Reading Time: 5 minutes

So apparently Paul Saladinos and Mikhaila Peterson have recently been talking about me on a podcast.🤨

I haven’t had a chance to listen to the podcast, and I probably won’t. But apparently it had something to do with my statements that the benefits of the carnivore diet are caused by calorie restriction.

So I will make my thoughts clear about this. There are probably five main mechanisms of the carnivore diet.

Calorie restriction
Antigen elimination
FODMAPs, etc.

First. Calorie restriction.

People might remember that @joerogan brought up that point with Mikhaila. @chriskresser agreed on a later podcast. And so did @foundmyfitness on yet another later podcast.

So I’m not alone.

Why? Because calorie restriction has long been robustly associated with anti-inflammatory effects. For instance, here from CALERIE 2:

And this is only CHRONIC calorie restriction, producing a lean body type. Chronic calorie restriction causes chronic reductions in inflammation.

But what’s more, there is a long literature on the ACUTE effects of fasting on rheumatoid arthritis. You can find that literature here:…

In a word, fasting has long been known to acutely cause remission of the symptoms of rheumatoid arthritis and other autoimmune conditions, almost immediately. Start fasting, and watch the symptoms disappear. It works for many people.

Of course it is not sustainable in the long-term without periodic refeeds, which will cause symptoms to return.

What are the mechanisms for this? It could be ketones. There is a conflicting literature on the supposed anti-inflammatory effects of ketones, which I am writing about for a review right now.

It could also be inhibition of many anabolic/inflammatory proteins associated with lower cellular energy levels.

It could also be the withdrawal of an antigen that the body responds to too strongly.

We do not know, but calorie restriction has profound anti-inflammatory effects and would be expected to help substantially for people with inflammatory conditions.

Incidentally, a ketogenic diet might also mimic some of the effects of the fasted state, and in doing so, might have an important therapeutic benefit for autoimmunity–similar to how it does for epilepsy.

But this still remains speculative. A definitive test for this might be done in a clinical trial:

A ketogenic diet
A diet that is carbohydrate-restricted with a very low glycemic load but no ketosis
A baseline diet with supplemental ketone esters
A baseline diet

Run it in random crossover format and watch the symptoms. Maintain stable bodyweight. Make sure the diets are as identical as possible except for the characteristics above.

An RCT like this would pick apart the antigenic effects, versus the ketotic effects, versus the glycemic effects, versus full ketosis. Somebody write a grant~

A pilot would just test ketogenic versus baseline diet. Anyway…

Mechanism two. Protein.

Protein has profound metabolic effects. It increases lean muscle mass. It causes isocaloric remission of fatty liver. It promotes improved overall body composition.

Through these mechanisms, protein is also anti-inflammatory. More muscle and less liver and muscle fat will increase the “energy sink” of the body, and this will increase the homeostatic regulatory capacity of the body in response to energy intake, i.e. smaller post-prandial fatty acid and glucose spikes. This will spare the cardiovascular system and the immune system will secrete fewer inflammatory molecules. The brain will “feel” this. So will the joints, etc.

How BIG the impact of this is is anyone’s guess. We don’t know.

However, a caveat: it probably depends on the source of protein.

Three. Antigenic restriction.

This one is obvious. The carnivore diet is hypo-antigenic. It is an elimination diet.

We have long known that elimination diets, e.g. the Elemental Diet, can be used to successfully treat inflammatory conditions. See:…

The Elemental Diet is kind of like Medical Soylent. It is all the nutrients a person needs, but with no proteins–just dissociated amino acids. No complex carbs either–just glucose, etc. And vitamins, fatty acids, etc.

It is as hypo-antigenic as a diet can be.

I remember my Master’s advisor telling me about the elemental diet when I was a Paleoish Internet diet warrior. I was appalled. OMG NOT REAL FOOD.

It doesn’t matter.😆The point is that restricting antigens works. We know that.

Four. FODMAPs.

Fermentable oligosaccharides, disaccharides, monosaccharides and polyols, or FODMAPs, are carbohydrates in many plant foods that irritate the gut and cause inflammation. When restricted, they can treat irritable bowel syndrome, see here. FODMAPs and other carbohydrates like fiber might also modulate gut immunity in ways that science still has a long way to understanding.

Five. Placebo.

We know that the mind has a profound impact on immune function, predominantly via the vagus nerve. Example:

A really great book discussing this is Jo Marchant’s Cure. Highly recommended.

Incidentally, the same might be true for weight loss. Witness:

I do think that placebo might have a profound influence on how a diet is experienced. If a diet is expected to be anti-inflammatory, I do wonder if it might in fact be anti-inflammatory.

There is a psychological defense mechanism called conversion. I used to experience it. When I was a child, I used to have seizures. When the doctors gave me an EEG, we found that I was not having seizures.

I was having pseudoseizures. Thus the moniker “conversion”: conversion of psychological stress into bodily symptoms. According to psychoanalysts, conversion is an immature, narcissistic psychological defense. It focuses on the self.

So from my own personal experience, I really believe in the mind-body connection. It can be profound. It can create profound distortions in experience.

Jo Marchant’s book shows that these effects can extend beyond the psychological and manifest in physical illness (or cures) via modulation of immunity.

So these are my 4 mechanisms that I would hypothesize personally.

The reason this is important to talk about is that, once we know the mechanisms, we can then change and optimize the diet and have people helped even more by it.

There are stories floating about of people on a carnivore diet who are refusing statins but continuing to have CVD progression.

What if the carnivore diet does not work for everyone and could be harmful for some people? Does Mikhaila think that is possible?

If so, what if we could get all of the benefits of the carnivore diet by isolating mechanisms without some of the potential downsides?

I still strongly suspect that the high red meat content is not optimal. Red meat might be nutritious in some ways–sure–but I strongly suspect that large quantities are probably not optimal for whole body oxidative stress and cardiovascular disease risk.

So if we can pull apart the mechanisms and determine which are helping people on the carnivore diet, then we can use these mechanisms with more flexible dieting strategies, producing the same effect with fewer downsides.

Let me add one last thing.

There is a big difference in worldview between most doctors and many carnivore dieters (the same could probably be said of many plant-based dieters, etc.).

For the medical way of thinking, every intervention has benefits and risks. There is no perfect intervention. Knowing the mechanism of an intervention allows us to get rid of everything else that is not relevant to the mechanism, and thus reduce potential harms.

Thus, mechanisms are necessary to explore to try to maximize the benefits while minimizing the risks.

On the other hand, among many people in various dieting communities, lifestyle interventions are “wholly good”.

I don’t believe anything that humans do is wholly good. There are good and bad parts.

It is true that there are some things that humans do that are better than other things.

But I don’t think there are many “final goods” that solve all problems with no downsides, and I think we should be skeptical of anyone who claims to have found such a good.

And I think we are right to be skeptical. And I think if anyone says we shouldn’t be skeptical, that we should just believe–well, that is very problematic to say the least, and it is a lot like religion.

Science says that we should explore and understand. That is what I think we should do.

That is all.

This post was adapted and edited with some additional content from a popular Twitter thread, here.


Support me here.

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.


Reading Time: 6 minutes

This represents an early draft of a section of an upcoming scientific review.

One of the most exciting series of findings involves reduction of xenograft growth in mouse cancer models among animals given the ketogenic diet. A much-celebrated meta-analysis of mouse cancer models by Klement et al., 2016 (using at least a 2:1 ketogenic ratio and included controls with 50% of energy without additional treatment and reported tumor growth and survival endpoints) showed a robust reduction in tumor growth was found in mice fed the ketogenic diet compared to mice fed standard rodent chow [1]. However, severe methodological problems may have caused this meta-analysis and the studies it includes to poorly represent the preclinical efficacy of the ketogenic diet. Among the twelve studies included in this meta-analysis, nine used ketogenic diets with protein content (as a percent of total kilocalories) ranging from 61% to as low as 22% of that in the control diets, or in other words, involving between a half and a four-fold protein restriction (with a mean protein intake of 42% that of the control diet) [2–11]. This is important because it has long been known that protein restriction causes a robust delay of chemically induced and xenograft tumor growth [12–16]. Methionine restriction, which also occurs during protein restriction, achieves the same effect [17–19], including among several types of glioma xenografts [20], the most prominent and much-celebrated cancer type to ostensibly respond to the ketogenic diet in the ketogenic diet literature [1]. Therefore, the positive results of these nine ketogenic diet studies are confounded by protein restriction, and it is unclear what role the ketogenic component of the diet played in the results reported.

