Just got the December issue of the American Journal of Clinical Nutrition (AJCN), which prints a letter debate on the harmful effects (or lack thereof) of saturated fats. I’m going to print the debate in its entirety below so that you can listen in. I want to you see first hand the narrow mindedness of a true believer of the lipid hypothesis.
The inspiration for this debate came from an editorial written by Martijn Katan about a paper published last May by Ronald Krauss and his group. (I wrote a fairly extensive post on this same paper as soon as it came out.) Katan is a fervent advocate of the lipid hypothesis who writes editorials espousing it whenever he gets the chance. Since these editorials seem always to advance the same issues despite any evidence to the contrary I’ve begun referring to them as the Katanic Verses.
A taste of this (typical) Katanic Verse:

This study is valuable because it extends our knowledge of dietary protein and blood lipids. Evidently, proteins lack the triacylglycerol-elevating effect of carbohydrates. However, lipoproteins are now a less pressing problem than is obesity. Low-fat, high-carbohydrate diets have failed to produce long-term weight loss, but we should not be overly optimistic about the alternatives. Obesity is a societal disease caused by an overabundance of food and mechanization, and diets high in protein or fat are unlikely to reverse the trend. We also do not know whether the consumption of large amounts of protein is safe for the kidneys and bones; trials to determine this are urgently needed. We have a way to go before we know as much about protein as we do about unsaturated fats. Clinical trials have shown that high intakes of unsaturated fatty acids reduce the risk of heart attacks, a finding that is consistent with their favorable effects on lipoproteins and with the inverse associations between unsaturated fat intake and heart disease. In comparison, the evidence that high-protein diets prevent heart disease is still slim.

Dr. Uffe Ravnskov wrote a letter to the editor of the AJCN about this editorial and the article to which it referred. Before we get to the actual letters, let me tee up the informal ground rules for such letter exchanges in academic journals. Typically it goes this way: Professor A publishes a paper. Professor B has a question or takes exception to a conclusion that Professor A has drawn. Professor B writes a letter to the editor of the journal saying something along the lines of: I read Professor A’s paper with great interest and wondered if he had considered blah blah blah. Professor A responds to Professor B’s letter by saying: I appreciate Professor B bringing this to my attention. What I perhaps didn’t make clear was blah blah blah. It’s all very clubby and congenial.
Dr. Ravskov’s letter is in such a congenial spirit.


Saturated fat does not affect blood cholesterol

Uffe Ravnskov
Magle Stora Kyrkogata 9
S-22350 Lund

Dear Sir:
The most striking observation from the study by Krauss et al (1) is the finding that a diet rich in saturated fatty acids (SFAs)results in a lower or a steady state concentration of total and LDL cholesterol and an increase in the concentration of HDL cholesterol, regardless of whether the diet has a reduced energy content. Similar effects on blood lipids have been observed in 4 weight-reducing trials with high intakes of SFAs (2-5)(Table 1) and in many similar trials with unrestricted intakes of SFAs.
[Table 1 goes here. I don’t have enough technical know-how to copy it from the paper. It is a summary of the above references 2-5 presenting data showing the lack of cholesterol elevation brought about by dietary saturated fat in doses of up to 50 percent of calories consumed.]
In 1973, Reiser (6) questioned the effects of SFA intake on serum cholesterol. In a thorough review of the relevant experiments, he noted several methodologic and interpretational errors. The most important errors are probably the attribution of differences between SFAs and polyunsaturated fatty acids to the former, when the effect could have been due to the latter, and the use of vegetable oils saturated by hydrogenation instead of natural SFAs.
A possible reason why the effects were more pronounced before weight reduction than after weight reduction in the study by Krauss et al was the difference in metabolism between the normal-weight and overweight subjects. Cornier et al (7) recently found that total and LDL-cholesterol concentrations decreased more with a low-carbohydrate than with a low-fat, calorie-restricted diet. Interestingly, the overweight subjects with reduced insulin sensitivity, but not those with normal insulin sensitivity, had an increase in cholesterol with the low-fat diet but a decrease with the low-carbohydrate diet. In both groups, the changes in lipids were more beneficial with a low-carbohydrate diet than with a low-fat diet. Therefore, the different lipid responses before and after weight reduction in the study by Krauss et al may have been because the loss of weight may have improved the participants’ insulin sensitivity and thus their lipid response.
Because the main reason for restricting the intake of SFAs in all official guidelines is to change blood lipids, demonizing these nutrients seems inappropriate. In his editorial, Katan (8) claims that high intakes of unsaturated fatty acids reduce the risk of heart attacks, but his evidence is based on a meta-analysis that had ignored 4 unsuccessful trials (9). Two meta-analyses of all controlled clinical trials in which the only intervention was a change in dietary fats found no effect on coronary or total mortality (10).
The author had no vested interest in the subject of this letter.

  1. Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr 2006;83:1025–31.
  2. Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents. J Pediatr 2003;142:253–8.
  3. Hays JH, DiSabatino A, Gorman RT, Vincent S, Stillabower ME. Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease. Mayo Clin Proc 2003;78:1331–6.
  4. Meckling KA, O’Sullivan C, Saari D. Comparison of a low-fat diet to a low-carbohydrate diet on weight loss, body composition, and risk factors for diabetes and cardiovascular disease in free-living, overweight men and women. J Clin Endocrinol Metab 2004;89:2717–23.
  5. Sharman MJ, Gomez AL, Kraemer WJ, Volek JS. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr 2004;134:880–5.
  6. Reiser R. Saturated fat in the diet and serum cholesterol concentration: a critical examination of the literature. Am J Clin Nutr 1973;26:524–55.
  7. Cornier MA, Donahoo WT, Pereira R, et al. Insulin sensitivity determines the effectiveness of dietary macronutrient composition on weight loss in obese women. Obes Res 2005;13:703–9.
  8. Katan MB. Alternatives to low-fat diets. Am J Clin Nutr 2006;83:989–90.
  9. Ravnskov U. The diet-heart idea is kept alive by selective citation. Rapid response. BMJ 8. December 2003.
  10. Ravnskov U. Diet-heart disease hypothesis is wishful thinking. BMJ 2002;324:238.

