GCBC Reference Check ~ Part IV of ? ~ Kipnis

In a recent post, following up on discussion of Grey & Kipnis as  in the Fasting Insulin & Weight Loss post,  I noted that G&K was  but one study (of many) where calories were controlled that demonstrated definitively that it was calories, and only calories, and not carbohydrates or any hormonal effect thereof, that determined weight loss/stability.

Taubes made the slanderous claim on his blog:

... the value of controlling variables in a scientific experiment is something that a reasonably well-educated child supposedly understands. And what I want to know is why don’t nutritionists understand it and those researchers out there doing diet trials and studying obesity and weight regulation. Because their failure to do so — and I would argue that it may be a willful failure — has led to what may be another of the great misconceptions in modern nutrition research.

I ended my post with the following:

Now I realize 1971 is a bit too contemporary for Mr. Taubes, but since he did reference a text published in 1972 he could have found this study were he interested.

I think Mr. Taubes owes Drs. Grey and Kipnis an apology for his unprofessional, unethical, and downright below the belt assaults on their scientific abilities and integrity! Don't you?

In a "gotcha" moment, regular commenter Christian had this to say:

Hmm, the only problem is that

a) Taubes read the study and

b) also interviewed the researcher and

c) the researcher himself comes to a different conclusion regarding his own study than you do.

Let me begin by saying that, although I've read GCBC, and some sections multiple times, my many waking hours spent stalking {} have kept me from my GCBC Reference Memorization drills.  It seems to me that G&K is just the type of study Taubes laments will never happen, only it did 30 years earlier.   At this point I'm not surprised that he came across it, and even cited it.  It's been all downhill from Reshef when it comes to looking into Gary's references.

To (a):  I would point out that, by his own admission, citing a study or reference is no indication that Taubes has actually read it, let alone viewed it with a critical eye.  (Apparently one of the things I got Gary to do was actually read Keith Frayn's text!  See, I'm useful for something after all.  Phew!)

The funny thing about G&K is that it's a rather poor quality scan of an old article.   So more than with the  fancy PDF's and nice HTML texts - where you often have to click to view tables - these graphs practically leap off the pages at you.  If you even skim the article, knowing nothing of the dietary interventions you are presented with fasting insulin vs. bodyweight.  Graphs that CLEARLY show no correlation!!

So let's see what Gary Taubes had to say about this study in GCBC.  I've included the two paragraphs preceding his mention of this Grey & Kipnis study for context:  

Since none of this research is particularly controversial, it’s hard to imagine why obesity researchers would not take seriously the hypothesis that carbohydrates have a unique ability to fatten humans—or, as Thomas Hawkes Tanner put it in The Practice of Medicine almost 140 years ago, that “farinaceous and vegetable foods are fattening, and saccharine matters are especially so.” Researchers who study carbohydrate metabolism have found this science compelling. In 1991, the Belgian physiologist Henri-Géry Hers, an authority on what are known as glycogen-storage diseases, one of which is named after him, put it this way: “Eating carbohydrates will stimulate insulin secretion and cause obesity. That looks obvious to me….” But this simple chain of cause and effect has nonetheless been rejected out of hand by authority figures in the field of human obesity, who believe that the cause of the condition is manifestly obvious and beyond dispute, that the law of energy conservation dictates that obesity has to be caused by eating too much or moving too little.

George Cahill, a former professor at the Harvard Medical School, is a pedagogical example. Cahill had done some of the earliest research on the regulation of fat-cell metabolism by insulin in the late 1950s, and had coedited the 1965 Handbook of Physiology on adipose-tissue metabolism. In 1971, when Cahill gave the Banting Memorial Lecture at the annual meeting of the American Diabetes Association, he described insulin as “the overall fuel control in mammals.” “The concentration of circulating insulin,” he explained, “serves to coordinate fuel storage and fuel mobilization into and out of the various depots with the needs of the organism, and with the availability or lack of availability of fuel in the environment.” When I interviewed Cahill in 2005, he told me it was true that “carbohydrate is driving insulin is driving fat.” But Cahill did not consider this chain of cause and effect to be a sufficient reason to speculate that carbohydrates drive obesity. Nor did he consider it a possibility that avoiding carbohydrates might reverse the process. Rather, he believed unconditionally that positive caloric balance was the critical factor. When it came to weight regulation, Cahill repeatedly told me, “a calorie is a calorie is a calorie.” He acknowledged that the obese ate no more, on average, than the lean, and this is why he believed that the obese must be fundamentally lazy and this was the proximate cause of their obesity.*121 There was no reason to test competing hypotheses, Cahill said, because any competing hypothesis would contradict the laws of physics as he understood them.

When clinical investigators tried to unravel the connection between diet, insulin, and obesity in human subjects, as the University of Washington endocrinologist David Kipnis did in the early 1970s, the results were invariably analyzed in light of this same preconception. Kipnis had fed ten “grossly obese” women a series of three-and four-week diets that were either high or low in calories, and high or low in carbohydrates. The fat-rich diets lowered insulin levels, Kipnis reported in The New England Journal of Medicine in 1971, and the carbohydrate-rich diets raised them, regardless of how many calories were being consumed. Even when these women were semi-starved on fifteen hundred calories a day, a high-carbohydrate content (72 percent carbohydrates and only 1 percent fat) still increased their insulin levels, even compared with the hyperinsulinemia of these obese women on their normal diets.  

