries. He was in agony even trying to sit in a chair for an hour.

He said that he used the meditation to focus on the back pain (which was part of the practice) and he’d seen a significant improvement in his back. He said the pain reduction alone was worth the investment in the ten-day course.

Accommodations

The Massachusetts center is a dedicated facility, owned and built by a not-for-profit for the purpose. It started out as tents in a field, often during the pouring rain, but the facility is now complete. Everyone has their own room and bathroom with a shower, and while it’s not luxurious, it’s certainly sufficient. I was on the outside of the circular facility facing the walking trails, so I had a nice view of the woods. One little quirk, as it’s run by volunteers, you are expected to clean up your own room at the end of the stay. This was not a big deal, and is consistent with their financing philosophy (more later), but be aware. By the time you are finished, you are happy to do so.

The dining hall was a cafeteria, and was adequate to the purpose. You were expected to bus your own table and to wash your dishes before they go in the commercial washer for sterilization. Again, not a big deal.

The Founder

Of course they say the founder was the Buddha, Siddhartha Gautama. (I read Siddhartha, Herman Hesse’s novel written in the 1920s when I was a kid; I recommend reading this before attending the course.) But the Vipassana Meditation Center was started by S.N. Goenka (known as Goenkaji, “-ji” being a suffix denoting respect and endearment). Goenkaji was a wealthy Hindu businessman of Indian descent living in British Burma, who came down with migraines. After exhausting the ability of the local physicians to treat it—they had him on morphine, and told him it would end badly—he travelled to Switzerland, the U.S., and Japan looking for a cure. No luck. A friend suggested he attend a local Buddhist meditation class, suggesting that his migraines were psychosomatic (all in his head), so maybe mediation would be beneficial. Goenkaji probably was having stress migraines, IMHO.

Goenkaji was skeptical, but having tried all Medicine had to offer, and facing the prospect of morphine addiction, he gave it a shot. His family was horrified, they were Hindi, and he was a prominent member of the Hindi community. They didn’t want him to join some Buddhist cult, and neither did he! He nearly dropped out on the second day of the ten-day course, but was convinced to stay.

He wound up as a student of the technique for the next thirteen years. After Burma left British rule behind, he travelled to India to teach his parents (who had moved back to India), as his mother was having psychiatric difficulties. He taught his parents, and 12 other students, and word-of-mouth spread. He quickly had more students, and spent the rest of his life teaching the technique, as he calls it. His teacher had told him the technique had been lost to India over the centuries, but there was a prophecy that someone would bring it back, and that this was his destiny. Shades of Star Wars.

Goenkaji died in 2013. My daughter thought I should travel to India to experience the full thing, but it turns out that the course in Massachusetts relied heavily on videos of Goenkaji made in India. I would have seen the same videos if I had been in India. He’s clearly a smart guy and quite funny. Each evening at 7pm we would listen to 1.5 hour “discourses”, Goenkaji talking about the day’s progress and what we would be doing tomorrow.

In one discourse he mocks himself for being such a bad guru, saying that he doesn’t have a ™ symbol on his forehead, he doesn’t make any money from it, and he looks like a “straight”, the derogatory hippie term for businessmen.

To give you an idea of the impact he has had, he was asked to address the UN in 2000.

I looked forward to the discourse each day, and paid rapt attention to each one. More below.

So How Was It?

Yuto had said that the first three or four days were brutal, but if you could get through that, you’d be fine. I was actually looking forward to time away from my phone (the most I’ve had since the 1990s), and didn’t really mind the prospect of not talking to anyone for ten days. While I did get a bit loopy on day three, and it progressed from there; I didn’t find that aspect brutal. Your experience may vary.

As I mentioned, there’s no reading material allowed or provided, with the exceptions of a board where the rules and schedules are posted. They also post some FAQ answers, and some special notifications. I paid close attention to the board, as it was the only thing to read, and they did have some schedule changes.

So on day four (Day four!), the board announced that it was Vipassana Day, “today you will find out what Vipassana is!”

Wait, what? I’ve been here three days and NOW I’m going to find out what Vipassana meditation is? What the heck!

It turns out for the first three days you have been practicing what is called anapana meditation. On day four they show you how to do Vipassana meditation.

Part of the reason the course is so effective is that it operates in a progressive fashion. They don’t tell you up front what you will be doing each day or how the course is structured. Each evening they tell you what you will do the following day. You spend the day practicing it, with maybe a little more guidance in the morning. In the evening discourse, Goenkaji explains what you have experienced during the day, and answers questions. This part was a bit spooky. Mind, Goenkaji has been dead for 13 years, and most of the videos were at least 20 years old. He had done so many of these courses, and he knew so well what the students would be going through, that he was able to correctly anticipate what we would go through and what we would need to hear. One old student, who has attended five courses in the last two years, said that even after five courses he was still getting new information from the discourses, answers to questions he hadn’t even considered in the previous courses.

When Vipassana Day arrived on day four, and Goenkaji finally told us how to do Vipassana meditation, I was frankly staggered by what I experienced.

The rest of the course was about advancing our meditation technique, and further understanding the goals of the technique.

The Purpose

Vipassana comes from a Buddhist, and thus Hindu, background. Things like ahimsa and the vegetarian diet clearly reflect this heritage. But the purpose is not to convert you to Hinduism. Goenkaji goes on at length several times that this is not a religion, and thus there is nothing to convert to. He did not want converts. You can be of any religion and get benefits.

The purpose (again, deriving from Hindi theology, but stick around) is essentially to die a happy death. This requires that you live a happy life, and in order to do so you must learn how not to be miserable. In Hindi theology, this means that you may leave the circle of life and attain Nibbana (Sanskrit: Nirvāṇa). But, as Goenkaji said, “If you do not believe in the next life, or the previous one, it does not matter. Consider this one, it’s right in front of you!”

Goenkaji observes that this is a technique with universal application, that it derives from the Golden Rule, which he says all religions endorse.

“Therefore all things whatsoever ye would that men should do to you, do ye even so to them: for this is the law and the prophets.”—Matthew 7:12

The means to this end is to train your subconscious mind to react thoughtfully to events, and not instinctively. The goal is to avoid creating cravings, or aversions to events that have no lasting significance. “This too shall pass”; a concept in Pali, the language of the early Buddhist teachings is called “anicca”, or impermanence.

The course is structured, in a way, to trick you into practicing this technique, hence it is not explained up front. It’s a great teaching technique, and I am doing Goenkaji no justice in describing it here. He’s a master instructor.

“If you think you could not live this way, consider: that is what you having been doing for the last ten days!”—Goenkaji

(No note taking was allowed, so all these quotes are from memory.)

He claims that once you control the creation of new cravings or aversions, you will begin to address those that are already built up in your mind, and that once you have done that, you will have eliminated misery, and what will be left will be happiness.

Scientific Basis

Goenkaji relates how many ancient Indian ideas have played out in Western science. The Jains, for instance, deduced the existence of microbes thousands of years before scientists could see them under microscopes.

He goes on at length about this, but ultimately does not insist on any causal pathway. What matters is if you get benefit. He’s very much the businessman in this respect, and insists that if the class offers no benefit it’s useless.

Metformin, the most-commonly prescribed diabetes medication, for instance, ameliorates the disease through a mechanism that is not yet understood. And let’s not even get into psychiatry, which operates on a scientific basis that is little more sound than the Buddhist ruminations that Goenkaji has to offer, but without the thousands of years of practice. Psychiatry is the least scientific branch of Medicine, and many have argued that it’s not scientific at all. So looking to a traditional treatment is reasonable.

Reward Pathway

If I was going to put the mechanism in modern, scientific terms I would do so through the emerging science around the reward pathway. This is the mechanism by which the endocannabinoid/dopamine system creates cravings (like addiction) and aversions. This is a huge social issue today.

“How Does Social Media Cause Depression: The Science

Vipassana should be thought of as a training system to deal with meaningless stimulations like those we see on the internet. They’re not impactful, they’re going to go away, but we get all spooled up by them instinctively in a way that is very harmful. Advertising depends on the ability to send signals to our reward system to creating cravings for impermanent things.

The practice of Vipassana is to become impervious to these things.

Goenkaji does not advocate Vipassana as a cure for addictions, but he does note that many people find that it is an effective treatment for, say, alcoholism. Is this credible? The two most effective treatments we have for alcoholism are rehabilitation centers, and Alcoholics Anonymous, a system designed after Christianity to help control cravings. The ten-day Vipassana course includes both of those elements: isolation and a somewhat faith-based program to control cravings.

I said to some of the guys as we were discussing this that there are so many elements to the course that it’s hard to isolate what’s driving the effect. Goenkaji comments that one of his friends in the early days said he loved the course, but he hated the hour-long group “sittings”, called “Sittings of Great Determination”. “If you got rid of those, it would be perfect!”

I hated them too.

Goenkaji’s response was that if you don’t include those, the technique doesn’t work.

And I see his point. I definitely got the most out of the the group sittings, even as I dreaded them and had to struggle to stay in lotus position for an hour. (On the first day, my legs would start to go numb after ten minutes. By the tenth day, I could go 35 minutes, but that’s still not an hour.)

So is it the isolation? Not talking? Clearly it’s not the cell phone avoidance, as the course long predates cell phones. Would you get the same effect if you locked up 120 people in a building for 10 days where they couldn’t talk, but did no meditation? (There is a Vipassana in prisons program.) It’s hard to tell.

It has been studied a little, but the scientific evidence is thin:

“Seven (7) mainly poor-quality studies were identified. Three (3) neuro-imaging studies suggested that VM practice could be associated with the activation of the prefrontal and the anterior cingulate cortex during meditative periods, and with increased thickness in cortical areas related to attention as well as increased subcortical gray matter in right insula and hippocampus in long-term meditators. Three (3) clinical studies in incarcerated populations suggested that VM could reduce alcohol and substance abuse but not post-traumatic stress disorder symptoms in prisoners. One (1) clinical study in healthy subjects suggested that VM could enhance more mature defenses and copying styles.”

“Vipassana Meditation: Systematic Review of Current Evidence”

So, mechanisms aside, does it work?

Discourses

From 7:30pm to 9 each day we listened to a video of Goenkaji instructing us. His Indian accent is strong, so that’s a bit of a handicap, but I was paying such attention there were only a few times when it was really an issue. And there was a Q&A afterward or after lunch the next day you could ask the teacher questions.

As I said before, the videos were amazing. Twenty years old, and it was like he was reading your mind. Really remarkable as a pedagogical effort: he knew exactly what effect what he was doing had on the students, and what he needed to say to address their questions and concerns. I’ve never experienced anything quite like it.

The funniest anecdote: One poor fellow got some indigestion, and couldn’t stop burping. This went on for a couple of days, but really got bad on the third day. Just a continuous escape of gas. I got to the point where I was stifling laughter, but the guy behind me couldn’t. He burst out laughing, and had to leave the hall, pursued by the staff. Not a good scene.

Then comes the discourse. Goenkaji discusses being in the hall, listening to the others’ intestinal noises. “…Sneezing, coughing, burping. Do not laugh at them, but consider their discomfort, their illness. Practice compassion.” We all laughed when he said “burping”, but he was spot on. Recorded 20 years earlier. Like I said, spooky. Yuto said something similar happened in his class in 2019.

The idea behind the pedagogy is, again, an old Buddhist one that makes a lot of sense. Basically, it’s that there are three kinds of learning; hearsay (what you are told), what you understand, and what you have experienced. Only the last one matters.

So you may have been told something, and you think you understand what was told to you, but then you try it yourself and it does or doesn’t work. N=1 science, in other words.

So the trick of this course is to give you the experience first, and then explain what has happened to you and why. Then do it again for the next day. Very effective, much more so than a lecture with practice later; but very frustrating when you’ve been doing anapana meditation for three days only to discover that it’s not the Vipassana you came for!

There is a book of the discourses, but I think if you haven’t actually been through the course it would be pretty meaningless.

My Reaction

I left the course a happier person.

On the last day, when the noble silence is lifted, you can talk to the other students. There was a not a single naysayer, and many of the old students had taken many courses, one fellow had done five in two years.

Tom, one of the two people I’d talked to on day one, had said that a lot of the people were engineers or scientists, and the conversations I had at the end reinforced that. Thinkers get the most out of a class about controlling thinking, the “monkey mind”. (That was another amazing discourse.) You could think of it as group therapy for ADHD, in fact. There were a number of guys walking around with Google or Amazon t-shirts, and I heard many conversations about programming and AI on that day, in addition to talks about Vipassana and the course.

One fellow said specifically he had come back because he hadn’t kept up the practice, “And I want to feel that way again.”

My wife commented on how much happier and calmer I was after. The effect has persisted, and I have tried to do at least some meditation every day. It’s harder outside the course.

The course was definitely hard. It’s no vacation. By day three, as mentioned, I was getting loopy. My mind wandered away from the meditation, and I started making up jokes about the program. “On day 10 there’s a Sacred Cow BBQ! Only grilled vegetables…” I awaited other students to come to me and suggest we make a break for it, like in prison.

Vipassana Day was revelatory.

The next day, day five, I finally asked for a chair. I didn’t have enough time to get one. They’d announced that from that day on you would be expected to sit for one hour with no squirming. I was aghast—there was no way I could do that! I was ready to leave. The next morning on the message board was a letter from Goenkaji about the “Sitting of Great Determination”, explaining that while it was supposed to be difficult, and even uncomfortable, it was not torture. You could move around if you had to, but you should strive to improve. Well, that’s what I had been doing, so I decided to stay.

I noticed that I started talking to myself, at first in my head, silently. But increasingly aloud, without meaning to. Then I noticed everyone else was doing this too, and we all laughed about it at the end.

I really had no expectations going into this, so I can’t say if they were exceeded, but I am certainly glad I went. Will I do another course? Apparently the second time through is harder than the first…

At the end of the course Goenkaji tells you how to measure your benefit from attending the course. He’s a businessman, and he gives you a toolset to decide if you got value for your money. (Hah!) It’s very compelling that the whole thing is based on benefits received. Not only in the afterlife, but every day, and improving over time.

Downsides

They screen you for psychiatric and emotional problems, and make clear that this is not a replacement for medical care. One guy, an old student, left the meditation hall sobbing two different times. I never found out why.

The time it takes is a drag. It crawls. You have no distractions except the others’ gurgling intestinal tracts, on a vegetarian diet! A lot of gurgling. The message board lists the day; 1, 2, 3… I checked it each day to be sure where we were. At one point I forgot the day of the week.

On the other hand you definitely have a feeling of accomplishment once you get through it!

It’s definitely not a cult. If you’re looking for a cult, you should probably go elsewhere.

Then there’s the expense…

Economics

The course is free. That’s right, they put you up for 10 days in what would be a nice hotel, feed you, and won’t take a dime from you.

Imagine if your surgeon did a surgery on you and said, “Only pay me if you feel better.”

The centers have been going for decades. The one in Massachusetts that I went to was started in 1982, and there are 270 centers of varying size around the world, 90 outside India. From the beginning, Goenkaji had to convince the trustees the idea of offering it for free was a good idea. They said it was madness in a hungry nation like India. “If they are willing to come and work from 4am to 9pm, then we will feed them!” he replied.

All the funding comes from old students who pay after they leave the course. There’s no mechanism to pay before, and they won’t tell you the cost. You contribute what you can, and apparently some people contribute a lot.

The centers are all not-for-profit. They don’t share resources or send money back to India to enrich someone. (Again, I was worried about this being a cult, or a scam.) They’re run by volunteers, all old students. There are some permanent employees, like the kitchen director.

They do no advertising or promotion; it’s entirely word of mouth, and the courses fill up immediately.

Something is going on here—they’re doing something right. I recommended the course to my daughter and my wife, and now to you.

Goenkaji said that part of the point of having it be free is to put people in the position of beggars, to be grateful for what they are getting, and not to feel like they own the place just because they’re paying for the visit. It definitely works that way. I had an issue with the kitchen on day one, and the fact that I hadn’t paid for anything definitely affected how I interacted with the kitchen director—who was terrific.

Preparation

If you do decide to do one of these courses, I wouldn’t do too much research into it. I’ve probably said too much already. As I’ve indicated, the surprise is part of the pedagogy, and I’ve withheld enough (I hope) to preserve that surprise.

I would do a little preparation:

1. Bring an open mind. Don’t get turned off by Goenkaji’s discussions from Buddhist tradition about how this works. It’s interesting to hear and think about, but it doesn’t matter.

2. Read Siddhartha. I did this years ago and it was helpful to understand the Buddhist background of the discourses.

3. Practice sitting. At the very least be able to sit quietly, without moving, in a chair for an hour; but sitting lotus-style on the floor for an hour would be best. You’ll still be uncomfortable, so you won’t miss out on that! That said, I couldn’t sit still the whole way through even at the end, so it’s not a requirement. But meditation when you’re in agony is not possible. I wished I’d practiced.