The letter in response by Dr. Katan is the epitome of rudeness and non-collegiality. It is the standard in academic papers and letters to reference any categorical statements. Even if you say something generally accepted you do it. For example, if you wrote: ‘the incidence of obesity has risen greatly over the past 20 years in this country’ you would list a reference to one or more of the many papers showing such. If what you are saying is the least bit controversial, you always reference it. I’ll add my interjections to Dr. Katan’s response using brackets and italics.


Reply to U Ravnskov

Martijn B Katan
Vrije Universiteit
Faculty of Earth and Life Sciences Institute of Health Sciences
De Boelelaan 1085
1081 HV Amsterdam

Dear Sir:
Ravnskov’s suggestion that a reduction in the intake of saturated fat does not lower cholesterol is wrong. [Where is the citation?] At constant body weight, the replacement of saturated fat with other nutrients unequivocally lowers cholesterol concentrations; [citation?] all meta-analyses of controlled trials agree on this.[Citation?]
As for the effects of saturated fatty acids on heart disease, Ravnskov rightly notes that some clinical trials have failed to show that the replacement of saturated fat with unsaturated fat reduces heart disease. However, most clinical trials have shown a benefit. [Citation?] In addition, evidence from epidemiologic, metabolic, and laboratory studies confirms that high intakes of saturated fat do cause heart disease. [Citation?] Ignoring this evidence leads to absurd consequences. For instance, our knowledge of the ill effects of cigarette smoking rests purely on epidemiologic, metabolic, and laboratory studies, whereas evidence from clinical trials is largely lacking. The same holds true for the ill effects of physical inactivity, the failure to use seat belts, the consumption of toxic chemicals in foods, and asbestos exposure. None of these conditions has been proven to be unhealthy in clinical trials performed according to the standards for pharmaceutical drugs. I believe that, in all of these cases, we should consider the totality of the evidence, and the totality of the evidence overwhelmingly indicts saturated fat as a cause of heart disease, just as it indicts cigarettes. [If the totality of the evidence indicts heart disease, how come the Framingham data, the biggest study of all, shows no correlation. I would say that kind of blows the totality-of-the-data-overwhelmingly-indicts theory.]
Ravnskov has now published approximately 58 Letters to the Editor (1-58) that address publications about lipids and heart disease. His letters have been published in the Journal of the American Medical Association, the New England Journal of Medicine, the British Medical Journal, the Lancet, Science, Annals of Internal Medicine, the Journal of Clinical Epidemiology, the Quarterly Journal of Medicine, and several Scandinavian medical journals. All his letters have argued essentially the same point, namely that lowering blood cholesterol concentrations is of unproven value. I agree with the dozens of scientists who have carefully replied to his letters and who have shown that, by and large, his arguments are faulty. [The implication here is that scientists refute all of these 58 papers, which you’ll find isn’t the case if you read them.]
The author had no conflict of interest.

