What Gary Taubes Can Learn From Evolutionary Theory: An Open Challenge To His “Hypothesis”

Many of you already know that I have been highly critical in the past of Gary Taubes and his "alternative hypothesis" of obesity.  In fact, back in 2010 I had begun a chapter by chapter review of his Good Calories, Bad Calories book.  After reviewing only one chapter it was already very clear that Taubes was guilty of the many things he accused other obesity researchers of, namely leaving out data that did not conform to his beliefs and "cherry-picking."  On top of that, Taubes would selectively quote out-dated scientific data while ignoring more present, more reliable data that conflicted with his beliefs.  In fact, even some of Taubes's own references did not support the claims that he was making, and it made me wonder whether Taubes actually read his own references.  I was never able to continue on with my review as that pesky thing called life got in the way, but others, such as Eveyln over at the Carb-Sane Asylum and Dr. Stephan Guyenet have done an excellent job of refuting many of Taubes's tenets.

Of course, this has not stopped Taubes from continuing with his march with trying to gain some type of acceptance for his "alternate hypothesis;"  he recently published an essay in the British Medical Journal repeating many of his past claims regarding insulin, carbohydrate, and obesity.  His continuous push to try to gain acceptance of his "alternative hypothesis", despite overwhelming evidence against it, has made me question whether Taubes understands the entire scientific process of hypothesis testing.  Or perhaps he does, but is so emotionally and financially invested in his alternate hypothesis that he is unable to see the overwhelming evidence against it and how it is not consistent with many known observations about obesity.

29 Evidences for Macroevolution

If Gary Taubes wants to gain acceptance for his alternate hypothesis, then he needs to construct a thorough compilation of the predictions that his hypothesis would generate, and how those predictions are confirmed by existing scientific evidence.  He also needs to show how those predictions could be potentially falsified.  Falsification is an important component of the world of scientific hypothesis generation and testing, a component that seems to be missing from Taubes's many writings.

A perfect example of how to construct a hypothesis or theory, along with predictions, confirmations, and potential falsifications, is in Dr. Douglas Theobald's excellent series of essays entitled 29+ Evidences for Macroevolution: The Scientific Case for Common Descent.  In this series of articles, Dr. Theobald lays out a very thorough examination of all of the evidence that supports macroevolutionary theory.  He does so by laying out a  series of predictions that would be made by evolutionary theory.  He then provides the scientific evidence that confirms those predictions.  More importantly, he also describes how each prediction could be potentially falsified (and how none of the predictions have yet to be falsified).

Let's take a look at one example.  One of the most fascinating evidences that I've found for evolution is the shared presence of endogenous retroviruses  among organisms that share a common ancestor.  Here is how Dr. Theobald lays out the prediction, confirmation, and potential falsification:

Prediction 4.5: Molecular evidence - Endogenous retroviruses

Endogenous retroviruses provide yet another example of molecular sequence evidence for universal common descent. Endogenous retroviruses are molecular remnants of a past parasitic viral infection. Occasionally, copies of a retrovirus genome are found in its host's genome, and these retroviral gene copies are called endogenous retroviral sequences. Retroviruses (like the AIDS virus or HTLV1, which causes a form of leukemia) make a DNA copy of their own viral genome and insert it into their host's genome. If this happens to a germ line cell (i.e. the sperm or egg cells) the retroviral DNA will be inherited by descendants of the host. Again, this process is rare and fairly random, so finding retrogenes in identical chromosomal positions of two different species indicates common ancestry.


In humans, endogenous retroviruses occupy about 1% of the genome, in total constituting ~30,000 different retroviruses embedded in each person's genomic DNA (Sverdlov 2000). There are at least seven different known instances of common retrogene insertions between chimps and humans, and this number is sure to grow as both these organism's genomes are sequenced (Bonner et al. 1982Dangel et al. 1995Svensson et al. 1995Kjellman et al. 1999Lebedev et al. 2000Sverdlov 2000). Figure 4.4.1 shows a phylogenetic tree of several primates, including humans, from a recent study which identified numerous shared endogenous retroviruses in the genomes of these primates (Lebedev et al. 2000). The arrows designate the relative insertion times of the viral DNA into the host genome. All branches after the insertion point (to the right) carry that retroviral DNA - a reflection of the fact that once a retrovirus has inserted into the germ-line DNA of a given organism, it will be inherited by all descendents of that organism.

