Gary Taubes responds to George Bray
The May 2008 issue of Obesity Reviews, the journal of the International Association for the Study of Obesity, contained a review written by George Bray, M.D. of Gary Taubes’ book Good Calories, Bad Calories (GCBC). Gary Taubes has written a rebuttal that will appear in this same journal. Before we get to Gary’s response, I would like to spend a little time on Bray’s review, which I found interesting and troubling on a number of fronts.
Most reviews of books in academic journals are of academic books and are, at most, a page and a half, maybe two pages, long. The Bray review of GCBC was 13 pages long, including two plus pages of citations. And this for what is basically a popular book written for a general audience, not an academic tome. In all the reading I do of the medical literature, I’ve never seen a book review come even close to this in terms of length and comprehensiveness. Obviously Taubes’ work struck a chord.
George Bray, M.D. is probably the most renowned figure in the field of obesity research today. He is the Boyd Professor at the Pennington Biomedical Research Center (and former executive director) in Baton Rouge, LA; he holds numerous other professorships at various academic institutions; he has held leadership positions in virtually every academic obesity organization in existence; he has authored or co-authored more than 500 scientific papers; he has written at least a dozen books and authored chapters in many more; and he figures prominently in the recent history of how the academic ideas of the causes and cures of obesity are what they are today. It speaks volumes that someone of Dr. Bray’s academic stature would be tapped to write a review (a review, in fact, that is longer than most scientific papers) of a popular book. GCBC has gotten the attention of the academic community.
I don’t think there is anyone out there who would be less likely to pooh pooh the idea that there is an obesity epidemic today than George Bray, yet he starts out his review with a couple of quotes from two centuries ago juxtaposed with a sentence from GCBC (see below) in an attempt right at the get go to belittle Gary’s arguments.
I believe no age did ever afford more instances of corpulency than our own. (Short, T. 1727)
If the increase of wealth and the refinement of modern times have tended to banish plague and pestilence from our cities, they have probably introduced to us the whole train of nervous disorders, and increased the frequency of corpulence. (Wadd, W. 1810)
Some factor of diet and/or lifestyle must be driving weight upward, because human biology and our underlying genetic code cannot change in such a short time. (Taubes, G. 2007)
Early on in the review after describing how GCBC is laid out, Dr. Bray writes the following:
As I read through Good Calories, Bad Calories, I found a number of errors of omission or commission that are important when relating diet to disease. There is no mention in the Diet-Heart section of low-density lipoprotein-cholesterol (‘bad cholesterol’) or of high-density lipoprotein-cholesterol (‘good cholesterol’).
I find this comment curious for a couple of reasons. First, anyone who has read GCBC knows that LDL- and HDL-cholesterol are covered in depth. Second, this review is published in an academic journal read by pretty much only academics (as compared to, say, the New England Journal of Medicine, which is also academic but has a much higher general and medical readership), so why the need to identify LDL-cholesterol as ‘bad cholesterol’ and HDL-cholesterol as ‘good cholesterol’? Surely the readers of this journal – academic obesity researchers – would know what LDL- and HDL-cholesterol are. Even JAMA and the New England Journal of Medicine wouldn’t identify these molecules this way. I suspect the intent was for this review to have wide circulation in the popular press and, consequently, was made more understandable for the lay reader.
Bray goes on to clarify his own position as to the cause of obesity:
Let me make my position very clear. Obesity is the result of a prolonged small positive energy surplus with fat storage as the result. An energy deficit produces weight loss and tips the balance in the opposite direction.
Again, I find the notion of Dr. Bray’s laying out his own view of the cause of obesity to be curious. Isn’t this supposed to be a review of GCBC? I would think that it would be more important to lay out the position of the author of the book being reviewed. Which Bray does by mischaracterizing Taubes’ position. Taubes’ ideas, according to Bray’s interpretation of them, run counter to the laws of thermodynamics, which interpretation is the refuge for all those who can’t or won’t understand what Gary is trying to say.
Bray is saying that obesity is a matter of creating a positive energy balance, i.e., consuming more calories than are being burned off. He implies that obesity is simply a matter of overeating and under exercising. If you consume more calories than you burn over time, you get fat. Gary’s perspective is that fundamentally obesity is a disorder of fat accumulation. And that this disorder drives people to overeat. Obesity, the disease, drives people to overeat and be lethargic. Bray believes that people overeat and are lethargic and, consequently, bring on the disease of obesity.
I’ve met George Bray, I’ve read many of his publications, and I’ve heard him lecture numerous times. And I can tell you that George Bray believes that obesity is a disease. And he believes that it should be regarded as a disease and treated with drugs. In an interview in 2005, he said
Obesity is multifactoral, develops over time, and manifest differently among individuals. I define it as a relapsing, chronic neurochemical disease. No specific dietary regimen can change that. We must accept the fact that we cannot cure obesity with diets.
