Posts Tagged ‘low carbohydrate’

In the last post, I had proclaimed a victory for dietary carbohydrate restriction or, more precisely, recognition of its explicit connection with cell signaling. I had anointed the BMC Washington meeting as the historic site for this grand synthesis. It may have been a matter of perception — many researchers in carbohydrate restriction entered the field precisely because it came from the basic biochemistry where the idea was that the key player was the hormone insulin and glucose was the major stimulus for pancreatic secretion of insulin. We had largely ignored the hook-up with cell-biology because of the emphasis on calorie restriction, and it may have only needed getting everybody in the same room to see that the role of insulin in cancer was not separate from its role in carbohydrate restriction. (more…)

It was in July of 2012 that I suddenly realized that we had won, at least scientifically. It was now clear that we had a consistent set of scientific ideas that supported the importance of insulin signaling in basic biochemistry and cell biology and that there was a continuum with the role of dietary carbohydrate restriction in obesity, diabetes or for general health.  The practical considerations, how much to eat of this, how much to eat of that, were still problematical but now we had the kernel of a scientific principle. In fact, it was not so much that we had the answer as that we had the right question.  In science, the question is frequently more important than the answer.  Of course, winning wasn’t the original idea. When my colleagues and I got into this, about ten years ago, coming from basic biochemistry, we hadn’t anticipated that it would be such a battle, that there would be so much resistance to what we thought was normal scientific practice.

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“I may have killed a dozen men but I never stole a horse.”

— last words of outlaw in the American West before being hanged.

The principle known as Occam’s Razor is usually understood as a statement that a simple explanation is preferable to one that is more complicated. The principle has many variations. It might be interpreted as saying that you have to have a sense of priorities. Occam’s Razor is not exactly a scientific idea so much as a principle of aesthetics expressing the value of elegance in scientific explanations. Named for William of Ockham (c. 1285–1349) — it is also referred to as Ockham’s Razor — the idea can be described mathematically by saying that if the outcome, Y, of an experiment can be expressed with a rough sort of equation: Y = A + B + C +… and if A explains Y, then you don’t want to drag in B, C, etc unless you absolutely have to. (A more compelling description might be to consider the principle in terms of a power series and if you are inclined to mathematics, Wikipedia has excellent description and animation).

Where we’re going. The bottom line on this post is that for obesity, diabetes and general health, the predominant effect of diet, the major contribution to the outcome — A in the equation above — is provided by substituting fat (any fat) for carbohydrate (any carbohydrate). That’s what the science says. That will give you the best effect. The B contribution (type of fat, type of carbohydrate) is strictly secondary. The practical consequence: if for some reason, you want to reduce fructose in the diet, the best advice is to reduce carbohydrate across the board. You can then add the additional advice “preferably sugar and high fructose corn syrup” but even if B doesn’t kick in, you will surely get a benefit. Most of all, if you take out Pepsi® and put in Pepperidge Farm® Whole Wheat Bread, you may not accomplish much.

In practical terms, confronted with a phenomenon that has many controlling variables, make sure you can’t do with one before you bring in the others. In nutrition, when people say that the phenomenon is very complicated, they frequently mean that they don’t want to look at a simple explanation. On its practical side, if a patients in a dietary experiment responds to the level of carbohydrate, you have to assume that carbohydrate across the board is the controlling variable. If, however, you think that it is specifically the fructose in the diet that caused the effect, or if you think that it was an additional effect of fructose beyond its role as carbohydrate, then that is something that you have to show separately. Until you do, the fructose effect is sliced off by Occam’s Razor. In terms of policy, you don’t want to go after fructose unless you are sure that it is not primarily the role of fructose acting as a carbohydrate.

So, there is a logical question surrounding recommendations against sugar and especially against fructose. What we know well in nutrition is that if you replace carbohydrate with fat, as in Krauss’s experiment described in the previous post, things improve and this is why we suggest low-carbohydrate diets as the “default diet,” the one to try first for diabetes and metabolic syndrome and probably for cardiovascular risk. I have, however, received at least two emails from well-known nutritionists saying that “the type of carbohydrate is more important than how much carbohydrate” and, of course, Rob Lustig is everywhere telling us how toxic sugar is but never suggesting that a low carbohydrate diet is any kind of ideal. On the face of it, the idea doesn’t make much sense. Fructose is a carbohydrate so the amount and type are not easily separable.