The Felidae (i.e. cats) provide another example. The standard phylogenetic tree has small cats diverging later than large cats. The small cats (e.g. the jungle cat, European wildcat, African wildcat, blackfooted cat, and domestic cat) share a specific retroviral gene insertion. In contrast, all other carnivores which have been tested lack this retrogene (Futuyma 1998, pp. 293-294; Todaro et al. 1975).

Potential Falsification:

It would make no sense, macroevolutionarily, if certain other mammals (e.g. dogs, cows, platypi, etc.), had these same retrogenes in the exact same chromosomal locations. For instance, it would be incredibly unlikely for dogs to also carry the three HERV-K insertions that are unique to humans, as shown in the upper right of Figure 4.4.1, since none of the other primates have these retroviral sequences.

Molecular vestigial characters are also a fascinating piece of evidence for evolution.  For example, the gene required for vitamin C synthesis is present in humans, yet it is not functional.  However, the predicted ancestors of humans had this function; somewhere down the line, a mutation caused the function of this gene to be lost, and all descendants share this pseudogene.  This is why all present day primates have the gene to produce vitamin C yet it is not functional.  Here is how Dr. Theobald lays it out:

Prediction 2.3: Molecular vestigial characters

Vestigial characters should also be found at the molecular level. Humans do not have the capability to synthesize ascorbic acid (otherwise known as Vitamin C), and the unfortunate consequence can be the nutritional deficiency called scurvy. However, the predicted ancestors of humans had this function (as do most other animals except primates and guinea pigs). Therefore, we predict that humans, other primates, and guinea pigs should carry evidence of this lost function as a molecular vestigial character (nota bene: this very prediction was explicitly made by Nishikimi and others and was the impetus for the research detailed below) (Nishikimi et al. 1992Nishikimi et al. 1994).


Recently, the L-gulano-γ-lactone oxidase gene, the gene required for Vitamin C synthesis, was found in humans and guinea pigs (Nishikimi et al. 1992Nishikimi et al. 1994). It exists as a pseudogene, present but incapable of functioning (see prediction 4.4 for more about pseudogenes). In fact, since this was originally written the vitamin C pseudogene has been found in other primates, exactly as predicted by evolutionary theory. We now have the DNA sequences for this broken gene in chimpanzees, orangutans, and macaques (Ohta and Nishikimi 1999). And, as predicted, the malfunctioning human and chimpanzee pseudogenes are the most similar, followed by the human and orangutan genes, followed by the human and macaque genes, precisely as predicted by evolutionary theory. Furthermore, all of these genes have accumulated mutations at the exact rate predicted (the background rate of mutation for neutral DNA regions like pseudogenes) (Ohta and Nishikimi 1999).

There are several other examples of vestigial human genes, including multiple odorant receptor genes (Rouquier et al. 2000), the RT6 protein gene (Haag et al. 1994), the galactosyl transferase gene (Galili and Swanson 1991), and the tyrosinase-related gene (TYRL) (Oetting et al. 1993).

Our odorant receptor (OR) genes once coded for proteins involved in now lost olfactory functions. Our predicted ancestors, like other mammals, had a more acute sense of smell than we do now; humans have >99 odorant receptor genes, of which ~70% are pseudogenes. Many other mammals, such as mice and marmosets, have many of the same OR genes as us, but all of theirs actually work. An extreme case is the dolphin, which is the descendant of land mammals. It no longer has any need to smell volatile odorants, yet it contains many OR genes, of which none are functional — they are all pseudogenes (Freitag et al. 1998).

The RT6 protein is expressed on the surface of T lymphocytes in other mammals, but not on ours. The galactosyl transferase gene is involved in making a certain carbohydrate found on the cell membranes of other mammals. Tyrosinase is the major enzyme responsible for melanin pigment in all animals. TYRL is a pseudogene of tyrosinase.

It is satisfying to note that we share these vestigial genes with other primates, and that the mutations that destroyed the ability of these genes perform their metabolic functions are also shared with several other primates (seepredictions 4.3-4.5 for more about shared pseudogenes).

Potential Falsification:

It would be very puzzling if we had not found the L-gulano-γ-lactone oxidase pseudogene or the other vestigial genes mentioned. In addition, we can predict that we will never find vestigial chloroplast genes in any metazoans (i.e. animals) (Li 1997, pp. 284-286, 348-354).

