Thursday, 30 November, 2023
HomeDigital ClubbingLess lore and more science, please, Prof Noakes

Less lore and more science, please, Prof Noakes

NoakesProfessor Tim Noakes’ Lore of Nutrition is an extraordinarily heady mix of conspiracy theory, bad science, bad writing, and persecution complex, writes Dr Alastair McAlpine, in his first occasional column for MedicalBrief.

McAlpine writes: “The world of nutrition has become so polarised and vicious, that it really is difficult for members of the public to know what they should – and should not – be eating. What is desperately needed is leadership from a prominent scientist to cut through the white noise, identify the strong and weak points from all sides, and coalesce the good science into a guide that begins to lift the haze of confusion from nutritional science.

“Sadly, Lore of Nutrition, by Tim Noakes and Marika Sboros, isn’t that leadership. The same issues that have plagued Noakes’ recent career, plague the book.

“The conspiracy theories run thick and fast, the victim card is played extensively, the science is cherry-picked and unrepresentative, and the conclusions questionable. On top of this, a malicious streak runs through Lore of Nutrition: anyone not directly supportive of Noakes is a shill, an apologist for Big Food/Big Pharma, or an idiot. There simply isn’t room for legitimate disagreement in the world of Noakes, and this is unfortunate, because in among the nonsense, there are some genuinely interesting ideas that deserve exploration.

“The book begins properly with a description of Noakes’ ‘Damascene’ conversion to the low-carbohydrate, high fat (LCHF) diet in 2010. Not only did he lose weight, but his running improved, his headaches stopped, and his indigestion vanished. The diet cured his allergies, his bronchitis, his asthma, and improved his vision. He also stopped snoring. His explanations for these range from the prosaic (he lost weight, so had less neck fat, and therefore stopped snoring) to the bizarre (he claims a wheat gliadin allergy causes headaches – but a quick PubMed search revealed no studies to confirm this, and Noakes’ claim that 30% of us may have the medically-contested non-coeliac gluten sensitivity [NCGS] is not supported by his own citation, which estimates that its prevalence is slightly higher than 1%. This major misquoting of his own references occurs frequently. See below.

“Most of the rest of the section deals with the ‘push-back’ that Noakes experienced prior to the tweet that got him into trouble. This started with a letter written by prominent cardiologists and lipidologists expressing concern about the diet, to the UCT centenary debate against his ‘arch-nemesis’ Jacques Rossouw, to the University of Cape Town itself distancing itself from his views, to a letter from some cardiologists denouncing the LCHF diet and expressing concerns about Noakes’s ‘statin denialism.’

“What emerges from these chapters is that Noakes was clearly deeply hurt by the attitudes and actions of his colleagues and his university. He rails against academic bullying, and spends pages targeting cardiologists and their ‘unnecessary’ practices. But some general themes emerge here that are pervasive throughout the rest of the book: Anyone who criticises Noakes or his ideas has an agenda beyond mere scientific scepticism, or is simply too stupid to understand the brilliance of his ideas. Professor Dirk Blom, for example, is targeted, because he has done studies on statins (the evil, evil man).

“Dr Martinique Stilwell, who wrote a critical article about Noakes, is accused, without a shred of evidence, of having formed a ‘game plan’ with UCT critical thinking lecturer, Jacques Rousseau (the aim of this ‘plan’ is never elucidated, and Rousseau has, in his blog, declared that he barely knows Stilwell, having only briefly met her twice). Professors Bongani Mayosi and Lionel Opie, and essentially the entirety of the medical profession, are part of a bizarre ‘omerta’ (vow of silence) to suppress the truth. Why so many esteemed and decorated academics would willfully suppress information that could benefit their patients is anyone’s guess.