4. Practice the anapana meditation that you’ll be doing for the first three days. It’s an excellent way to quiet the mind to fall asleep at night!

I watched this video before going, and I’m glad I did.

If You’re Interested…

Normally when I do a post this long I’d insert a paywall. But in respect to Goenkaji and the folks in Massachusetts, this is free. If you want to pursue a course, here’s the site of the center in Massachusetts that I went to:

Vipassana Meditation Center – Dhamma Dharā

And here’s the main site, with a list of all the sites world-wide.

Vipassana Meditation

Peter from the Hyperlipid blog has recently retired, in which he shared his nickname “The Wizard”. (I recall that he posted a picture somewhere with this, but can’t find it now. Peter has left X, and seems to have deleted his account, unfortunately.)

It’s an appropriate nickname, IMHO. I’ve learned an enormous amount from him, and I’ve read every post he ever did on his blog.

Peter and I both agree that excess linoleic acid (LA) is a problem, causing obesity, diabetes, and probably many other ills.

However we disagree to some extent about the mechanism. (The nice thing is we’re both winning from this discussion, and often shared information back and forth, as we both share the same goal: the truth.)

In a nutshell, Peter thinks it’s related to how LA is handled in the mitochondria, specifically the electron transport chain (ETC); while I think it’s related to LA’s ability to peroxidize and become toxic, negatively affecting many aspects of cell functioning.

When it enters the body LA has, basically, three fates:

1. Disposal, via a variety of mechanisms.

2. Incorporation into cell membranes throughout the body.

3. Oxidized (different from peroxidized) for fuel.

(Oxidation is when a fuel like LA is, essentially, combusted, in the body to CO2 and water. Peroxidation is when an oxygen atom is added to a fuel molecule, often with a hydrogen atom, known as “hydroxy”, hydrogen + oxygen. Two entirely different fates.)

Peter’s position revolves around 3, mine around 2. In another nutshell, Peter thinks LA is inherently bad, due to it’s effect on intra-cellular insulin signalling via inadequate ROS generation in the ETC; while I think that while he’s probably correct as far as it goes, but that is overwhelmed by the primary mechanism for badness, which depends on LA’s tendency to turn into toxins like HNE (4-hydroxynonenal).

So while doing some Google Scholar queries spurred by Peter’s recent post:

“Insulin resistance (16) Yes. Vitamin E can cause weight loss.”

I came across this paper:

“Chaperonin Counteracts Diet-Induced Non-Alcoholic Fatty Liver Disease by Aiding Sirtuin 3 in the Control of Fatty Acid Oxidation.” (Weng, 2023)

This paper is looking at the effect of increasing the oxidation of fats to resolve metabolic disease, specifically non-alcoholic fatty liver disease (NAFLD, now also called MAFLD—Metabolic-Dysfunction Associated Fatty Liver Disease—maybe some other time I’ll explain why I’m not using that term…)

Chaperonin is the heat-shock protein 60 (HSP60), and while it has a number of roles, it turns out that one of them is to facilitate the oxidation of fats. In diseases like obesity, diabetes, or NAFLD, impaired oxidation of fats is often present, as is a reduced quantity of HSP60.

“Decreased HSP60 expression correlated with severe steatosis in human NAFLD biopsies and murine DIO….

Impaired fatty acid oxidation is a hallmark of obesity development [36], while promotion of lipolysis prevents increased adiposity and body weight gain [37, 38]. (Weng, 2023—All subsequent quotes will be bolded)

One of the effects of the diabetes drug metformin is to upregulate HSP60 production (Docrat, 2020).

So in (Weng, 2023) they fed the mice a high fat diet, D12331.

Annoyingly, the methods in (Weng, 2023) lists D12331 as coming from LabDiets, while in fact it is produced by Research Diets (Research Diets, Inc., 2006); although LabDiets produces a diet called 58R3, about which they say, “Originally manufactured as “D12331”. One of four diets in the Surwit Series” (TestDiet, Land O’ Lakes. 2023). So I’m just assuming this is D12331, and that the apparent misattribution is a typo, but even if they used 58R3, it appears to be a clone of D12331. It’s one of the diets produced by the obesity researcher Richard Surwit, is pretty commonly used in obesity research, but it has minimal LA, so is an interesting case study in what actually is causing diabetes.

Background

D12331 is the diet Peter discusses in his post above (Dobromylskyj, 2026):

“The Surwit diet does this.”

What Peter is referring to is this graph, from (Graham, 2023):

(Graham, 2023) is a paper we discussed with the first author here:

Dalton designed this paper based on a number of my posts and ideas, and—thank God!—it worked as expected.

In Peter’s post he observes that there seem to be two obesogenic triggers in the diet used in (Graham, 2023)—it’s not exactly D12331, but it’s close. Medium-Chain Triglycerides (MCT), from the coconut oil; and LA. Vitamin E blocks the LA-induced obesity, but not the MCT-based obesity. Adding Vitamin E to the Surwit-derived diet + 8% LA (red triangles) reduces obesity to the level of the 1% LA Surwit diet (yellow squares).

It appears to cancel out most of the LA-induced obesity.

(We’re not going to worry for the moment about MCT-induced obesity here, as a) I have never seen evidence that coconut fat causes obesity in humans, and b) mice aren’t humans.)

In the comments to (Dobromylskyj, 2026) I observed that this effect is similar to that seen in (Chang, 2023), also fed D12331, but via an entirely separate mechanism—or is it?

How do we reconcile your comments about the diets above with this paper (Chang, 2023), which is able to similarly reduce the fat effect of LA in the 1% LA Surwit diet?…

Comparing the outcomes, it looks like there are two distinct obesogenic effects of Surwit (D12331): MCT and LA. Either vit. E or increased ALDH2 will ameliorate the effect of LA on obesity, while leaving the effect of MCTs untouched.

Both vit. E and ALDH2 are addressing the lipid peroxidation pathway...

In (Graham, 2023) Vitamin E reduces body weight from ~38 to ~32g (eyeballing it). In (Chang, 2023) the ALDH2 stimulator AD-9308 reduces body weight from ~35 to ~30g (again, eyeballing it) in the wild-type (WT) mice, and from ~38 to ~30g in the human genetic mutation knock-in (KI) mice.

We discussed (Chang, 2023) in this podcast:

What’s fascinating here is the common denominator. Vitamin E has an effect because it prevents LA from becoming peroxidized, and AD-9308 cleans up peroxidized LA via stimulating the detoxification pathway aldehyde dehydrogenase (ALDH2).

In (Graham, 2023), Dalton measured levels of malondialdehyde (MDA), which made me sad, because I prefer to look at HNE. HNE can only be produced from Ω-6 fats like LA, while MDA can also be produced from Ω-3 fats. HNE is a better signal for Ω-6-specific toxicity. Dalton didn’t have the budget for HNE testing.

We can see that MDA is reduced by vitamin E. Depending on the details of how the TBARS test for MDA is done, it can also produce a positive result for oxidized LA.

“These data show that the substances reacted with TBA in our system are unsaturated fatty acid hydroperoxides.” (Ohkawa, 1978)

We know from other work that vitamin E can prevent the production of lipid hydroperoxides (L-OOH, such as hydroxyoctadecadienoic acid (HODE), a peroxidized LA:

Which are precursors to HNE:

“L-OOHs undergo further oxidation, e.g., as an iron-dependent Fenton reaction, which generates various oxidation products with electrophilic properties, such as 4-HNE…” (Saito, 2021)

We can thus safely infer that HNE is also being reduced in (Graham, 2023).

Back to HSP60

(Weng, 2023) in my opinion reconciles the two approaches above. It forces LA from the pathway 2 described above, “Incorporation into cell membranes throughout the body”, to the pathway 3, “Oxidized for fuel”. If the cause of obesity and insulin resistance is insufficient ROS signalling from LA, this should exacerbate it (confounded by the fact that more fat may be being oxidized for fuel).

The authors use a transgenic mouse that over-produces HSP60, and in these mice both obesity and insulin resistance are reduced, despite a higher flux of fat through the electron transport chain.

“Hsp60-Tg mice developed less body fat, had reduced serum triglyceride levels, lower levels of insulin resistance and higher serum adiponectin levels than wild-type mice upon HFD feeding.”

They additionally had smaller adipocytes.

The transgenic mice had a lower respiratory exchange ratio (RER), a measure of fat oxidation. So HSP60 is indeed promoting fat oxidation.

The control diet (CD) WT-mice had a high RER (black line) because they were burning mostly carbohydrates. Interestingly the biggest increase in fat burning was in the WT mice fed a high-carb diet.

And, significantly, they had a lower production of HNE.

The electron transport chain is a significant source of HNE, due to being susceptible to dietary manipulation of fatty acids which alters the fat composition of the lipids holding the chain together, specifically the mitochondria-specific cardiolipin (Zhong, 2014).

HNE given alone produces larger adipocytes, through, it seems, damage to various proteins in the adipocyte during differentiation.

“As compared to the control (treatment with the 4-HNE vehicle DMSO), treatment with 1 μM 4-HNE inhibited the adipogenic differentiation of uncommitted ASCs, as ascertained by either contrast phase microscopy or Oil Red O staining by day 14 after the addition of a supplementation medium (Figure 3).” (Murdolo, 2023)

All the rest of the adipocyte disruption follows from excess HNE concentration—that’s a long post, for another time.

But, to make the point, (Murdolo, 2023) also look at HNE levels in normal and type-2 diabetic obese human adipocytes:

Another study looking at the same effect found similar results.

“Our data report for the first time impairment of the adipogenic capacity of OM preadipocytes taken from obese and morbidly obese IR individuals (including T2DM patients) compared to their IS counterparts, with a potential role of 4-HNE accumulation in this impairment.” (Jaganjac, 2017)

HNE and HSP60

So how could HNE and HSP60 interact to cause these effects? The primary route of damage via HNE to cells is via binding to proteins forming adducts, which damage the protein and ultimately the cell (Ishimura, 2008).

One of the proteins HNE binds to is HSP60. Interestingly, in atherosclerosis, macrophages react to HNE-HSP60 adducts as they would to an antigen, stimulating the auto-immune reaction that typifies later atherosclerosis.

“Upon exposure to HNE, HNE-LDL, and LDL oxidized with CuSO4, but not to native LDL, HNE-HSP60 adducts were formed in THP-1 cells at levels well higher than in basal conditions.” (Arcaro, 2015)

Autoimmunity is typical of atherosclerosis, and macrophage infiltration into adipose tissue is another aspect in which the two processes share similarities.

Clearly one of the mechanisms by which HNE damages cells is by damaging this specific protein, which would explain why reduced levels are found in human disease related to HNE.

The Foundation

Read more

“Is Seed Oil Intake Correlated With Bad Health?” (Lasker, 2025)

(A note about Lasker and his nom de plume Crémieux: I respect that some folks have a need for anonymity on the ‘net. Lasker has already been outed by, among others, The Guardian, in an article so idiotic and typical it should be read to be believed, but probably isn’t worth the time (Wilson, 2025).)

Words he’s going to live by:

Remember: I am the one who cites all the RCTs, genetic evidence, *and* the epidemiological evidence. I look over *all* of the evidence… (Lasker, 2026)

The Gish Gallop is a fundamentally dishonest rhetorical technique:

The Gish gallop is a rhetorical technique in which a person in a debate attempts to overwhelm an opponent by presenting an excessive number of arguments, without regard for their accuracy or strength, with a rapidity that makes it impossible for the opponent to address them in the time available.

It’s dishonest because you can’t have an honest debate over the details, and in an article, it attempts to overwhelm the reader by pummeling them with unverifiable information.

It’s telling that Lasker’s first sentence is a Gish Gallop:

Genetic evidence and trials suggest seed oils are not harmful: they don’t make people fat, they don’t cause inflammation, they don’t cause cardiovascular disease, and so on. (Lasker, 2025

I’ve included the various studies linked below. I’m not going to go through them all, but will address them by type or specifically as is relevant.

Epidemiology

Epidemiology is the lowest form of evidence, although it is invaluable. Many relationships between environmental variables (like, for instance, vitamin consumption) and diseases (like, heart disease) have been identified by epidemiology, and then tested and found not to be true when doing an experiment (like a randomly-controlled trial (RCT)).

One of the more famous examples was the attempt to treat oxidative damage from consuming seed oils on heart disease by taking vitamin E. Vitamin E impedes the oxidation of the Ω-6 fats in seed oils and was thus thought could prevent heart disease.

Unfortunately, when this was actually tested in an experiment, this was found not to work.

Mendelian Randomization

Lasker includes seven Mendelian Randomization (MR) studies. MR is an effort to “strengthen” epidemiology (Davey Smith, 2024). It has several issues, however, not least of which is that:

“A second explosion has been in complex mendelian randomisation methods that are difficult for most readers and co-authors to scrutinise.” (Davey Smith, 2024)

And thus:

“Considerable circumspection should be applied to interpretation of all published non-linear mendelian randomisation papers, and further stress-testing of the new non-linear mendelian randomisation method is required before its findings are accepted.” (Davey Smith, 2024)

MR should thus “…should always be situated within a triangulation of evidence framework.” (Davey Smith, 2024)

So these studies don’t really add anything. The relevant variable, linoleic acid, is solely provided through the diet, and all the genetic studies can only show is what happens after it is consumed. There’s certainly variability there, as we discussed in this podcast:

There’s a more fundamental problem with epidemiology such as this, however: ubiquity.

“…When a risk factor is ubiquitous in a population, it may strongly influence the population incidence of a disease, but may not identify high-risk individuals within a population. This is technically correct, e.g. in a society where everyone smokes, smoking will not identify high-risk individuals for lung cancer.”

“So can the role of near-ubiquitous risk factors be studied and their importance for disease causation quantified? Yes they can, but it’s not easy, and they cannot always be studied with our ‘standard’ methods such as randomized controlled trials, cohort studies or case–control studies….

First, it may be possible to identify important risk factors by comparisons between populations or comparisons over time.” (Pearce, 2011)

Virtually all epidemiological studies are conducted in industrialized countries with capable research universities. All such countries (except Japan) have been consuming seed oils with linoleic acid for decades before nutritional epidemiology became widespread. So the question is: where do you find the subjects without exposure?

So looking at seed oils, the populations that do not consume them do not suffer from cardiovascular disease, and this is true both for current, primitive populations, and across time in countries like the United States (Levenstein, 1975; Balsbag, 2011).

So ‘simple’ comparison like those used in MR, where all the population has long been exposed, will not necessarily be enlightening.

“However, the problem is that too often the major population risk factors will not be hypothesized (and therefore will not be studied) when they are ubiquitous.” (Pearce, 2011)

This is illustrated by the lack of MR papers (I can find none) looking at the ALDH2*2 mutation, linoleic acid, and heart disease, despite many papers finding clear links epidemiologically or experimentally.

“In particular, a number of studies have reported an association between the ALDH2 polymorphism and increased risk of coronary artery disease (CAD) risk (Xu et al., 2018; You, Li, Zhao, Wang, & Cui, 2018). In 2012, a GWAS study in the Japanese population corroborated these findings by identifying increased susceptibility to CAD in individuals who carry the ALDH2 mutant allele (Takeuchi et al., 2012). In further support of these findings, a meta-analysis of 5644 Chinese subjects from nine individual studies revealed a significant association between the ALDH2 rs671 polymorphism and CAD however, the authors acknowledged their meta-analysis included only a limited number of large-scale or prospective studies (Li et al., 2018). Furthermore, serum ALDH2 levels could be influenced not only by the ALDH2 polymorphism, but also by environmental factors and metabolic diseases such as obesity, diabetes mellitus, hyperlipidemia and hypertension. Researchers have also evaluated whether the ALDH2 polymorphism is an independent risk factor for worse outcome following AMI. Overall, numerous experimental and clinical studies support this notion…” (Lamb, 2024)

Lasker doesn’t discuss this at all.

Bogus RCTs

There are a number of studies that looked at how seed oils might be protective against cardiovascular disease (CVD). Virtually all failed, showing instead that seed oils increase CVD risk.

Lasker includes a number of meta-analyses (studies of studies) looking at this phenomenon, but only one RCT, the Oslo Diet-Heart Study (ODHS) (Leren, 1970).

Lasker does not include the most rigorous meta-analysis, done by the NIH (Ramdsen, 2016).

Ramsden excluded ODHS from their main analysis, because, importantly, ODHS is not a trial solely of seed oils.