A final piece of evidence that has always been interesting to me is the presence of atavisms in living organisms.  Atavisms are the reappearance of a lost character specific to a remote ancestor, but not observed in the parents or recent ancestors of the organism.  Atavisms are extremely rare.  Examples of atavisms include the rare formation of extra toes in horses, similar to what was seen in their ancestors, living whales and dolphins found with hindlimbs (whales descended from terrestial mammals, and thus hindlimbs would be a characteristic of the ancient ancestors of whales) , including femurs and tibias, and humans found with tails (the ancient ancestors of humans had tails).  You can read here how Dr. Theobald lays it out; I'll only repost a section here due to the length:

Prediction 2.2: Atavisms

Anatomical atavisms are closely related conceptually to vestigial structures. An atavism is the reappearance of a lost character specific to a remote evolutionary ancestor and not observed in the parents or recent ancestors of the organism displaying the atavistic character. Atavisms have several essential features: (1) presence in adult stages of life, (2) absence in parents or recent ancestors, and (3) extreme rarity in a population (Hall 1984). For developmental reasons, the occasional occurrence of atavisms is expected under common descent if structures or functions are gradually lost between ancestor and descendant lineages (Hall 1984Hall 1995). Here we are primarily concerned with potential atavistic structures that are characteristic of taxa to which the organism displaying the structure does not belong. As a hypothetical example, if mutant horses occasionally displayed gills, this would be considered a potential atavism, since gills are diagnostic of taxa (e.g. fish) to which horses do not belong. As with vestigial structures, no organism can have an atavistic structure that was not previously found in one of its ancestors. Thus, for each species, the standard phylogenetic tree makes a huge number of predictions about atavisms that are allowed and those that are impossible for any given species.


Many famous examples of atavisms exist, including (1) rare formation of extra toes (2nd and 4th digits) in horses, similar to what is seen in the archaic horses Mesohippus and Merychippus, (2) atavistic thigh muscles in Passeriform birds and sparrows, (3) hyoid muscles in dogs, (4) wings in earwigs (normally wingless), (5) atavistic fibulae in birds (the fibulae are normally extremely reduced), (6) extra toes in guinea pigs and salamanders, (6) the atavistic dew claw in many dog breeds, and (7) various atavisms in humans (one described in detail below) (Hall 1984).


Potential Falsification:

These are essentially the same as for vestigial structures above.

To expand further on the "potential falsification" line, basically if we found atavisms that we would not expect in an organism because of its known ancestry, this would be potential falsification for evolutionary theory.  For example, if we found horses with gills, this would be a problem for evolutionary theory since gills were not part of any of the ancestors of horses.

Predictions, Confirmations, and Potential Falsifications for Gary Taubes's "Alternate Hypothesis"

If Gary Taubes's "alternate hypothesis" of obesity should hold any scientific validity, he should be able to set it up just as Dr. Theobald has set up his evidences for macroevolution.  He should be able to outline the evidences for his hypothesis, the predictions made, the confirmations of those predictions, and the potential falsification of those predictions.

For example, one of the crux's of Gary Taubes's hypothesis is that insulin is the mechanism behind how carbohydrates are uniquely fattening.  If this was true, a series of predictions could be made from this.  A couple of these predictions would be:

  • Prediction 1:  Hyperinsulinemia, or high insulin levels, should predict weight gain
  • Prediction 2:  Other substances that promote high levels of insulin secretion should promote weight gain

Let's take a look at prediction 1.  Confirmation of prediction 1 would mean studies should show that hyperinsulinemia is predictive of weight gain, and potential falsification would be that it is not, or even the reverse being true.  When you look at the data, the reverse of prediction 1 is true.  High insulin levels have been found to be predictive of less fat gain, not more.  Thus, already we have one prediction that would be made by Gary Taubes's hypothesis that has been falsified by the scientific data.

Let's take a look at prediction 2.  We know that carbohydrate is not the only substance that promotes insulin secretion; something that Gary Taubes has seemingly continued to miss is that protein is a powerful stimulus for insulin secretion.  In fact, the amino acid leucine will directly stimulate pancreatic beta cells to produce insulin.  Dairy products, are in fact, quite insulinemic and can cause just as much, if not more, insulin release than white bread.  Thus, based on prediction 2, we would predict that dairy products should also be uniquely fat promoting.  However, the scientific data does not support this.  When you look at the data on the whole, dairy either has no effect on weight gain, or has been found to promote weight loss.