There are all kinds of strange things in nutrition. People actually say that the type of diet you are on is less important than whether you stay on the diet. While true, it is like saying that if you are baseball player, whether you get a hit depends less on who’s pitching than whether you remember to show up for the game. But anyway, I decided to ask the question about relative importance of type and amount of carbohydrate on facebook and on a couple of blogs where things like Hizzona’ Michael Bloomberg’s Big Bottle Ban or related questions was being discussed. Here’s how I put it.

For general health, should you change the type of carbohydrate or replace the carbohydrate with fat (any natural fat, no trans-fat)? It’s a thought experiment (not real world situation with subtleties). You only get three choices: For general health (no change in calories):

1. Change type of carbohydrate
2. Replace carbohydrate with fat
3. It doesn’t matter

Strangely enough, I did not get very many answers. I think that people didn’t like the question and even when they voted, they wanted to put in disclaimers:

ANS: 2. Replace carbohydrate with fat But I want to add; not replacing ALL the carbs. Only the worst ones. You know; Sugar, grains (bread and pasta) potatoes and rice.

RDF: You can do that in a real case but the question is about first-order strategies. You only get 3 choices.

ANS: okej 2. Replace carbohydrate with fat.

And James Krieger jumped in:

“Feinman, your ‘thought experiment’ is essentially a false trichotomy…same thing as a false dichotomy except you’ve arbitrarily limited it to 3 choices rather than 2, when in fact there are many more. This is why you aren’t getting answers…because you’re committing a common logical fallacy.”

I explained that

“It’s called Occam’s Razor…. I’m simply asking: if you could theoretically do only one thing, 1. or 2., which would be better? There are many other choices but in a thought experiment you imagine these to be held constant or to be the higher order terms in a power series.”

But, of course, Krieger was right. The question is not really answerable. Not because it is false so much as because it is confused. Fructose is a carbohydrate and whatever its unique contribution, it is hard to say it is more important than the contribution of the fructose as a carbohydrate. It is a screwy idea but, again, that’s how it was phrased to me in emails and probably in print someplace. Researchers in this field say: “it is not carbohydrate per se (or glycemic index/load) that is involved in adverse metabolic effects of dietary carbohydrates, but rather the type of carbohydrate,…” The kind of evidence that is used to support such an idea, the kind of result that is used to support fructophobia is in the paper by Stanhope, et al.

Stanhope, et al. measured the effects of chronic consumption of either glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks in overweight and obese subjects. The figure below shows the superimposed outcomes in the response of triglycerides in the course of a day (red lines = fructose, blue = glucose). It is obvious that there is a difference — people consuming fructose had higher triglyceride responses (although fasting levels were not different). Looking at the figure, though, there is big variation in the data and it is not clear that everybody showed big differences between the glucose and fructose curves: the error bars represent standard error of the mean (SEM) which, while it shows you that there may be a statistically significant difference between the trials, doesn’t display very well the spread of the individual values, that is, whether a few individuals biased the grouped data. To convert to standard deviation, which gives you a better feel for the variation, you multiply, in this case, by about 4. In other words, there must have been big overlap between the fructose people and the glucose people.

So there is an effect of type of carbohydrate. But what to compare it to? The study of Krauss in the previous post showed much bigger changes when you substituted fat for carbohydrate and, in fact, those were fasting triglycerides which, in the fructose experiment, didn’t change at all but this is a different kind of experiment. So for comparison, we can look at a study from Jeff Volek’s lab where carbohydrate was replaced with fat in the carbohydrate restricted diet (CRD) in comparison to a low-fat diet (LFD). I described this study previously because it showed how carbohydrate, rather than dietary saturated fat, was actually controlling saturated fat in the blood. Here is what the responses to meals as seen in plasma triglycerides:

Maybe it’s the Fructose.