Furthermore, while Klement et al., 2016 reported positive findings for the remaining three studies, two of these findings occurred in comparison to a high-fat diet [3,5], which has been shown in several studies to increase the rate of xenograft tumor growth [21,22]. In fact, in these same two papers, a comparison with a third group of mice fed standard rodent chow was reported, and this showed no significant difference with the ketogenic diet-fed mice (except for a small difference at day 39 in one paper, which favored the standard chow mice) [3,5]. Surprisingly, the comparison with this control group of mice, which would suggest no efficacy of the ketogenic diet beyond simply being better than a high-fat diet, was for some reason not reported by Klement et al., 2016, further biasing the meta-analysis.

The third of the three diets that matched for protein did see a beneficial effect for the ketogenic diet, but this version of the ketogenic diet was highly unusual, with non-ketogenic carbohydrate kilocalorie % and ketogenesis driven by supplemental medium-chain triglycerides (Martuscello et al., 2016). Interestingly, Martuscello’s MCT group had a 5% higher protein as % of macronutrients than control (21% vs 26%) and may have consumed more food: they gained more weight than the other groups.

This finding is promising, but future studies will need to confirm these results with less confounded feeding designs. Of note, one high-profile mouse study published last year in Nature also used a highly restricted protein intake in the ketogenic group—a mere 25% of the intake of the control group (Hopkins et al., 2018), perhaps exemplifying the prevalence of this design flaw in the ketogenic diet literature. Other recent papers, such as one that showed normalization of the metabolome in a breast cancer xenograft model with the administration of a ketogenic diet, are also confounded by profound protein restriction (Licha et al., 2019).

A list of studies discussed in this article can be found below:

This image has an empty alt attribute; its file name is Screen-Shot-2019-09-06-at-4.52.13-PM.png

Note: the 2013 Poff article listed in the spreadsheet above refers to a different study (but published in the same year) than that examined by Klement et al., 2016, with a slightly different macronutrient composition than that listed. This difference does not substantially change the analysis or conclusion.

1.        Klement, R.J.; Champ, C.E.; Otto, C.; Kämmerer, U. Anti-tumor effects of ketogenic diets in mice: A meta-analysis. PLoS One 2016, 11, 1–16.

2.        Zhou, W.; Mukherjee, P.; Kiebish, M.A.; Markis, W.T.; Mantis, J.G.; Seyfried, T.N. The calorically restricted ketogenic diet, an effective alternative therapy for malignant brain cancer. Nutr. Metab. (Lond). 2007, 4, 5.

3.        Freedland, S.J.; Mavropoulos, J.; Wang, A.; Darshan, M.; Demark-Wahnefried, W.; Aronson, W.J.; Cohen, P.; Hwang, D.; Peterson, B.; Fields, T.; et al. Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate 2008, 68, 11–9.

4.        Otto, C.; Kaemmerer, U.; Illert, B.; Muehling, B.; Pfetzer, N.; Wittig, R.; Voelker, H.U.; Thiede, A.; Coy, J.F. Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides. BMC Cancer 2008, 8.

5.        Mavropoulos, J.C.; Buschemeyer, W.C.; Tewari, A.K.; Rokhfeld, D.; Pollak, M.; Zhao, Y.; Febbo, P.G.; Cohen, P.; Hwang, D.; Devi, G.; et al. The effects of varying dietary carbohydrate and fat content on survival in a murine LNCaP prostate cancer xenograft model. Cancer Prev. Res. (Phila). 2009, 2, 557–65.

6.        Rieger, J.; Bähr, O.; Maurer, G.D.; Hattingen, E.; Franz, K.; Brucker, D.; Walenta, S.; Kämmerer, U.; Coy, J.F.; Weller, M.; et al. ERGO: a pilot study of ketogenic diet in recurrent glioblastoma. Int. J. Oncol. 2014, 44, 1843–52.

7.        Maurer, G.D.; Brucker, D.P.; Bähr, O.; Harter, P.N.; Hattingen, E.; Walenta, S.; Mueller-Klieser, W.; Steinbach, J.P.; Rieger, J. Differential utilization of ketone bodies by neurons and glioma cell lines: a rationale for ketogenic diet as experimental glioma therapy. BMC Cancer 2011, 11, 315.

8.        Abdelwahab, M.G.; Fenton, K.E.; Preul, M.C.; Rho, J.M.; Lynch, A.; Stafford, P.; Scheck, A.C. The ketogenic diet is an effective adjuvant to radiation therapy for the treatment of malignant glioma. PLoS One 2012, 7, e36197.

9.        Hao, G.-W.; Chen, Y.-S.; He, D.-M.; Wang, H.-Y.; Wu, G.-H.; Zhang, B. Growth of human colon cancer cells in nude mice is delayed by ketogenic diet with or without omega-3 fatty acids and medium-chain triglycerides. Asian Pac. J. Cancer Prev. 2015, 16, 2061–8.

10.      Martuscello, R.T.; Vedam-Mai, V.; McCarthy, D.J.; Schmoll, M.E.; Jundi, M.A.; Louviere, C.D.; Griffith, B.G.; Skinner, C.L.; Suslov, O.; Deleyrolle, L.P.; et al. A Supplemented High-Fat Low-Carbohydrate Diet for the Treatment of Glioblastoma. Clin. Cancer Res. 2016, 22, 2482–95.

11.      Dang, M.T.; Wehrli, S.; Dang, C. V.; Curran, T. The ketogenic diet does not affect growth of Hedgehog pathway medulloblastoma in mice. PLoS One 2015, 10.

12.      Fontana, L.; Adelaiye, R.M.; Rastelli, A.L.; Miles, K.M.; Ciamporcero, E.; Longo, V.D.; Nguyen, H.; Vessella, R.; Pili, R. Dietary protein restriction inhibits tumor growth in human xenograft models of prostate and breast cancer. Oncotarget 2013, 4, 2451–2461.

13.      Hawrylewicz, E.J.; Huang, H.H.; Liu, J.M. Dietary protein, enhancement of N-nitrosomethylurea-induced mammary carcinogenesis, and their effect on hormone regulation in rats. Cancer Res. 1986, 46, 4395–9.

14.      Appleton, B.S.; Campbell, T.C. Inhibition of aflatoxin-initiated preneoplastic liver lesions by low dietary protein. Nutr. Cancer 1982, 3, 200–6.

15.      Appleton, B.S.; Campbell, T.C. Dietary protein intervention during the postdosing phase of aflatoxin B1-induced hepatic preneoplastic lesion development. J. Natl. Cancer Inst. 1983, 70, 547–9.

16.      Appleton, B.S.; Campbell, T.C. Effect of high and low dietary protein on the dosing and postdosing periods of aflatoxin B1-induced hepatic preneoplastic lesion development in the rat. Cancer Res. 1983, 43, 2150–4.

17.      Gao, X.; Sanderson, S.M.; Dai, Z.; Reid, M.A.; Cooper, D.E.; Lu, M.; Richie, J.P.; Ciccarella, A.; Calcagnotto, A.; Mikhael, P.G.; et al. Dietary methionine restriction targets one carbon metabolism in humans and produces broad therapeutic responses in cancer. bioRxiv 2019, 627364.

18.      Kokkinakis, D.M.; Schold, S.C.; Hori, H.; Nobori, T. Effect of long-term depletion of plasma methionine on the growth and survival of human brain tumor xenografts in athymic mice. Nutr. Cancer 1997, 29, 195–204.