“While conflicts of interest (COI) in science are real, and have been shown to influence the results of studies, to assert that an expert cannot be trusted simply because he or she has accepted money to perform an industry-funded trial, without actually demonstrating any bias, is lazy science. The charge could equally be turned on Noakes (in fact it was, when an editorial of his was withdrawn due to his failure to disclose his COI), and this book could be dismissed based on the idea that Noakes and his foundation make money promoting the LCHF diet. It would be unfair to do so, but Noakes frequently employs this tactic to dismiss his colleagues.

“Noakes also fails to acknowledge his own role in the poisoned relationship between some of these professionals, including his own ‘academic bullying’. Noakes famously ‘fat shamed’ respected UK-based dietitian Catherine Collins, tweeting that he would ‘believe her when she lost weight’. He has consistently sneered at other ‘overweight dietitians’, and has erroneously claimed that the profession is in the ‘pocket of Coca Cola’. He frequently derides sceptical medical colleagues as ‘The Anointed’, and ‘Statinators’, while claiming that people like Australia’s celebrity chef, ‘Paleo’ Pete Evans (who bizarrely thinks that drinking milk ‘sucks calcium from your bones’) knows more than most MDs.

“This segues into the next section, and one of the overarching themes of the book: That the current diet-heart hypothesis – where whereby cholesterol, specifically low-density lipoprotein (LDL) cholesterol, which is considered a primary cause of atherosclerotic cardiovascular disease (CVD) – is the ‘biggest mistake in modern medicine.’ Now let’s be clear: it is entirely possible that the harms of saturated fat over the past few years have been exaggerated, and that it is not as bad for us as previously thought (The recent PURE study showed no association between saturated fat intake and CVD or mortality).[1] It is also likely that how much saturated fat we eat has less effect on LDL levels than previously anticipated.

“But to claim that this link has been ‘destroyed’ is to misrepresent the best evidence we have, which is that saturated fat may be harmful, and that keeping its consumption low, while eating other, healthier fats, is probably the best way to go at present. As for LDL, its link with CVD is extremely well described, and accepted by every heart association on the planet. While there are certainly elements that are unknown (the effect of smaller vs. larger particles, the effect of apoB, the effect of triglycerides, etc.), to describe LDL as being unrelated to heart disease is to come off as being dogmatic, rather than reasonable. To wit, a recent consensus statement, released by the European Atherosclerosis Society, which examined over 2m participants, in many different study types, over 20m person years, showed that LDL ‘unequivocally causes CVD’.[2]

“The bad guy in all of this is Ancel Keys, who developed the idea that saturated fat causes heart disease through his famous ’seven countries’ study.[3] Noakes (and Sboros) go out of their way to claim that his study is invalid because it ignored the data from 15 other countries, but fail to realise that even with the data from those other countries included, the correlation, despite what Gary Taubes has repeatedly said, still holds, and is significant (p=0.02).[4]

“Further studies are trotted out, such as the Lyon Heart Study, which showed that a Mediterranean diet was superior to a standard low fat diet, but Noakes conveniently ignores the fact that the Mediterranean diet was lower in fat than the standard one (30% vs 32%), and that carbohydrate consumption was similar (52% vs 51%). He claims that Bueno’s recent meta-analysis[5] showed the superiority of LCHF vs Low Fat, but fails to mention that the difference in diets at one year was on average less than a kilogram, with a significant increase in LDL on the LCHF diet. Was this weight loss difference statistically significant? Yes. Clinically significant for someone with obesity? No.

“He states that many people have ‘normal’ cholesterol levels at the time of heart disease diagnosis, but fails to point out that a drop in serum cholesterol levels immediately after an episode of cardiac disease is well described, which confounds much of the data.[6]

“His second big theory is that arterial, and many chronic, diseases are caused by insulin resistance (IR), which is exacerbated by carbohydrate ingestion. The high levels of insulin prevent fat from being released from cells and provoke constant hunger, he writes. This causes obesity, and fat deposition, especially in the liver, resulting in the development of non-alcoholic fatty liver disease (NAFLD), which then causes dyslipidaemia, and arterial disease, including heart attacks.

