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Anyone who is active on social media has come to expect a certain degree of tribalism around the issues of the day: guns, climate change, abortion, politics, and the like. We’ve been surprised to see it creep into the online conversation about nutrition science, especially the discussion about low-carbohydrate, high-fat diets. Even more surprising to us is that such advocacy sometimes comes from health professionals, scientists, and journalists, from whom we would normally expect a certain degree of objectivity.

These diets aren’t new. William Banting described in 1863 how a low-carbohydrate diet helped him lose weight, and since the 1970s the low-carb Atkins and South Beach diet books have sold millions of copies. Emerging data show that low-carb, high-fat diets can lead to reduced weight and better control of blood sugar, insulin, triglycerides, and possibly blood pressure. But they may increase cholesterol in the bloodstream, which has been associated with an increased risk of heart disease. That doesn’t necessarily mean low-carb, high-fat diets increase the risk of heart attack in everyone — or even in those with high cholesterol — because of the many potential benefits associated with these diets.

It’s a classic issue of balancing benefits and risks, one complicated because it isn’t clear if, how much, or in whom an increase in cholesterol even matters. That’s why there is general consensus that rigorous clinical trials are needed to answer this critical question.


The role of advocates who work on behalf of a cause or group can be essential to the success of these movements. But advocates also inflame the bitterness inherent in these battles. Given the current discourse in nutrition science, it can be hard to disentangle science from advocacy.

The idea that a dietary intervention might affect heart attack risk isn’t complicated or controversial. According to the cholesterol hypothesis, too much low-density lipoprotein (the so-called bad cholesterol) in the blood leads to its deposition in artery walls; the resulting plaque can block arteries and lead to heart attack or stroke. This theory has been bolstered by decades of evidence ranging from epidemiological associations to genetic studies and interventional drug trials. There may be no better studied pathway in modern medicine.


We believe in low-carb, high fat nutrition. One of us (E.J.W.) advises a company that uses this approach to treat individuals with type 2 diabetes and also recently co-founded a company using this approach for weight loss. The other (N.G.) uses low-carb, high-fat nutrition with her own patients and is the principal investigator of multiple studies of low-carb, high-fat nutrition in type 1 and 2 diabetes. We see this approach to nutrition as an exciting tool in the management of weight and cardiometabolic disease.

Yet we are disturbed by the discourse surrounding these diets, which often feels less like science and more like cheerleading. To be sure, nutritional tribalism is not limited to discussions about the relative merits or demerits of low-carb, high-fat diets. The evidence that nutrition has become a team sport is found in Twitter handles of individuals rooting for their favorite nutritional movement, such as small plant emojis in the Twitter handles of vegan advocates or a Ó in those promoting carnivore-type diets.

To bolster their cause for low-carb, high-fats diets, these advocates, including some scientists and doctors, claim that the cholesterol hypothesis is a conspiracy led by pharmaceutical companies in an effort to sell more drugs. Others have suggested that cholesterol may actually protect against cardiovascular disease. This goes on and on.

The effort to discredit the role of cholesterol in cardiovascular disease is striking because the evidence linking elevated cholesterol to heart attack risk is so strong. This makes us wonder why advocates might take this approach.

It’s possible that acknowledging an unknown risk might undermine or discredit the benefits of low-carb, high-fat nutrition. But that kind of thinking ignores a central tenet of medicine: Everything we do in medicine — from appendectomies to cancer chemotherapies to diet therapy — has benefits and risks. If a chemotherapy has a 10% chance of a side effect, that doesn’t make it any less likely to cure the cancer. So why would we treat the science of nutrition any differently? Perhaps because science has morphed into advocacy. Successful advocacy demands a clear narrative, yet science and biology are inherently gray.