19.      Latimer, M.N.; Freij, K.W.; Cleveland, B.M.; Biga, P.R. Physiological and molecular mechanisms of methionine restriction. Front. Endocrinol. (Lausanne). 2018, 9.

20.      Hoffman, R.M.; Kokkinakis, D.M.; Frenkel, E.P. Total Methionine Restriction Treatment of Cancer. Methods Mol. Biol. 2019, 1866, 163–171.

21.      O’Neill, A.M.; Burrington, C.M.; Gillaspie, E.A.; Lynch, D.T.; Horsman, M.J.; Greene, M.W. High-fat Western diet-induced obesity contributes to increased tumor growth in mouse models of human colon cancer. Nutr. Res. 2016, 36, 1325–1334.

22.      Lloyd, J.C.; Antonelli, J.A.; Phillips, T.E.; Masko, E.M.; Thomas, J.A.; Poulton, S.H.M.; Pollack, M.; Freedland, S.J. Effect of Isocaloric Low Fat Diet on Prostate Cancer Xenograft Progression in a Hormone Deprivation Model. J. Urol. 2010, 183, 1619–1624.

23.      Hopkins, B.D.; Pauli, C.; Xing, D.; Wang, D.G.; Li, X.; Wu, D.; Amadiume, S.C.; Goncalves, M.D.; Hodakoski, C.; Lundquist, M.R.; et al. Suppression of insulin feedback enhances the efficacy of PI3K inhibitors. Nature 2018, 560, 499–503.

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 3 minutes

Nutrition science is challenging. In its own way, it is the most challenging of the sciences. But also the greatest.

(This quote is mainly lifted from Nicola Guess, who says that nutrition science drives people mad. She is right.)

Could it possibly be argued otherwise?

This difficulty comes from the fact that we are deeply biased about the act of eating, in a few ways:

Psychological. We are emotional about the act of eating, and we crave certainty about how we do it. We all eat, and eating is one of our most primary life functions. We form strong emotional attachments to the habits that fulfill primary life functions: food, sex, work, family, etc. When the emotional attachments to such habits of life–in this case, our eating habits–are challenged, we respond emotionally. The tendency to respond emotionally to biases our interpretation of the objective facts about nutrition. We also develop polarized thinking. Good-bad, right-wrong, natural-unnatural. Emotional, polarized thinking leads to a desire for certainty: if something so important is either good or bad, then we need it to be clearly one or the other, since making a mistake about something so important has serious implications. And yet…

Scientific. The objective facts of nutrition science, i.e. how we should eat, are unclear. Our strong emotions and craving for certainty about food are frustrated by the fact that the objective facts in nutrition science are incomplete and cannot fulfill these desires. We do not and will not have randomized controlled trials testing many of the most important hypotheses in nutrition science for the foreseeable future. Instead, we rely on surrogate or indirect tests of most of the hypotheses of nutrition science. Because these surrogate or indirect tests are many but also flawed, with different methods giving contradictory results, the results of many or most of these tests are debatable on the grounds that they do not and cannot provide the certainty that we psychologically crave. In fact, nutrition science does the very opposite and assures us that we can know little. What nutrition science can offer us (very little of certainty) is in direct conflict with deep-felt psychological needs (that is, a desire for certainty). This causes us to impute into nutrition science what is not there, or alternatively to become frustrated when definitive, practicable answers are not forthcoming–and to seek alternative sources of certainty, in the form of gurus, anecdotes, knowledge-through-self-knowledge, etc.

Politico-economic. The government and diet industry make authoritative but seriously conflicting recommendations. This leads to group identity and financial conflicts of interest. Because eating is one of our primary life functions, how we eat is important for health. To promote health, the government makes recommendations. Because we desire certainty and simplicity, they provide these recommendations in a simplified and authoritative form. Because these broad recommendations are not detailed, individualized, or explained well, an industry of practical advice has sprung up to provide more detailed, individualized, and better communicated recommendations. Because the advice of these authorities is conflicting, an emotionally charged conflict over food choices emerges. Shared feelings about food lead to the formation of groups of like-feeling people, in turn creating a sense of group identity. This sense of group identity further biases the way we receive the already fragmentary and difficult to interpret objective facts. Furthermore, because there are livelihoods to be made in this industry, financial conflicts of interest further bias the communication of the objective facts.

How should we evaluate and understand nutrition science so as to minimize these challenges and the impact of our biases on the interpretation of the facts? Is there any method or approach that is most reasonable that we can systematically follow to achieve this?

I think there might be. In evaluating this chapter, I hope to articulate the outlines of what that might look like. This systematic approach to the evidence will not enable us to fulfill our psychological desire for certainty about what we eat, but it might help people who want to understand how nutrition scientists think and work and where nutrition recommendations come from. Not much if anything of what I will write here will be new. It will only communicate what I have learned from my reflections on what nutrition scientists have told me and what I have read as a nutrition scientist-in-training.

But what I want to point out here is that nobody seems yet to be popularly endorsing or communicating a systematic approach for looking at nutrition science. That is part of the problem, and part of what this series is going to try to do.

For those who have followed this, I want this to be something bigger and more serious than just Diet Wars, or polyunsaturated or saturated fats, etc. That kind of argument is simply not interesting to me. I agreed to look at the chapter itself. So let us look at the chapter. And take it very seriously.


You can find me on Twitter and Instagram. You can help support me here.

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 4 minutes

I have had a few exchanges with Paul Mason over the past couple of months. Most of the time he has explained concepts well, and I agree with his explanations.

What he gets wrong is the level of confidence that he has that these concepts are true. This is like much in the low-carbohydrate dieting space: plausible hypotheses are frequently passed as scientific fact, while everyone else is held to a much higher standard.

One would think that, given the consternation of the low-carbohydrate diet community at the weakness of evidence for, e.g. the American dietary guidelines, that this very same community would itself be very careful with the evidence. They are not. They have chosen to fight what they think to be fire with their own fire.

My own consternation came to a head recently, when, after seeing Paul tweet about his newly published chapter in Karim Khan and Peter Brukner’s Sports Medicine textbook, I pointed out that even the very first quote of Hippocrates in the book chapter was not something that Hippocrates actually said:

Snarky sure. So I beg forgiveness: snark is how I survive on Twitter, which is a veritable madhouse. Besides, in the Harvard Grant Study, humor was among the healthiest of ways to deal with psychological stress. So that’s my humor.

But, it’s also true: what does a misquote say about the factual soundness of the rest of the chapter? I mean, if your opening quote is contrived, what about the rest?

So Paul went on the offensive, and rightly…

This image has an empty alt attribute; its file name is Screen-Shot-2019-07-28-at-9.19.25-AM.png

I didn’t think I could give it a take that would result in a productive discussion. So I didn’t want to try. But Paul persisted, and I accepted.

I read the first few pages, and my eyes nearly rolled out of my head: it was exactly what I had expected. One weakly defensible hypothesis after another, presented as scientific fact, which, according to Paul, fools, conspirators, and other actors in bad faith from The Establishment had committed to suppressing through a deadening avalanche of bad science. And then, one criticism of dissenting views after another, presented as definitive. Next, references that provided weak support or used poor methods presented as conclusive. It goes on.

I thought: it will take 200 hours of digging, picking apart the distortions, and correcting them. And who will read it anyway? So I sat on it, planning to write something but procrastinating, mostly despairing of being able to do anything meaningful about this.

Paul decided to go on the offensive, again, here:

And here:

And the rest of that thread consists of Paul haranguing me about saturated fat and polyunsaturated fat and trying to pigeonhole me about my “views”. I mostly tried not to engage.

But what I realized is this: if I could do that work and break down Paul’s chapter, and demonstrate why it is a misuse of evidence, and people would actually commit to reading it, it might be worth my time. I wouldn’t be writing for myself. And if I feel confident that I can persuade intelligent people–and I do feel confident–then this could actually be quite a fulfilling exercise.

It would also help me to work out my own thoughts about what constitutes an impartial evaluation of nutrition science.