“There are a number of problems with the insulin-obesity hypothesis, but Noakes never addresses these.

“Firstly, there are multiple studies[7,8] that show weight loss is possible on diets that provoke high insulin levels. One of these was done by David Ludwig, a fellow low-carb advocate, which makes the likelihood of industry tainting quite low. Second, studies that look at the obese show an increased release of fat from the adipocytes compared to the lean.[9] This contradicts the idea that hormones like insulin are ‘trapping’ fat in cells. There is also the inconvenient fact that in many countries (like China and the UK), sugar and carbohydrate consumption has fallen in recent years, but obesity continues to rise. Finally, a recent study by Kevin Hall showed that there was no intrinsic metabolic advantage to low carbohydrate diets, which is fairly devastating to the insulin-obesity hypothesis.[10] Noakes responds in LoN that the advantage lies not in an altered metabolism, but in increased satiety. He does not offer a citation to back this up, and the evidence I found suggests that both carbohydrate and fat have similar effects on satiety, with only protein really suppressing it.[11] There is also evidence that low fat diets offer better satiety control than LCHF, especially in the early stages.[12]

“The ‘NAFLD causes dyslipidaemia idea’ is also complicated by the fact that the relationship is bidirectional,[13] often making it difficult to tell which came first, the dyslipidaemia, or the NAFLD. More research is ongoing, but the point remains: Noakes’ description is oversimplified, and potentially wrong.

“The second part of the book is written by Sboros and covers the Health Professions Council of South Africa (HPCSA) trial over his tweet that advised weaning infants from breast milk to the LCHF diet. Sboros covers proceedings blandly but methodically. It should be noted that there is simply no way this tweet was worthy of the attention paid to it by the HPCSA, and their bizarre insistence that he was entering a ‘doctor-patient relationship’ by responding is nonsensical, and was appropriately demolished by Noakes’ lawyers.

“Sboros and Noakes clearly believe that there were dark games and hidden agendas afoot, and there may have been, but her description leaves one mostly convinced that the HPCSA was simply over-enthusiastic, and woefully underprepared, rather than engaged in the world’s most inept conspiracy. There is apparently a ‘smoking gun’ in the form of an email chain tantalisingly mentioned at one point, but we are never actually exposed to these, making it difficult to know how damning they are.

“A few points need to be covered here. Firstly, Noakes does some major goal post shifting in justifying his tweet. He claims that when he said ‘LCHF’, he assumed that people would know he just meant ‘real food.’ But he spends large swathes of the book telling us he doesn’t think saturated fat is bad, and that it is not causative in any health problems. So to then claim that when he said they should go ‘LCHF’, he didn’t mean to imply that infants should go on a diet high in saturated fat, is simply disingenuous.

“Second, the whole concept of ‘real food’ needs to be addressed. Some LCHF advocates use it synonymously with the LCHF diet, and Noakes himself is evidently fond of the phrase, but the point remains that the term itself is meaningless.

“It is never properly defined, and for good reason. If your definition is ‘unprocessed food and drink’, then butter, sausages, milk, beer, coffee, and wine are all out. If your definition is ‘doesn’t come in a box or a tin’, then you’ll have to explain why this disqualifies some foods which have almost identical nutritional qualities to their untinned counterparts.

“Perhaps for these reasons, Noakes never offers an explanation of what ‘real food’ really is, but his appropriation of the phrase to replace ‘LCHF’ when he feels like it is cynical in the extreme (Noakes is not alone in this. The phrase is consistently used in LCHF circles, without any sort of attempt at a definition.)

“The final section is called, ‘The Science’, and is perhaps the most disappointing of the three. There isn’t enough space to cover all the problems with this part here (it would probably require a book), but some examples may suffice.