  1. Ravnskov U, Rosch PJ, Sutter MC, Houston MC. Should we lower cholesterol as much as possible? BMJ 2006;332:1330–2.
  2. Ravnskov U, Rosch PJ, Sutter MC. High-dose statins and the IDEAL study. JAMA 2006;295:2476, 2478–9.
  3. Ravnskov U. [Misleading advice on cholesterol reduction.] Lakartidningen 2006;103:568, 569 (discussion).
  4. Ravnskov U. [Treatment of hypercholesterolemia—lower is not better.] Ugeskr Laeger 2006;168:1665.
  5. Understrup AG, Ravnskov S, Hansen HC, Fomsgaard IS. Biotransformation of 2-benzoxazolinone to 2-amino-(3H)-phenoxazin-3-one and 2-acetylamino-(3H)-phenoxazin-3-one in soil. J Chem Ecol 2005;31:1205–22.
  6. Ravnskov U, Rosch PJ, Sutter MC. Intensive lipid lowering with atorvastatin in coronary disease. N Engl J Med 2005;353:93–6.
  7. Ravnskov U. [Should cholesterol levels be reduced more aggressively?] Lakartidningen 2005;102:2583–4.
  8. Ravnskov U. Europe in transition: dietary fat is not the villain. BMJ 2005;331:906–7.
  9. Ravnskov U, Sutter MC. Aggressive lipid-lowering therapy and regression of coronary atheroma. JAMA 2004;292:38–40.
  10. Ravnskov U. Inflammation, cholesterol levels, and risk of mortality among patients receiving dialysis. JAMA 2004;291:1833–5.
  11. Ravnskov U. [High cholesterol level may protect against infections and probably also atherosclerosis.] Lakartidningen 2004;101:1215–7, 1218 (discussion), 1221–2.
  12. Ravnskov U. [Hasty conclusions on cardiac mortality in Norway.] Tidsskr Nor Laegeforen 2004;124:2153.
  13. Ravnskov U. [Karl Popper and the cholesterol hypothesis.] Tidsskr Nor Laegeforen 2004;124:2517.
  14. Ravnskov U. ASCOT-LLA: questions about the benefits of atorvastatin. Lancet 2003;361:1986.
  15. Ravnskov U. Lipoproteins and cardiovascular risk. Lancet 2003;361:1988–9./li>
  16. Ravnskov U. [Too many calories and too little exercise cause obesity not intake of fat.] Lakartidningen 2003;100:3255–6.
  17. Ravnskov U. High cholesterol may protect against infections and atherosclerosis. QJM 2003;96:927–34.
  18. Ravnskov U. Dietary fat intake and risk of stroke: allegations about dietary fat are unfounded. BMJ 2003;327:1348.
  19. Ravnskov U, Allen C, Atrens D, et al. Studies of dietary fat and heart disease. Science 2002;295:1464–6.
  20. Ravnskov U. Diet-heart disease hypothesis is wishful thinking. BMJ 2002;324:238.
  21. Ravnskov U. [Surrogate research on heart disease and risk factors.] Lakartidningen 2002;99:1507.
  22. Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM 2002;95:397–403.
  23. Ravnskov U. [The debate in science: dietary guidelines against myocardial infarction are defended by wrong citations.] Lakartidningen 2002;99:2673.
  24. Ravnskov U. A hypothesis out-of-date. the diet-heart idea. J Clin Epidemiol 2002;55:1057–63.
  25. Ravnskov U. [Millions of healthy people can be considered ill because of the American cholesterol policy.] Lakartidningen 2001;98:4574–7.
  26. Ravnskov U. [Lipid lowering doesn’t affect the development of atherosclerosis in peripheral artery disease.] Lakartidningen
  27. Ravnskov U. Cholesterol and all-cause mortality in Honolulu. Lancet 2001;358:1907.
  28. Ravnskov U. VAT and fat. Evidence is contradictory. BMJ 2000;320:1470.
  29. Ravnskov U. [Misleading cholesterol statistics.] Lakartidningen 1999;96:1947.
  30. Ravnskov U. Why heart disease mortality is low in France. Authors’ hypothesis is wrong. BMJ 1999;319:255–6.
  31. Ravnskov U. [Experts ask for priorities when it comes to interpretation. Ravnskov answers in the debate on dietary fats.] Lakartidningen 1998;95:1022–3.
  32. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. J Clin Epidemiol 1998;51:443–60.
  33. Ravnskov U. [Excellence of the “Mediterranean diet” is a myth. There is no evidence that monounsaturated fats prevent myocardial infarction.] Lakartidningen 1998;95:4749–50.
  34. Ravnskov U. [On honesty and monounsaturated fat.] Lakartidningen 1998;95:4966.
  35. Ravnskov U. [Do cholesterol-lowering drugs cause cancer?] Lakartidningen 1996;93:2040.
  36. Ravnskov U. American College of Physicians guidelines on cholesterol screening. Ann Intern Med 1996;125:1010–1.
  37. Ravnskov U. [Fatty acids and confusing signals.] Ugeskr Laeger 1995;157:1534–5.
  38. Ravnskov U. Quotation bias in reviews of the diet-heart idea. J Clin Epidemiol 1995;48:713–9.
  39. Ravnskov U. Implications of 4S evidence on baseline lipid levels. Lancet 1995;346:181.
  40. Ravnskov U. Beneficial effects of simvastatin may be due to non-lipid actions. BMJ 1995;311:1436–7.
  41. Ravnskov U. Hypercholesterolemia does not cause coronary heart disease–evidence from the nephrotic syndrome. Nephron 1994;66:356–9.
  42. Ravnskov U. Ischaemic heart disease and cholesterol. Optimism about drug treatment is unjustified. BMJ 1994;308:103.
  43. Ravnskov U. [Do polyunsaturated fats cause male sterility?] Lakartidningen 1994;91:2308.
  44. Ravnskov U. [Uncritical review of articles on cholesterol.] Ugeskr Laeger 1994;156:4479–80.
  45. Ravnskov U. Is intake of trans-fatty acids and saturated fat causal in coronary heart disease? Circulation 1994;90:2568–9.
  46. Ravnskov U. Doing the right thing: stop worrying about cholesterol. Circulation 1994;90:2572–3.
  47. Ravnskov U. What do angiographic changes after cholesterol lowering mean? Lancet 1994;344:1297.
  48. Ravnskov U. [Doubtful advices on cholesterol screening in children.] Ugeskr Laeger 1993;155:1886–7.
  49. Ravnskov U. Reducing serum cholesterol. Lower cholesterol of doubtful benefit to anyone. BMJ 1993;307:125.
  50. Ravnskov U. [New trends from the USA. The cholesterol campaign is questioned.] Lakartidningen 1993;90:2528–9.
  51. Ravnskov U. Coronary atherosclerosis on angiography—progress or regress, and why? Circulation 1993;88:1358–60.
  52. Ravnskov U. [Decreased cholesterol level shortens life.] Ugeskr Laeger 1993;155:3679–80.
  53. Ravnskov U. [Stop the cholesterol campaign!] Lakartidningen 1993;90:4587–8, 4589–90 (discussion).
  54. Ravnskov U. [What is the correct answer in the cholesterol debate?] Ugeskr Laeger 1992;154:1716–8.
  55. Ravnskov U. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. BMJ 1992;305:15–9.
  56. Ravnskov U. Frequency of citation and outcome of cholesterol lowering trials. BMJ 1992;305:717.
  57. Ravnskov U. [Are polyunsaturated fats useful?] Lakartidningen 1991;88:1058.
  58. Ravnskov U. An elevated serum cholesterol level is secondary, not causal, in coronary heart disease. Med Hypotheses 1991;36:238–41.