So I created a reading challenge. Here’s the gist of it. If you are a hardcore carnivore/LCHF type but open-minded, you can sign up for the reading challenge and commit to reading one hour of what I write.

Tit-for-tat with each such commitment, I myself will commit to an hour of research and writing.

So if I get 100 sign-ups, I will commit to researching and writing for 100 hours. And I work at a minimum rate of 10 hours per month, which is sustainable for me. So no concerns about spending tons of time writing for no reason:

Lo-and-behold, I received 90 commitments. So now I am committed to 90 hours. This will be the first post fulfilling that commitment. For those signed up, I will be sending out an email with an update when the first 10 hours are over and each month when the work is complete thereafter. When I have written an hour’s worth of reading content (as measured by an algorithm), people who have already signed up will also be able to sign up a second time.

If you are stumbling across this post from outside of Twitter, take a moment to read the Twitter thread. If you meet the criteria to sign-up and want to commit, please do. The sign-up form is at the end of the thread.

For those who do not meet the criteria but still want to follow this series and receive updates about it, please sign up using the form here.

Now, why the title? This is about Paul Mason and Daniel Freedman’s book chapter, isn’t it? It is. But after looking through the chapter, it is obvious to me that Paul’s book chapter actually represents “current low-carbohydrate thinking”, in general. All of the contentious claims about fiber, saturated fat, red meat, macronutrient intakes, epidemiology, etc.: everything is there.

Thus, I want to use Paul’s chapter to scrutinize “low-carb science” as a whole. But I don’t want to just say the chapter is wrong. I want to go deeper. I want to get to the heart of current methodological controversies within nutrition science itself. And I want to explain why “low-carb science” does it wrong. And I want to do it in the most minute, meticulous detail, point-by-point, error-by-error, explaining painstakingly why they are errors and what a better way might (or might not) be–to a degree nobody has done before.

It’s a big thing to take on. That’s why I asked for a commitment before starting this. Thank you for starting on this journey with me. If I continue to get commitments, I will be continuing this series throughout the entire remainder of my Ph.D. I would be honored and excited to do so.


You can find me on Twitter and Instagram. You can help support me here.

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 4 minutes

A narrative has sprung up on the Internet, largely fueled by mainstream media organizations like Vice, CNN, etc., that meat consumption in the developed world is causing deforestation of the Amazon.

This narrative is false.

In this blog, I will cover two issues:

  1. Brazilian beef and who consumes it
  2. Brazilian soy and who consumes it

It is true that the Amazon is being deforested for wood, soy, and livestock. The soy in turn is being fed to livestock, so the Amazon is being deforested, more substantially, for wood and livestock.

But who is buying that soy? Who is buying that livestock? Who, in other words, is economically (and morally) responsible for environmental devastation that these commodities are a product of?

According to CNN, the breakdown of Brazilian beef exports is as follows:


So far, this is true.

Now, total production of beef in Brazil is ~22 billion pounds. 1.64 million metric tonnes or ~3.61 billion pounds is exported.

This means that 3.61/22 or 16.4% of Brazilian beef is exported. In turn, this means that Brazilians consume 84% of Brazilian beef domestically.

64 million pounds are exported to America, according to USDA:

This roughly confirms the CNN figures: 64 million is a little less than 2% of 3.61 billion. This amounts to ~0.3% of total Brazilian beef production.

On the other hand, the amount exported to China and Hong Kong combined amount to 43% of exports, which is 43% of 16%:

Or 7% of total Brazilian beef production.

This means that together, Brazilians and Chinese consume about 91% (84% + 7%) of Brazilian beef. So the narrative that the “world” is driving the fires in the Amazon is just wrong. The Brazilians and Chinese are driving the fires. And largely the Brazilians.

Europeans by the way consume about 7% of Brazilian exports, mainly Italians. This amounts to 1.1% of total Brazilian beef production.

So together, the EU and USA consume about 1.4% of Brazilian beef.

Brazilians and Chinese consume about 91%.

So we should definitely stop Brazilian beef importation completely, but we aren’t the main problem.

There is also a narrative about Brazilian soybeans, i.e. because Americans don’t send their soybeans to Brazil, we are somehow responsible. How do Americans and Europeans fit in there?

Almost 80% of Brazilian soybean exports are to China, and exports to China from the United States actually increased in 2019, while Brazilian exports to China dropped by almost 15%. (Source.)

But it gets worse, because while 80% of Brazilian soybean exports are to China, about 80% of Brazilian soybeans are NOT exported, probably mainly to feed Brazilian livestock. (Source.)

This means that about 96% of Brazilian soybeans are either consumed domestically (i.e. by livestock) or exported to China (also to feed livestock). I’m not sure that America and Brazil trade soybeans at all.

So if the Amazon rainforest fires are driven by beef and soybeans, and we want to blame anyone this, again, it’s overwhelmingly China, Hong Kong, and Brazil.

Together, China, Hong Kong, and Brazil consume about 91% of Brazilian beef and 96% of Brazilian soybeans.

Indeed, emissions from animal agriculture in the advanced world have declined for the past 30 or 40 years. However emissions from developing countries have massively increased, fueled by their own domestic production and importation of beef.


Industrialized countries should set an example and stop consuming so much beef. They should also help developing countries use more efficient means of production, and penalize countries that are high emitters.

But while about 15% of total global emissions are from livestock, in industrialized countries like America, only 4% of American emissions are from agriculture, and we have little role in the emissions from developing countries.

This is because about 92% of beef consumed in the United States is from American-produced beef. We simply don’t import very much beef, and the beef we do import is mainly from Canada and Mexico.

What this means is that if Americans want to combat global emissions from themselves, they should use less transport energy and less electricity. That is the bulk of emissions from Americans.

If they want to combat emissions and deforestation from China and Brazil, they should support economic and foreign policies that penalize China and Brazil for their bad and worsening environmental records and incentivize better behavior.

There is a notion that if Americans consumed less beef, we could send our soybeans to other countries so they could avoid deforestation. This is really questionable, though, because it implies that Americans should change our behavior to stop bad behavior from others–as if by being held hostage.

The fact is, Americans should consume less beef and reforest. And Brazilians and Chinese should also consume less beef and also reforest and stop deforestation.

Everyone should do something, but Americans are responsible for their own bad behavior, not the bad behavior of others. The bad behavior of Americans is mainly in using too much electricity and too many cars. The bad behavior of Brazilians is in burning down their own forests, largely for production of beef that they themselves consume.

Not every bad thing is linked to Americans eating meat. When you want to make everything about One Thing, that is called an ideology. Ideologies are bad because they distort and prevent behavior that can actually achieved the desired outcomes.

— Kevin

Like what I write? Support me at

Find me on Twitter and Instagram.

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 9 minutes

I eat a mostly plant-based diet and I think most people should do the same. But it is important not to spread ideas that are not true. This leads to distortions in behavior–compared to what would happen if people had correct information–and worse outcomes. As we shall see.

Without further ado.

Those who focus primarily on food without changing other aspects of their lifestyle are fooling themselves.

According to EPA, agriculture accounts for only a tiny fraction of emissions of carbon emissions. This includes methane from livestock. 9% of carbon emissions are from agriculture. Maybe half are from animals (4.5%). Transportation and electric power produce 29% and 28%, respectively. From a carbon emissions POV, green energy and transport is way more important than abstaining from meat.

Below is a table giving the emissions figures for agriculture. Note that a substantial proportion of agricultural emissions are actually from growing crops to feed animals. Even if this proportion were relatively high, it still would be on the order of 10% of transportation and energy.

This does not mean that meat consumption is not important for CO2 emissions. It does mean however that those who focus primarily on food without changing other aspects of their lifestyle are fooling themselves.

To fight global warming, American meat consumption is largely not what counts.

I am not alone in pointing this out. Michael Mann points it out as well.

I do think that animal agriculture can be environmentally destructive, especially with respect to land use (the idea of sequestering carbon with livestock is largely unsubstantiated except with the weakest evidence).

I also think there are some serious animal ethics issues associated with, e.g. pig and chicken farming, and sometimes with cows as well.