The conversation about low-carb, high-fat nutrition is being painted as binary without room for nuance, when nuance is exactly what is required. The choice for individuals following low-carb, high-fat diets isn’t should they quit the diet or ignore the science. There are other choices, such as seeking testing to better define cardiovascular risk or taking a statin or other medication if needed. It’s also possible to change the types of high-fat foods in the diet, emphasizing those with unsaturated fats such as olive oil, salmon, avocado, or nuts while eating fewer foods with saturated fats such as butter, cream, and bacon. These approaches aren’t anti-low-carb, high-fat nutrition.

Nutrition science may be especially ripe for advocacy because of the linked epidemics of obesity and type 2 diabetes that so clearly stem from our changing lifestyles. And everyone has a stake in nutrition. But that is all the more reason we should be clear-eyed about what we know, even if what we know is “we don’t know.” We all have to eat, and make our choices based on imperfect evidence.

Of course, if a high-quality, large-scale, randomized control trial showed conclusively that the risks of the low-carb, high-fat approach outweighed the benefit, as health professionals and scientists we would accept that. In the other direction, if low-carb, high-fat diets were shown to protect against cardiovascular disease — regardless of their effect on LDL cholesterol — then that should be accepted and integrated into clinical practice.

We believe that the intrusion of advocacy into science has led to reductionism and the creation of false dichotomies. We believe that scientists, health care professionals, and journalists must avoid intentionally confusing or alarming the public in an attempt to discredit legitimate science, ultimately in the name of advocating for an agenda.

In addition to being dangerous, such ostensible advocacy appears to be an intentional attempt to degrade the public’s trust in science. One need look no further than the tragedy of the false story linking vaccines to autism as an example of what can and will result.

Nicola Guess, Ph.D., is a registered dietitian, associate professor of nutrition at the University of Westminster in London, head of nutrition at the Dasman Diabetes Institute in Kuwait, and a director of CityDietitians, a private clinical and consultancy company based on London. Ethan J. Weiss, M.D., is a preventive cardiologist and associate professor of medicine at the University of California, San Francisco.

Guess reports having received research or fellowship funding from Diabetes UK, the Medical Research Council, Diabetes Research and Wellness Foundation, American Overseas Dietetic Association, Chronic Disease Research Foundation, Winston Churchill Memorial Trust, and Oviva, and speaking or consultancy fees from Sanofi, Boehringer Ingelheim, and Fixing Dad (a low-carb app). Weiss reports having received research funding from the National Institutes of Health, Pfizer, and Lilly. He is an advisor to Virta Health and a co-founder and advisor to Keyto, Inc.

  • “This theory has been bolstered by decades of evidence ranging from epidemiological associations to genetic studies and interventional drug trials. There may be no better studied pathway in modern medicine.” Every RCT has failed to bolsterd this theory. Look at the data, not the author’s biased conclusions.

    The WHO committee declaration that meat is a carcinogen is based mostly on confounded food-survey epidemiological studies. These WHO members are a tribe of vegetarians and vegans.

  • Carbohydrates directly cause obesity, cancer, heart disease, liver disease, diabetes and dementia (brain shrinkage).

  • I eat very few processed foods with a low-carb diet. Could it be that the grain and processed food industry has for decades used lobbying power over politicians and government regulators, pushing the high carb/low fat diet for monetary rewards? My guess is that the profit margin just isn’t very high on unprocessed vegetables, fat, and meat.

    • If you look back at what the nutrition doctors handed to the government back when the first food pyramid was established, a politician committee took that model and spit something else out entirely. pressured by lobbyists.

      You’ll also find sugar companies that those that make sugary products (like coke) funded research and counter research to blame fat for the rise in obesity, diabetes, etc. Now its so ingrained that we should eat lots of bread/pasta/rice/potatoes that even after my friends saw me lose 95lbs and turn my blood pressure, blood sugar, and LDL down to extremely low levels, they still won’t try my LCHF diet. And they think they’re eating “whole grains” when they aren’t eating wheat berries and whole groats unless they are ground up into a fine flour.