This letter, like Katan himself, is a nasty piece of work that shouldn’t be legitimized in the pages of a prestigious scientific journal. That it is speaks volumes to the notion that the editors are on board with Katan and his anti-saturated fat jihad. At least you can see what kind of bias need be overcome in presenting an opposing viewpoint to the lipid hypothesis.


  1. Hi Mike,
    I guess it would be a breach of the ‘clubby and congenial’ code for a third party (such as yourself?) to write to the editor pointing out the glaring defects in Katan’s response? (btw I like “Katanic Verses!)
    Hi Malcolm–
    These things are usually a one off kind of deal.  People don’t write in criticizing the response of one party to the other.

  2. I believe it was George Mann who called the lipid hypothesis the biggest fraud ever perpetuated on the public. Makes me pretty cynical about government, academia, corporations, and (no offense intended, Mike) mainstream medicine. Big government, big business, big U, and big medicine–that’s a hard combo to beat!
    Hi Paul–
    No offense taken; I don’t consider myself a part of mainstream medicine.

  3. Well, having been a research scientist myself (in physics), and I can testify that the sort of dogmatic insistence displayed by Katan is all too common, regardless of the scientific field. The good news is that the truth ultimately prevails, though it can take a long time, especially once the government gets involved.
    Here’s a question: have you ever actually gotten a response to requests for references demonstrating the validity of the lipid hypothesis? Or do “they” just poo-poo you off as a nut? I’d be curious to know what papers the lipid folks believe provide support to their position. I’ve been asking around, and gotten no response (maybe not surprisingly).
    Hi Dave–
    No, I haven’t gotten responses to requests for references substantiating the lipid hypothesis. If asked, the pro-lipid-hypothesis people act like they’ve been asked for references as to whether or not gravity exists. If you look up the references when pro-lipid-hypothesis statements are made in scientific journals, the papers referenced are always papers that make the same kind of statements that are themselves referenced to other identical papers. I’ve never spent the time required to take it all the way back. But, someone else has.
    Gary Taubes, of New York Times What if it’s all been a big fat lie fame, has written a book on this very subject, and he has tracked it back. I’m reading his book in manuscript form right now, and I can tell you that a) he is incredibly thorough, and b) there ain’t no substance to the lipid hypothesis. He’s tracked it all the way back, and when you get back there it’s like that highly touted episode on Geraldo a few years back where he was going to open Al Capone’s secret vault that had been discovered and hadn’t been opened since Al was around. After much hoopla, Geraldo opened the safe only to find it empty. When Taubes tracked the lipid hypthesis back to its origins, he found the same thing.
    When Gary’s book hits the stands in several months, you’ll be able to read all about it and a lot more to boot.

  4. I’m so jealous you get to read Taubes’ book! I’ve been looking forward to it for a long time (I’ve read Ravnskov’s book and am getting through Colpo’s).
    Hi Anna–
    It’s my second time through.  The first time was 700+ pages; this time around it’s a mere 400 or so after all the editing cuts.  The book is well worth waiting for.  An incredible amount of work went into it.

  5. I was going to do a similar thing for my own curiosity using the “Cholesterol Facts” paper (http://circ.ahajournals.org/cgi/reprint/81/5/1721.pdf). But after I found out that on the 4th page where it says, “a 1% reduction in an individual’s total serum cholesterol level translates into an approximate 2% reduction in CHD risk,” they claim that some studies support even greater reduction, and then reference the 30-year follow up of Framingham that showed for every 1 mg/dl DECREASE in cholestrerol there is a 14% INCREASE in CHD, I just laughed and stopped there. I have better things to do with my time.
    Hi Neal–
    Taubes has done it all and saved us all a lot of effort.

  6. I wonder if Katan even READ the Ravnskov’s letters that he referenced so ‘exhaustively’. Because his reference 5 isn’t even a Uffe paper. It’s by some other Ravnskov, and has nothing to do with lipid arguments at all.
    It was just a fast Google hash job.
    I think Gary Taubes was right, many of the most ‘prominent’ researchers in this field are among the worst scientists there are.
    Hi Walt–
    Good to hear from you.  I noticed the faulty reference as well.  And of the references that are from the correct author, many are not  dissed as Katan would have us believe.
    I don’t think Gary Taubes is right–I know he’s right.

  7. It seems as the Emperor becomes aware that he is about to be naked he becomes very irrate and irrational. I was recently reading an article on Dr. Passwater’s site (www.drpasswater.com) where he interviewed Dr. Bill Judy about his research with CoQ10 and working with Dr. Folkers. Fascinating stuff and infuriating stuff. After doing trials on CHF patients and getting very positive results, he was told he could no longer do research on CoQ10. There were people who were given 2-3 months to live and after receiving the Q10 were alive several years later. Now I’m just a lowly chiropractor, but in my 10 years in practice I don’t ever think I’ve ever heard a cardiologist or GP tell their heart patients to take Q10 or anything that would actually make their biochemistry work more efficiently. OK, I’ve vented and feel a little better, sorry.
    Hi Robert–
    No problem.  You’re welcome to vent any time.  In today’s medicine there is plenty to vent about.

  8. Ah Ha, so you’re the one with the Taubes manuscript, ehhh?
    😉 We need the precious…
    Hi Karen–
    All in good time. It will be well worth the wait. If I thought it would make Katan and his ilk invisible, I would send ‘the precious’ to them ASAP.

  9. Ack! We still have to wait for the Taubes book for several months!
    Frankly, because he does have a reputation as an investigative science writer, I expect it to make a big splash. It’s one thing to tar Atkins and Protein Power as being in it for the money in this cynical world, but it’s going to be hard to do that to Taubes.
    Expect him to be investigated for any kind of conflict of interest after this comes out.
    Hi LC–
    It will be worth the wait.  It’s an excellent, in depth, read.
    I’m certain eyebrows will be raised and teeth will be gnashed.  Many upper lips will be have to be stiffened as countless drudges see the results of their careers spent currying favor with the mainstream dashed before their eyes.
    I can hardly wait.