And, again, I think eating less meat and more plants produces better health for other reasons. Suffice to say, less hyperprocessed food is also a high priority here.

But I don’t think that animal agriculture is a CO2 issue.

Our way of life is the CO2 issue, and going vegan to fight global warming is substantially a distraction from that. The focus on meat to combat global warming in this sense is in fact harmful. We do not have much time to turn this ship around. That means focusing on what counts. Meat is not insubstantial, but it is not the major issue. To fight global warming, American meat consumption is largely not what counts.

You can find the EPA document here: ‪‬


Some people have sent me IPCC data suggesting that the global emissions footprint is larger than the modest figure suggested by EPA.

While global animal agriculture emissions are a substantial proportion of total emissions (25%), emissions from countries like the United States (OECD-1990) are actually a remarkably small proportion of the total annual greenhouse gas emissions from agriculture.

For instance, here is a graph from a recent IPCC report:

Where AFOLU stands for “agriculture, deforestation, and other land use change.”

What is clear here is that about 25% of global carbon emissions equivalents are from agriculture. Why are these figures different from those from the EPA?

It is important to note that the EPA is showing emissions only from the United States. Let’s take a look at a figure showing a breakdown by global region.

MAF: Middle East and Africa
LAM: Latin America
EIT: Economies in Transition

What is most striking here is that while AFOLU emissions from non-OECD countries has increased substantially, AFOLU emissions from high-income countries in the OECD from the past several decades have been stable. Additionally, it is clear that emissions AFOLU emissions from countries like the United States (OECD-1990) are actually a remarkably small proportion of the total annual greenhouse gas emissions from agriculture.

In other words, the IPCC data seem to be consistent with the EPA data. Although countries like the United States are responsible for the lion’s share of greenhouse gas emissions, this share in fact derive from animal agriculture but from other sectors.

Less than 10% of beef in the United States is not domestically produced, meaning that the United States contributes to a very small fraction of the large proportion of greenhouse gas emissions from beef from other countries.

At least not directly, one might object. What accounts for these emissions in these other countries? Could these emissions be from industries that US consumers use–thus the US emissions levels are in fact underestimated by such graphs above?

At first sight, this seems possible. After all, the largest proportion of total agricultural emissions does come from deforestation, and we have been told that the world is deforesting in order to provide for agriculture (especially livestock):

If we look at trends in land use, this seems to further reinforce this story, with land put aside for “cattle and buffaloes” declining in countries belonging to the OECD (such as the United States) but rapidly increasing elsewhere:

And indeed, the FAQ section of the IPCC report suggests much the same thing: about half of greenhouse gas emissions are driven by deforestation.

However, the notion that this deforestation globally (due to beef production, etc.) is on behalf of the United States cannot be right, either. According to this Michigan State University agricultural extension website, less than 10% of beef consumed in the United States is not domestically produced, meaning that the United States contributes to a very small fraction of the large proportion of greenhouse gas emissions from beef from other countries.

Indeed, most of the foreign beef supply is from countries like Mexico and Canada–not from, say, the Amazon:

Similarly, the USDA estimates that almost 90% of US food consumption is domestically produced:

In 2016, 87.3 percent of food and beverage purchases by U.S. consumers, including both grocery store and eating out purchases, were from domestic production. The remaining 12.7 percent were imported food and beverages such as produce from Chile or wines from France.–made-food-produce/article_a76f95f0-5857-11e8-8922-47f84163101f.html

American greenhouse gas emissions are not substantially from agriculture; our forestry problems are not from deforestation; and our food does not come from countries that do produce large agricultural emissions. If climate is your priority, go carless first, then talk about reducing meat consumption.

Finally, if we look at the estimate mitigation potentials for forestry in the IPCC report, we see that the vast bulk of mitigation potential in OECD countries is from better forest management, while preventing deforestation is the priority in other countries (such as in the Middle East, Africa, and Latin America):

In other words, our greenhouse gas emissions are not substantially from agriculture; our forestry problems are not from deforestation; and our food does not come from countries that do produce large agricultural emissions.

While agriculture might account for ~25% of emissions globally, people in the developed world are actually contributing only 10% of their emissions from agriculture. If we want to point our fingers about agriculture, we should point them at other countries. And if we want to make a change in total emissions at home, we need to start with transportation.

I still think people should consume a predominantly plant-based diet and reduce their meat and animal product consumption, but not for reasons of climate.

If climate is your priority, go carless first, then talk about reducing meat consumption.


The following thread was linked in response to my post:

Richard’s main argument is as follows:

Even though the United States produces relatively few emissions as a proportion of total emissions (10% of total emissions is from agriculture and perhaps only about 5% from livestock) and only contributes to a very small fraction of total greenhouse gases from agriculture…

If consumers in the United States were to stop consuming so much beef, say 1/3, but continue to export to other countries, these countries which are producing the lion’s share of emissions could start producing less, because they are receiving American beef and don’t need to produce as much of their own.

But this argument relies on many assumptions that are not justified. I can count at least four (and there are probably more):

1) that there is an upper-bound to meat demand globally and other countries will stop producing as much just because we produce more;

2) that we can export all of the meat we produce;

3) we will continue to produce the same amount of beef for exportation.

But the fourth assumption is the most important: that even if the above 3 assumptions hold, the amount of beef that the United States produces is enough to substantially offset the amount of beef produced elsewhere.

This assumption does not hold up, and therefore Richard’s argument does not hold up. Here is why.

According to USDA, America produced 26.87 billion pounds of beef in 2018. (See:

Let us round that up to 27 for the sake of math. One-third of 27 is 9.

9 billion pounds that the US can export and provide to the world.

Worldwide food balance for beef in 2013 according to the Food and Agricultural Association was 147.3.

Let us round that down for the sake of math.

147 billion pounds that the world produces.

147 – 9 = 138 billion pounds vs. 147 billion pounds, or a 6% decline in beef production worldwide from a one-third drop in American beef consumption.

OK. Now according to the UN Food and Agricultural Association emissions from livestock are 14.5% of total emissions, and beef and milk account for 65% of that:

That means we have about 9.5% potential emissions to mitigate via this one-third decline in American beef (and milk) consumption.

6% of 9.5% is what?

0.57% of total emissions.

Assuming the first assumptions were correct, the fourth assumption–that declines in American beef are substantial enough to offset total GHG–is false. And the fact that the first three assumptions will to some degree not hold makes the fourth assumption even more erroneous. 0.57% is the best-case scenario (and includes milk and favorable rounding).

And this is not accounting for the future increases in beef production in other countries, either. (The assumption that everyone else won’t produce more beef is not reasonable.) Here’s why. Americans produce almost 20% of the world’s beef, yet are only 4% of the world’s population.

What do you think the world is going to do as they continue developing? Keep their beef production at a standstill?

The world will keep increasing its consumption of beef, and this is all the more reason to believe that American reductions in beef won’t make a dent.

Let’s compare that to the other 96% of the American greenhouse gas emission equivalents. About 96% of American emissions are not from animal agriculture, because 9% of American emissions are from agriculture, and about 42% of those are from animals. 42% of 9% is 3.8%. 3.8% represents the total % of American emissions from animal agriculture. This New York Times article gets the numbers right, which are consistent with EPA and other sources.

OK, 96%, right? Let’s reduce that by one-third. How much would that directly impact worldwide emissions (and not by any assumptions)?

Well, the United States produces about 15% of total emissions, according to EPA:

One-third of that is about 5% of total global emissions.

So reducing beef by one-third is about 0.5% in the best case scenario. (It probably would have a substantially smaller impact.) Reducing everything else by one-third is about 5%, or at least ten times more effect.

If everyone in America stopped eating beef and milk tomorrow, and we could magically ship all of this beef and milk somewhere else, and nobody would produce more beef and milk to replace it, it would cause a 1.5% reduction in emissions–at best. And livestock emissions worldwide would drop from 14.5% to 13%.

It’s actually not the worst idea in the world.