Since we don’t fully understand the causes of obesity, we should take the patient’s responsibility out of it. Rather than focusing on the gluttony, sloth, and moral issues, it is far better to address the neurochemical imbalance and why it occurs. [In other words, let's give them drugs.]
But in this review we have Dr. Bray telling us that obesity is “the result of a prolonged small positive energy surplus.” He has definitely taken on the mantle of George you’re-fat-because-you-overeat Bray. It does make one wonder.
Enough of my preamble. You can decide for yourself.
Here is the link for the full-text version of George Bray’s review: bray-review-of-gcbc
Take a look about two thirds of the way down the right-hand column of the third page. Bray takes off on a riff about thermodynamics while completely missing the point Gary makes in GCBC. Unfortunately, the academics who read this, most of whom know little or nothing about thermodynamics, will swallow it hook, line and sinker and think they’ve been enlightened.
And here is Gary’s response: taubes-response-to-bray-ob-reviews
Enjoy.
ItsTheWoo,
Leptin won’t help (they’ve tried it) because if your insulin is chronically high, so is your leptin. And leptin resistance goes hand in hand with insulin resistance. So giving leptin to fat people is like giving insulin to hyperinsulinemic people. They unfortunately already have too much leptin but their brain won’t listen to its signals.
I should know. I was one of those people.
Fortunately, bringing excess leptin down and making brain more sensitive to leptin takes just the same measures as bringing high insulin down and making the tissues more sensitive to insulin: eating foods that don’t require much insulin. I.e. low carb foods. I’ve reduced my insulin levels almost by 500% in just 5,5 months. No drug can do that. You can imagine the weight loss that followed …
And talking about drugs, maybe pharmaceuticals can help with weight maintenance. But why use pharmaceuticals when you can use Protein Power or other similar plans to achieve the same goal and even surpass it?
Xenia – Oh I know leptin won’t do anything for weight LOSS… weight maintenance is another story. The weight reduced obese are leptin deficient, and this is a major cause of weight maintenance failure and a return of cravings/hunger that leads to diet failure.
When you give leptin to weight reduced people they can maintain weight much more easily.
An article about a study in june which demonstrates leptin allows people to maintain weight after a diet
I speak not only hypothetically but from personal experience. I have lost over 100% of my body weight. This has left me with a leptin level that is almost non-existent and I have all symptoms of leptin deficiency (other than obesity, of course). I am pariticpating in a study for hypothalamic amenorrhea which involves leptin replacement. Since starting a very low dose leptin all of my symptoms (including infertility) are much, much better! I feel like a normal weight person, it is very easy to eat normal calories, my glucose tolerance is better (less hypoglycemia) and I have so much more energy. I have had menses again when I haven’t had them in four years (after all the weight loss).
Don’t get me wrong – a low carb diet (like protein power) is essential to STOP obesity, and to reduce weight… but this obesity thing is a lot more complex and permanent than insulin stuffing food in fat cells. I believe that insulin damages the fat tissue, possibly because insulin makes too many fat cells grow in morbid obesity (sort of like a tumor). Google “insulin adipocyte hyperplasia”.
Because of how insulin changes the fat tissue permanently, dieting alone will not allow you to maintain a low fat mass normally (i.e. without metabolic consequences). Your depleted fat tissue will behave as if starving because the glut of depleted fat cells does not make leptin normally (even if your absolute fat mass is within a healthy range, your number of fat CELLs are not in normal range so you have a whole lot of small fat cells that act as if starving).
This is not something I”m making up… I actually had blood tests and it was all verified. My leptin level was extremely low.
Low carb will bring your insulin down and stop the disease process.
However, once developed, obesity is intractable because insulin changes the body and fat tissue in such a way that a high weight becomes “normal” weight. Leptin supplementation is a major, major part in allowing the previously obese to achieve a normal weight without starvation symptoms.
to maintain a weight loss where leptin is low,would liposuction be a good choice?
i,ve often thought that because obesity causes a growth in the number of fat cells(appears to be permanent)then one of the best therapies should be to reduce the total number of fat cells.
reduce through a low carb diet along with permanent fat cell removal through lipsuction.this should return the system to normal.
any thoughts?
What are we to do (as physicians) to at the very least open the eyes of our colleagues to the flawed minimally-based ‘theories’ (ie Bray) of obesity, weight gain/loss and nutritional health? Merely by asking these questions among my colleagues and with my patients (and friends for that matter!) has caused a flurry of consternation… If this is what it takes to stimulate a re-evaluation based on sound scientific method then count me in….