  10. Do you think there’s any chance that the fat phobia falls within the next years?
    I have trouble seeing such an abrupt change.
    Maybe in the 2010’s… Although with the Internet and the quick spread of information, maybe things will get better quicker.
    I could be mean and say that it’s natural selection doing its work, but it would not be true. There are plenty of very intelligent individuals who have been shown the lipid hypothesis again and again as something so obvious that it goes to make itself a place in the subconcious, just next to our natal language. The brain then tries to prevent its self destruction by bypassing the logic skills of these people.
    I don’t know anything about Gary Taubes. Will his book be something that will grab the attention of the public? Or will he be seen as “yet another quack”… Faith is so much stronger than logic.
    Hi Max–
    Gary Taubes is a well-respected science journalist.  He kicked off the latest round of low-carb controversy with a front page article in the
    New York Times a few years ago titled What if it’s all Been a Big Fat Lie?
    His book is being published by Knopf, the most prestigious book house in the US, so it will get plenty of attention.  Taubes doesn’t have a diet plan to sell or an axe to grind, so he will be given plenty of credibility.

  11. Does anyone know why saturated fat increases cholesterol? why the addition of a few hydrogen molecules increases the likelihood a healthy person will keel over and die? I have searched google many times and never ever found any evidence for this, i continually get the same information: “saturated fat is bad, it raises cholesterol.” But no-one ever explains WHY, i get so irate with this statement which equates to “it is, because i say so”. what’s the mechanism?, where’s the evidence? tell me why! epidemiological studies are not good enough, im sure people could correlate sesame seeds with cancer becuase they’re widely consumed on top of macdonalds burgers.
    I often think all the real scientists went into physics or chemistry and all the drugged up hippies when into nutrition.
    Either PROVE saturated fat is bad or shut the F*** UP!
    Hi Proove_it_or_lose_it–
    Actually it has been shown that increasing dietary saturated fat as part of a regular diet can raise cholesterol levels.  What hasn’t been shown is that raising cholesterol levels causes an increase in heart disease.  And it has been shown that increased consumption of saturated fat as part of a low-carb diet doesn’t even cause an increase in cholesterol.

  12. Hi. Is the mechanism by which saturated fat raises cholesterol understood at all? Particularly the effects in the presence/absense of dietary carbohydrate?
    Hi Dave–
    I don’t know if the actual mechanism for the saturated fat-increased cholesterol has been worked out.  That’s not to say it hasn’t, it’s just that if it has been, I’m not aware of it.  And I don’t really care about it enough to spend the time tracking it down.

  13. Good point – if cholesterol doesn’t cause CHD, then why sweat it’s relationship to saturated fat?
    But I’m a curious monkey, so I started following the trail from the link you posted on the sat-fat/cholesterol connection. I didn’t have to go far before encountering a dizzying array of research which attempted to understand in great detail the effects of various fatty acids on the size, structure, composition, etc. of cholesterol and the corresponding potential implications for CHD. I wasn’t interested enough to dig much deeper, but it certainly sounded like they’re busily adding parameters to the model in an attempt to prove their hypothesis, without much success (surprise!).
    But that’s what you get when you presume the truth of a hypothesis before actually testing it: a nice long and expensive trip to nowhere.
    Hi Dave–
    It’s like Eskimos having 29 different words for snow.  If your life is cholesterol–which it is for most lipid-hypothesis nerds–you have to come up with multiple types, sub-types, and fractions in an effort to find some part of it somehow that fulfills your expectations.
    A thousand roads leading nowhere…

  14. I interviewed David Kritchevsky a year and a half back for an article in the Irish Times and he willingly acknowledged that his early experiments with cholesterol meant very little, though they did encourage the American edible oil industry to develop and promote the Prudent Diet. He now attributes atherosclerosis to chlamydia and the like. Equally I interviewed Luise Light about how the Food Pyramid was first constructed – she was Director of Nutrition Education at the USDA when the pyramid was proposed. She has an interesting story about the first draft – recommending vegetables as the main source of nutrition and recommending restricting grains to very small quantities. She was over-ruled and what we got instead was a high carb diet recommending we stuff ourselves with 6 – 11 helpings of grains a day.
    Not only is much of the mainstream cholesterol science bad the vested interestes are quite clear. It’s a political problem but I have found as a journalist it is next to impossible to tel this story. TV and newspapers really want to believe the pasta generation is right.
    You’re right.  It’s almost impossible to get the true story.  Gary Taubes’ new book will lay it out in detail.  He spent 5 years of constant research and writing, and based on my many conversations with him, it wasn’t easy coming up with the info.
    Thanks for writing.

  15. Hi
    A recent article in UK paper said that
    ‘a cholesterol level of 7.5 which would warrant treatment for a middle aged man with heart disease but would be completely normal in a fit person in their 70’s and beyond’
    Is this correct ??
    Hi Philip–
    A cholesterol reading of 7.5 mmol/L translates into a cholesterol of about 290 mg/dL.  The statement is both true and false.  It’s true in that a cholesterol of 290 would be okay for a person 70 years old or older (even the pro-lipid hypothesis people agree with this), but in my opinion that same cholesterol level would be okay for someone with heart disease.  Why do I say this?  Because I don’t believe that elevated cholesterol is the driving force behind heart disease.  Plus, even if one is a believer in the lipid hypothesis, it would depend on what that 290 mg/dL of cholesterol was composed of.  If it contained 90 mg/dL of HDL it would be great.  Total cholesterol by itself doesn’t indicate anything.