      My diet is simple: drink water with an exemption for my morning coffee with cream and sugar (takes me over a year to go through a bag of sugar), don’t eat foods with a high glycemic index (whole groats are 50GI, instant oatmeal is 70, white table sugar is 67) which brings me to the form of the food as much as whats in it. I drink no shakes or smoothies or in the above case, groats that have been steamed and rolled, etc. Whole cuts of meat, whole vegetables, raw if that works, and an occasional piece of whole fruit, and blueberries. Cook with avocado oil for high heat and olive oil for cold/low heat foods, and plenty of irish grass fed butter. No potatoes, rice, pasta or finely processed foods. And if you look at the nutritional profile of brown vs white rice, you’ll see there’s barely any difference. I WILL make pasta but its about half a cup or less with a nice sauce full of vegetables and sausages, meatballs or a meat sauce. I WILL put my thai curry full of veggies, meat and coconut fat over a quarter cup of rice.

      The trick is avoiding drinking 1000 calories a day without really thinking about it, eating high GI foods that spike your blood sugar, and eating foods such that it’ll take a while for them to digest and release calories and nutrients.

  • For years I gained a pound or two a year and then 40 after a back injury.

    Over the years I did vegan, vegetarian, low fat, ornish, and everything else.

    Then I tried low carb. Loved what I was eating and I lost 95lbs in six months. 20 of it crept back in because I started eating pasta, rice and bread a little and I just went back to <100g of carbs per day and lost 30lbs in two months.

    Now I have to buy all new clothes…

  • Very well put. This is exactly how I feel about the climate change that is being rammed down our throats.

    • James, this is a false dichotomy. The nutrition science is far from settled. The science of climate change is absolutely settled to anyone who isn’t using motivated reasoning. Questioning climate change/global warming is akin to challenging that HIV causes AIDS. Sorry, but it’s just plain denialism.

    • James, I hope you’ve given more thought to nutrition science than you have to climate science.
      Yes the saturated fat and cholesterol expert advice was badly wrong, and had unintended consequences, but that doesn’t mean that man didn’t land on the Moon, that smoking doesn’t cause lung cancer, that Al Qaeda didn’t attack the Twin Towers, and so on.
      One thing being right or wrong doesn’t have any bearing on the truth of other, unrelated things.
      But let’s keep them unrelated – I for one would like to see everyone who is or has been wrong about animal fat shut up about planetary health – the climate scientists would be a lot more convincing without them.

  • Damned if you do or damned if you don’t. You’re going to die of something or another, so as always, what do you have to lose,
    pun intended. 🤘

  • While I agree with the basic premise of your contentions, the fact that you seem to be focusing your rhetoric on one-side of the advocacy discussion tends to give your arguments a ring that sounds like bias, if not outright hypocrisy.

  • It’s a mistake to think that, because LCHF diets that are plainly life-saving can raise LDL (they only really do this to any great extent in healthy people – the higher the risk, the more likely it is that they’ll lower LDL, and I’d like to see research into why this difference exists), that therefore a drug that lowers LDL is always bogus.
    Statins block the cholesterol synthesis pathway stimulated by excess insulin and leptin – so whatever their different effects on LDL, statins and LCHF are working in similar beneficial ways to lower the intracellular cholesterol pool when it’s been over-driven by excess energy. The difference is that LCHF, by lowering insulin, TGs and glucose, also decreases macrophage cholesterol retention and optimises reverse cholesterol transport (This can be clearly seen if we use the atherogenic index of plasma as our marker of RCT activity – again, the movement of cholesterol under different metabolic conditions is something that can usefully be researched).
    To some extent the LCHF pushback against statins exists because statins are being oversold by advocates and pushed in the media by zealots with little sense of nuance or context or much curiosity as to why their drugs work or not. This emphasis makes LDL cholesterol a shibboleth in contexts where it ought to be irrelevant – when the healthiest of the healthy are being offered drugs, something has gone wrong.
    LDL cholesterol rises a great deal during a fast in healthy people – no-one has ever suggested that fasting causes atherosclerosis. It rises when healthy people eat fats with myristic or lauric acid, yet these saturated fatty acids have more beneficial associations with CHD than the saturated fatty acids that do not raise LDL. This list can go on – coffee, SGLT2 inhibitors. However, some heavy metal toxins may raise both LDL and the risk of CHD, as do some genetic variants that also interfere with LDL trafficking.
    The efficacy of statins, which seems real enough in secondary prevention, if overstated for everyone else, seems to have nailed in place a well-outdated prejudice against doing anything that might increase LDL. But this is a case of false equivalence; for example, in the diet-heart RCTs there was no benefit, for CVD or all-cause mortality, from lowering LDL across similar time periods as those showing benefits from doing the same with statins.
    Interventions that could have raised LDL by increasing fat-burning simply weren’t tested. However, when epidemiologists have pooled the existing low-carb trial literature for CVD outcome data, there is none, which is not a signal indicating high risk.

