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. Stephen 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:
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. 1982; Dangel et al. 1995; Svensson et al. 1995; Kjellman et al. 1999; Lebedev et al. 2000; Sverdlov 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).
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:
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. 1992; Nishikimi 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. 1992; Nishikimi 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).
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:
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 1984; Hall 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).
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.