  16. Hi Michael
    First, Thank you for your sharp analysis of my correspondence with Katan.
    I would like to comment on the question about how saturated fat is able to raise the cholesterol. To be very short: I don´t think it does!
    Already 30 years ago Raymond Reiser analyzed 40 trials and found that instead of using natural satfat many authors had used vegetable oils saturated by hydrogenation, and in the trials where they did use original satfat the effect on cholesterol could as well have been due to a lowering of polyunsaturated fat. The latter seems very likely because in at least ten lowcarb trials where fat was substituted for carbs, no effects were seen on total or LDL cholesterol although some of them used satfat intakes that covered between 20 % and 50 % of the calorie intake.
    Hi Uffe–
    Thanks for writing. Thanks to your letter to Katan, I dug out the Reiser paper (Large pdf) and read it for the first time as well as the the absolutely vicious attack (Large pdf) on it written by Ancel Keys and published several months later. Keys’ vitriol makes Katan look like a school child. To paraphrase Shakespeare, Methinks the gentleman doth protest too much. I also read Reiser’s rebuttal to the Keys diatribe. Gentle, but well done.
    You are right; the studies cited by Reiser do seem to indicate that the effect of saturated fat on cholesterol could have been occasioned either from the hydrogenated vegetable oils or from the decrease in polyunsaturated fat. Maybe even the generally accepted idea that natural saturated fat raises cholesterol is false as is the idea that a rise in cholesterol increases the risk for heart disease.

  17. Many thanks to Dr. Ravnskov for the reply. I suspected as much, but never would have found the time to dig into the topic in detail. While I was looking for an answer to the underlying cause for the supposed sat. fat/cholesterol connection, I could find nothing. Odder yet, in papers discussing (in incredibly gory detail) the various aspects of LDL and its putative effects on CHD, there is NO mention of the mechanism by which cholesterol might be raised by diet.
    I’m sure somebody talks about it somewhere, but I couldn’t find it (admittedly, I didn’t look that hard, especially after reading Dr. Ravnskov’s
    “The Cholesterol Myths”
    ). After 50 years, you think some progress would have been made on this front; or, you’d think the community at large would have put it together that maybe the hypothesis was wrong in the first place.
    It’s going to be very interesting if the research decribed in
    this article
    holds water. I think it would be immensely ironic if low carb made it into the nutritional and legislative mainstream because a direct cause/effect relationship could be established between high carbohydrate intake and increased cholesterol level. Even more irony to be found if it is realized that high cholesterol wasn’t the culprit in the first place, but rather CHD was caused by damage do to high blood sugar.
    Hi Dave–
    I’ve got the Nature paper that the ScienceDaily article discusses, but I haven’t had time to read it in depth.  When I do, I’ll probably post on it if it really has merit.  I never trust journalistic interpretations of scientific papers.
    I’m in an interesting situation.  I have my money on San Francisco +10, but I want the Broncos to win.  So, root for a Bronco win and a SF cover.
    Happy New Year!

  18. Pre-orders are now being taken for Gary Taubes book, to be titled “The Quality of Calories: Challenging the Conventional Wisdom on Diet, Weight Control, and Disease.” I kind of liked the “Big Fat Lie” title better 🙂
    Release date is September 18, 2007. I was hoping for something sooner, but better late than never. Here’s the Link to the publisher’s site.
    Hi Dave–
    I’ve been involved in an intense email exchange with Gary over this title.  I don’t like it, and I don’t think he particularly does either.  Once you read the book, though, the title makes more sense.  But I still don’t like it.  I could have been so much better.

  19. The effectiveness of statins seemingly lends strong support to the standard picture of the role of cholesterol in coronary disease. Indeed (continuing with links to PubMed abstracts),
    “Statins, therefore, have unequivocally shown the importance of cholesterol lowering in the prevention of morbidity and mortality due to coronary disease.” (Am Heart J. 2002)
    And there you have it, and stated with certitude. However, just offhand, I’d thought that the promptness of mortality reduction in response to statins would be odd, for an intervention that merely slows a decades-long process of accumulation. And indeed, this turns up:
    “The effectiveness and rapidity of statin-induced decreases in coronary events led to the speculation that statins possess cholesterol-independent effects… we describe the numerous beneficial pleiotropic effects of statins that could modulate atherogenesis.” (Curr Drug Targets Cardiovasc Haematol Disord. 2005)
    “[H]ave unequivocally shown the importance of cholesterol”? Ooops. Further:
    “…the demonstration that statins can inhibit inflammation and encourage angiogenesis offers other possibilities for action.” (Arthritis Res. 2002)
    “Statins were originally developed as lipid-lowering drugs… statins may provide beneficial effects outside of reductions in low-density lipoprotein and triglycerides.” (Drug News Perspect. 2005)
    So, “statins may provide” additional beneficial effects? This is a very cautious statement, given the repeated documentation of their anti-inflammatory effects.
    If the statin data gives support to the standard picture of the role of cholesterol, that support is surprisingly weak, and not just in a statistical sense, but in the deeper sense of suffering from enormous and seemingly inescapable confounding effects.
    By the way, aside from their rare but serious side effects, and the evident confusion about their mode of action, what is wrong with liberal prescription of statins?
    Hi PubMed Diver–
    What’s wrong with liberal prescription of statins, eh.  Only that they are raising the cost of health care to us all.  Statins are extremely expensive – about $1300-$1400 per year – and most people who take them have drug cards as part of their insurance.  These increased expenses run all of our insurance rates up.  And the ‘rare’ side effects create more medical expenses that add to the burden.  All this could be justified if it reduced the all cause morbidity and mortality, but it doesn’t.  In only serves to cost us all more money for which we get very, very little in return.