“He begins by misunderstanding evolution when he claims that we were ‘designed’ (we weren’t designed; we evolved) for ‘carnivory’ (sic). This is odd, considering the many enzymes in our gut, like lactase, maltase and sucrase, whose sole purpose is for carbohydrate metabolism. Our molars have evolved for grinding grass and grains, and our relatively long short intestine mirrors other omnivores. In all, anyone looking at the history of human evolution would draw one conclusion: we evolved to eat both meat and carbohydrates.

“He also misunderstands our sociological history. Noakes claims we evolved as meat-eaters because we hunted ‘big prey’ for their nutritious meat and fat, but as Noah Yuval Harari demonstrates in Sapiens, up until 70 000 years ago, humans languished in the middle of the food chain, eating small rodents, insects, and tubers. We were predominantly the ‘hunted’, not the ‘hunters’. There simply hasn’t been enough time to evolve from this omnivorous diet to a predominantly carnivorous one, as Noakes claims.

“He then trots out a whole bunch of hoary old colonial ‘experts’ to show us that back in the day the good old ‘natives’ were super healthy, didn’t have cancer, lived long lives, etc. This is odd because early on in the book, Noakes says that ‘observational studies’ cannot prove anything, or demonstrate causation, yet he essentially uses the ‘observations’ of a few individuals to prove how healthy our old diets were.

“One of his ‘experts’ (Weston Price) has already faced accusations in the literature of promoting the myth of the ‘healthy savage’. It is disappointing that Noakes extends these. The notion, however, that all chronic disease and cancer can be linked to insulin resistance and the current diet is simply nonsense. Cancer exists in all societies, and occurs in everyone from babies to old men. But cancer occurs most commonly in the elderly (50% in folk over the age of 70). The likeliest reason these ‘experts’ didn’t see any cancer in these societies is because, firstly, people died of things like pesky infectious diseases before they contracted it and, secondly, everyone with cancer probably died fairly quickly.

“He also talks about how ketones for the baby brain are ‘essential’. There is simply no evidence for this. The fact that infants move in and out of an extremely mild state of ketosis is likely due to the lack of consistent feeds in early life. The ketones are a ‘back up’ mechanism, but Noakes makes the mistake of assuming that because they are there, they must be good. Even if it were true, it remains factual that glucose is the primary fuel source for the infant brain, which is why breast milk is high fat (3-5%) and high carb (7%).[14]

“These are but a few of the issues in this section. He legitimises pseudoscience by endorsing diagnoses that don’t exist (‘Leaky Gut Syndrome’), promoting fake statistics (that child health in SA is deteriorating. In reality, the under-five mortality rate is improving) and advising against exercise for weight loss (which is baffling as the evidence is clear: a combination of diet and exercise is the key to losing weight). What is disappointing is not that Noakes sometimes gets the science wrong, but his refusal to even present the counter-arguments, or legitimate concerns, about his viewpoints. What we are left with is not so much a review of the ‘science’, but Noakes’ take on the science, with cherry-picked articles and unsubstantiated conclusions.

“Noakes should be commended, however, for alerting us to many issues that may have remained hidden. It is now abundantly clear that the low-fat diet is a poor option for many, especially when products that contained fat were neutered by the addition of sugar to replace that fat. Similarly, for many, the LCHF diet works very nicely, and seems to be well tolerated. We’ve always known sugar was bad for us, and while Noakes goes overboard with his claim that it is ‘addictive’ (evidence is weak and conflicting), the fact that many of us are relooking at the amount of sugar we consume can only be positive. Finally, the trial has shown that the HPCSA, as an organisation, needs to strongly look at its archaic attitudes towards social media, and what it spends its money on. From start to finish, the trial was an unfortunate circus. There are serious issues that the HPCSA should be focusing on; spending millions going after a silly – but fairly harmless – is is not one of them.