    • Nigel, is this really a spot for sealioning?
      Ethan and Nicola haven’t made their article heavy on citations. They are intelligent enough to know what I’m talking about, and I trust curious enough to check anything new and question why things should be so.
      As for most of the other people in this thread, they couldn’t even read the article clearly, so what would they want with citations?
      They are backing the right horse, for the right personal reasons, but with all the wrong arguments.
      The best I can do is give them facts to go on with, in the hope that this stimulates someone’s curiosity.

    • As sealioning is expecting citations to support personal preferences (e.g. “I can’t stand sealions”), I’m not sealioning, but thanks for the strawman. I’m talking about *you* (and other commenters) making claims, unsupported by citations.

      As for LCHF/keto saving lives, *any* diet which eschews the overconsumption of over-refined/processed food products saves lives.

      I’ve linked to multiple citations which show that LCHF/keto isn’t the panacea it’s made out to be. Are you going to try to refute any of my evidence, or just continue giving unsupported opinions?

      They are backing the wrong horse & Ethan J. Weiss has trashed his carbohydrate tolerance (see #5 in my list) i.e. made himself *less* metabolically flexible. This is supposed to be an improvement?

  • Yes, never mind that some studies, including those done by some leading universities, have been funded and rigged by companies that would lose money if keto was to go mainstream.

    To add, your argument that more studies are needed doesn’t hold any water. People have for centuries experimented on themselves and others with little to no concern if what they are doing is detramental to their health. Now you feel you must stop people from finding a solution to their health issues because there is not enough studies confirming benefits of high fat, low carb diet.

    Your honesty is suspect.

    So why are there no major universities and corporations funding these studies? Most of your argumenta are studies done to just reiterate same old that got us where we are with obesity epidemic.

    Your article doesn’t propose any solution to those struggling to lose weight.

  • You have to understand that LDL cholesterol isn’t the problem, and in fact your liver naturally makes LDL cholesterol for its bodily needs. It’s when that LDL cholesterol gets oxidized that it becomes an issue.

    Hyperinsulinemia & hyperglycemia can both oxidize your cholesterol, both of which could be resolved with a ketogenic diet & intermittent fasting. Other things keto folks avoid such as vegetable oils, trans fats, and margarine can also oxidize your cholesterol. Also, the nature of saturated fats (such as butter) make them heat-stable and thus are much more resistant to oxidation compared to unsaturated fats and oils when cooked.

    The villain here was never LDL cholesterol, but its oxidized counterpart. It’s actually a bit scary how bad even mildly oxidized LDL is for you.

    A study in this video found, ‘mildly’ oxidized LDL cholesterol is almost as bad as LDL cholesterol which has been massively oxidized with copper:

    “…so the took the L1, L2, and L3 [non-oxidized LDL cholesterol] from both people and it did not cause any endothelial distress.”

    “…[minimally oxidized LDL] killed 40% of the endothelial cells in culture.”
    “So they then got LDL and oxidized with copper and massively oxidized it and they found out it only killed around 45% of the cells.”

    The endothelial cells are the cells that line the inner surface of your blood vessels.

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