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disagree with my views if you want, but my ideas get NIH grants, peer-reviewed publications, and presentations at professional conferences. I do make mistakes sometimes, but I am not a bullshit artist, nor am I dumb or attempting to mislead. Stephan Guyenet, PhD
Sam Feltham conducted recently four interviews, three of them with three CICO (Calories In Calories Out theory) supporters: Stephan Guyenet, PhD, carbsane and David Katz. The fourth interview is with himself.
I’m going to focus on Stephan Guyenet, PhD. The problem I find in this guy is that, too often, he misrepresents information or his arguments are blatantly wrong, and also that, too often, when I check the links he uses to back his arguments I feel I’ve been deceived.
Calories In Calories Out
Stephan Guyenet, PhD (extracts from the video):
just to make this explicit, I think it boïls down to calories in calories out […] ultimately the amount of fat in your body is determined by the amount of calories entering and the amount of calories leaving (see)
for the average person, or at least for the average person that was included in that study, it doesn’t matter whether it’s carbohydrate or fat, it’s the same amount of fat gain when the calories are controlled, […] if you look at the weight loss studies, it’s the same thing: calories seem to matter, composition doesn’t seem to matter. It doesn’t seem to matter what happens to insulin levels. There is no effect independent of calories, as far as you can tell. (see)
If you specifically look at the highest quality studies available, they consistently suggest that, as far as we know, the calorie value of food is the only food property that has ever been demonstrated convicingly to impact body fat mass. There is no other food property that has ever been demonstrated to impact body fat mass (see)
The idea that calories determine the amount of fat in our body is moronic, as I’ve explained over and over again in the blog (see,see,see,see). But that’s no surprise coming from Stephan Guyenet, PhD, since he is a well-known supporter of these ideas (and that is indeed the reason why Sam Feltham has interviewed him). Am I saying that a researcher, with a PhD in neurobiology, is making a childish reasoning mistake? I don’t know to what extent the fact that this guy has an academic degree makes his opinions better. Would my opinions be better if I put PhD after my name? But he is not just wrong: he is deceiving people, may be because he is a liar or may be because he is ignorant: the calories of the food have never been proved to determine body fat. There are plenty of scientific studies in which different isocaloric diets produce quite different outputs (see,see,see) or other studies in which people who are overfed by exactly the same amount of calories gain very different amounts of body fat (see,see,see,see). The ingested calories do NOT determine the body fat gain. Neither it is true that there are no other food properties that have been shown to affect body fat, as I’ve posted repeatedly in the blog. For example this study, this one or this review of studies conducted in metabolic wards. More examples can be found in the Por Temas section of this blog, mostly written in spanish language. I insist: it is false that calories have been demonstrated to determine body fat and it is false that there are no other properties of food, other than calories, that can affect the amount of body fat that we gain or lose.
The problem, as I see it, is that this guy is basing his career as a scientist on the hypothesis that the brain regulates the amount of body fat. And it seems to me that to be able to exploit that line of work he has to deny/ignore studies published in the scientific literature that contradict his working hypothesis. This guy has bet his career to one specific hypothesis (that we are fat because we eat too much because the food is too rewarding), one hypothesis that would be diluted if the insulin hypothesis were accepted as correct.
And, by the way, Stephan Guyenet, PhD, didn’t defend the CICO theory when in a recent study by Hall et al. it was proclaimed —fraudulently, in my opinion— that low-fat diets were more effective than low-carb diets for weight loss (see). That fantasy from the authors of the article would have as a corollary that the CICO theory is false, as the main author of that article conceded on twitter (see). It would seem that the composition of the diet did matter in that study. Stephan Guyenet, PhD, a believer in the god calorie, is not such a practicing believer when it suits his purposes.
Untruths about Gary Taubes
There are more interesting things in the video:
the insulin hypothesis of obesity, that Gary Taubes for example supports, he is not saying insulin resistance causes obesity, he is saying elevated insulin and increased insulin action causes obesity (see)
In 2011, three years before this video, Tom Naughton interviewed Gary Taubes. Below I reproduce two of Taubes’ answers:
As I discuss in GCBC, it’s quite likely that sugar — by which I mean a roughly 50-50 mixture of glucose and fructose — is the trigger that first sets off insulin resistance and then the vicious cycle from eating all carbs that leads to obesity, diabetes, etc. (see)
That’s exactly the possibility I’m discussing. Once you become insulin resistant, your body responds to carbs by secreting more insulin. So it is quite possible —and laboratory work backs this up— that sugar causes the initial insulin resistance because of the effect of the fructose on the liver. So if we never had sugar, we’d be able to eat the other carbs with relative impunity. But being possible doesn’t mean it’s true. I suspect it is, but I’m not sure exactly how this can be tested. (see)
From another interview, also from year 2011 (minute 39:35):
Sugar might be the trigger, if we didn’t eat sugar… and by sugar I mean sucrose or high-fructose corn syrup, may be the rest of the carbs would be relatively harmless, and that you need the glucose-fructose combination to trigger insulin resistance, and there is plenty of laboratory evidence that suggests that is the case, although it tends to be mostly in animals, and, yeah, to me insulin resistance is the fundamental problem. You know, once you become insulin resistant, hyperinsulinemic, then everything else follows.
But according to Stephan Guyenet, PhD, Taubes doesn’t talk about insulin resistance… I think that it is indifferent whether Guyenet lies or he is sincerely ignorant about the opinion of Taubes. In both cases he would be trying to deliberately mislead people. Given that in a recent post on his blog he clearly manipulated Taubes’ words to make them sound dogmatic (and thus to be able to attack them), the hypothesis of being ignorant doesn’t stand up.