These are just a couple examples of the predictions that could be derived from Gary Taubes's alternate hypothesis, predictions that are not supported by the available data.  There are many other predictions that can also be derived that I won't go into here, but it is safe to say that many of these predictions do not hold either.

My Challenge to Gary Taubes

If Gary Taubes wants his alternate hypothesis to be accepted by the scientific community, he should easily be able to lay it out just as Dr. Theobald has done.  This means examining all of the available data, offering the predictions that would be made by his hypothesis, offering the confirmatory data, and also describing the potential falsification, and being honest about that falsification if the contradictory data exists.  However, I have my doubts that we will ever see it laid out like this, given that if he were to do this, it would become very apparent just how flawed his alternate hypothesis really is.


18 Responses to “What Gary Taubes Can Learn From Evolutionary Theory: An Open Challenge To His “Hypothesis”

  • It is intensely interesting that the Taubes critics invariably focus upon his Carb-Insulin thinking and not the first part of his thesis- his historically rooted criticism of the reigning Energy Balance paradigm. Just because his Carb-Insulin idea may be invalid does not invalidate his criticisms. The reigning paradigm is riddled with problems– the discovery of irisin, the role of the microbiome, the overwhelming evidence of setpoints as clear proof homeostasis in energy balance. Krieger’s piece is at best interesting linkbait, at worst pandering marketing. Taubes is not a scientist, he is journalist. Krieger’s thesis is a straw man. And Taubes has started a foundation and raised money to advance the state of research, far more than what Krieger has done…

    • Sanjeev Sharma
      6 years ago

      > Krieger’s piece is at best interesting linkbait, at worst pandering marketing

      That is rich. Really. Who’s the one offering “eat infinite calories of the food you love most and lose weight easily”?

      Yet JAMES is pandering … riiiiight.

      your comment is so error riddled it leaves me speechl

    • his historically rooted criticism of the reigning Energy Balance paradigm

      Taubes’s criticism of the energy balance paradigm is based on a strawman caricature of it. This is why these criticisms have no validity.

      Just because his Carb-Insulin idea may be invalid does not invalidate his criticisms.

      When your criticisms are based on strawmen, yes, it does invalidate them.

      the discovery of irisin, the role of the microbiome, the overwhelming evidence of setpoints as clear proof homeostasis in energy balance.

      Obesity researchers are very well aware of all these factors, and more that Taubes never talks about. It is Taubes who leads you to believe that obesity researchers ignore all of these things.

      Taubes is not a scientist, he is journalist. Krieger’s thesis is a straw man.

      Taubes’s occupation is irrelevant. He has created a hypothesis just like any other scientific hypothesis. Thus, it should be judged like any other scientific hypothesis. Therefore, my thesis is not a strawman.

      And Taubes has started a foundation and raised money to advance the state of research, far more than what Krieger has done…

      Taubes could raise a billion dollars for obesity research but that is irrelevant to whether his arguments and hypothesis are sound. And one thing that I have done, which Taubes has not, is have actually published obesity research, as well as directly counseled numerous obese people. Taubes may be raising the money, but I, and others like me, are the ones in the trenches doing the work. And thus, people like me are in a far better position to understand obesity and the research that goes into it.

    • Taubes turned down a researcher friend of mine who’s an expert in cognitive science & has access to 2 separate labs designed to investigate environmental factors that drive eating behaviors (like Brian Wansink’s work). This would have been awesome for Taubes since we know from a half-century of experiments that a caloric deficit takes weight off, every–single–time. What we don’t have a grip on is the full range of behavioral factors driving chronic overeating & weight re-gain. Apparently, the purpose of Taubes’ project is not investigation, but rather confirmation of his pre-existent beliefs. That’s hugely ignorant of you to insult James by claiming Taubes has made more noble strides toward advancing the state of research. That’s the most idiotic thing I’ve read in a long time. And trust me, I come across some spectacularly stupid shit.

      • Jared Carr
        6 years ago

        When you get into a knife fight, best to bring a knife. The one who brings their buddy instead quickly finds they will either run or serve to delay the impending truth.