The fructose experiments can be shaved with Occam’s razor — insofar as we can tell, reducing carbohydrate across the board is more effective than changing type of carbohydrate. But how do we know that the effect of reducing carbohydrates wasn’t due to removing fructose — fructose is a carbohydrate so carbohydrate restriction may be due to the de facto removal of the fructose? Well, we don’t. It’s unlikely but possible. Where does this leave us? Wikipedia cites Bertrand Russell’s variation of Occam’s Razor: “Whenever possible, substitute constructions out of known entities for inferences to unknown entities.” This is a pompous way of saying: “don’t make things up.”

Another way of looking at Stanhope’s experiment is to recognize that it does not show, as the title says, “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids… in overweight/obese humans.” What the paper really is about is “Consuming fructose-sweetened, not glucose-sweetened, beverages as part a high carbohydrate diet (55 % of energy) increases….” In other words, you don’t know whether you would get any benefit in changing from fructose to glucose if the total carbohydrate were lower.  In terms of our Occam’s Razor equation, you can’t say that you have proved that your results are due to A  (the major controlling variable (carbohydrate)) when all you have studied is A with the specific change in  the term (secondary effect of the type of carbohydrate). Stanhope’s experiment shows: if you are on a high carbohydrate diet, replacing glucose with fructose will make things worse but that’s different than saying that fructose is toxic. From a practical point of view, if you are on a high carbohydrate diet and it is not giving you the health benefit you want, replacing sugar with starch may give you disappointing results compared to simply cutting down on carbohydrates.

How to Reduce Fructose Consumption.

If you want to encourage fructose reduction, encourage carbohydrate restriction (this is where we have the most information) with the additional proviso of recommending fructose reduction as the first carbohydrate to remove (may also help but we have less data).

Flawed Studies.

In combination with the previous post, a summary of things to look for in a study to make sure that the authors are not misleading you and/or themselves:

1. Understatement is good. “Healthy” is a value judgement. “Fructose-sweetened” is not the same thing as “fructose-sweetened in a high carbohydrate diet.”

2. Where are the pictures? The author has an obligation to make things clear. A graphic representation is usually an indication of a desire to explain.

3. Has Occam’s Razor been applied? Are secondary effects taken as primary?

Crabtree’s Bludgeon

Finally, we should not forget Crabtree’s Bludgeon which is described by Wikipedia as “a foil to Occam’s Razor” and “attributed to the fictitious poet, Joseph Crabtree, after whom the Crabtree Foundation is named.” It may be expressed as:

‘No set of mutually inconsistent observations can exist for which some human intellect cannot conceive a coherent explanation, however complicated.’

Doctor:    Therein the patient

  Must minister to himself.

Macbeth: Throw physic [medicine] to the dogs; I’ll none of it.

— William Shakespeare, Macbeth

The quality of nutrition papers even in the major scientific and medical journals is so variable and the lack of restraint in the popular media is so great that it is hard to see how the general public or even scientists can find out anything at all. Editors and reviewers are the traditional gate-keepers in science but in an area where rigid dogma has reached Galilean proportions, it is questionable that any meaningful judgement was made: it is easy to publish papers that conform to the party line (“Because of the deleterious effects of dietary fructose, we hypothesized that…”) and hard to publish others: when JAMA published George Bray’s “calorie-is-a-calorie” paper and I pointed out that the study more accurately supported the importance of carbohydrate as a controlling variable, the editor declined to publish my letter.  In this, the blogs have performed a valuable service in providing an alternative POV but if the unreliability is a problem in the scientific literature, that problem is multiplied in internet sources. In the end, the consumer may feel that they are pretty much out there on their own. I will try to help.  The following was posted on FatHead’s Facebook page:

 How does one know if a study is ‘flawed’? I see a lot of posts on here that say a lot of major studies are flawed. How? Why? What’s the difference if I am gullible and believe all the flawed studies, or if I (am hopefully not a sucker) believe what the Fat Heads are saying and not to believe the flawed studies — eat bacon.