The ODHS has often been represented as a test of the replacement of SFA with an LA-rich vegetable oil (soybean oil). However, in addition to soybean oil, the intervention group received a very large dose (≈5 grams per day) of n-3 EPA+DHA from provision of sardines canned in cod liver oil, and was advised to restrict sugar intake and to replace refined carbohydrates with less processed selections. Since EPA+DHA (and sugar) are reported to influence CHD risk by mechanisms independent of serum cholesterol lowering, it is not possible to determine which intervention components were responsible for study results. (Ramsden, 2016)

Thus it cannot answer the question here. Why not include some of the other trials?

Oslo is included in (Mozaffarian, 2010), a meta-analysis that Lasker does include. However, two other meta-analyses that Lasker also includes, (Hamley, 2017) and (Hooper, 2018) also both note that Oslo is not a trial of seed oils.

“Multifactorial dietary interventions: ODHS and STARS both used a multifactorial dietary intervention, in which the dietary advice given to the experimental group included much more than just replacing SFA with mostly n-6 PUFA. Other dietary differences besides TFA intake included: 1) a higher intake of long chain n-3 PUFA (2.0% vs. usual intake (ODHS) and 0.21 vs. 0.10% (STARS); 2) advice to consume more whole plant foods (ODHS and STARS); 3) advice to moderate sugar consumption and to increase fish and shellfish (ODHS); 4) sardines canned in cod liver oil that were supplied to the experimental group (ODHS); 5)...

Hooper et al. judged ODHS and STARS as having a ‘high risk’ of bias related to being ‘free of dietary differences other than fat’, but included ODHS as a fat modification trial and STARS as a reduced and modified fat trial.” (Hamley, 2017)

Hooper in their 2018 paper states they excluded “Oslo Diet Heart 1966 as it increased both omega-3 and omega-6 fats and included a multivitamin in the intervention group (so was multifactorial).”

So Lasker is sloppy, doesn’t understand the study, or is being disingenuous in included only this one trial, which, one can see from the Ramsden analysis above, is an outlier.

Bogus Meta-analyses

Lasker, while excluding the most definitive meta-analysis, as mentioned above, does include a number of others. (Mozaffarian, 2010) has come in for a number of criticisms. Hooper, 2018) is another meta-analysis he includes, here’s what Hooper had to say about Mozaffarian in 2010:

“So might relevant studies have been missed? Yes, several studies, such as a trial by Houtsmuller et al (which randomised newly diagnosed diabetics to a usual diet or a fat-modified diet, reporting myocardial infarctions over 6 years), and similar, more recent studies are missing from this analysis. An ‘excluded study’ randomised people who had recently had a myocardial infarction to remain on their usual diet or to follow a low-fat diet with added corn or olive oil. Corn oil versus control diet would seem an appropriate comparison for the systematic review, but the results do not appear. This lack of inclusion of all relevant studies may cause the suggested bias in the funnel plot. With only eight data sets used in the analysis, the ability of the subgrouping and meta-regression to identify relevant relationships is limited.” (Hooper, 2010)

Hooper also notes that they “…do not explain how much of the PUFA consist of ω-3 fats in each trial.” (Hooper, 2010) This conflation of beneficial Ω-3 fats with apparently harmful (Ramsden, 2016) Ω-6 fats is a typical tactic of those seemingly trying to obfuscate the relative effects of the two series.

My own notes on (Mozaffarian 2010) include the following:

• Rose 1965—Rose Corn Oil: “Multiple interventions”. Intervention was reduction of SFA and increase polyunsaturated fat (n-6 via corn oil) or olive oil in two separate wings.
  Excluded: Negative result.
  vs. Burr 1989—DART: 3 separate wings, one was reduction of saturated fat an increase of unspecified polyunsaturated fat. Same intervention as Rose.
  Included: Positive result.

• Woodhill 1978—Sydney Diet Heart: “No CHD endpoint” is reason given for exclusion. Title of study is “Low fat, low cholesterol diet in secondary prevention of coronary heart disease.” CHD was the primary endpoint.
  Excluded: Negative result.

• De Lorgeril 1994—Lyon Diet Heart: “Multiple interventions”. This did have multiple interventions, one of which was a REDUCTION in n-6 PUFA, along with other fats; increase in n-3 PUFA (large decline in CVD with REDUCTION in PUFA).
  Excluded: Negative result.
  vs. Watts 1992—STARS included: “Multiple interventions” included reduction in total fat and SFA, increase in n-6 and n-3 PUFA, increase in fiber. n-6 and n-3 not measured or defined.
  Included: Positive result.

Hamley 2017 sums up the problem with this meta-analysis thus:

“Mozaffarian et al. [19] was the only meta-analysis to find a significant reduction in risk for CHD mortality, which is mostly due to their inclusion of FMHS and their exclusion of SDHS.”

I’ve discussed my problem with Mozaffarian and his research methods and bias in the following:

Just for starters. Search for more.

Bogus Review

Lasker links to “Perspective on the Health Effects of Unsaturated Fatty Acids and Commonly Consumed Plant Oils High in Unsaturated Fat” (Petersen, 2024). I’ll confess I hadn’t seen this previously, although the list of authors has a lot of overlap with those discussed in this post:

It’s basically an update of that previous paper. Significantly, the abstract notes the following:

“Epidemiological evidence indicates that higher PUFA intake is associated with lower risk of incident CVD and type 2 diabetes mellitus (T2DM). Additionally, replacement of SFA with PUFA is associated with reduced risk of CVD and T2DM. Clinical trials show higher intake of UFA from plant sources improves major CVD risk factors, including reducing levels of atherogenic lipids and lipoproteins. Importantly, clinical trials show that increased n-6 PUFA (linoleic acid) intake does not increase markers of inflammation or oxidative stress.” (Petersen, 2024)

Oddly, they fail to note the strongest evidence: the multiple human trails that show seed oils increase the rate of CVD evidence. I discussed this in the post above.

I’d like to note the funding sources:

This work was supported by the Soy Nutrition Institute Global, United Soybean Board, Corn Refiners of America, National Corn Growers Association, Canola Council of Canada and USA Canola Association. These funders had no role in the design, analysis or writing of this article. K. S. P., K. C. M., P. C. C., M. A. B., M. M., C. F. K. and W. S. H. conducted literature searches and wrote sections of the manuscript, K. S. P. & M. M. drafted the manuscript, all authors critically reviewed the manuscript. Financial support for K. S. P., K. C. M., M. A. B., C. F. K., and W. S. H. was provided by the Soy Nutrition Institute Global, United Soybean Board, Corn Refiners of America, National Corn Growers Association, Canola Council of Canada and USA Canola Association…. Over the last 3 years, K. C. M. has received research funding and/or consulting fees from… Cargill… P. C. C. acts as an consultant/advisor to… Bunge, Cargill… M. A. B. serves on the American Society for Nutrition board of directors and has received research funding from the United Soybean Board. M. M. is employed by Soy Nutrition Institute Global, which is funded by the United Soybean Board and membership dues from organisations involved in the manufacture and/or sale of soy foods or soy ingredients. C. F. K. is an employee of Midwest Biomedical Research and has no additional conflicts of interest to report beyond those disclosed for K. C. M., except that she serves on the National Lipid Association Board of Directors. W. S. H. holds stock in OmegaQuant Analytics, LLC, a laboratory that offers fatty acid testing. (Petersen, 2024).

The bolded organizations have a direct financial interest in seed oil production, with the exception of the National Lipid Association (NLA). Cargill and Bunge are the two largest producers of seed oils on Earth. The most recent annual report of the NLA is 2020, as listed on their foundation’s website. Their funding is predominantly from the pharmaceutical industry:

Specifically from Amgen, Esperion, and Novartis.

I can’t tell you how odd it is that nothing more recent is listed. Why wouldn’t they want you to know their financial state and funding sources?

Petersen (the first author) includes the following on her bio:

“Petersen is currently a member of the American Heart Association’s Nutrition Committee and a liaison to the Council on Lifestyle and Cardiometabolic Health. She has been a member of several AHA scientific statement/advisory writing groups including a scientific statement describing how popular diets align with AHA Dietary Guidance. Petersen was also a member of the writing group for the 2023 National Lipid Association Nutrition Interventions for Adults with Dyslipidemia Clinical Perspective.”

The AHA of course has been perpetrating the fraud that seed oils prevent heart disease since 1956, despite their own research showing this isn’t true.

Harris (the last author) doesn’t mention he’s part of the FORCE consortium, which is funded by Unilever, in part, to fund research into “THE OMEGA-6 FATTY ACIDS PROJECTS”. Unilever produces highly-processed foods which include seed oils, has a long history of funding and writing pro-seed oil research, and was one of the largest producers of seed oils until they sold that business to Bunge (see above).

“In conclusion, authoritative health and scientific organisations recommend intake of n-6 PUFA-containing vegetable oils, including seed oils, as part of healthful dietary patterns. Specifically, vegetable oils rich in UFA should be consumed instead of rich sources of SFA, such as butter, tallow, lard, palm and coconut oils, duck fat and ghee.” (Petersen, 2024)

You can see where they’re coming from. The idea that seed oils provide a benefit in cardiovascular disease over natural fats consumed when heart attacks were unknown was thoroughly debunked in the 1960s and 70s.

A Shill?

Lasker doesn’t like it that I call him a shill for promoting seed oils.

Given that he’s uncritically promoting research from the industry, I think it’s a fair description. He’s clearly promoting this research, and not providing any context that would allow one to judge it.

That’s Just the First Sentence!

Lasker goes on to cite some epidemiological evidence to support his title. The problem is that epidemiological evidence is useless to establish causation, especially when there are well-designed and executed human randomized controlled trials looking at the question, and contradicting the epidemiology.

To quote famed epidemiologist George Davey Smith again, commenting on a study titled “Butter and Plant-Based Oils Intake and Mortality” (Zhang, 2025)

“It is now more than 30 years since these authors published two high profile papers back to back in the New England Journal of Medicine claiming that vitamin E supplement use would reduce heart disease risk by 40%. The claims were incorrect, but many people believed them – the story was the headline news in the New York Times – and started taking vitamin E.”

As in the conclusion of my blog on the same authors’ “dark chocolate” paper, the interesting question this paper raises is “why do supposedly legitimate journals keep publishing papers like this?”.” (Davey Smith, 2025)

Ironically, vitamin E was promoted as a cure to the well-established role of seed oils in promoting cardiovascular disease.

During its incubation with cells, the LDL particle undergoes a large number of structural changes that alter its metabolism in important ways. All these changes, however, depend on a common initiating step — the peroxidation of polyunsaturated fatty acids in the LDL lipids. As shown independently by Steinbrecher et al. and by Morel et al., the modification of LDL by cells is totally inhibited by antioxidants, such as butylated hydroxytoluene or vitamin E. (Steinberg, 1989)

Unfortunately, it turns out that vit. E acts as a pro-oxidant for seed oils in circulation (Santanam, 1995), and the human RCTs that followed those epidemiological studies demonstrated vit. E supplementation increased heart disease.

On the basis of all the available data, we believe that vitamin E supplements cannot be recommended for patients with coronary heart disease. (Ness, 1999)

Vit. E is thus no longer promoted for that purpose, yet seed oils, which have similar effects in human RCTs, still are.

Conclusion

Lasker’s claim that he cites “all” the evidence is just pretty conclusively false. As I’ve demonstrated here, he cites the evidence that other pro-seed oil parties, including the industry, cites, and nothing that might cast another light on the matter.

Don’t listen to the shills.

Gish Gallop Studies

Note the studies are not in the same order as they were referenced in Lasker’s sentence, as he did not group them as they are grouped here. Those I discuss are in bold, those I specifically discuss include the reference code.

Epidemiology

Mendelian Randomization (MR)

“Genetic evidence”:

• “Mendelian Randomization of Circulating Polyunsaturated Fatty Acids and Colorectal Cancer Risk”
  doi:10.1158/1055-9965.EPI-19-0891

• “Mendelian Randomization Analysis of n-6 Polyunsaturated Fatty Acid Levels and Pancreatic Cancer Risk”
  doi:10.1158/1055-9965.EPI-20-0651

• “Polyunsaturated fatty acids and prostate cancer risk: a Mendelian randomisation analysis from the PRACTICAL consortium”
  doi:10.1038/bjc.2016.228

• “Phenome-wide Mendelian randomisation analysis of 378,142 cases reveals risk factors for eight common cancers”

  doi:10.1038/s41467-024-46927-z

• “Effect of linoleic acid on ischemic heart disease and its risk factors: a Mendelian randomization study”
  doi:10.1186/s12916-019-1293-x

• “Pro-inflammatory fatty acid profile and colorectal cancer risk: A Mendelian randomisation analysis”

  doi:10.1016/j.ejca.2017.07.034

• “Polyunsaturated Fatty Acid Levels and the Risk of Keratinocyte Cancer: A Mendelian Randomization Analysis”
  doi:10.1158/1055-9965.EPI-20-1765

Experiment

Crossover

• “they”: “Comparison of dietary conjugated linoleic acid with safflower oil on body composition in obese postmenopausal women with type 2 diabetes mellitus”
  doi:10.3945/ajcn.2008.27371

Randomly-Controlled Trial (RCT)

• “don’t”: “Overfeeding Polyunsaturated and Saturated Fat Causes Distinct Effects on Liver and Visceral Fat Accumulation in Humans”
  doi:10.2337/db13-1622

• “make”: “Overfeeding polyunsaturated fat compared with saturated fat does not differentially influence lean tissue accumulation in individuals with overweight: a randomized controlled trial”
  doi:10.1016/j.ajcnut.2024.04.010

• “people”: “Overeating Saturated Fat Promotes Fatty Liver and Ceramides Compared With Polyunsaturated Fat: A Randomized Trial”
  doi:10.1210/jc.2019-00160

• “fat”: “Overfeeding polyunsaturated fat compared with saturated fat does not differentially influence lean tissue accumulation in individuals with overweight: a randomized controlled trial”

  doi:10.1016/j.ajcnut.2024.04.010

Other

• “don’t”: (Leren, 1970) “The Oslo Diet-Heart Study : Eleven-Year Report”
  doi:10.1161/01.CIR.42.5.935

Meta-analysis

• “they”: (Mozaffarian, 2010) “Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials”
  doi:10.1371/journal.pmed.1000252

• “cause”: “Effect of Interventions Aimed at Reducing or Modifying Saturated Fat Intake on Cholesterol, Mortality, and Major Cardiovascular Events: A Risk Stratified Systematic Review of Randomized Trials”
  doi:10.7326/ANNALS-25-02229

• “cardiovascular”: (Hamley, 2017) “The Effect of Replacing Saturated Fat with Mostly N-6 Polyunsaturated Fat on Coronary Heart Disease: A Meta-Analysis of Randomised Controlled Trials”
  doi:10.1186/s12937-017-0254-5

• “disease”: (Hooper, 2018) “Omega‐6 fats for the primary and secondary prevention of cardiovascular disease”
  doi:10.1002/14651858.CD011094.pub3

• “and”: “Reduction in Saturated Fat Intake for Cardiovascular Disease”
  doi:10.1002/14651858.CD011737.pub2

• “on”: “Health Effects of Various Edible Vegetable Oils: An Umbrella Review”
  doi:10.1016/j.advnut.2024.100276

Review

• “so”: (Petersen, 2024) “Perspective on the health effects of unsaturated fatty acids and commonly consumed plant oils high in unsaturated fat”
  doi:10.1017/S0007114524002459

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References

Blasbalg, Tanya L., Joseph R. Hibbeln, Christopher E. Ramsden, Sharon F. Majchrzak, and Robert R. Rawlings. 2011. “Changes in Consumption of Omega-3 and Omega-6 Fatty Acids in the United States During the 20th Century.” The American Journal of Clinical Nutrition 93 (5): 950–62. https://doi.org/10.3945/ajcn.110.006643.

Davey Smith, George, and Shah Ebrahim. 2008. “Biosocial Surveys, Ch.16: Mendelian Randomization: Genetic Variants as Instruments for Strengthening Causal Inference in Observational Studies.” In Biosocial Surveys, edited by Maxine Weinstein, James W. Vaupel, and Kenneth W. Wachter. National Research Council., edited by Committee on Advances in Collecting and Utilizing Biological Indicators and Genetic Information in Social Science Surveys. National Academies Press (US). https://www.ncbi.nlm.nih.gov/books/NBK62433/.

Davey Smith, George, and Shah Ebrahim. 2024. “Mendelian Randomisation at 20 Years: How Can It Avoid Hubris, While Achieving More?” The Lancet. Diabetes & Endocrinology 12 (1): 14–17. https://doi.org/10.1016/S2213-8587(23)00348-0.

Davey Smith, George. 2025. “Expert Reaction to Study Looking at Butter or Vegetable Oils and Mortality.” Blog. Science Media Centre, March 6. https://www.sciencemediacentre.org/expert-reaction-to-study-looking-at-butter-or-vegetable-oils-and-mortality/.