Hey Doc–
Glad to have you join the fray. I’m sure it will prove to be an interesting ride for you.
Cheers–
MRE
That was an amazing rebuttal by Taubes!
Ouch, guys. It’s “renowned.” Don’t you folks have copy editors?
We do now. Thanks. At least is wasn’t ‘reknowned.’
Cheers–
MRE
“I would suspect that Dr Bray does not want to bite the hand that feeds him.”
Exactly. I’m sure that a defense of his own career is the least of Dr. Bray’s conflicts of interest. Just one more pseudoscientist in the pocket of larger interests.
The discussion about leptin (above) begs the NEXT question:
Assuming the ‘insulin connection’ is dealt with, what can an obese (Or FORMERLY obese) person do to NATURALLY increase his/her leptin sensitivity?
I would expect that time at the new lower weight would help, but I don’t know for sure. I don’t think the issue has been studied. And I would make sure to keep my triglycerides low so that the leptin I did have could easily get into my brain.
This has been a very interesting discussion. I’ve had to read more and think more to try to understand. It seems that Taubes and many of you are pointing out that Bray is missing the point that, in some cases, the body preferentially stores available energy as fat rather than keeping it readily available for daily activity. So, even though the obese individual expends more energy than his thinner counterpart, the body is focussing on feeding the fat cells, not emptying them to cover the excess energy requirements. The individual feels low on energy and hungry enough to keep eating, even though he doesn’t appear to need additional calories or nutrition. This is the context, I think, of the assertion that overeating and sedentary habits can be a consequence of weight gain rather than the cause. Have the studies been done to test this hypothesis from end to end, with no missing links? It seems it would be very subtle and complicated to prove or disprove.
I read “Dr. Neal Barnard’s Program for Reversing [type II] Diabetes”, in which he focusses on the role of fat stored in muscle cells in causing insulin resistance in individuals who have a tendancy to store fat in their muscle cells (who also tend to have relatives with type II diabetes). This can lead to the whole metabolic syndrome spiral. He has clinical trial results that show his good carbs, VERY low-fat vegan diet with exercise is effective for weight loss, improved insulin sensitivity and improved cholesterol.
In the other corner is Dr. Richard Bernstein, whose “[type I or II] Diabetes Solution” involves “a low carbohydrate diet and exercise”. There are studies that support his approach for weight loss, blood sugar control, and improved blood lipids.
So there is more than one way to skin a cat. When Bray says “Weight loss is related to adherence to the diet, not to its macronutrient composition.” he is rolls several valid ideas into that one statement, but misses issues that statement does not address. Like — what influences adherence to the diet, do some diets just make weight loss more difficult, and why can’t everyone lose weight on a Michael Phelps diet?
“what influences adherence to the diet, do some diets just make weight loss more difficult, and why can’t everyone lose weight on a Michael Phelps diet?”
I gave up on dieting because I was so hungry and so tired all the time. I couldn’t adhere to a lowfat or calorie restricted diet very long. When I started eating fewer carbs the constant hunger went away, my appetite was cut in half.
It’s really amazing. I suppose we’ll gradually learn more about why some people do better on one type of diet than another, while others seem fine on any kind of diet.
Hi , Dr Eades.
You’d think that Dr. Bray being a doctor (who probably is a statinator) would realize that statins have 11 other very strong effects besides mere cholesterol lowering.
You’d think he could figure out that non – statin cholesterol lowering trials have been complete failures for reducing CAD deaths. And that dietary cholesterol lowering clinical intervention trials also have been failures. You’d think he’d take note of the JUPITER and ENHANCE trials. You’d also think he would know (as Dr. Uffe Ravnskov points out ) there is no dose response with statins.
You’d think he’d realize any ( slight ) reduction in CAD deaths amoung patients WITH CAD from the use statin drugs is enitrely due to these 11 effects , epsecially in light of the above mentioned evidence.
It really amazes me just how many doctors can’t seem to grasp that just because statin drugs (which lower cholesterol, but also do a myriad of other things ) lower CAD death rates amoung patients WITH CAD a little bit, doesn’t mean cholesterol lowering is the mechanism. They can’t seem to seperate mere cholesterol reduction from the use of statin drugs. Cholesterol lowering trials using non statin drugs (which have no pleotropic effects) and their lack of benefit should make this blatantly obvious to them , you would think.
For example The Lipid Research Clinics Coronary Primary Prevention Trial found that out of 3,086 pateints those taking cholestyramine had 30 CAD deaths vs 38 in the controls. Total mortality was 68 in the treatment group vs 71 in the controls. Another non – supportive result amoung many for the cholesterol theory proponents.
If anything statin drugs strongly challange the lipid hypothesis.
Take Care,
Razwell
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