  20. Even the Ads by gooooooooogle (top left) are in on the act!!
    But seriously… it seems all is clear to those who look for the real truth as in the letters above.
    Is there any research coming out of the knowledge that there is little useful benefit of cholesterol levels and CHD, in terms of:
    a) what IS increasing CHD in middle aged men in western cultures? and
    b) just how bad are polyunsaturated (+/- hydrogenation) fats that have become so integrated into supposed ‘healthy’ living over the past half century or so?
    Like your work, btw.
    Hi Toby–
    Sorry it’s taken me so long to post this–you got caught up in my spam filter, so I just found your comment today.
    First, I don’t really think CHD is increasing.  Deaths from CHD are falling, but CHD is kind of holding its own.
    Second, I think polyunsaturated fats of the omega-6 variety are dreadful in the amounts people typically consume today; trans fats are even worse. We don’t need any trans fats (of the commercially prepared variety–some of the naturally occurring ones, CLA, for instance, are actually good for us), but we do need a little omega-6.  Just not anywhere near the amounts we’re getting today.

  21. I have seen people die of heart disease. I believe it must have a cause. The current debate about dietary fat and cholesterol is very welcome, because it may show that what really counts is oxidized LDL, not the absolute level of native LDL.
    Has anyone heard of Sir Harry Himsworth, who was the first to show a strong link between sat fats and diabetes, way back in 1936? The huge historic rise in sat and trans-fat intake in industrial nations was noted by an astute Oxford biochemist, Dr Hugh Sinclair, who was aware of Himsworth’s findings, and who left the world a simple formula that explains chronic disease in the West.
    In his landmark letter to The Lancet in 1956, Sinclair proposed that a high dietary ratio of [Sat + Trans] to Essential Fatty Acids (EFA) might cause a vital deficiency of EFA in cell membranes throughout the body, including mitochondrial membranes.
    His ratio, also known the other way around, as the Poly/Sat, or P/S ratio, is rather clever, because it explains how fatty diet can oxidize LDL (without raising total LDL very much), and also oxidize the Good Guy HDL, rendering the latter dysfunctional and dangerous, as well as more abundant!
    What causes this crucial oxidation in vascular disease? Sinclair’s mitochondrial membranes, rendered EFA-deficient by fatty diet, are the most likely source of this oxidation, because EFA deficiency causes respiratory uncoupling in mitochondria–a potent source of superoxide free radicals and hydrogen peroxide, which easily oxidize lipoproteins, and also promote vascular inflammation.
    Those who (quite rightly) question the importance of dietary fat in heart disease must remind themselves that fat intake, especially from between-meal and late-night snacks, is seriously underestimated by most “Free Range Liars”!
    Animal experiments show quite clearly that fatty diet causes insulin resistance, reduced membrane unsaturation, raised glucose and insulin, increased triglycerides and blood pressure, obesity and inflammation.
    Sinclair’s cell membrane hypothesis, when applied to pregnancy, also explains the curious syndrome of chronic anxiety, Metabolic Syndrome and Deadly Lipid Triad, seen in 20-30% of Westerners. Fatty maternal diet (low P/S Ratio) in pregnancy causes gestational diabetes (or subclinical pre-diabetes), which are known causes of shyness (anxiety disorder) in the offspring.
    At least half of all Type 2 Diabetics and heart patients have this syndrome, showing as anxiety, visceral obesity, hypertension, glucose intolerance, and Deadly Lipid Triad (low HDL, small dense LDL, raised trigs).
    These are the ones who often simply drop dead, from anxiety-induced lethal arrhythmias; if they live and reach hospital, they will be noted as coronary cases whose total cholesterol was normal or only slightly raised–thereby starting a great argument.
    It is quite possible that such anxious folks do badly on low-fat, high-carb diets, which may raise their trigs even more. But their anxiety drives them to over-eat sweet fatty foods like chocolate, pastries and cakes, so in practice their hi-carbs are usually hi-fat too.
    What these folks need is a quick fix for their anxiety and their binge-eating, which will also cure the Deadly Lipid Triad. One simple molecule will do all this–the simple glucose isomer Inositol, abundant in all seeds, whole grains, nuts and legumes, and also found in citrus and rock melon.
    Inositol magically reverses anxiety by inhibiting Serotonin 2A receptors in the brain stress circuits, thereby stopping stress-related over-eating; and it raises HDL, and lowers trigs, by lowering peripheral stress hormone activity (less cortisol and noradrenaline).
    The world needs more Psycholipidologists, who will treat calm folks eating fatty diet, with a simple low-fat diet; but who will detect anxious cases (“Were you a shy child?”), and treat their Deadly Lipid Triad, their weight problem and their anxiety–all in one Big Hit–by recommending a low-fat, grain- and legume-rich diet. Problem solved!
    I wouldn’t say the problem is solved all that categorically.  In fact I don’t think a low-fat, grain- and legume-rich diet will solve the problem at all.  And I suspect that all the speculation on oxidized LDL is simply another ad hoc hypothesis to somehow salvage the lipid hypothesis. 
    I do agree that stress is a major cause of heart disease and should always be considered as a causative force.