Hamley, Steven. 2017. “The Effect of Replacing Saturated Fat with Mostly N-6 Polyunsaturated Fat on Coronary Heart Disease: A Meta-Analysis of Randomised Controlled Trials.” Nutrition Journal 16 (1): 30. https://doi.org/10.1186/s12937-017-0254-5.

Hooper, Lee. 2010. “Meta-Analysis of RCTs Finds That Increasing Consumption of Polyunsaturated Fat as a Replacement for Saturated Fat Reduces the Risk of Coronary Heart Disease.” Therapeutics. BMJ Evidence-Based Medicine 15 (4): 108–9. https://doi.org/10.1136/ebm1093.

Hooper, Lee, Lena Al‐Khudairy, Asmaa S. Abdelhamid, et al. 2018. “Omega‐6 Fats for the Primary and Secondary Prevention of Cardiovascular Disease.” Cochrane Database of Systematic Reviews, no. 7. https://doi.org/10.1002/14651858.CD011094.pub3.

Kaplan, Hillard, Randall C. Thompson, Benjamin C. Trumble, et al. 2017. “Coronary Atherosclerosis in Indigenous South American Tsimane: A Cross-Sectional Cohort Study.” The Lancet 389 (10080): 1730–39. https://doi.org/10.1016/S0140-6736(17)30752-3.

Lamb, Reece J., Kayleigh Griffiths, Gregory Y. H. Lip, et al. 2024. “ALDH2 Polymorphism and Myocardial Infarction: From Alcohol Metabolism to Redox Regulation.” Pharmacology & Therapeutics 259 (July): 108666. https://doi.org/10.1016/j.pharmthera.2024.108666.

Lasker (ndp Cremieux), Jordan. 2026. “That’s pretty funny Remember….” Post. X, April 5. https://x.com/cremieuxrecueil/status/2040938613114814924.

Lasker (ndp Cremieux), Jordan. 2025. Is Seed Oil Intake Correlated With Bad Health? Blog. March 12.

Cremieux Recueil

Is Seed Oil Intake Correlated With Bad Health?

Genetic evidence and trials suggest seed oils are not harmful: they don’t make people fat, they don’t cause inflammation, they don’t cause cardiovascular disease, and so on…

Read more

3 months ago · 82 likes · 13 comments · Cremieux

Leren, Paul. 1970. “The Oslo Diet-Heart Study: Eleven Year Report.” Circulation 42 (5): 935–42. https://doi.org/10.1161/01.CIR.42.5.935.

Levenstein, J. H. 1975. “Historical Perspective of Myocardial Infarction.” South African Medical Journal = Suid-Afrikaanse Tydskrif Vir Geneeskunde 49 (39): 1585–90. https://doi.org/10520/AJA20785135_24168.

Mozaffarian, D., R. Micha, and S. Wallace. 2010. “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 Medicine 7 (3): e1000252. https://doi.org/10.1371/journal.pmed.1000252.

Ness, Andy, and George Davey Smith. 1999. “Mortality in the CHAOS Trial.” The Lancet 353 (9157): 1017–18. https://doi.org/10.1016/S0140-6736(05)70733-9.

Pearce, Neil. 2011. “Epidemiology in a Changing World: Variation, Causation and Ubiquitous Risk Factors.” International Journal of Epidemiology 40 (2): 503–12. https://doi.org/10.1093/ije/dyq257.

Petersen, Kristina S., Kevin C. Maki, Philip C. Calder, et al. 2024. “Perspective on the Health Effects of Unsaturated Fatty Acids and Commonly Consumed Plant Oils High in Unsaturated Fat.” British Journal of Nutrition 132 (8): 1039–50. https://doi.org/10.1017/S0007114524002459.

Ramsden, Christopher E., Daisy Zamora, Sharon Majchrzak-Hong, et al. 2016. “Re-Evaluation of the Traditional Diet-Heart Hypothesis: Analysis of Recovered Data from Minnesota Coronary Experiment (1968-73).” Research. BMJ 353 (April). https://doi.org/10.1136/bmj.i1246.

Santanam, N., and S. Parthasarathy. 1995. “Paradoxical Actions of Antioxidants in the Oxidation of Low Density Lipoprotein by Peroxidases.” The Journal of Clinical Investigation 95 (6): 2594–600. https://doi.org/10.1172/JCI117961.

Steinberg, D., S. Parthasarathy, T. E. Carew, J. C. Khoo, and J. L. Witztum. 1989. “Beyond Cholesterol. Modifications of Low-Density Lipoprotein That Increase Its Atherogenicity.” The New England Journal of Medicine 320 (14): 915–24. https://doi.org/10.1056/NEJM198904063201407.

Wilson, Jason. 2025. “US Natalist Conference to Host Race-Science Promoters and Eugenicists.” US News. The Guardian, March 3. https://www.theguardian.com/us-news/2025/mar/03/natal-conference-austin-texas-eugenics.

Zhang, Yu, Katia S. Chadaideh, Yanping Li, et al. 2025. “Butter and Plant-Based Oils Intake and Mortality.” JAMA Internal Medicine, ahead of print, March 6. https://doi.org/10.1001/jamainternmed.2025.0205.

it turns out that there’s an epidemiological relationship between fevers and cancer:

“Since the 19th century, it has been repeatedly observed that spontaneous cancer regressions were coincided with acute infections and the cancer patients had a remarkable disease-free history before the onset of cancer [1]–[4]. In the 20th century, an inverse association between infectious diseases, particularly febrile ones, and cancer risk has also been consistently found for malignant melanoma and glioma using modern epidemiological methods [1], [3], [5]–[7].

“With the widespread introduction of antibiotics and antipyretics since the beginning of the last century, however, the critical role played by fever has often been overlooked, resulting in considerable changes to the clinical course and magnitude of the immune response that develops following acute infections [1], [8]. These changes may be part of the reasons for the substantial increase in the age-adjusted incidences or mortalities of malignant diseases during the early part of the last century in western countries [9] and in the late of the last century in China [10]. It has been observed that every 2% reduction in infectious disease mortality was followed by a 2% increase in cancer mortality over a 10-year interval from 1895 to 1963 in Italy [9].” (Su, 2012)

Medicine, like Economics, is full of unintended consequences. It wouldn’t surprise me at all to discover that messing with the immune system messes with the immune system in unexpected ways...

Original post: May 23, 2012.

References

Su, Yi, Lu-Ying Tang, Li-Juan Chen, et al. 2012. “Joint Effects of Febrile Acute Infection and an Interferon-γ Polymorphism on Breast Cancer Risk.” PloS One 7 (5): e37275. https://doi.org/10.1371/journal.pone.0037275.

Yikes.

“Obesity levels have risen dramatically in research animals and others living close to humans, suggesting environmental factors are encouraging everyone to gain weight, according to new findings…” (Arnold, 2010)

The authors of the paper looked at in this news article (Klimentidis, 2010) essentially looked at animals that are wholly under the control of the human food environment:

• Three populations of rhesus macaques (a monkey) in research labs.

• Chimpanzees in captivity.

• Vervet monkeys in captivity.

• Marmoset monkeys in captivity.

• Lab rats and mice.

• Domestic dogs.

• Domestic cats.

• Wild rats, urban and rural.

I'll note that all the animals in this study are eating diets provided by humans, or derived from human diets (feral rats). Even rural rats likely live in areas around humans and eat human crops.

What about wild animals eating traditional diets?

They didn’t look at any of those.

Scientists can be so dense...

Additionally, one of those macaque populations, in Wisconsin, was part of a reconciled diet-longevity study. You’ll note from the graph above that they had different levels of weight gain. Want to guess which group was eating corn oil?

I’ll cover that some other time.

After going paleo/primal myself, I did the same for my dog, after noting most of the available dog foods are all grain, soy, and veggie oils. He didn't overeat, and didn't have an ounce of fat on him.

My current dogs are the same. They eat until they are full, and then walk away from the plate, even if it has more food sitting on it.

They gain no weight.

Original post December 8, 2010.

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References

Arnold, Carrie. 2010. “Animals Are Getting Fatter, Too.” The Scientist, November 25. https://www.the-scientist.com/animals-are-getting-fatter-too-42960.

Klimentidis, Yann C., T. Mark Beasley, Hui-Yi Lin, et al. 2010. “Canaries in the Coal Mine: A Cross-Species Analysis of the Plurality of Obesity Epidemics.” Proceedings of the Royal Society B: Biological Sciences 278 (1712): 1626–32. https://doi.org/10.1098/rspb.2010.1890.

I’m not going to discuss possible causes in this post, just therapies that worked very well for me.

My first choice would be to walk or run uphill, and ensure your heel touches the ground at each step, while wearing zero-drop shoes, or barefoot. This is what I’ve used for Achilles’ tendon issues in my bad leg. (My bad leg is now my good leg, at least for the time being.)

If you can’t for whatever reason do that, an eccentric heel drop is the exact same movement.

But, since it’s come up, folks have asked for some decent videos.

I’d first suggest listening to this podcast by the (insane) Doctor Håkan Alfredson who invented the eccentric heel drop while trying to rupture his Achilles’ tendon so his boss would have to operate on it and relieve him of his Achilles tendonopathy.

Instead, he cured it. Whoops.

Having listened to that, and determining that you most definitely do not want Dr. Alfredson scraping your tendons to sever the nerves, you can try his exercises.

The videos below are the training for a study to evaluate the usefulness of orthotics for treating achilles tendinopathy (Munteanu, 2009).

“Achilles tendinopathy is a common condition that can cause marked pain and disability. Numerous non-surgical treatments have been proposed for the treatment of this condition, but many of these treatments have a poor or non-existent evidence base. The exception to this is eccentric calf muscle exercises, which have become a standard non-surgical intervention for Achilles tendinopathy.”

The videos look useful, and are based on Alfredson’s protocol. I’d skip the marshmallow shoes shown in the video, and do them barefoot. I’d also avoid orthotics... But that’s just me.

(I’d also avoid taking any medical advice from any doctor from Latrobe University, where this study is being conducted, as the quack Dr. Payne is a professor of podiatry there. I’ll not link to Dr. Payne’s site again, but you can find it at the bottom of that link.)

I’ll also note that Dr. Alfredson says that the bent-knee heel drops are crucial. Did I mention that you should listen to his podcast before trying out these exercises?

One more observation: I’m not a doctor, or a physical therapist, just a foot-deformed westerner trying to run the way I was born to. Also, you should never believe anything you read on the internet, it’s all crap.

OK, now that the caveats are out of the way, here are the videos. I’ll note that the videos are also available for download in the study—search for m4v in (Munteanu 2009).

P.S. Lest you think I’m being too tough on Latrobe, and podiatrists, Dr. Munteanu, who is conducting the aforementioned study, has this advice:

“...If you are a runner, ensure that you have your footwear professionally fitted and replace your runners [sneakers] at least every 500km/6 months....”

I wonder if that’s been shown to be effective? Anyway...

Part 1:

Part 2:

Part 3:

Part 4:

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Original post December 20, 2011.

References

Munteanu, Shannon E., Karl B. Landorf, Hylton B. Menz, Jill L. Cook, Tania Pizzari, and Lisa A. Scott. 2009. “Efficacy of Customised Foot Orthoses in the Treatment of Achilles Tendinopathy: Study Protocol for a Randomised Trial.” Journal of Foot and Ankle Research 2 (1): 27. https://doi.org/10.1186/1757-1146-2-27.

Yasui, Youichi, Ichiro Tonogai, Andrew J. Rosenbaum, Yoshiharu Shimozono, Hirotaka Kawano, and John G. Kennedy. 2017. “The Risk of Achilles Tendon Rupture in the Patients with Achilles Tendinopathy: Healthcare Database Analysis in the United States.” BioMed Research International 2017 (1): 7021862. https://doi.org/10.1155/2017/7021862.

Nick asked me to do a YouTube livestream to go over some research he had been doing. He drilled down on a reference in a high-profile cardiology guideline article and discovered that the authors had inverted the research finding in the referenced paper to claim the inverse of what it actually showed.

We discussed this, and then I gave some more context about the matter and one of the authors.

We discussed this post:

Guest info

“Nick Jikomes is a neuroscientist, plant chemistry researcher, data scientist, and podcast host. He received a PhD in Neuroscience from Harvard University and a Bachelor of Science in Genetics from the University of Wisconsin. Nick currently works in the legal cannabis industry in the US.”

https://www.nickjikomes.com/about

Home page, with links to writing and podcasts.

https://www.nickjikomes.com/

Tucker Goodrich

Substack:

Tucker Goodrich: yelling Stop

Building a Healthy Diet & Lifestyle.

Twitter: https://twitter.com/TuckerGoodrich

Youtube: https://www.youtube.com/tuckergoodrich0

Apple podcast:

Spotify podcast:

Podcast: https://sites.libsyn.com/408758

Blog (deprecated, but still a lot there!):

http://yelling-stop.blogspot.com/

If you have any questions about sources for things discussed please ask in the comments.

When Stephan Guyenet recommended I read Gary Taubes’ Good Calories, Bad Calories (Taubes, 2008: All quotes in bold and italic, unless otherwise cited), he warned that it was a little dry. I found it to be a page-turner, and quickly finished it. I was new to the topic of diet and health, and the Taubes hypothesis of that era (that carbohydrates caused obesity and perhaps the related diseases) sounded pretty good after one read Gary’s book.

My experience was a little different from that described in the book, however. While Taubes emphasized the dangers of sugar in that book, I had been on a low-sugar diet quite diligently since 1986 or so, when my dentist had told me that I could stop getting cavities if I stopped eating so much sugar. I despise visits to the dentist, and countless cavities and eight pulled teeth had given me ample opportunities to learn that dislike.

So cutting out sugar seemed like a no-brainer to me. I learned to like coffee without sugar, stopped drinking soft drinks, and diligently started reading labels and avoiding anything with added sugar (you can even find jelly without added sugar, for my formerly beloved peanut butter & jelly sandwiches).

It worked.

Since 1986 or so I have had a single, minor cavity—due to the unfortunate introduction of a mint bowl at the office—and my dental health is excellent. Since my current dentist is also my father-in-law, I get excellent feedback on how things look.

However, I also got fat and sick, in the manner Taubes attributes to sugar.

When I finally started to learn about diet, and fixed all my chronic diseases, I actually wound up increasing my sugar consumption, since I learned that the cavity-healing diet described by Weston Price (Price, 1938) actually had more sugar in it than I was eating!

So I took the book with a grain of salt, so to speak.

There’s a corollary to Knoll’s Law of Media Accuracy (above), which is Michael Crichton’s Gell-Mann Amnesia. This is the effect where having noted that a particular bit of reporting with which you have knowledge is nonsense, you immediately forget that the source is unreliable, and go on to read the rest as if it were faultless. I probably should have kept that in mind when reading GCBC.

What Causes Obesity?

So Gary and I have a disagreement here. I’ve done a few posts about it in the past:

And recently:

I won’t go into that discussion any further here, but it has led to further discussion, from me an others.

The Bigger Picture

In a thread started on X by Gary about how low-carb used to be standard medicine (which is true), he got a response from (@exfatloss on X):

“This worked before so many people were PUFA'd with seed oils”

Gary replied:

And in another fork of the thread replied:

I replied with a quote from (Taubes, 2008).

Gary dismissed it:

“…While this is an example of Key's hypothesis failing an experimental test, and of the selection bias used to establish it as dogma, that's about all this study is good for.”

The “experimental test” was that increasing seed oils would reduce the rate of heart disease. Here’s the next paragraph after the quote above:

“As I implied earlier, we can only know if a recommended intervention is a success in preventive medicine if it causes more good than harm, and that can be established only with randomized, controlled clinical trials. Moreover, it’s not sufficient to establish that the proposed intervention reduces the rate of only one disease—say, heart disease. We also have to establish that it doesn’t increase the incidence of other diseases, and that those prescribed the intervention stay healthier and live longer than those who go without it.”

So what these studies showed is that increasing seed oils caused an increase, not a decrease, in heart disease.

Gary is claiming this study isn’t able to show that seed oil Ω-6 PUFA is harmful, it doesn’t meet his request for “evidence that it actually causes harm”, yet it shows exactly that according to his criteria in GCBC.

Good Calories, Bad Calories

So I went back and took a look at what Gary had said in the book that made his career.

“The only way to establish cause and effect with any reliability is to do ‘controlled’ experiments, or controlled trials, as they’re called in medicine. Such trials attempt to avoid all the chaotic complexities of comparing populations, towns, and ethnic groups. Instead, they try to create two identical situations—two groups of subjects, in this case—and then change only one variable to see what happens.”