One interpretation of these results is that we could remove the carbohydrates from the diet and replace them with fat, and weight would be lost, perhaps without hunger, because insulin levels would drop, even if the total calories consumed did not. Kipnis’s results, as the University of Heidelberg clinicians Gotthard Schettler and Guenter Schlierf wrote in 1974, underlined the “necessity of restricting carbohydrates in obesity in order to restore insulin levels to normal, thus hopefully decreasing appetite and fat deposition….”

Kipnis, however, refused to believe that carbohydrates might cause obesity, or that avoiding carbohydrates might ameliorate the problem. When I interviewed him over thirty years later, he described the findings of his research as “very obvious.” “You manipulate the amount of carbohydrates you give a human,” he said, “you can manipulate his or her basal insulin level.” He also said that “insulin causes deposition of fat in fat cells.” But when it came to the cause of human obesity or weight gain, Kipnis rejected the relevance of these physiological phenomena. “Most people are obese because they eat more than they need to sustain the energy requirements that they have,” he said. “They eat too damn much.”

As an aside, the opening paragraphs and those that precede it make clear that, in this place in this book, Taubes is making the case that calories have nothing to do with weight gain/loss - it's the carbohydrates.  Skipping down to the last two paragraphs regarding Kipnis, Taubes - for a refreshing change of pace - doesn't mischaracterize Kipnis' position on this matter.  But he does, however, paint him as an ideological zealot who can't see the forest for the trees that it is insulin that makes you fat by causing fat deposition into the fat cells.  Kipnis knew, OTOH, from conducting this study, that these subjects were indeed eating "too damn much".  And Kipnis, although he and Grey weren't specifically looking at this aspect in their study, knew that the obese young ladies maintained weight when they ate an energy balance level of calories (irrespective of whether Carb/Fat/Pro was 62/18/20 or 25/53/22), and lost weight predictably on a 1500 cal CRD (again irrespective of the extremes of carb or fat content that were more extreme in this leg -- essentially zero fat v. zero carb, ~25% protein).

But Gary says "One interpretation of these results is that we could remove the carbohydrates from the diet and replace them with fat, and weight would be lost, perhaps without hunger, because insulin levels would drop, even if the total calories consumed did not."


Really??

Nope.  Gary is just pulling another one from his nether-regions in this "analysis".  Did he read G&K and conclude that when insulin levels dropped weight was lost?  I'll repeat the scatter plot of G&K's results that need not even be constructed if one looks at the graphs they did provide, but is instructive nonetheless.

Not only do the insulin levels reported in either leg of this study correlate one iota with weight changes, this is a particularly damning piece of evidence that definitively denounces Taubes' carbohydrate hypothesis.  Because when calories were reduced, subjects lost weight.  Period.  When carbohydrate was varied from as little as 135g to as much as 650g on weight stable caloric intake, the subjects maintained weight.  And weight loss was not impeded by just under 300g carbs on the 1500 cal CRD and weight loss.

In this regard, Gary misrepresents what G&K really demonstrated, and then portrayed Kipnis as one of those willful failures amongst all the other hapless scientific researchers.  I think Taubes owes Grey and especially Kipnis an apology for this.  

So as to point (b) from the outset of this post, one might want to have been a fly on the wall (or bug in the phone) for this conversation, as it would have been interesting to note what Kipnis said regarding his research.  We'll never know.  Imagine how Kipnis must feel with the amount of their conversation Taubes left on the "cutting room floor" that ultimately portrays him in such an unfavorable light in print.  But I digress ...

As to point (c), I don't see that Kipnis came to a different conclusion than I do, nor how this is relevant.  Firstly, tons of blogs and bloggers thrive on "debunking" or otherwise tearing to shreds various studies and the conclusions drawn by the hopelessly biased and paid off by Big ________ (fill-in-the-blank) researchers.  Secondly, tons of secondary research is published every day (everywhere from peer review journals to research blogs to research papers in academia) of this sort.  Kipnis seems to be a calorie guy in his interview with Gary (so we agree) and doesn't come to his "different" conclusion in a manner that has any bearing on the validity of mine.

The conclusion that fasting insulin bears no correlation to weight loss is solid.  Also solid is the conclusion that fasting insulin is not only not *the* factor that determines weight loss, but probably not even *a* factor.  

I doubt Gary read this paper, or if he did he did so with his usually biased eye:  that being one looking for evidence to support one's hypothesis while avoiding inconvenient evidence refuting it along the way.  Here in G&K Gary had a study that demonstrated that in the already "grossly obese", very dramatic swings in dietary content  - utterly inconsistent with what these obese were eating before the study (avg. 48/38/14 carb/fat/pro) - can influence basal insulin levels for relatively short periods of time.  He jumped the gun.

Too bad for him he provides the reader with evidence directly countering his hypothesis.  I'd call this extraordinary.  :-)