        Research is that knife and relying on expert opinion is a dangerous game. Guerin although i understand where your trying to come from, it will serve you better to be more objective of any evidence put in front of you.

        By the way good article James, i always greatly enjoy your stuff and will shortly subscribe.

        As for Alan, maybe a topic for your next AARR, the effects of p-ratio and fat and muscle cell depletion/atrophy on the mechanisms that drive appetite and hunger, especially after a period of dieting? I sure found it interesting, especially for the relevance it has in chronic exercise and diet prescription.

      • Can we be careful with the “every-single-time” sort of rhetoric? That isn’t true, and it isn’t what the data shows. In a “Healthy Person”…sure. However, when talking about energy balance what we are saying is that “the average person” at Bodyweight X, with a certain amount of activity will lose weight.

        I’ll offer up my wife who has a tumor in her hypothalamus. She will go from weight stable at a fair caloric range to unable to function to the point of not being able to get out of bed. However she will be incapacitated long before she starts losing significant weight. Yes, she is the exception. Yes, Caloriesin-caloriesout applies in that her TDEE is dropping because her metabolic output drops so much. But that doesn’t change the fact that “eat less” doesn’t work for her. She can strength train, she can put on impressive amounts of muscle, she can improve her over all composition but fat loss is a nightmare.

        When you say something like “every–single–time” you ignoring the exceptions, even if they only make up 1% or less of the over-weight community.

        • Funny how you call that rhetoric, then attempt to counter it using someone with a hypothalamic tumor. Well, guess what – that rule still applies to her, and I did not make any specification about reducing energy in; I said a CALORIC DEFICIT.

  • As always well done James!

    To Guerin I would simply say you gotta be kidding me! For Taubes it is always been about insulin and carbs = insulin = obesity. Have you read GCBC??

  • *Dr. Stephan Guyenet.

    Good article.

  • Hello,
    when I am fed up with internet broscience, what advice should I follow regarding diet and weight training? I know what’s wrong, but is there a book that would include real world advice on what to eat for your goals and how to realistically, sustainably weight train? It would be refreshing to understand what is important for non-professional “bodybuilder” and leave, because even though the debate is interesting, I suspect the real-life plans of what to do didn’t change very much over the last 30 years, we just understand the underlying biochemistry and physiology better. The rest is endless minutae debate while many miss the foundation.

    I found Brad Schoenfeld’s book Max Muscle Plan to be great, but maybe too equipment dependent, could you recommend something else as well, maybe more suitable to modify to dumbbell training?

    On diet, I read an excellent analysis on Paleo by Alan Aragon. In the articles of Lou Schuler, I realised that Paleo is wrong theoretically, but practically mostly right when one still uses that 80/20 rule, includes dairy and tubers etc.I try to follow what Alan said in that presentation, without counting calories, which is essentially the same thing Matt Stone recommends in Diet Recovery 2. Still, more info wouldn’t hurt.

    Could the effective approach be summed up briefly?


  • This is biochemistry, so while I follow the argument (well done James), I am afraid you will have to forgive me if I tend to ignore the detail!

    I was a scientist for 15 years (fisheries) and often came across the fine line between good science and bad science.

    The former follows the basic principles of finding the right question to ask, and then uses scientific methodology to find the answer – ensuring at each step of the process that objectivity is maintained as much as is humanly possible.

    The latter is does not adhere to sound scientific methodology, but instead applies inductive reasoning to a subjective belief. In doing so it extrapolates from poor foundations (data) and so the veracity of the conclusions reached are jeopardized. If this “bad” science relates to a popular issue, then it will tend to draw popular conclusions that seem justified to the majority of the non-scientific community and so these conclusions become false “truisms”.

    As in the fable the Emperor Wore No Clothes.

    We all know throughout history that people will tend to believe what they are lead to believe, especially if it is what they want to believe or need to believe.

    Perhaps the telling difference between good science and bad science is that the “good” scientist will accept the null hypothesis if significance levels support it. The “bad” scientist will engineer the situation to “neutralize” the data that gave rise to accepting the null hypothesis and continue blithely on.

    all the best

  • So glad you took the time to really clarify the scientific method of prediction>evidence>falsification/confirmation. There’s plenty of pseudo-scientific crap out there, but without explaining why a theory is flawed, the arguments against it just sound like bluster and venom. This article was very interesting and beneficial for someone like myself with little background in the sciences.

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