  22. I am of the view that all this preoccupation with cholesterol has more to do with business than good science, and sad to say our conventional Doctors are going along with it. Best practice…who sets the agenda for best practice..it seems to me it is big pharma. I am also surprised that there is so little discussion here of the research that has been done over the decades concerning the proven relationship between vitamin c deficiency and atherosclerosis. The logic of this relationship, and the vitamin c status of those who do not consume mega doses of Vitamin c is inescapable, and to me and many others lies at the root cause of chd. Why do so many make a life’s preoccupation of analysing the cholesterol theory, when the much more rewarding vitamin c connection is there to very probably resolve the issue.
    I have researched the Vitamin C connection for the past 5 years and believing in it have followed the Linus Pauling recommendations and have taken between 10 and 20 gms per day together with 4 gm l-lysine and 1gm l-proline. I do also take a broad spectrum of other suppliment nutrients, following a MI in Feb. 2002. Blood tests, ecg, and echocardiogram confirmed. Angiogram showed complete blockage at bottom of LAD and 40% mid vessel in RCA. Over a period of 1 – 2 years all signs of MI resolved and I am now told following echo and ecg that my heart is normal function and that performance at ecg is that of a young fit person (14 mins 40 secs. standard Bruce test) with no deviations. I am 63 yrs. next month. I was initially on the usual meds. of Beta blocker, Ace Inhibitor, Plavix, Aspirin, Lipitor (10mg). All the meds. were the minimal doses. I have been taken off everything except the 75mg of Aspirin and the 10 mg of Lipitor. My blood pressure off BP meds. is now typically between 110/70 and 120/80 ish. Doctors have expressed surprise at the recovery made and my current status as being untypical, but only show mild interest when I tell them how I believe it was achieved. I despair sometimes, but keep propounding. Please give some time to studying this most probable cause of CHD and, if you become convinced as I, to promoting knowledge of it.
    Hi Liam–
    I’m happy that your coronary artery disease has improved, although it was unclear in  your comment whether you had had a bypass, a stent, angioplasty or medical therapy only.  I have spent a fair amount of time studying the vitamin C/heart disease issue.  As of yet, I’m not as convinced as you are of its efficacy.

  23. Thanks for the analysis!
    I found this link through the fasting yahoo group. Apparently, it references an article in the same issue, December 2006. I’ve been following a 19-hour fasting plan and was rather dismayed to read about IGF levels increasing with low carb, as I follow very low carb myself, under about 40 grams per day. Any comments you have about this research would be welcome! Again, it appears to be referencing the same journal of clinic nutrition, December 2006.
    Hi Jill–
    A couple of things…
    First, this report states that high levels of IGF-1 increase the growth of cancers that are already in place. At no point does it posit that IGF-1 causes the cancers in the first place. I would bet that a good quality low-carb diet, especially one followed on an intermittent fasting schedule would reduce the incidence of cancer formation, so the levels of IGF-1 are immaterial.
    Second, there is free IGF-1 and bound IGF-1. And there is a world of difference between the two. Free IGF-1 is the active hormone whereas bound IGF-1 in inactive. When one measures total IGF-1 levels one gets the sum of both the free and the bound hormone, which tells very little about what’s going on.  I haven’t looked at this paper in a while (and don’t have access to it right now since I’m traveling), but as I recall the researchers measured total IGF-1, not free IGF-1.
    Chronically elevated insulin levels as are found in those following high-carb diets cause the liver to make LESS IGFBP (IGF binding protein), meaning that there will usually be more free IGF circulating since there is less IGFBP for it to bind to.  This can lead to the situation where the total IGF-1 is low, but the free IGF-1 is high.  A low-carb diet that leads to less insulin drives the liver to synthesis MORE IGFBP, which means more bound and less free IGF-1.  This is a condition in which the total IGF-1 is high, but the free (or active) IGF-1 is actually low.
    I hope this clarifies things.

  24. Dr. Eades
    I have ALWAYS questioned the anti saturated fat campaign , just from the way a low saturated fat meal made me feel. Very hungry . bad mood , completely unsatisfied. I ALWAYS felt like crap after skim milk
    On the other hand berries and red meat , grass fed (the way nature intended with the n3 n6 ratios balanced) has me feeling great
    I always felt like crap after skim milk.
    I can’t believe anyone would be taken by this type of a “grasping at straws attempt to explain the cause of CHD”. Nature sure does not evolve to kill itself off. Saturated fat was available to our ancestors and they sure ate it. Along with leafy greens nuts fruits.
    To rail against a natural and healthy food source is beyond dumb. I mean its basic intelligence example – do Lipid Hypothesis proponents really think Bear Grylles would survive in the wilderness with no saturated fat and protein? Lipid Hypothesis proponents INVENT “paradoxes” and ignore the evidence of the Maasai, Dinkas , Samburu , French, Inuits , Tokeluans and many more .
    Take Care,
    Hi Razwell–
    You’re preaching to the choir.

  25. Whoever posted the bit about inositol and anxiety was spot-on. I couldn’t quite follow where the post went from fat to inositol, but between a low-carb diet and 5-7g/day of inositol supplementation, my panic attacks have been almost nonexistent.
    When I cheat, though, I get them bad… exactly 2 nights later. Perhaps the serotonin drop off that follows the spike?
    Hi Keenan–
    Thanks for relating your experience.  I guess I’ll need to read up a little on inositol.

    1. Insolitol as a lecithin is bio-available to humans. Insolitol in certain fruits. Not from grains or plants unless they are highly processed, or you are a ruminant.
      Interestingly enough, it’s been used to cut cocaine and treat anxiety.
      Once it was actually studied using randomized controlled trials(2004), it proved to be ineffective for depression, anxiety, bi-polar disorders. It really does appear to be ‘a spoonful of sugar’.

  26. I should add that they were only spot on about the inositol. The rest of the post seemed a bit ridiculous and the whole thing was completely incoherent.

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