“Finally, a note on Noakes’ references. They are shoddy. In many instances, the references are quoted incorrectly, or he makes extrapolations beyond the scope of the study cited. Both he and Sboros link to YouTube videos and quack conspiracy websites (Like Russ Greene’s frankly bizarre conspiracy article on Coca Cola). For a book that purports to be the ‘final word’ on nutrition, this is especially disappointing.

“In all, Lore of Nutrition could have been a valuable addition to nutritional knowledge from a respected scientist and journalist. Unfortunately, it comes off as an awkward mishmash of ideas from two individuals who simply cannot conceive that their paradigm is flawed. The HPCSA trial against Noakes was clearly a farce, but rather than allow him time to reflect, it only seems to have made him even more dogmatic. If you’re a devout Tim Noakes fan, you’ll lap this up, I suspect. The rest of us, sadly, will be hoping for less ‘Lore’ and more ‘Science’ in the inevitable sequel.”

Declaration of interest: I should declare that I have been a state doctor my entire career. I have no ties to any pharmaceutical companies and I have never even entertained a drug rep. I have no books to sell and no profits to be made from this review or my position.

Follow McAlpine on Twitter @AlastairMcA30

[link url=""]1. Dehghan M, Mente A, Zhang X, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017;390(10107):2050-2062.[/link]
2. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-2472.
3. Keys A, Taylor HL, Blackburn H, Brozek J, Anderson JT, Simonson E. CORONARY HEART DISEASE AMONG MINNESOTA BUSINESS AND PROFESSIONAL MEN FOLLOWED FIFTEEN YEARS. Circulation. 1963;28:381-395.
[link url=" (accessed 5 January 2018)"]4. Minger D. The Truth About Ancel Keys: We’ve All Got It Wrong 2012.[/link]
[link url=""]5. Bueno NB, de Melo IS, de Oliveira SL, da Rocha Ataide T. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. Br J Nutr. 2013;110(7):1178-1187.[/link]
6. Fresco C, Maggioni AP, Signorini S, et al. Variations in lipoprotein levels after myocardial infarction and unstable angina: the LATIN trial. Ital Heart J. 2002;3(10):587-592.
7. Sichieri R, Moura AS, Genelhu V, Hu F, Willett WC. An 18-mo randomized trial of a low-glycemic-index diet and weight change in Brazilian women. Am J Clin Nutr. 2007;86(3):707-713.
[link url=""]8. Ebbeling CB, Leidig MM, Feldman HA, Lovesky MM, Ludwig DS. Effects of a low-glycemic load vs low-fat diet in obese young adults: a randomized trial. Jama. 2007;297(19):2092-2102.[/link]
[link url=""]9. Makimura H, Stanley TL, Suresh C, et al. Metabolic Effects of Long-Term Reduction in Free Fatty Acids With Acipimox in Obesity: A Randomized Trial. J Clin Endocrinol Metab. 2016;101(3):1123-1133.[/link]
[link url=""]10. Hall KD, Bemis T, Brychta R, et al. Calorie for Calorie, Dietary Fat Restriction Results in More Body Fat Loss than Carbohydrate Restriction in People with Obesity. Cell Metab. 2015;22(3):427-436.[/link]
11. Rolls BJ. The role of energy density in the overconsumption of fat. J Nutr. 2000;130(2S Suppl):268s-271s.
[link url=""]12. Hopkins M, Gibbons C, Caudwell P, Blundell JE, Finlayson G. Differing effects of high-fat or high-carbohydrate meals on food hedonics in overweight and obese individuals. Br J Nutr. 2016;115(10):1875-1884.[/link]
[link url=""]13. Ballestri S, Zona S, Targher G, et al. Nonalcoholic fatty liver disease is associated with an almost twofold increased risk of incident type 2 diabetes and metabolic syndrome.
14. Ballard O, Morrow AL. Human milk composition: nutrients and bioactive factors. Pediatr Clin North Am. 2013;60(1):49-74.

MedicalBrief — our free weekly e-newsletter

We'd appreciate as much information as possible, however only an email address is required.