It’s just that 1.5% is a drop in the bucket compared to our 15%. And so long as we focus on that 1.5% and not that 15%, we will get to keep our cars, planes, etc. while telling ourselves we are doing good for the planet by being vegan.

Nothing could be further from the truth. That is why, in the context of the climate debate, the focus on veganism is wrong: it is a false, self-complacent surrogate for authentic commitment to stopping climate change.

Follow me on Twitter:


Support me:


Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 6 minutes

This is a draft of a subsection that I have written for an upcoming review paper on the ketogenic diet. This is comprehensive look at what we know about the usefulness of the ketogenic diet for the treatment of overweight and obesity. The review of which this subsection is a part will be published later this year.

Without further ado…

Ketogenic diets show appetite suppression

The most well-known application of ketogenic dietary therapy (KDT) is for weight loss. This form of KDT popularly takes the form of a diet high in meat, eggs, dairy, high-fat nuts, non-starchy vegetables, and restricted in foods containing carbohydrate (such as most fruits, grains, legumes, etc.) (Volek, Phinney, Kossoff, Eberstein, & Moore, 2011). Less commonly, plant-based versions of this diet rich in seeds, nuts, and oils—so-called Eco-Atkins—are also possible (Jenkins et al., 2014). Acute dosing studies using exogenous ketones suggest that ketones may cause appetite suppression owing to lower ghrelin secretion peripherally (possibly via activation of GPR41 on enteroendocrine cells), as well as direct effects on the brain (Stubbs et al., 2018). One study investigating the changes caused by the classical KD for refractory epilepsy in children have found an even more robust chronic reduction in ghrelin (Marchiò et al., 2019). Still another study showed that, after 13% weight loss over 8 weeks in 39 individuals, reintroduction of a carbohydrate containing diet over two weeks caused increases in ghrelin and hunger to above baseline, whereas prior to reintroduction, ghrelin and hunger had remained suppressed at baseline levels, defying typical changes in ghrelin during weight loss (Sumithran et al., 2013). Correspondingly, systematic review and meta-analysis suggests a modest reduction in self-reported hunger and increase in self-reported fullness and satiety during adherence to the ketogenic diet compared to baseline, pre-diet levels (Gibson et al., 2015).

Ketogenic diets may or may not provide a metabolic advantage

Findings from a recent Mendelian randomization study have further suggested that reduction in post-prandial plasma insulin levels as achievable by KD (Hall et al., 2016) might be capable of reducing the prevalence of between 1 and 10% of obesity at the population level (Astley et al., 2018). Consistent with this, (Ebbeling et al., 2018a, 2012) reported a “metabolic advantage” of isocaloric carbohydrate restriction that may substantially increase energy expenditure. However, in a widely circulated critical re-analysis by Kevin Hall and Juen Guo available in pre-print (Hall & Guo, 2019), the latest of these findings have been contested on a number of technical grounds. Moreover, as shown by recent meta-analysis, the findings of these studies (Ebbeling et al., 2018b, 2012) are themselves extreme outliers among more than 30 similar controlled feeding studies, which on average show a slight metabolic advantage in fact for low-fat diets (Hall & Guo, 2017).

Twelve-month weight loss: low-carb vs. low-fat diets

More importantly, the highest-quality reviews of free-living trials comparing 12-month outcomes of low-carbohydrate versus low-fat diets in free-living conditions show negligible weight loss difference—less than a kilogram—which might itself be fully accounted for by the glycogen- (and thus water-) depleting effect of the diet (Churuangsuk, Kherouf, Combet, & Lean, 2018). That the above mechanistic advantages do not seem to translate into a clinically substantial weight loss advantage for the KD may be indicative that such advantages are short-lived (Stubbs et al., 2018) or that other factors, such as socioeconomics, social support, and other life circumstances (Hall, 2018), in the context of chronic hyperpalatable food cue exposure (Lutter & Nestler, 2009), are more biologically important. Indeed, according to a recent study, among the high-quality systematic reviews with meta-analyses on low-carbohydrate diets (Churuangsuk et al., 2018), only one used for its study inclusion criteria a carbohydrate intake sufficiently low to produce ketonemia (Bueno, de Melo, de Oliveira, & da Rocha Ataide, 2013), and in only one RCT of the included 13 were low-carbohydrate dieters still in the ketogenic range of carbohydrate intake by study end, with a 59% completion rate (Brinkworth, Noakes, Buckley, Keogh, & Clifton, 2009). The DIETFITS trial, which had 609 participants and a 79% completion rate, had subjects start well into the ketogenic range (<20g) in the low-carbohydrate group for 8 weeks, adding carbohydrates back to their diets in increments of 5-15g/week “until they reached the lowest level of intake they believed could be maintained indefinitely”. By the twelfth week, just four weeks later, dieters were on average consuming nearly twice the carbohydrate grams as is generally recommended to maintain nutritional ketosis, and by twelve months, nearly triple (Gardner et al., 2018).

Adherence is the central issue for all diets, including the ketogenic diet

Indeed, as with other weight loss regimens, studies on low-carb diets show, on average, the start of progressive weight regain between 6 and 12 months (Athinarayanan et al., 2019; Hall, 2018), with the subjects exiting the ketogenic carbohydrate intake range earlier (Hallberg et al., 2018). Accordingly, while at 6 months the ketogenic diet shows a weight loss advantage, at 12 months the results for the KD are similar to those for other well-formulated diets that attempt to exclude hypercaloric, high-reward, low-satiety foods, and there is little or no significant detectable difference in 12-month weight loss in the best designed studies and highest quality reviews (Churuangsuk et al., 2018; Gardner et al., 2018), and the postulated mechanisms above of appetite suppression and metabolic advantage may not be clinically relevant for this reason, or if they are, they may only be relevant in marginal cases not yet captured by the RCT literature. It is possible that in the context of an adequately characterized and implemented behavioral modification intervention, the above-postulated mechanisms may prove to make ketogenic diets superior to other approaches. However, what is most striking about the literature given current crude approaches to behavioral modification is that the macronutrient composition—beyond a focus on whole foods—is relatively insignificant a factor for determining the degree of long-term weight loss.

Conclusion: leveraging ketogenesis for weight loss will require addressing the adherence problem

Astley, C. M., Todd, J. N., Salem, R. M., Vedantam, S., Ebbeling, C. B., Huang, P. L., … Florez, J. C. (2018). Genetic evidence that carbohydrate-stimulated insulin secretion leads to obesity. Clinical Chemistry, 64(1), 192–200.

Athinarayanan, S. J., Adams, R. N., Hallberg, S. J., McKenzie, A. L., Bhanpuri, N. H., Campbell, W. W., … McCarter, J. P. (2019). Long-Term Effects of a Novel Continuous Remote Care Intervention Including Nutritional Ketosis for the Management of Type 2 Diabetes: A 2-Year Non-randomized Clinical Trial. Frontiers in Endocrinology, 10, 348.

Brinkworth, G. D., Noakes, M., Buckley, J. D., Keogh, J. B., & Clifton, P. M. (2009). Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo. The American Journal of Clinical Nutrition, 90(1), 23–32.

Bueno, N. B., de Melo, I. S. V., de Oliveira, S. L., & da Rocha Ataide, T. (2013). Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. British Journal of Nutrition, 110(7), 1178–1187.

Churuangsuk, C., Kherouf, M., Combet, E., & Lean, M. (2018). Low-carbohydrate diets for overweight and obesity: a systematic review of the systematic reviews. Obesity Reviews, 19(12), 1700–1718.

Ebbeling, C. B., Feldman, H. A., Klein, G. L., Wong, J. M. W., Bielak, L., Steltz, S. K., … Ludwig, D. S. (2018a). Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial. BMJ (Clinical Research Ed.), 363, k4583.

Ebbeling, C. B., Feldman, H. A., Klein, G. L., Wong, J. M. W., Bielak, L., Steltz, S. K., … Ludwig, D. S. (2018b). Effects of a low carbohydrate diet on energy expenditure during weight loss maintenance: randomized trial. BMJ (Clinical Research Ed.), 363, k4583.