Sure enough, (Frantz, 1989) fits the bill:

“The Minnesota Coronary Survey was a 4.5-year, open enrollment, single end-time, double-blind, randomized clinical trial that was conducted in six Minnesota state mental hospitals and one nursing home. It involved 4393 institutionalized men and 4664 institutionalized women.” (Frantz, 1989)

It was a RCT (randomized, controlled trial) in other words, exactly what Gary is looking for.

“The Minnesota Coronary Survey was, by far, the largest diet-heart trial carried out in the United States…”

Those quotes are from the section of (Taubes, 2008, Chapter 2, “The Inadequacy of Lesser Evidence”) in which he discusses the evidence for what’s known as the Diet-Heart Hypothesis, which I discussed in this post:

By Gary’s standards, this test should be the gold standard. It’s an RCT, it’s well-conducted, it’s large, and it’s only testing one intervention. Gary himself implies that this should be a valid bit of evidence.

“Proponents of Keys’s hypothesis who considered the Helsinki Mental Hospital Study reason enough to propose a cholesterol-lowering diet for the entire nation, never cited the Minnesota Coronary Survey as a reason to do otherwise.”

A “cholesterol-lowering diet” is a diet high in seed oils (Nelson, 1995; Taubes, 2008), so according to Gary, the MCS is a valid experiment showing that it is harmful.

But we begin to run into some problems.

What Are We Testing?

The Diet-Heart Hypothesis changed the goalposts as it evolved. Originally it was an idea that fat caused increased cholesterol, and hence we should pursue a low-fat diet. However, experimental evidence soon showed that this was not accurate. The “Keys” Gary mentioned above was of course Ancel Keys.

“Keys eventually accepted that animal fats tend to raise cholesterol and vegetable fats to lower it, only after he managed to replicate Groen’s finding with his schizophrenic patients in Minnesota.”

They still, however, thought that cholesterol in the blood was what was driving heart disease. So the focus shifted from a low-fat diet to a moderate-fat, high-polyunsaturated-fat diet.

In the 1961 paper in which the American Heart Association kicked off the diet revolution (a point on which Gary and I agree), the AHA (including Keys) recommended “a diet moderate in calories and fat”, but only for “coronary-prone persons”.

Gary describes this repeatedly as a low-fat diet.

The two AHA interventions are:

1. Moderate-fat diet

2. Substitute polyunsaturated fat (PUFA) for saturated fat (SFA).

As Gary puts it:

“…the new report argued the opposite—“the best scientific evidence of the time” strongly suggested that Americans would reduce their risk of heart disease by reducing the fat in their diets, and replacing saturated fats with polyunsaturated fats.”

Research Committee Trial

“Only these two trials ever tested the benefits and risks of the kind of low-fat diet that the American Heart Association has recommended we eat since 1961, and that the USDA food pyramid recommends when it says to ‘use fats and oils sparingly.’”

However these diets are not “the kind of low-fat diet” that the AHA recommended.

The second of these trials, which is quite well-known, compared two groups:

“One group was placed on a low-fat diet, while the control group continued with their normal diet.”

However:

“The nature of the fat consumed was not altered, nor were any additional unsaturated fats given.” (A Research Group, 1965)

That’s an average of 20% of energy as fat vs 43%. So the AHA diet recommendation (25% to 35%) is indeed moderate; and the diet tested here is not the diet that the AHA recommended, on either count.

So with a similar intake of type of fat, but a large decrease in quantity of fat, no change was noted, and the authors observe, as Gary quotes:

“A low-fat diet has no place in the treatment of myocardial infarction.”

Who could resist quoting that?

(Why Mischaracterize These Diets?)

A bit of an aside here, because it bothers me that Gary is not accurately representing these diets. I think it’s a bit of a tell…

In 1995, another study looked at the effect of a strictly-controlled low-fat diet on serum cholesterol (they found no effect), and used 22% vs 39% fat as the low- and high- fat diets (Nelson, 1995).

And since we’re talking about Ancel Keys, he looked at the diets of the groups in the Eight Countries he was researching (Yugoslavia split into Serbia and Croatia during the study) and found a range of fat consumption, from almost 50% in the U.S. to 13.2% in Japan. 13.2% is a low-fat diet! But Italy was at 32.8% (Kromhout, 1995). That’s solidly in the moderate fat range, and is certainly not low fat. You’ll note it’s the high end of the AHA prudent diet, discussed next. (Keys retired to Italy, by the way, and lived to a ripe old age.)

I don’t know why Gary calls what are pretty objectively not low-fat diets as being such throughout his book. But it’s a bad sign, in my opinion. It’s a sign of his innate bias.

Mystifyingly, in chapter nine, Gary states:

“Diets that lowered cholesterol by replacing saturated fat with polyunsaturated fats would have accomplished such a balancing act, but there was legitimate concern that polyunsaturated fats were carcinogenic, and so the AHA had simply recommended fat reduction in general.”

The AHA has been recommending increased PUFA consumption from 1956 to the current day. We can let the AHA itself address what its recommendations are:

“A common misconception is that the AHA currently recommends the intake of large quantities of polyunsaturated fats. It is true that the recommendation is to increase the mean intake for the U.S. public from its present 5-6% to an upper limit of 10%.” (Grundy, 1982)

End aside.

Anti-Coronary Club Trial (Prudent Diet)

“In all the other trials, cholesterol levels were lowered by changing the fat content of the diet, rather than the total amount of fat consumed. Polyunsaturated fats replaced saturated fats, without altering the calorie content.”

This is also not correct.

Gary notes:

“In total, the prudent diet was barely 30 percent fat calories, and the proportion of polyunsaturated to saturated fat was four times greater than that of typical American diets.”

It’s described by the authors:

“The diet contains about 30% to 33% of total calories as fat with a ratio of polyunsaturated to saturated fatty acids of 1.25-1.50 compared to the P/S ratio of 0.3-0.4 for the American diet…. (The P/S ratio, without consideration of technical qualifications, is substantially the amount of polyunsaturated fatty acids divided by the amount of saturated fatty acids present in a given diet pattern.)” (Christakis, 1966)

While it is, again, not low-fat, it’s a direct trial of the AHA diet at the time of the AHA recommendation.

Despite what Gary said above, this trial also reduced fat consumption. That was a crucial part of the AHA prescription at this point.

At inception, fat consumption for the intervention group ranged from 36% to 40% (Singman, 1980).

Gary misses another crucial point about this trial. It was the only trial that was running at the time of the writing of (Page, 1961), the AHA’s diet recommendation. It’s the only trial that are listed in what Gary notes were “a half-page of ‘recent scientific references on dietary fat and atherosclerosis’” in (Page, 1961). It was testing the AHA diet recommendation, the so-called Prudent Diet.

“In the mid-1950s, Irvine Page, Norman Jolliffe, Ancel Keys… and others devised a diet, which was called the “Prudent Diet” [115], to test the lipid–heart hypothesis.

This diet, which was introduced to the American public in 1956 in a nationally televised fundraiser for the AHA…

The Anti-Coronary Club Study (1957–1966) was a 10-year study of the Prudent Diet… with and without diagnosed heart disease.” (Newport, 2024)

So how did this high-seed-oil, moderate fat diet work out?

“…In November 1966, just nine months later, the Anti-Coronary Club investigators published a second article, revealing that twenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent. Eight members of the club died from heart attacks, but none of the controls.”

I’ve characterized this trial as seed oils vs. smoking.

“At the initiation of the study, smoking was not stressed as a CHD risk factor. Our data indicated that there were significantly more smokers at entry in the control group than in the active experimental group at both age levels. In the 50 to 59-year-old group 17.7% of the active experimental group and 36.0% of the control group smoked (P = 0.00 1). In the younger age category 25.9% of the active experimental group smoked compared to 44.3% of the control group (P = 0.03).” (Singman, 1980)

So a high-seed-oil, ‘prudent’ diet is worse for you than smoking and eating imprudently.

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Good work, AHA, one can see why they don’t like to talk about this study (AHA, 2024).

Good work, Gary, for not recognizing what the results of this study tell us.

The “Mortality Problem”

After discussing the Anti-Coronary Club, Gary wrote:

“This mortality problem was the bane of Keys’s dietary-fat hypothesis, bedeviling every trial that tried to assess the effects of a low-fat diet on death as well as disease.”

Here’s where Gary’s bias matters. In none of these trials was the low-fat diet the intervention, it was high seed oil consumption, as he has noted. But he’s so gung-ho on proving his ‘hypothesis’ that he can’t even grasp the significance of his own research.

As he notes, this is a consistent effect, seen across multiple human RCTs performed by various different investigators. This is the highest level of scientific evidence.

Minnesota Coronary Survey, Again

He then discusses a pretty good series of trials. I’m not going to run through them all here, as I have already discussed them elsewhere, and Gary does a pretty good job except for the sloppiness above, and continuously mischaracterizing this intervention as low-fat. Back to the MCS.

What’s the Intervention?

“Two diets were served. The control diet involved little departure from the institutional diet served before the trial. The treatment diet represented a compromise between the B and C diets of the National Diet-Heart Study, with target values of 45% of calories from fat, a polyunsaturated/ saturated fat (P/S) ratio of 2.5, and less than 150 mg of cholesterol daily.”

So by this point, Keys & Co. had completely abandoned the low-fat idea. The intervention diet was planned to be 44.9% fat, compared to the control at 42.4%. Perhaps, in part, because the lowest-fat wing of the Seven Countries Study, the Japanese, had the highest rate of mortality, as Gary notes.

In practice, however, the intervention wound up 37.8% fat, and the control was 39.1%.

You’ll note that’s the median fat intake from the Seven Countries Study.

“Traditional American foods were used for the control diet, and foods high in polyunsaturated fat and low in saturated fat and cholesterol were used for the experimental diet…. The experimental diet goal was to provide 18% to 20% of calories from polyunsaturated fat, to limit saturates to less than 9%, and to maintain the ratio of polyunsaturated to saturated fats at more than 2:1.” (Frantz, 1989)

There’s that P/S Ratio again.

A few more important points on the MCS.

“In October 1961, The Wall Street Journal reported that the NIH and the AHA were planning a huge National Diet-Heart Study that would answer the ‘important question: Can changes in the diet help prevent heart attacks?’ Fifty thousand Americans would be fed cholesterol-lowering diets for as long as a decade, and their health compared with that of another fifty thousand individuals who continued to eat typical American diets.”

A cholesterol-lowering diet is typically a high-seed-oil diet, remember.

The Anti-Coronary Club trial, aside from failing to prove the hypothesis, had some methodological problems that prevent it from being a proper RCT. The AHA decided to fix that defect, and this was how they were “dotting the final i”.

Gary discusses it a little bit, but again, misses some crucial details. He noted earlier:

“The Minnesota Coronary Survey was, by far, the largest diet-heart trial carried out in the United States… The principal investigator on the trial was Ivan Frantz, Jr., who worked in Keys’s department at the University of Minnesota.”

But the NDHS initial report explains:

“The design of the feasibility study involves the recruitment of approximately 1,500 healthy, male volunteers. (Dr. Frantz's study will be conducted in a controlled, hospital environment; the other studies involve men living at home.)” (Baker, 1963)

In doing his research for his interview of Frantz, Gary seems to have missed this detail:

“The trial [MCS] was an outgrowth of the National Diet-Heart Feasibility Study.” (Frantz, 1989)

The MCS was, in other words, the continuation of the National Diet-Heart Study.

Gary states that after the National Diet-Heart Study failed (it showed no difference), that there were only two studies that continued it.

“As a result, the NIH agreed to spend only $250 million on two smaller trials that would still constitute the largest, most ambitious clinical trials ever attempted. One would test the hypothesis that heart attacks could be prevented by the use of cholesterol-lowering drugs. The other would attempt to prevent heart disease with a combination of cholesterol-lowering diets, smoking-cessation programs, and drugs to reduce blood pressure. Neither of these trials would actually constitute a test of Keys’s hypothesis or of the benefits of low-fat diets.”

This is wrong. The MCS continued. And it was not only a test of Keys’ hypothesis, he was a co-principal investigator with Frantz (Newport, 2024; Ramsden, 2016)—another detail Gary missed.

However, he almost gets the point:

“Overall, the cholesterol-lowering diet was associated with an increased rate of heart disease.

Again, cholesterol-lowering diet = high-seed-oil diet.

And this was a nice bit of reporting.

“When I asked Frantz in late 2003 why the study went unpublished for sixteen years, he said, ‘We were just disappointed in the way it came out.’”

This should have been the final nail in the Keys’ and AHA’s hypothesis.

Keys, with the aid and support of the AHA, had a hypothesis that increasing seed oils and decreasing saturated fat would decrease heart disease. In a classic example of why we don’t trust epidemiology, he did an epidemiological study that seemed to show this relationship. Then he conducted, with colleagues, not one, but three RCTs to demonstrate that this hypothesis was valid. All three failed.

If they hadn’t hidden the data, the evidence would have been pretty clear.

Lyon Diet Heart

The single Diet-Heart trial that actually succeeded in lowering rates of CVD was the only one that targeted lowering Ω-6 fats, while increasing Ω-3 fats. It also lowered saturated fat intake and total fat intake, two interventions we know are ineffective.

“In the present trial, a reduction in coronary events and cardiac deaths of close to 70% was achieved without a reduction of serum cholesterol, triglycerides, or an increase in HDL compared to controls.” (Lorgeril, 1994)

Oddly Gary doesn’t discuss it at all in the context of Diet Heart. You’d think to be fair to the hypothesis he should have brought it up.

It was presented as a direct test of the AHA prudent diet and thus Keys’ idea of the polyunsaturated/saturated ratio.

“Even in primary prevention with a diet rich in polyunsaturated (P) and low in saturated (S) fat (P/S), the rates of coronary events and deaths were not decreased.” (Lorgeril, 1994)

Gary mentions it in passing in chapter 9, in a side discussion of monounsaturated fats.

“When they [monounsaturated fats, oleic acid] finally were tested in two clinical trials in the 1990s—the Lyon Diet Heart Trial and an Italian study known as GISSI-Prevenzione—both supported the contention that the diet prevented heart attacks, but neither provided evidence that it did so by either raising HDL or lowering LDL, which was how it was now alleged to work.”

Talk about burying the lede. Oleic acid was an incidental change in this study.

“The increase in intake of oleic acid, less susceptible to peroxidation, and in natural antioxidants, probably also play a protective part.” (Lorgeril, 1994)

Conclusion

While muddling the waters by misrepresenting diets as low-fat when they are not, and referring to a cholesterol-lowering diet when a high-seed oil diet would be more accurate, Gary’s GCBC nevertheless makes it clear (with careful reading and some research) that the “mortality problem” that plagued Keys’ hypothesis was not due to the low-fat nature of the interventions, as they were not low fat, but to the high levels of Ω-6 polyunsaturated fat.

Subsequent research has confirmed these results. CVD initialization and progression depends on the presence of rancid Ω-6 fats from seed oils (Steinberg, 1989). The “cholesterol-lowering” effect of seed oils are due to the presence of rancid Ω-6 fats in the liver, which refuses, sensibly, to create rancid cholesterol-carrying lipoproteins (Pan, 2004).

The standard model of how CVD progresses thus begins with these rancid fats in LDL (oxLDL).

One of Gary’s favorite quotes is from Richard Feynman. It’s the second quote opening the Epilogue of GCBC:

“The first principle is that you must not fool yourself—and you are the easiest person to fool.”

It’s ironic, because that seems to be exactly what Gary has done: fool himself about the low-fat diet, and fool himself about the role seed oils has played in causing heart disease.

References

American Heart Association. 2024. “Historical Timeline of the American Heart Association.” Advertisement. American Heart Association, January 24. https://www.heart.org/-/media/files/about-us/history/history-of-the-american-heart-association.pdf.

Borén, Jan, M. John Chapman, Ronald M. Krauss, et al. 2020. “Low-Density Lipoproteins Cause Atherosclerotic Cardiovascular Disease: Pathophysiological, Genetic, and Therapeutic Insights: A Consensus Statement from the European Atherosclerosis Society Consensus Panel.” European Heart Journal 41 (24): 2313–30. https://doi.org/10.1093/eurheartj/ehz962.

Christakis, George, Seymour H. Rinzler, Morton Archer, and Arthur Kraus. 1966. “Effect of the Anti-Coronary Club Program on Coronary Heart Disease Risk-Factor Status.” JAMA 198 (6): 597–604. https://doi.org/10.1001/jama.1966.03110190079022.

Frantz, I. D., E. A. Dawson, P. L. Ashman, et al. 1989. “Test of Effect of Lipid Lowering by Diet on Cardiovascular Risk. the Minnesota Coronary Survey.” Arteriosclerosis (Dallas, Tex.) 9 (1): 129–35. https://doi.org/10.1161/01.atv.9.1.129.