Where are the true studies that are NOT flawed…. and how do I differentiate? : /

 My comment was that it was a great question and that it would be in the next post so I will try to give some of the principles that reviewers should adhere to.  Here’s a couple of guides to get started. More in future posts:

 1“Healthy” (or “healthful”) is not a scientific term. If a study describes a diet as “healthy,” it is almost guaranteed to be a flawed study.  If we knew which diets were “healthy,” we wouldn’t have an obesity epidemic. A good example is the paper by Appel, et al. (2005). “Effects of protein, monounsaturated fat, and carbohydrate intake on blood pressure and serum lipids: results of the OmniHeart randomized trial,” whose conclusion is:

“In the setting of a healthful diet, partial substitution of carbohydrate with either protein or monounsaturated fat can further lower blood pressure, improve lipid levels, and reduce estimated cardiovascular risk.”

 It’s hard to know how healthful the original diet, a “carbohydrate-rich diet used in the DASH trials … currently advocated in several scientific reports” really is if removing carbohydrate improved everything.

Generally, understatement  is good.  One of the more famous is from Watson & Cricks’s 1953 paper in which they proposed the DNA double helix structure. They said “It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material.”  A study with the word “healthy” is an infomercial.

2. Look for the pictures (figures).  Presentation in graphic form usually means the author wants to explain things to you, rather than snow you.  This is part of the Golden Rule of Statistics that I mentioned in my blogpost “The Seventh Egg”  which discusses a very flawed study from Harvard on egg consumption. The rule comes from the book PDQ Statistics:

“The important point…is that the onus is on the author to convey to the reader an accurate impression of what the data look like, using graphs or standard measures, before beginning the statistical shenanigans.  Any paper that doesn’t do this should be viewed from the outset with considerable suspicion.”

The Watson-Crick  paper cited above had the diagram of the double-helix  which essentially became the symbol of modern biology.  It was drawn by Odile, Francis’s wife, who is described as being famous for her nudes, only one of which I could find on the internet.

Krauss, et. al. Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia.

The absence of a figure may indicate that the authors are not giving you a chance to actually see the results, that is, the experiment may not be flawed but the interpretation may be misleading, intentionally or otherwise.  An important illustration of the principle is a paper published by Krauss. It is worth looking at this paper in detail because the experimental work is very good and the paper directly — or almost directly — confronts a big question in diet studies: when you reduce calories by cutting out carbohydrate, is the effect due simply  to lowering calories or is there a specific effect of carbohydrate restriction.  The problem is important since many studies compare low-carbohydrate and low-fat diets where calories are reduced on both. Because the low-carbohydrate diet generally has the better weight loss and better improvement in HDL and triglycerides, it is said that it was the weight loss that caused the lipid improvements.

So Krauss compared the effects of carbohydrate restriction and weight loss on the collection of lipid markers known collectively as atherogenic dyslipidemia.  The markers of atherogenic dyslipidemia, which are assumed to predispose to cardiovascular disease, include high triglycerides (triacylglycerol), low HDL and high concentrations of the small dense LDL.

Here is how the experiment was set up: subjects first consumed a baseline diet of  54% of energy as carbohydrate, for 1 week. They were then assigned to one of four groups.  Either they continued the baseline diet, or they kept calories constant but reduced carbohydrate by putting fat in its place.  The three lower carbohydrate diets had 39 % or 26 % carbohydrate or 26 % carbohydrate with higher saturated fat.  After 3 weeks on constant calories but reduced carbohydrate, calories were decreased by 1000 kcal/d for 5 week and, finally, energy was stabilized for 4 weeks and the features of atherogenic dyslidemia were measured at week 13.  The protocol is shown in the figure from Krauss’s paper:

The Abstract of the paper describes the outcomes and the authors’ conclusions.

Results: The 26%-carbohydrate, low-saturated-fat diet reduced [atherogenic dylipidemia]. These changes were significantly different from those with the 54%-carbohydrate diet. After subsequent weight loss, the changes in all these variables were significantly greater…(my italics)

 Conclusions: Moderate carbohydrate restriction and weight loss provide equivalent but non-additive approaches to improving atherogenic dyslipidemia. Moreover, beneficial lipid changes resulting from a reduced carbohydrate intake were not significant after weight loss.