Ebbeling, C. B., Swain, J. F., Feldman, H. A., Wong, W. W., Hachey, D. L., Garcia-Lago, E., & Ludwig, D. S. (2012). Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance. JAMA, 307(24), 2627–2634.

Gardner, C. D., Trepanowski, J. F., Del Gobbo, L. C., Hauser, M. E., Rigdon, J., Ioannidis, J. P. A., … King, A. C. (2018). Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion. JAMA, 319(7), 667.

Gibson, A. A., Seimon, R. V., Lee, C. M. Y., Ayre, J., Franklin, J., Markovic, T. P., … Sainsbury, A. (2015). Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Obesity Reviews, 16(1), 64–76.

Hall, K. D. (2018). Maintenance of Lost Weight and Long-Term Management of Obesity. Medical Clinics of North America, 102(1), 183–197.

Hall, K. D., Chen, K. Y., Guo, J., Lam, Y. Y., Leibel, R. L., Mayer, L. E., … Ravussin, E. (2016). Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men. The American Journal of Clinical Nutrition, 104(2), 324–333.

Hall, K. D., & Guo, J. (2017). Obesity Energetics: Body Weight Regulation and the Effects of Diet Composition. Gastroenterology, 152(7), 1718-1727.e3.

Hall, K. D., & Guo, J. (2019). Carbs versus fat: does it really matter for maintaining lost weight? BioRxiv, 476655.

Hallberg, S. J., McKenzie, A. L., Williams, P. T., Bhanpuri, N. H., Peters, A. L., Campbell, W. W., … Volek, J. S. (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study. Diabetes Therapy, 9(2), 583–612.

Jenkins, D. J. A., Wong, J. M. W., Kendall, C. W. C., Esfahani, A., Ng, V. W. Y., Leong, T. C. K., … Singer, W. (2014). Effect of a 6-month vegan low-carbohydrate (‘Eco-Atkins’) diet on cardiovascular risk factors and body weight in hyperlipidaemic adults: a randomised controlled trial. BMJ Open, 4(2), e003505.

Lutter, M., & Nestler, E. J. (2009). Homeostatic and Hedonic Signals Interact in the Regulation of Food Intake. The Journal of Nutrition, 139(3), 629–632.

Marchiò, M., Roli, L., Lucchi, C., Costa, A. M., Borghi, M., Iughetti, L., … Biagini, G. (2019). Ghrelin Plasma Levels After 1 Year of Ketogenic Diet in Children With Refractory Epilepsy. Frontiers in Nutrition, 6, 112.

Stubbs, B. J., Cox, P. J., Evans, R. D., Cyranka, M., Clarke, K., & de Wet, H. (2018). A Ketone Ester Drink Lowers Human Ghrelin and Appetite. Obesity, 26(2), 269–273.

Sumithran, P., Prendergast, L. A., Delbridge, E., Purcell, K., Shulkes, A., Kriketos, A., & Proietto, J. (2013). Ketosis and appetite-mediating nutrients and hormones after weight loss. European Journal of Clinical Nutrition, 67(7), 759–764.

Volek, J., Phinney, S. D., Kossoff, E., Eberstein, J. A., & Moore, J. (2011). The art and science of low carbohydrate living : an expert guide to making the life-saving benefits of carbohydrate restriction sustainable and enjoyable. Retrieved from

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: < 1 minute

1. If a quack is promoting an underused but scientifically legitimate therapy and helping people, critics have the moral responsibility to promote this intervention themselves or they do not have the right to criticize the quack about what the quack says about the intervention. This applies even if the quack’s explanation of the science is wrong.

2. Nobody has the moral responsibility or right to withhold scientific information from the public just because it can be abused by quacks.

3. However, scientists and other public figures have the moral responsibility to denounce the misuse by prominent quacks of the science they have produced.

4. Scientists and other public figures who associate with and support quacks share moral responsibility in the misinformation and harm these quacks cause.

* A note on quacks: A quack is someone who makes a livelihood from exaggerated or false claims about what the science says about health. Quacks can include academics, activists, popular media figures, university press release office workers, etc., and is not limited to the traditional figure of the “snake oil salesman”.

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 6 minutes

A dream

I wake up at 7AM, alarm clock blaring. As I get to my feet, I look around frantically. Just a moment earlier, I had been hunched in a bunker, preparing for rocket launch as the bomb sirens blared.

I had been dreaming.

Blinking, I realize I am in my bedroom. And the rocket sirens? My alarm clock.

My tensed shoulders relax and I exhale.

After going to the bathroom and grabbing coffee, I sit down at my computer, beginning my morning ritual of checking Twitter–and my Oura ring’s sleep tracking data.

Throughout the entire sleep cycle, the Oura ring had been tracking every heartbeat and every hand movement. And because the heart’s activity is modulated by the vagus nerve, so the theory goes, the Oura ring can track brain activity by tracking heart activity. And according to company claims, by tracking the brain’s activity via heart activity, it can track sleep stages.

A nightmare

As I look down at my Oura ring’s data about my sleep stages on my smart phone, I see a depressingly familiar sight:

  • A sleep-scape pockmarked by white spikes, indicating night-time waking events–I have been nearly 2 hours awake while I had thought I had been sleeping
  • 16 minutes of total REM sleep out of more than eight hours in bed “asleep”
  • An impressive, nearly 3 hours of deep sleep. Well that’s nice at least

Great. I have a serious sleep disorder.

Then I looked at my overnight heart rate:

Not bad, except for the frequent gigantic spikes. (My wife claims that I often engage in somnolent, heated invective against dream opponents.)

Was that me thrashing about? Awake or asleep? Was I punching the air in the face? I muse.

Then I remember my dream and see that while I was dreaming, the ring recorded me as awake.

Hmm, I think, my brow furrowed.

This calls for PubMed

So I start trawling through PubMed. Here is what I found.

The Oura ring has been compared to polysomnography–the gold standard in sleep staging. While the company boasts that the ring is “scientifically validated” for sleep staging, we should use that term rather loosely. Scientifically validated just means scientifically studied. It actually pretty much sucks for sleep staging.

Here is a graph from a “validation” paper (link):

On the X-axis is the gold standard of polysomnography, and on the Y-axis is the deviation. N3 is deep sleep, and REM is, well, REM. What we see for N3 deep sleep is a nearly 200 minute range of deviation around the actual gold standard value. And these blue dots are not clustering around the 0 on the Y-axis with just a few outliers. No, most of the blue dots are significant outliers.

The same goes for REM sleep. In fact, two of the subjects showed literally 3 hours fewer REM sleep than they actually got. If one of those subjects was me, and I was receiving such values on a consistent basis, then my sleep architecture might in reality be dysfunctional for getting too much REM rather than too little.

In other words, without knowing which blue dot that I am, I have no idea how good or bad my sleep actually is.

From the abstract of the above study, we see rather meager figures:

“From EBE analysis, ŌURA ring had a 96% sensitivity to detect sleep, and agreement of 65%, 51%, and 61%, in detecting “light sleep” (N1), “deep sleep” (N2 + N3), and REM sleep, respectively. Specificity in detecting wake was 48%.”

Specificity in detecting wake was 48%! If this was a medical test, it would never be approved by FDA.

A specificity of 48% means that there is a 48% chance that someone is awake when the device says they are asleep.

That is horrible.

But is it reliably bad? We don’t even know that.

In a recent interview with Matthew Walker, podcaster Peter Attia asked whether, once establishing a baseline, the Oura ring was reliable at least for predicting changes in sleep. A user of the ring, Peter presumably wanted to be reassured that the ring data had some utility. Without elaborating–and I suspect to assuage Peter’s fears–Dr. Walker responded coolly in the affirmative.

But even this is not known. From my searches, nobody has ever actually scientifically studied how reliable the ring is from night to night versus polysomnography. That is to say, nobody knows whether the biases the ring shows on one night for one user are necessarily replicated the following night. Nobody knows whether what it is estimating as sleep is anymore than a very rough estimate that changes substantially from night to night based on factors that are irrelevant to sleep.