Grundy, Scott M., David Bilheimer, Henry Blackburn, et al. 1982. “Rationale of the Diet-Heart Statement of the American Heart Association. Report of the AHA Nutrition Committee.” Arteriosclerosis: An Official Journal of the American Heart Association, Inc. 2 (2): 177–91.

Kromhout, D., A. Menotti, B. Bloemberg, et al. 1995. “Dietary Saturated and TransFatty Acids and Cholesterol and 25-Year Mortality from Coronary Heart Disease: The Seven Countries Study.” Preventive Medicine 24 (3): 308–15. https://doi.org/10.1006/pmed.1995.1049.

Lorgeril, M. de, S. Renaud, N. Mamelle, et al. 1994. “Mediterranean Alpha-Linolenic Acid-Rich Diet in Secondary Prevention of Coronary Heart Disease.” Lancet (London, England) 343 (8911): 1454–59. https://doi.org/10.1016/s0140-6736(94)92580-1.

Nelson, Gary J., Perla C. Schmidt, and Darshan S. Kelley. 1995. “Low-Fat Diets Do Not Lower Plasma Cholesterol Levels in Healthy Men Compared to High-Fat Diets with Similar Fatty Acid Composition at Constant Caloric Intake.” Lipids 30 (11): 969–76. https://doi.org/10.1007/BF02536280.

Newport, Mary T., and Fabian M. Dayrit. 2024. “The Lipid–Heart Hypothesis and the Keys Equation Defined the Dietary Guidelines but Ignored the Impact of Trans-Fat and High Linoleic Acid Consumption.” Nutrients 16 (10): 10. https://doi.org/10.3390/nu16101447.

Page, Irvine H., Edgar V. Allen, Francis L. Chamberlain, Ancel Keys, Jeremiah-6 Stamler, and Fredrick J. Stare. 1961. “Dietary Fat and Its Relation to Heart Attacks and Strokes.” Circulation 23 (1): 133–36. https://doi.org/10.1161/01.CIR.23.1.133.

Pan, M., AI Cederbaum, YL Zhang, HN Ginsberg, KJ Williams, and EA Fisher. 2004. “Lipid Peroxidation and Oxidant Stress Regulate Hepatic Apolipoprotein B Degradation and VLDL Production.” The Journal of Clinical Investigation 113 (9). https://doi.org/10.1172/JCI19197.

Price, Weston. 1938. Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects. Benediction Classics. http://gutenberg.net.au/ebooks02/0200251h.html.

Ramsden, Christopher E., Daisy Zamora, Sharon Majchrzak-Hong, et al. 2016. “Re-Evaluation of the Traditional Diet-Heart Hypothesis: Analysis of Recovered Data from Minnesota Coronary Experiment (1968-73).” Research. BMJ 353 (April). https://doi.org/10.1136/bmj.i1246.

Steinberg, D., S. Parthasarathy, T. E. Carew, J. C. Khoo, and J. L. Witztum. 1989. “Beyond Cholesterol. Modifications of Low-Density Lipoprotein That Increase Its Atherogenicity.” The New England Journal of Medicine 320 (14): 915–24. https://doi.org/10.1056/NEJM198904063201407.

A Research Committee, K.P. Ball, Edda Hanington, et al. 1965. “Low-Fat Diet in Myocardial Infarction: A Controlled Trial.” The Lancet, Originally published as Volume 2, Issue 7411, vol. 286 (7411): 501–4. https://doi.org/10.1016/S0140-6736(65)91469-8.

Singman, H. S., S. N. Berman, C. Cowell, E. Maslansky, and M. Archer. 1980. “The Anti-Coronary Club: 1957 to 1972.” The American Journal of Clinical Nutrition 33 (6): 1183–91. https://doi.org/10.1093/ajcn/33.6.1183.

Taubes, Gary. 2008. Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health. Penguin RandomHouse. https://amzn.to/3ZdNHVB.

“...Conclusions: Linoleic acid [LA] has a pro-inflammatory effect on cartilage whereas oleic acid and palmitic acid seem to inhibit cartilage destruction. These results indicate that altered fatty acid levels may influence loss of cartilage structure in OA.”

Monounsaturated and Saturated, but Not Ω-6 Polyunsaturated Fatty Acids Decrease Cartilage Destruction under Inflammatory Conditions (Bastiaansen-Jenniskens et al, 2013)

There’s another way to read that, of course, if one assumes that high levels of LA are not normal....

This next study is hilarious; yes, if you assume that high levels of LA (which don’t exist naturally) are “normal” this would be a mystifying result:

“We report here the finding that normal, young cartilages, in distinction from all other tissues examined, have unusually high levels of n-9 eicosatrienoic (20:3 cis-i5’8”) acid [Mead acid] and low levels of n-6 polyunsaturated fatty acids (n-6 PUFA)....

“...The finding of low levels of n-6 PUFA and high levels of unusual n-9 fatty acids, characteristic of EFA deficiency, in normal cartilage is remarkable in view of the fact that normal levels of EFA are present in serum, muscle, liver, kidney, and bone of the same animals (Tables 1-4). To properly understand this finding, it is important to recognize that when tissue from an EFA-deficient animal is transplanted into a nutritionally normal recipient, the EFA-deficient tissue rapidly recovers and regains a normal fatty acid profile within a period of 5 days (19). Thus it seemed implausible that a tissue should exhibit features characteristic of EFA deficiency in an animal with normal levels of EFA in its other tissues. Yet this phenomenon was consistently seen in normal cartilage of all species so far investigated (chicken, calf, human, rabbit, and pig).”

Unique Fatty Acid Composition of Normal Cartilage: Discovery of High Levels of N-9 Eicosatrienoic Acid and Low Levels of N-6 Polyunsaturated Fatty Acids (Adkisson et al, 1991)

If high LA is not normal, but is a result of a novel diet, these studies might be alarming.

Especially if we’d been seeing a rise in the incidence of injuries to cartilage.... (Mall et al, 2014)

More to come...

Original post February 25, 2016.

References

Adkisson, H. D., Risener, F. S., Zarrinkar, P. P., Walla, M. D., Christie, W. W., & Wuthier, R. E. (1991). Unique fatty acid composition of normal cartilage: Discovery of high levels of n-9 eicosatrienoic acid and low levels of n-6 polyunsaturated fatty acids. The FASEB Journal, 5(3), 344–353. https://doi.org/10.1096/fasebj.5.3.2001795

Bastiaansen-Jenniskens, Y. M., Siawash, M., van de Lest, C. H. A., Verhaar, J. A. N., Kloppenburg, M., Zuurmond, A.-M., Stojanovic-Susulic, V., Van Osch, G. J. V. M., & Clockaerts, S. (2013). Monounsaturated and Saturated, but Not n-6 Polyunsaturated Fatty Acids Decrease Cartilage Destruction under Inflammatory Conditions: A Preliminary Study. CARTILAGE, 4(4), 321–328. https://doi.org/10.1177/1947603513494401

Mall, N. A., Chalmers, P. N., Moric, M., Tanaka, M. J., Cole, B. J., Bach, B. R., & Paletta, G. A. (2014). Incidence and trends of anterior cruciate ligament reconstruction in the United States. The American Journal of Sports Medicine, 42(10), 2363–2370. https://doi.org/10.1177/0363546514542796

“The most recent American Dietary Guidelines (2020–2025) recommend shifting dietary fats from solid saturated fats to unsaturated oils. Dietary oils contain different compositions of unsaturated fatty acids (UFA). Oleic acid (OA) and linoleic acid (LA) are the most common UFA in dietary oils. How individual UFA in oils regulate immune cell function and cancer risk remains unclear.” (Jin 2021—all quotes from this source in Bold and Italic.)

This is certainly a neat paper.

Going all the way back to the 1960s, it’s been observed that there was a connection between increased consumption of seed oils and increased rates of cancer. Immigrants to the U.S. often see an increased rate of certain types of cancer (breast and colon, for instance), until their cancer risk ultimately matches the American population.

And it’s well recognized that the seed oil metabolite 4-HNE can cause mutations, notably to the P53 tumor-suppressor gene, especially in colon and liver cancer.

See this post for a model where our favorite obesogenic rodent diet, D12492, causes liver tumors.

When I first started reading about nutrition and disease, there was an English researcher, Barry Groves, who stated that early organ-transplant surgeons had used seed oils to suppress the immune systems of patients, but had to stop because of the increased rates of cancer they saw.

“But the transplant doctors were then astonished to see how quickly their patients developed cancers and the treatment was stopped.” (Groves, 2007)

It’s certainly true that immune suppression causes increased rates of cancer in transplant patients.

“The most significant cancer-related risk for organ transplant recipients, however, is associated with the very immunosuppressive medications that are required to prevent rejection of the organs but also can render the immune system less able to identify and kill tumor cells or battle cancer-linked infections….

A 30-year cohort study in Finland that examined roughly 6500 transplant recipients, for example, found that nearly 1 in 4 eventually contracted cancer; this translated to a 3.6-fold higher risk. For non-melanoma skin cancers, such as basal cell and squamous cell carcinomas, the rate is even higher: Studies have documented anywhere from a 25- to 250-fold increase in risk.” (Nelson, 2025)

But I had never seen a paper demonstrating what the mechanism might be for seed oils impeding immune function, until now.

Linoleic vs. Oleic

This is just what we want to see. A pretty straight-forward bake-off.

They’re using three diets, low-fat (LFD) with 10% soybean oil, a linoleic acid diet (Safflower) with 10% soybean oil and 35% safflower oil, and an oleic acid diet (Olive) with 10% soybean and 35% olive oil

They even give us the fatty-acid composition of the two added oils. Safflower has a lot more LA than even a high-LA olive oil would, so it’s a clear delineation. (In the graphs to follow, Safflower or LA are red. 18:2 is LA, 18:1 is OA.)

Remember, the body makes saturated and monounsaturated fats in the proportions in which they are needed, and so the LFD diet is effectively a lower-LA diet, with the SFA and MUFA made from carbs and the Ω-3 in soybean oil.

They do tell us the effect of the diets on the mice in terms of body weight:

The higher-LA diet produces more obesity in this model, but neither curve looks like what you would get with D12492. Visceral fat is also higher in Safflower as one would expect, but insulin is a smidge lower, which Peter (Hyperlipid) will appreciate.

Safflower Kills Cancer-Killing Cells

We have a variety of white blood cells, and two of them are the T cells, CD8 and CD4. They’re like a sniper team: CD8 is the killer, and CD4 is the spotter, or helper cell, as it’s known. These cells are produced in the thymus, and then released into the general circulation. They go through a period where they are “naive”, which is to say they’ve not been assigned something to kill.

One of the things that these cells can kill is cancer cells. In fact, in several types of cancer better survival is associated with higher numbers of these cells. In HIV, a higher ratio of killer to helper cells is associated with a lower incidence of cancer.

So it seems that killing these cells would be a bad thing.

Sure enough, Safflower kills off the T cells, both as they’re developing in the thymus and after they’re released while they’re still naive.

Fewer Killer Cells Means More Cancer Cells

This isn’t an ideal model. The mice don’t get cancer in this model, they’re given it. They implant E0771 breast cancer cells into the mammary tissue of the three groups of mice, and see how they do.

“…We observed a significant acceleration of mammary tumor growth in the safflower oil–fed mice compared with the olive oil–fed or LFD-fed mice (Fig. 3A).”

And they note that it wasn’t just obesity that was driving tumor growth.

“This observation of uncoupling obesity from tumor growth in mice on the olive oil diet suggests that not all dietary oil-induced obesity is tumorigenic.”

You’ll note that Olive is a smidge higher than LFD, as one would expect from the higher LA percentage.

Fewer Killer Cells, and Weaker Too

After COVID, we’ve all heard of cytokines. Tumor Necrosis Factor Alpha (TNFa) is a cytokine that is produced by CD8 cells, and it is an anti-cancer drug, to oversimplify things. It can cause cancer cells to die (via apoptosis, a controlled cell death) and it also damages the blood cells that feed the tumor.

Unfortunately, Safflower also reduces production of TNFa.

“In line with in vivo data collected from safflower oil–fed or olive oil–fed mice, LA, but not OA induced significant death of CD8+ and CD4+ T cells (Fig. 4A and B). Intracellular staining showed that LA treatment in vitro significantly inhibited the production of TNFa…”

“Altogether, our data indicate that LA in safflower oil–fed mice and in culture negatively affect naive T-cell survival and TNFa production.”

Having your T cells unable to make an anti-tumor chemical is unfortunate.

How Did The T Cells Die?

There are basically three pathways describing how cells die (assuming it’s not from physical injury, like a wound). They are apoptosis, mentioned previously; necrosis, an uncontrolled cell death where the contents of the cells often escape into the general circulation; and ferroptosis, which is defined (erroneously, I think) as an iron-dependent type of cell death.

Next they gave T cells three chemicals which prevent each of the three types of cell death, and then exposed them to LA or OA.

Apoptosis, it turns out, is the culprit.

LA caused an increase in Reactive Oxygen Species (ROS) in the cells. N-acetylcysteine (NAC) is a ROS inhibitor. It is a precursor for glutathione, the most powerful antioxidant in the body.

As you can see, NAC almost totally inhibited the lethality of LA in both CD4 and CD8 T cells. Now here’s the crux of the analysis.

“LA impairs T-cell responses by promoting mitochondrial dysregulation….

“Interestingly, when we measured the production of mitochondrial ROS (Mitosox) in T cells treated with LA, OA, or BSA, we found that LA treatment significantly promoted mitochondrial ROS production in both CD8+ T and CD4+ cells compared with BSA or OA-treated groups (Fig. 5A–C). In line with increased mitochondrial ROS production, LA treatment increased mitochondria, but did not affect peroxisomes in T cells (Fig. 5D). In contrast, OA treatment did not induce significant increase of mitochondria in CD8+ and CD4+ T cells (Fig. 5E and F).

This suggests to me that the mitochondria are trying to compensate for LA-induced damage via lipid peroxidation (fats going rancid), but OA does not induce damage or the need to adapt to it.

Cardiolipin (CL) is a unique fat structure that’s only found in mitochondria, and is an essential part of the energy generation function of the electron transport chain.

“Given that 18:2 LA was the predominant composition of CL, a unique class of phospholipids in mitochondrial inner membrane, and 18:2 LA was more sensitive to ROS-mediated lipid peroxidation than 18:1 OA, we postulated that treatment with LA, but not OA, would induce mitochondrial lipid peroxidation. Indeed, 4-HNE, a common byproduct of lipid peroxidation, was significantly upregulated in both CD8+ and CD4+ T cells in response to LA treatment (Fig. 5G–I). These data demonstrated that LA specifically induced mitochondrial ROS and lipid peroxidation, thus leading to mitochondrial dysfunction in T cells.”

4-HNE is of course only produced from Ω-6 fats, and is highly toxic to cells.

We saw a similar destruction of mitochondria upon seed oil consumption in this study.

Since N-acetyl-L-cysteine (NAC) is an important antioxidant that neutralizes ROS and is a scavenger of α,β-unsaturated aldehydes, we used it to abolish the formation of 4-HNE adducts…. The data indicated that NAC is a reliable 4-HNE-scavenging agent. (Manea, 2015)

“Scavenging” means it removes 4-HNE, and its ability to do damage; and allows it to be excreted harmlessly.

It’s known that 4-HNE is produced from high-LA cardiolipin (Liu, 2011), and that oxidized LA in cardiolipin induces apoptosis (Kagan, 2005).

So the pathway appears to be: increased LA → increased LA in cardiolipin → iron-catalyzed peroxidation of cardiolipin → production of 4-HNE → inducement of apoptosis.

“…CL was the only mitochondrial phospholipid that underwent peroxidation during apoptosis.” (Kagan, 2005)

I’m rather pleased with this finding, as this was exactly the pathway that I described back in 2016:

Blocking Linoleic Acid Prevents T Cell Death and Impedes Tumor Growth

Fatty Acid Binding Protein (FABP) is a protein that transports fats like LA or OA into the cell. E-FABP is a version that is found in large number in T cells.

T cells from mice without E-FABP (E-FABP-/-) are unable to take up LA when cultured with it. This causes several changes to the cell, including a reduction in uncoupling protein 2 (UCP2), which is part of the LA disposal pathway.

“Importantly, E-FABP deficiency significantly reduced mitochondrial lipid peroxidation in T cells (Fig. 6K). Accordingly, LA-induced T-cell death in [wild-type] T cells was significantly reduced when E-FABP was absent (Fig. 6L).”

I discussed disposal of LA as an indication of its toxicity and UCP as a disposal pathway in this post.