More poor reasoning
In the video he also says (see) that if high insulin inhibited lipolysis, obese people would have less free fatty acids in the blood, compared to lean people, and not normal or even high levels as is the case. He had previously said the same on his blog (see):
CIH [Carbohydrate-Insulin Hypothesis] proposes that obesity is due to a reduction in the ability to release fatty acids from fat stores. What the evidence shows is the opposite: the more fat mass a person carries, the more fatty acids their fat tissue releases.
As we will see next, it is untrue that fatty acids release is increased, and in no way the data presented by Stephan Guyenet, PhD, demonstrates a contradiction in the insulin hypothesis of obesity.
According to him, the evidence shows that the more fat mass you have the greater is the release of fatty acids, a fact that, according to him, would contradict the idea that insulin causes obesity through a reduction in lipolysis. It is not easy to explain all the problems with his reasoning, because he mixes up a lot of things. Let’s focus for a moment on a first deception: talking only about the lipolysis rate (i.e. rate of release of free fatty acids coming from triglycerides in the adipocytes), when what really matters when talking about the accumulation of fat is the difference between lipolysis and lipogenesis (i.e. creation of triglycerides from free fatty acids). The net fat accumulation comes from the difference between fat uptake and fat release, and the absolute values of both rates, input and output, separately are not that important. Regarding to fat accumulation, is the difference between them what counts. And, as far as I can tell, nobody argues that insulin increases lipogenesis and reduces lipolysis (see).
Insulin signalling enhances lipid storage in adipocytes by both stimulating triacylglycerol synthesis and inhibiting its breakdown.
I will come back to this later.
The truth is that the article he linked as proof of his hypotheis shows precisely the opposite of what he is saying: “The rate of FFA release into plasma per unit of FM progressively decreased with increasing FM“). That is, that an increase in fat mass, and supposedly higher levels of insulin in blood, is associated with a decay in capability of the adipocytes to release free fatty acids. Less release per unit of fat mass. Therefore, it isn’t true what Stephan Guyenet, PhD, is saying and there is no such contradiction between the data from that experiment and the insulin hypothesis.
However, think about it this way. What really determines whether your fat mass is increasing or decreasing is the total amount of fat going into vs out of fat cells, not the amount per unit fat mass. So in the obese, the total amount of fat fat tissue is greater than the total amount exiting exiting to read a person’s fat tissue.
suppression of fatty acid release due to elevated insulin cannot explain the development or maintenance of obesity, because total fatty acid release increases in parallel with body fat accumulation.
Stephan Guyenet, PhD, said that adipocytes weren’t releasing less fatty acids as fat mass increased, a fact demonstrated by the increased release of fatty acids. We have already seen that his claim was false. In this new commentary he adds the term “total“. The total release is indeed increased, as in this study obese people have adipocytes that release less acids fatty (a fact consistent with the antilipolytic action of insulin), but have more fat mass. Altogether the effect is a bigger total release of fatty acids, but that fact doesn’t show a contradiction in the insulin hypothesis, as demonstrated by the fact that the release of fatty acids in the fat cells is indeed reduced. If we assume homogeneity —and I see no reason not to assume that as the authors of the article give us data normalized per unit of body fat— whatever happens to an adipocyte is what happens globally, but scaled by a factor. Talking about the total fatty acids release contributes nothing to the knowledge of what happens to an adipocyte.
I insist that this is just the rate of fatty acids release, i.e. lipolysis. It is not the net release of fatty acids. Although he falsely says it is increased in the obese people, t doesn’t matter if it is increased or reduced, if we don’t also know what’s happening with the lipogenesis. It is the difference between those two rates what really matters, at the cellular level or globally for all the fat mass. You can’t really draw conclusions as Stephan Guyenet, PhD does, from just the knowledge of what happens to the release of fatty acids.
The explanation from Guyenet seems alarmingly devoid of logic, as neither a clear reduction of lipolysis per unit of body fat mass shows a contradiction in the well-known role of insulin as a lipolysis inhibitor, nor has he shown to us any argument that would justify his claim that a insulin-mediated reduction of lipolysis (and an increase in lipogenesis, I would add) can’t explain the development of obesity. Does anyone believe that an increase in the total fatty acids release rate when you are fat demonstrated that high insulinemia hasn’t caused a net accumulation of fat in that person while the fat mass increase happened? Does that fact tell us anything about the temporal evolution suffered by both rates while the fat mass was increasing? I don’t think so. The rate of lipolysis is decreased, as therefore so has to be the rate of lipogenesis, if the amount of body fat in that person is stable. And while that person became fatter lipogenesis was bigger than lipolysis, a difference perhaps caused primarily by abnormally high levels of insulin? Nothing in this study says it can’t be so.
One quote (see):
we find, across the studies, a marked negative relationship—that is, as fat mass increases, so NEFA release per unit weight of adipose tissue decreases. There was a similar strong relationship when plotted against fasting insulin (Fig. 3B), suggesting that the hyperinsulinemia of insulin resistance, or long-term adaptation to hyperinsulinemia, are means by which fatty acid release is downregulated.
SG, PhD has repeatedly claimed that the insulin hypothesis is dead (see, see, see) and, as a curiosity, has been disrespectful to a person who doesn’t share his views saying that he is “utterly confused” and has “cognitive dissonance” (see). The answer he got was anything but friendly (see) and things didn’t get any better as time went by (see).
As a final remark, it seems that fortunately Sam Feltham has learned nothing from Stephan Guyenet, PhD:
“Biochemistry leads and physics follows”
- Insulinic regulation of the adipose tissue metabolism
- The role of insulin in the adipocyte
- Insulina, obesidad, zombis y fanatismo (2/2)