The bitter truth: all sleep trackers suck

What about compared to my other sleep tracking device: the Garmin Fenix 5S?

2 hours and 57 minutes of REM sleep! Or 11-fold more REM sleep than my Oura ring.

19 minutes deep sleep! Or 8-fold less deep sleep.

8 minutes awake! Or 14-fold fewer minutes awake.

Which one is right? The answer: they both suck. Because it turns out that many wrist sleep trackers have been validated as well. And they all suck. According to one study, the Fitbit Charge 2 is actually better than the Oura ring. Here are its data:

It still really sucks.

Again, the question isn’t even what the average agreement between these sleep trackers and polysomnography is. The question is WHICH BLUE DOT ARE WE?

Even if these trackers are, say, 60% accurate, that doesn’t mean it is going to be accurate 60% of the time for us. It could be much worse for us than average. Or better. How would we know?

We cannot trust the sleep tracker’s data independent of data from a sleep lab. We cannot even trust it to be biased in a consistent manner. Because those data do not exist either.

The science is clear: if you want to track your sleep, go to a sleep lab

Sleep trackers have the veneer of science. Thus we think the results they report are meaningful. But just because someone has studied a given sleep tracker does not mean that the sleep tracker is reliable. It might be (and in the case of the Oura ring is) shown to be terribly unreliable.

The science of HR tracking of sleep phases is not weak. In fact, at the current stage of technology, the science is that these trackers are demonstrably not reliable.

So unless you have access to a sleep lab that you can use for several nights over a period of time, you have zero idea how accurate your sleep tracker is for you. It might be accurate or it might be terribly inaccurate.

Nocebo is a health risk for using the Oura ring

Companies like Oura that offer sleep tracking should also be very clear about the serious if not disqualifying limitations of their technology. And I now believe that devices with sleep tracking should give the option to users to disable the sleep tracking feature.

Given the evidence of demonstrated nocebo from biomarker tracking in multiple scientific studies, the option to disable sleep tracking on these devices would be prudent indeed.

According to the above study, sleep trackers like the Oura ring can exert nocebo effects that affect our cognition and potentially our health. In the above study’s case, the nocebo affected cognition.

According to other studies, simply receiving genetic data causes our body’s physiology to change in the direction of what that genetic data would predict.

But because nocebo can also affect immunity and a diverse range of other physiological processes (for example, see Jo Marchant’s book Cure or take a look at the research of Harvard professor Ted Kaptchuk), nocebo from sleep tracking technology has the potential to cause chronic health harm on stress or immunity.

When we wake up feeling good, look at our sleep tracker data and see we have had a terrible night of sleep, we might suddenly start not feeling so good–and the ring data itself might be inducing these effects.

We should demand that Oura give the option to disable sleep tracking

Therefore, given this potential negative effects on a broad scale on users experiencing negative (and substantially false) sleep data, the Oura ring company should include the option to disable displaying sleep tracking data altogether.

Why do I keep using my Oura ring? Because nighttime HRV, resting heart rate, and temperature are awesome. But the sleep staging? Not so much.

Besides, even if we find out our sleep is in fact actually terrible, despite keeping a consistent schedule, etc.–what can we actually do about it? It is questionable to what degree the data–even if they were not fatally flawed–are even actionable.

Share this post and demand to Oura that they make sleep staging a feature that can be disabled. For many of us, it should be.

Enjoy this post? Help me smash the wellness industry by supporting me here:

Eternal graduate student,
Someday physician,
Always yours,

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.

Reading Time: 4 minutes

I want to make a case for the way science should be done in the health sciences–in a way that is totally different from physics–and I want to make this case using some of the evidence available on the link between animal protein and cardiovascular disease. I will use this as a particular example of the use of scientific inference, as is used in medicine to make a case that many might find persuasive, but which would be dismissed in other so-called hard sciences. I want to explain in particular why this kind of scientific inference is necessary for medicine–owing to its practical orientation–as compared to such other sciences.

Rabbits LDL levels increase with animal protein. Rabbits get atherosclerosis with animal protein via LDL. Humans increase LDL with animal protein (here and here). Humans get atherosclerosis via LDL.

We might infer therefore that animal protein causes atherosclerosis in humans.

To be clear, I’m not suggesting that animal protein definitely causes atherosclerosis in humans. But if it doesn’t, and if one accepts the lipid hypothesis, one would need to postulate some protective factor from animal protein that could counter its LDL-producing effects.

It follows that the more parsimonious (simpler) explanation is that animal protein is atherogenic in humans, and that is why an association between animal protein and cardiovascular disease is found in many (but not all) epidemiological studies.

This interpretation as far as I can tell is the simplest explanation comporting with the evidence. Again, I’m not saying it is true or that the evidence is strong. Clearly, the evidence is weak; direct human evidence in RCT would be strong. But it is the evidence that we have.

And here’s where the philosophy of science comes in. The health sciences (which includes nutrition science) are not like cosmology. In cosmology, conclusions don’t much matter, because nobody has to make decisions based on these conclusions. One can be agnostic and reserve one’s judgment on many issues.

However, in the health sciences, one must make a decision: do I take X action or not-X? What about Y? And Z? In the case of nutrition science, one must eat and thus while one can be scientifically agnostic, one must come to some practical conclusion. Because one cannot choose not to eat.

In such muddy sciences as the health sciences, it is not that we should be scientific idiots and go with any weak evidence to form some loaded and unjustified conclusions–some popular writers look to portray us in exactly in this way.

It is that as practical people who live in the real world, we must make decisions.

In medicine, we must make a decision based on incomplete information.

If the question of animal protein were a cosmological question with no practical relevance, I would be coming to a conclusion based on insufficient evidence to justify it. My conclusion would in fact be partly speculative: I am filling in the gaps in evidence (specifically, an RCT demonstrating an effect of animal protein on cardiovascular disease risk) with logic. In a formal sense, that isn’t science.

However, because this is about life and death and a decision I must make one way or the other, what constitutes good or bad reasoning in this particular domain is entirely different than what constitutes good or bad reasoning in cosmology.

Let us use an example to illustrate the case, and to more clearly illuminate what health science is, compared to a science like cosmology.

What if all politicians based their policy decisions on RCTs, with perfect design, generalizability, power, etc.? No decisions would ever be made.

This is exactly the situation in many areas of health science, medicine, nutrition science, etc.

That is why comparing medicine to physics and decrying the former for not measuring up to the latter is asinine. It totally misses the point of what medicine is about: making practical decisions.

When the point is making practical decisions, evidentiary standards radically shift: they go from a) austere scientific principles to b) making use of whatever is at hand to accomplish the task in the most competent way available.

I’m not the first person to say these things. They are obvious.

As a final note, this does not mean that we should abandon careful scientific principles. On the contrary, the difficulty of coming to good conclusions because strong evidence is so often absent requires us to double down on rigor and try to produce more of it–to ground the decisions we must make in increasingly strong evidence. It is precisely because we often have such little good evidence that we should take good science so seriously.

But given the flaws in the science, how do we deal with it scientifically *now*? This is a philosophical question and a lot more comes into play than I have just addressed. But I wanted to make a bare-bones case explaining one point of view.

Also: I’m not saying that the effect of animal protein in rabbits is the basis of my views. Rather, I’m saying indirect evidence such as that suggested by animal models has a greater role to play in forming conclusions in the health sciences than one like cosmology or physics. In the latter, such evidence would be frustrating. In health science, such evidence is sometimes necessary!

It’s nothing mind-blowing, but I guess these things sometimes need to be said–or rather, these assumptions about the way we approach science should be articulated because that’s the first step to understanding–both of each other and ourselves–and discussion at a deeper level.


Help me communicate good science–and how to think about it–by supporting me at

— Kevin

Producing high-quality scientific work like this takes many hours of work. This is made possible through the support of readers and viewers like you. Please consider donating below.

In just a few clicks, sign up to donate $5 monthly here:
Or $20 monthly here:

For one-time donations, or to become a patron on Patreon, click here.