Next they fed E-FABP genetic knock-out mice Safflower to see what would happen. This genetic modification did not protect from obesity, but they did have higher levels of CD8 and CD4 T cells, and those cells were able to produce more TNFa than the unmodified mice were.

Then they injected mice with and without E-FABP with breast cancer cells, as above. Mice without E-FABP had a 50% lower tumor load than normal mice.

“These results clearly demonstrated that E-FABP expression in CD8+ T cells was critical in mediating safflower oil-impaired T-cell responses.”

Conclusion

Given:

• The many similarities between mice and men when it comes to the effects of seed oil consumption.

• The demonstrated increase of certain types of cancer when people immigrate to a high-seed-oil-consumption country like the U.S.

• The demonstrated effect impairing immune-system function has on cancer incidence in humans.

It seems wise to avoid seed oils to reduce the risk of cancer.

For the first time, I can also conclude that if you have cancer, elimination of seed-oil consumption should be a first-order alteration to diet, as the potential increase of killer T cells could help fight the disease.

Sadly this also implies that the diet offered in hospitals, in which seed oils are the primary source of fat, should be considered a cancer-promoting diet.

“Dietary Fats High in Linoleic Acids Impair Antitumor T-cell Responses by Inducing E-FABP–Mediated Mitochondrial Dysfunction” (Jin, 2021

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References

Groves, Barry. 2007. “Immunity to Infections: Part 2: Polyunsaturated Fats Suppress The Immune System.” Blog. Second Opinions, February 20. http://www.second-opinions.co.uk/immunity2.html.

Jin, Rong, Jiaqing Hao, Yanmei Yi, et al. 2021. “Dietary Fats High in Linoleic Acids Impair Antitumor T-Cell Responses by Inducing E-FABP–Mediated Mitochondrial Dysfunction.” Cancer Research 81 (20): 5296–310. https://doi.org/10.1158/0008-5472.CAN-21-0757.

Kagan, Valerian E., Vladimir A. Tyurin, Jianfei Jiang, et al. 2005. “Cytochrome C Acts as a Cardiolipin Oxygenase Required for Release of Proapoptotic Factors.” Nature Chemical Biology 1 (4): 4. https://doi.org/10.1038/nchembio727.

Liu, Wei, Ned A. Porter, Claus Schneider, Alan R. Brash, and Huiyong Yin. 2011. “Formation Of 4-Hydroxynonenal From Cardiolipin Oxidation: Intramolecular Peroxyl Radical Addition And Decomposition.” Free Radical Biology & Medicine 50 (1): 166–78. https://doi.org/10.1016/j.freeradbiomed.2010.10.709.

Manea, Adrian, Simona-Adriana Manea, Andra Todirita, et al. 2015. “High-Glucose-Increased Expression and Activation of NADPH Oxidase in Human Vascular Smooth Muscle Cells Is Mediated by 4-Hydroxynonenal-Activated PPARα and PPARβ/Δ.” Cell and Tissue Research 361 (2): 593–604. https://doi.org/10.1007/s00441-015-2120-0.

Nelson, Bryn, and William Faquin. 2025. “Amid a Boom in Organ Donation, a Heightened Focus on Cancer Risk in Transplant Recipients: Immunosuppression, Transmissible Infections and Tumors, and Improved Long‐Term Survival Among Organ Recipients Are Requiring More Vigilance for Skin Cancers and Other Malignancies.” Cancer Cytopathology 133 (2): e22932. https://doi.org/10.1002/cncy.22932.

Introduction

It’s well-known that lipid peroxidation is involved in aging and longevity. But what can we do about it? Dr. Shchepinov has been researching using deuterium to ‘shore up’ the PUFAs like those in seed oils to prevent them become toxic metabolites. He’s had some interesting successes, and we discuss at length his new book: “Breaking the Chains of Aging”

Amazon link:

https://amzn.to/46A29KX

Book website

https://www.breakingaging.com

Research:

https://scholar.google.com/citations?user=0kQp8lEAAAAJ&hl=en

Biography:

Mikhail Shchepinov trained in Moscow (PhD, Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, 1994), then moved to Oxford to work on DNA microarray technology, combinatorial chemistry, and oligonucleotide dendrimers.

He worked in academia and biotech in Oxford, UK and San Diego, USA, and is affiliated with several universities.

From: https://www.breakingaging.com/author

Tucker Goodrich

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If you have any questions about sources for things discussed please ask in the comments.

If you haven’t been paying attention, he’s mentioned about 1700 times in the Jeffrey Epstein email release. I’m not going to attempt to link to all the interesting emails, I’m sure you all can find them easily enough, there are only a few.

Apparently, he was in contact with Epstein from 2014 to 2019, and had a number of meetings and visits with him. Most of the emails, apparently, are about arranging meetings.

It’s important to note: at this point nothing in the emails so far disclosed suggests any illegal activity.

While my initial reaction was that this really wasn’t that big of an issue if he had a medical relationship with Epstein, Attia has released a statement saying that he was not Epstein’s doctor.

Physicians traditionally have an obligation to treat anyone who comes to them for help, or at least to try to get them help (an eye doctor won’t be much help for your cancer diagnosis, for instance, but he might help you find a specialist).

If he had been trying to help Epstein with some health problem, this would have been a fair explanation of his relationship with him.

In my opinion, that fact that this was not a medical relationship makes it worse for Attia.

So someone offered to introduce Attia to Epstein. Peter says that he was aware of Epstein’s conviction, but proceeded anyway.

Don’t Fraternize with Felons

I am reminded of a job interview I did once. We were looking for a consultant to work on our accounting system. The fellow we interviewed came highly recommended from a consulting firm we had used for years. He was very intelligent, and while he didn’t have specific knowledge of our system, his general knowledge of accounting was peerless. He had been a foreign exchange trader at a bank.

But it was rather odd that a fellow like this would want a short-term, gig like this, which seemed pretty far below his pay grade.

So of course I Googled the guy. It took about a half an hour, and would have been shorter if I hadn’t read a bunch of the documents that turned up.

It turned out that he had been convicted of bank robbery, and was awaiting sentencing (!).

He had done this by manipulating the bank’s accounting system to get paid bonuses for profits he had never made.

Hence his deep knowledge of accounting systems and principles.

The idiot who recommended him didn’t initially understand why we were so upset that he had sent this guy to us. The relationship never recovered.

Now let’s imagine that we had hired the felon. Can you imagine what the response of our investors and the regulatory authorities would have been?

Do Your Homework

Obviously asking the bank robber wouldn’t have been a good idea. “So, do you plan on using your access to our system to rob us?” That wouldn’t have cut it.

“Shortly after we met, I asked him directly about his 2008 conviction. He characterized it as prostitution-related charges.”

That’s from Attia’s mea culpa. As due diligence, it’s a joke. By 2014 there were lots of accounts online discussing what exactly he’d been convicted of.

Instead, Attia waited until a 2018 article came out: “In 2018 I came to learn this was grossly minimized…”

Attia could have saved himself a lot of trouble with the query above.

No Evidence of Criminal Behavior.

Attia points out in his mea culpa that he didn’t do anything criminally wrong with Epstein. There’s no evidence that he did, in the DOJ document release, or anywhere else.

That’s a low bar for a physician.

Does Poor Judgement Matter In A Physician?

It’s well understood that we have an epidemic of opioid overuse and overdose in the U.S.

What’s not so well understood is that the critical failure that led to this epidemic was not Purdue Pharmaceutical’s fraudulent claims about the alleged non-addictive nature of their OxyContin. It was that physicians as a class largely failed us—one can also note the Sackler brothers who owned Purdue were all physicians. Physicians have a monopoly on prescribing these drugs, and they are supposedly trained to evaluate the claims and evidence that pharmaceutical companies use to justify prescribing a new drug to the physicians’ patients. Instead they accepted weak or nonexistent marketing evidence from Purdue, along with “branded promotional items such as OxyContin fishing hats, stuffed plush toys, and music compact discs (‘Get in the Swing With OxyContin’)” (Van Zee, 2009). They exercised poor judgement, believed some absurd claims, and kicked off an opioid-abuse epidemic that at last accounting, had resulted in 600,000 deaths, and still continues.

So yes, judgement matters in a physician.

Promoting Dubious Longevity Drugs

I’ve listened to Attia’s podcast since he started producing it. He’s had some terrific guests on, and a number of the episodes have been quite educational. But one theme that has been pretty consistent is Attia’s infatuation with various drugs that have been proposed to be longevity enhancers, particularly metformin and rapamycin. In the episodes that he’s produced with experts on these drugs, they’ve been far more measured in their evaluation of the drugs than Attia has, in fact, a good part of the reason I’m skeptical about these drugs (rapamycin especially) was from listening to these experts! Rapamycin may be proved to be a longevity drug at some point, but the evidence does not exist yet. Attia stopped taking metformin after realizing that it was harmful for adaptation to exercise, and a big part of his longevity protocol is low-grade aerobic exercise. There’s no good evidence for metformin as a longevity drug, and while he’s ceased promoting it, It boggles my mind that he ever did.

I’m not a physician, I don’t have the training he has, and I don’t have access to the research team and experts that he does. So if I’m able to figure out before he does that metformin is a bad idea, why would I want his health information?

“Avoid the obvious mito-toxins, like seed oils, statins, metformin, and feed yourself correctly.”

Promoting Incorrect Health Information

I was shocked to hear Attia say in one of his podcasts that running was bad for your knees. This is misinformation that has been known to be such for decades, and a physician who brags about his research team should know better. This is, unfortunately, a medical myth that ill-informed physicians continue to propagate.

Worse are his views on cardiovascular disease. He said in one podcast that cardiovascular disease is essentially a part of our genetic heritage, which is the logical conclusion of the belief that the lipoprotein ApoB causes heart attacks.

Unfortunately this idea was pretty definitively debunked in the 1960s.

One of the better interviews Attia did was with Dr. Eric Topol. This is what Topol had to say about Attia’s mea culpa.

“…But the man you are today vs 10 years ago has not changed w/r to arrogance. Moreover, these days you are riddled with conflicts as a huckster for David Bars, AG-1 supplement, and so many other things that diminish your credibility. That's a shame.”

I don’t even know what the AG-1 supplement is, and based on Attia’s previous infatuations, I don’t really care. Guilt by association.

However…

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So I follow Attia’s podcast for his guests, which have been excellent, if very conventional. But as compared to other physicians, he’s not terrible. His basic advice is to eat well, get exercise, and it’s pretty hard to agree with those views. He’s probably better than the average physician, in fact.

Conclusion

So Attia’s problem is that he’s got poor judgement, basically. Does he have worse judgement than the average physician? As we can see from the OxyContin fiasco, there are lots of physicians with poor judgement, who get suckered by claims that shouldn’t fool a “trained professional”. The list of such claims are long, unfortunately, as most medical interventions are poorly supported by scientific evidence.

“Most medical decisions, however, come with far less certainty. The BMJ clinical evidence team reviewed 3000 treatments used in the UK’s National Health Service and found that about one half were of unknown effectiveness and only 11% were clearly beneficial.” (Mandrola, 2019)

Ultimately, Attia’s problem is that he’s a physician, and he was trained as a surgeon. Arrogance and over-confidence in Medicine is unfortunately typical of such professionals.

While I do know some good, conservative physicians, and I’m sure there are more out there, they are unfortunately the exception.

So ultimately the lesson of the Attia affair is to be wary of any over-confident physician, and always double-check their work.

(I did a little less referencing than usual on this one, to get it out the door. If you have any requests, let me know in the comments.)

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References

Mandrola, John, Adam Cifu, Vinay Prasad, and Andrew Foy. 2019. “The Case for Being a Medical Conservative.” The American Journal of Medicine 132 (8): 900–901. https://doi.org/10.1016/j.amjmed.2019.02.005.

Van Zee, Art. 2009. “The Promotion and Marketing of OxyContin: Commercial Triumph, Public Health Tragedy.” American Journal of Public Health 99 (2): 221–27. https://doi.org/10.2105/AJPH.2007.131714.

Looks like a good movie. But why is he on a juice fast?

Because vegan physician ‘Dr.’ Joel Fuhrman told him to eat this way. Poor Joe Cross.

In the trailer Joe describes how he likes to eat two pizzas. That’s not slices, he points out, that’s pizzas. Joe has a wheat belly, as you can clearly see.

Joe mentions that he’s got urticarial vasculitis, which is a rare, chronic auto-immune disease of unknown cause.

Hmm... Wheat belly and a chronic auto-immune disease. Could it be?

“Dermatitis Herpetiformis Presenting as Chronic Urticaria“ (Powell, 2004)

Dermatitis Herpetiformis is also known as celiac disease, which is a subset of wheat poisoning. Sure enough. Of course the juice diet wouldn’t include any wheat, one would imagine. Urticarial vasculitis and chronic urticaria seem to be two aspects of one disease (Krause, 2023).

Joe Cross is a perfect candidate for a paleo/primal diet. The fast he does in the movie is a high-fat diet, as he’s using the stored fat in his body to fuel himself. A low-carb paleo/primal diet replicates this, sustainably, unlike the mostly-vegan approach Fuhrman advocates, which starts out high-fat, but turns low-fat as soon as Joe runs out of body fat. High-fat diets are sustainable, low-fat diets are not.

Fuhrman’s diet, which is some ways is a vegan take on the paleo diet, is way better than the two-pizzas-a-day diet, but it’s not optimal.

And I feel for Joe, I really do. I did the Fat, Sick, and Nearly Dead thing myself, and it sucks.

P.S. How’s Joe doing?

“JC: At the beginning of the movie I was 310, after juicing for 60 days I lost about 80-85 pounds – thereabouts. I lost another 20 pounds for the next three months by just eating plant foods, such as fruits, vegetables, nuts, until I was off full medication. So that was five months of me like that and I was down to 210. Then since that – Feb. 8th – and three and a half years later – I’ve fluctuated 220 on the low side and 240 on the high side. Most of the time I sit at about 230. So that’s about a 85-90 pound consistent weight loss.”

“Chronic urticaria: A cutaneous manifestation of celiac disease”:

“Celiac disease, or gluten-sensitive enteropathy, is an immune-mediated disease of the small bowel that results in malabsorption. It classically presents with gastrointestinal symptoms including chronic diarrhea, weight loss, abdominal bloating and anorexia. It is becoming more frequently identified in asymptomatic patients with a diagnosis of deficiencies related to malabsorption of iron, folic acid, vitamin B12 and vitamin D. It is increasingly identified as a cause for early or refractory osteoporosis. Occasionally, celiac disease presents with cutaneous manifestations alone. Dermatitis herpetiformis is a well-recognized cutaneous manifestation of celiac disease. Other cutaneous manifestations include alopecia, angular stomatitis and aphthous ulcerations. Described here is a case of a 24-year-old woman who presented with intermittent urticaria and gastrointestinal complaints. She was found to have celiac disease on small-bowel biopsy. Both her gastrointestinal symptoms and urticaria resolved when she was put on a gluten-free diet, suggesting that her urticaria was a cutaneous manifestation of celiac disease.”

Original post March 8, 2011

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References

Krause, Karoline, Hanna Bonnekoh, Jannis Jelden‐Thurm, et al. 2023. “Differential Diagnosis Between Urticarial Vasculitis and Chronic Spontaneous Urticaria: An International Delphi Survey.” Clinical and Translational Allergy 13 (10): e12305. https://doi.org/10.1002/clt2.12305.

Powell, Gavin R., Anna L. Bruckner, and William L. Weston. 2004. “Dermatitis Herpetiformis Presenting as Chronic Urticaria.” Pediatric Dermatology 21 (5): 564–67. https://doi.org/10.1111/j.0736-8046.2004.21509.x.

Introduction

I am honored to be joined by John Speakman, a leading authority on energy balance in animals, and in the use of the doubly-labeled water method of determining energy balance. This has led him into the study of obesity, among other topics, where he has become a recognized expert.

We have an enlightening discussion on the potential role of deuterium in obesity and chronic disease.

Biography:

“John Roger Speakman (born 1958) FRS FRSE FRSB FRSA FMedSci FRSS is a British biologist working at the University of Aberdeen, Institute of Biological and Environmental Sciences, for which he was Director from 2007 to 2011. He leads the University’s Energetics Research Group, which is one of the world’s leading groups using doubly labeled water (DLW) to investigate energy expenditure and balance in animals. Between 2011-2020, he was a ‘1000 talents’ Professor at the Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, in Beijing, China, where he ran the molecular energetics group. In 2020 he moved to the Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences in Shenzhen, China where he works at the Center for Energy Metabolism and Reproduction and Head of the Shenzhen Key laboratory of Metabolic Health.”

https://en.wikipedia.org/wiki/John_Speakman

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Tucker Goodrich

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Show Notes

Boros, Laszlo, Que Collins, and Gábor Somlyai. 2018. “Deuterium and Metabolic Water Matter – What This Means Biochemically and Clinically.” September 24. https://www.science.org/doi/10.1126/sciadv.aat7314#elettersSection.

If you have any questions about sources for things discussed please ask in the comments.

Four weeks later I got cramps at work. I had to lie on the floor until it passed. Then I drove to my doctor’s office, and he told me that I had diverticulitis, and I had to go to the emergency room.

I drove myself, and barely made it. I was in agony; I nearly passed out again while they were interviewing me to see if it was “serious”.

That’s a good trick to get through triage quickly, by the way. I heard the nurse yelling “Medic!” A little while later I had a doctor screaming, “Morphine!” down the hall, I was in so much pain.

Turns out I had a perforated colon. That’s right, a hole in my colon, with bubbles of air trickling out to my abdomen. I spent the next four days in the pre-operative ward, so if it got worse they could cut me open immediately. I lost 10 pounds. Then I started bleeding from my behind, and I realized these were all the same symptoms that I had had 14 years before. My blood pressure got so low that the automated blood-pressure machine wouldn’t work, it thought I was dying, and would alarm immediately.

Diverticulitis is supposed to be age-related in industrial countries—people in non-industrial countries don’t get it (Trowell, 1981). 70% of of people have it by the time you reach 80, which is why all the old folks eat fiber. It usually starts occurring at 40; I had turned 40 a week earlier! But the first attack in the 20s... I mentioned to all three of the doctors I saw that I had had constant diarrhea for the last 14 years (Cohen, 2013), since the first attack, and they shrugged. They told me to eat more fiber, and whole wheat, even though that was what I had been eating for the last 20 years. So I avoided surgery, started eating salad with salad dressing (containing industrial seed oils) and lots of whole wheat. And lots of running, since I’d read running helped diverticulitis. (Got my 5k PR at that point, still haven’t beaten it. As I was telling people, I was running from a man with a knife!)

But the more salad and whole wheat I ate, the worse it got. I couldn’t understand why. Finally had to have eight inches of my colon removed. The diarrhea continued, so obviously the cause remained.

So in 2010, I stopped eating industrial seed oils (veggie oils). In two days the diarrhea stopped. Eat the oils, it started again. I no longer craved starch or sugar, so I didn’t eat any wheat for a week, without meaning to. Then I had a sandwich, felt like crap, and had diarrhea the next morning. Hmm... but I didn’t have a problem with wheat! I ate tons of it! How could I have a problem with wheat? Another week went by, and I had two slices of pizza. I thought I was having a heart attack. So now I could turn the symptoms of the last 16 years on or off, based on eating veggie oils or wheat. Wow!

Stephen Guyenet says that chronic intestinal issues are an excellent indicator of a wheat problem, and now I believe him. I read Nina Planck’s Real Food one year before my surgery, and now I realize that if I’d just followed what that woman said, I could have avoided the whole thing, most likely.

Now I’ve learned that diverticulitis is one of the most common misdiagnoses of celiac, and erroneous bowel resections are common for people who are subsequently found to be celiac—some have died (Arvanitakis, 1977). And the 14 years of chronic diarrhea? Chronic diarrhea of the sort I had (I’ll spare you the details) are also typical of a wheat problem.

And none of my doctors ever mentioned any of this as a possibility.

Lots of people have serious problems with wheat, and come back negative on celiac tests. I think celiac is just one aspect of wheat poisoning (yeah, I know, a strong term) for people with a specific immune system profile. Apparently wheat causes leaky gut syndrome in almost everyone... It took them over 2000 years just to figure out that celiac was caused by wheat! Science and Medicine know very little about it.

Hopefully this story will help my readers, but after going through all this, and then realizing not only I, but my wife and daughters, all have wheat problems, it’s been quite an eye-opener. And the veggie oils are just plain toxic. Not fit for human consumption.

So that’s just part of the introduction. Next I’ll go into more detail on how I figured out what was going on.

Original post August 17, 2010.

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Original Comments

References

Arvanitakis, Constantine. 1977. “Recurrent Colonic Ulcers in Celiac Sprue, an Unrecognized Fatal Complication: Report of a Case.” Diseases of the Colon & Rectum 20 (7): 613. https://doi.org/10.1007/BF02586629.

Cohen, Erica, Garth Fuller, Roger Bolus, et al. 2013. “Increased Risk for Irritable Bowel Syndrome After Acute Diverticulitis.” Clinical Gastroenterology and Hepatology 11 (12): 1614–19. https://doi.org/10.1016/j.cgh.2013.03.007.

Trowell, Hubert Carey, and Denis P. Burkitt. 1981. Western Diseases, Their Emergence and Prevention. Harvard University Press. https://www.hup.harvard.edu/catalog.php?isbn=9780674950207.

I was in shock.

This blog is about barefoot running and healthy, paleo-style diets, ultimately. These two topics have utterly changed my and my family’s life in the past five years prior to this news.

I learned about the barefoot running movement, like most of us, from Chris McDougall’s Born to Run.

I’ve gotten to know Chris, and Barefoot Ted, ran a race with Caballo Blanco, toured Dan Lieberman’s lab, helped design some shoes, and helped some folks fix their diets and change their lives.

I learned about Born to Run from an ad at the bottom of an item in Google Reader.

I clicked the link, watched the video, and at the end Chris put on a pair of Vibram Fivefinger Sprints. In the three years I’d had my Sprints, this was the only time I’d seen another human being who had a pair. I immediately bought the book. Thank God.

Through that book, I learned about the paleo diet from Justin Owings, who sent me a link to this post at Stephan Guyenet’s Whole Health Source. The fact that diet could control dental development (my dental development was seriously impaired growing up) blew my mind, and I started following that blog in Google Reader. Six months later, I fixed my diet and changed my life.

I had a stroke at 38, a colon resection after coming close to dying from a perforated colon at 40, and I strongly suspect I was getting osteoporosis. I don’t know where I’d be today.

Those problems are gone thanks to what I found by dumb luck through Google Reader.

“Our hypothesis (that we’ve been testing for the last 45 years) is that bioenergetic dysfunction lies at the nexus of the genetic and environmental “causes”; and that the “common-complex” diseases are bioenergetic diseases, and not anatomical diseases.” 7:07.

“Now each cell has hundreds of thousands of these mitochondrial DNAs, and they’re constantly replicating inside your cells right now. And if you doubt that they’re active and vital in there, talking to each other; tonight when it’s very very quiet and your spouse is not snoring if you just concentrate you’ll feel them wiggling in there.” 16:49

Discussing cells with different mitochondrial genotypes from mutation and division:

“Some with good mitochondrial DNAs and high energy, some with bad mitochondrial DNAs and low energy, and if it’s below the minimum energy for that tissue, then you will get a phenotype. The equivalent of a biological, a metropolitan brownout. So if there was a line voltage decline in LA, all the electrical systems wouldn’t fail at one time. The first thing that would go would be the fluorescent light bulbs, then certain elevators, then certain electrical motors, but the incandescent light bulbs would just get dimmer and dimmer.

“Well the same is true for your body. Different parts of your body rely on energy to different extents, so as the energy declines, you’re going to get organ-specific symptoms of a systemic defect.” 17:35

Noting the wild variation in expression between mitochondrial defects:

“If you inherit that from your mother you’re fine until midlife, and then you’ll lose your hearing (sensory-neural hearing loss). But if you get treated by aminoglycoside antibiotics, you’ll go deaf within a week. OK? Mutation in the tRNA leucine gene, another protein synthesis mutation at 3243; at 30 % mutant will give you diabetes, 50% mutant give your neuromuscular disease, 100% mutant and you are dead.” 18:55

He goes on with many more examples.

“So we have a quantitative genetics with totally different clinical phenotypes.” 20:15

“So why would there be tissue-specific symptomatology? Well because different tissues rely on mitochondrial energy for different extents [sic]... [Examples] ...So in fact when you think energetically, much of anatomy is about energetics, not anatomy.” 21:12

"If the, in fact, the cells are sick, they cannot undergo apoptosis, then the mitochondria are released into the bloodstream, and they are perfectly good bacteria, and you're going to get inflammation. And that's why we believe all of these diseases have an inflammatory component." 23:54

He doesn't discuss my favorite topic, the impact of omega-6 fats on mitochondria and therefore health, but it fits nicely with his hypothesis. For instance, the part of mitochondria that causes the immune reaction and inflammation he describes is cardiolipin released with oxidized linoleic acid into the blood stream. [2]

Do watch the whole thing!

Original post January 8, 2020.

Original Comments

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References

1. A Mitochondrial Etiology of Common Complex Diseases. UCLA CTSI; 2017.

. Accessed December 20, 2019.

2. Tuominen Anu, Miller Yury I., Hansen Lotte F., Kesäniemi Y. Antero, Witztum Joseph L., Hörkkö Sohvi. A Natural Antibody to Oxidized Cardiolipin Binds to Oxidized Low-Density Lipoprotein, Apoptotic Cells, and Atherosclerotic Lesions. Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26(9):2096-2102. doi:10.1161/01.ATV.0000233333.07991.4a

“Glycogen losses or gains are reported (2) to be associated with an additional three to four parts water, so that as much as 5 kg weight change might not be associated with any fat loss.”

From here:

“Glycogen Storage: Illusions of Easy Weight Loss, Excessive Weight Regain, and Distortions in Estimates of Body Composition.” (Kreitzman, 1992)

The referenced paper (2) in Kreitzman is:

Variation in Total Body Water with Muscle Glycogen Changes in Man. (Olsson, 1970)

Interesting. So how did they get to that number?

“The total body water increased 2.2 1 which is assumed to be caused by the glycogen storage in the muscles and the liver. The amount of glycogen stored was calculated to be at least 500 g, which means that 3—4 g of water is bound with each gram of glycogen.” (Olsson, 1970)

Emphasis mine. Wait, they assumed? Has anyone checked this?

Sure enough:

“In 1970, Olsson and Saltin… measured total body water after manipulating exercise and diet to supercompensate muscle glycogen stores in human skeletal muscle….

“Muscle water content expressed as mumol H2O lost/g wet tissue weight or made relative to protein content showed no consistent relationship to the glycogen content. These data, therefore, do not support the commonly accepted muscle glycogen-to-water ratio of 1.0:2.7 (g:g). Further work is necessary to quantify the exact amount of water that is actually associated with the glycogen complex.” (Sherman, 1982)

And here:

“The extent to which muscle glycogen concentrations can be increased during exposure to maximal insulin concentrations and abundant glucose was investigated in the isolated perfused rat hindquarter preparation.... Total muscle water concentration decreased during glycogen loading of the muscles.” (Richter, 1988)

I can’t find any evidence that anyone’s tried to confirm this assumption in man.

An assumption does not equal knowledge. It’s a guess, however educated. And a guess is not “science”.

I do think, however, that body weight can go up with glycogen increase. But the water’s not in the muscles, it’s in the gut, buffering the sugar that is generally used to replenish muscle glycogen:

“What he discovered was that if he drank sugary water, his body reacted to it by flooding his stomach with water.

“...Two lights went on over my head on hearing this. The first is that this explains diabetics’ frequent thirst and urination: they’re thirsty because diabetics consume a lot of sugar, which requires their bodies to dump water into their guts. They need to replenish this water in their systems, and perhaps drinking the water helps in diluting the sugar in their guts.” (Goodrich, 2013)

And going on a low-carb diet allows the body to lose the water that’s in the gut (doing you no good from a running performance perspective), not the muscles.

At least that’s n=1, not n=SWAG.

[Scientific Wild-Ass Guess]

P.S.

OK, it’s not just me:

“...Several attempts have been made to estimate the amount of water stored in muscle in association with glycogen, but this is not easily quantified. Early data suggested a value of about 3 g of water for each gram of glycogen (Olsson & Saltin, 1970). However, a subsequent study by Sherman et al. (1982), in which the muscle glycogen content of rats was manipulated by exercise and diet, suggested that there was no consistent association between the amount of glycogen stored in a muscle and the muscle water content. Richter, Hansen, and Hansen (1988) found a decrease in muscle water concentration after muscle glycogen loading. Nygren, Karlsson, Norman, and Kaijser (2001) have also suggested that glycogen loading may alter the disposition of water molecules within the muscle. These apparently conflicting data may result from different amounts of water storage with different structural forms of glycogen and changes in the proportions of these different forms as the total amount of glycogen changes.

“Notwithstanding the uncertainties, there is good evidence of gross changes in body mass as a consequence of diet and exercise manipulations designed to induce alterations in glycogen storage in humans. Any major change in the amount of glycogen stored in muscle will result in a change in body mass, with the major part of the mass change being a consequence of the storage of the associated water (Olsson & Saltin, 1970)....” (Maughan, 2007)

The studies they cite are the studies linked to above. They’re not particularly logical with that last statement, however, as there’s still no evidence for the proposition that glycogen is stored with water.

But that’s how scientific myths stay alive!

P.P.S.

The whole point of the glycogen molecule is to store glucose without water...

“Glycogen is also a suitable storage substance due to its insolubility in water, which means it does not affect the osmotic pressure of a cell.”

That was what Wikipedia said when I first wrote this post. Which as we can see is correct.

Wikipedia now quotes (Kreitzman, 1992), and says:

“Glycogen in muscle, liver, and fat cells is stored in a hydrated form, composed of three or four parts of water per part of glycogen associated with 0.45 millimoles (18 mg) of potassium per gram of glycogen.^[5]”

Sob. Wikipedia is a propaganda machine, not a reliable source of information.

P.P.P.S

I had a back-and-forth about this with Kevin Hall on X:

The first paper is (Geddes, 1977) which says in the abstract:

“Hydrodynamic studies indicated that all fractions of glycogen of mol.wt. exceeding 25 x 106 had about 1.1 g of water per g of polysaccharide associated with them.”

This sounds authoritative. However they clarify in the text:

“As pointed out by Ogston (1953), the amount of water which we have shown (1.1 g/g of polysaccharide) to be associated with the particles is some sort of average and could well be different under different hydrodynamic conditions.”

How did this water get into the glycogen in their experiment?

“Solutions of known glycogen concentration were prepared by dissolving an accurately weighed quantity of previously dehydrated glycogen in a known volume of pure water.” (Geddes, 1977).

Dehydrated glycogen. Right.

So it’s not a relationship, just an average, as the water is “loosely associated” (Geddes, 1977). Hall’s quote “extensively hydrated” isn’t to be found in either paper, but the second paper says “It is hydrated extensively [31]” (Channareddy, 1996). [31] is a reference to (Geddes, 1977), not so some separate demonstration.

Original Post: April 7, 2014, and the comments:

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References

Channareddy, Sreelatha, Sherilyn S. Jose, and Nathan Janes. 1996. “Ethanol Binding to a Model Carbohydrate, Glycogen.” Biochemical Pharmacology 52 (12): 1911–14. https://doi.org/10.1016/S0006-2952(96)00695-8.

Goodrich, Tucker D. 2013. “What Does Sugary Water Do To Your Body? Thoughts On Racing With A Water Balloon.” Blog. Yelling Stop, August 29. https://yelling-stop.blogspot.com/2013/08/what-does-sugary-water-do-to-your-body.html.

Kreitzman, S. N., A. Y. Coxon, and K. F. Szaz. 1992. “Glycogen Storage: Illusions of Easy Weight Loss, Excessive Weight Regain, and Distortions in Estimates of Body Composition.” The American Journal of Clinical Nutrition 56 (1 Suppl): 292S-293S. https://doi.org/10.1093/ajcn/56.1.292S.

Maughan, Ronald J., Susan M. Shirreffs, and John B. Leiper. 2007. “Errors in the Estimation of Hydration Status from Changes in Body Mass.” Journal of Sports Sciences 25 (7): 797–804. https://doi.org/10.1080/02640410600875143.

Olsson, K. E., and B. Saltin. 1970. “Variation in Total Body Water with Muscle Glycogen Changes in Man - Olsson - 1970 - Acta Physiologica Scandinavica - Wiley Online Library.” Acta Physiologica Scandinavica 80 (1): 11–18. https://doi.org/10.1111/j.1748-1716.1970.tb04764.x.

Richter, E. A., S. A. Hansen, and B. F. Hansen. 1988. “Mechanisms Limiting Glycogen Storage in Muscle During Prolonged Insulin Stimulation.” The American Journal of Physiology 255 (5 Pt 1): E621-628. https://doi.org/10.1152/ajpendo.1988.255.5.E621.

Sherman, W. M., M. J. Plyley, R. L. Sharp, et al. 1982. “Muscle Glycogen Storage and Its Relationship with Water.” International Journal of Sports Medicine 3 (1): 22–24. https://doi.org/10.1055/s-2008-1026056.