Now there is something odd about this.  It is the last line of the conclusion that is really weird. If you lose weight, the effect of carbohydrate is not significant?  As described below, Jeff Volek and I re-analyzed this paper so I have read that line a dozen times and I have no idea what it means.  In fact, the whole abstract is strange.  It will turn out that the lower (26 %) is certainly “significantly different from.. the 54%-carbohydrate diet” but it is not just different but much better. Why would you not say that?  The Abstract is generally written so that it sounds negative about low carbohydrate effects but it is already known from Krauss’s previous work and others that carbohydrate restriction has a beneficial effect on lipids and the improvements in lipid markers occur on low-carbohydrate diets whether weight is lost or not.  The last sentence doesn’t seem to make any sense at all.    For one thing, the experiment wasn’t done that way.  As set up, weight loss came after carbohydrate restriction.  So, let’s look at the data in the paper.  There are few figures in the paper and Table 2 in the paper presents the results in a totally mind-numbing layout.  Confronted with data like this, I sometimes stop reading.  After all, if the author doesn’t want to conform to the Golden Rule of Statistics, if they don’t want to really explain what they accomplished, how much impact is the paper going to have.  In this case, however, it is clear that the experiment was designed correctly and it just seems impossible from previous work that this wouldn’t support the benefits of carbohydrate restriction and the negative tone of the Abstract needs to be explained.  So we all had to slog through those tables.  Let’s just look at the triglycerides since this is one of the more telling attributes of atherogenic dyslpidemia.  Here’s the section from the Table:

Well this looks odd in that the biggest change is in the lowest carb group with high SF but it’s hard to tell what the data look like.  First it is reported as logarithms. You sometime take logs of your data in order to do a statistical determination but that doesn’t change the data and it is better to report the actual value.  In any case, it’s easy enough to take antilogs and we can plot the data.  This is what it looks like:

It’s not hard to see what the data really show: Reducing carbohydrate has an overwhelming effect on triglycerides even without weight loss.  When weight loss is introduced, the high carbohydrate diets still can’t equal the performance of the carbohydrate reduction phase.  (The dotted line in the figure are data from Volek’s earlier work which Krauss forgot to cite).

The statements in the Conclusion from the Abstract are false and totally misrepresent the data.  It is not true as it says “carbohydrate restriction and weight loss provide equivalent…” effects. The carbohydrate-reduction phase is dramatically better than the calorie restriction phase and it is not true that they are “non-additive”  Is this an oversight?  Poor writing?  Well, nobody knows what Krauss’s motivations were but Volek and I plotted all of the data from Krauss’s paper and we published a paper in Nutrition & Metabolism providing an interpretation of Krauss’s work (with pictures).  Our conclusion:

Summary Although some effort is required to disentangle the data and interpretation, the recent publication from Krauss et al. should be recognized as a breakthrough. Their findings… make it clear that the salutary effects of CR on dyslipidemia do not require weight loss, a benefit that is not a feature of strategies based on fat reduction. As such, Krauss et al.  provides one of the strongest arguments to date for CR as a fundamental approach to diet, especially for treating atherogenic dyslipidemia.

An important question in this experiment, however, is whether even in the calorie reduction phase, calories are actually the important variable.  This is a general problem in calorie restriction studies if for no other reason than that there is no identified calorie receptor.  When we published this data, Mike Eades pointed out that in the phase in which Krauss reduced calories, it was done by reducing macronutrients across the board so carbohydrate was also reduced and that might be the actual controlling variable so we plotted the TAG against carbohydrate in each phase (low, medium and high carb (LC, MC, HC) without or with weight loss (+WL) and the results are shown below

This is remarkably good agreement for a nutrition study. When you consider carbohydrates as the independent variable, you can see what’s going on.  Or can you?  After all, by changing the variables you have only made an association between carbohydrate and outcome  of an experiment. So does this imply a causal relation between carbohydrate and triglycerides or not?  It is widely said that observational studies do not imply causality, that observational studies can only provide hypothesis for future testing. It certainly seems like causality is implied here.  It will turn out that a more accurate description is that observational studies do not necessarily imply causality and I will discuss that in the next posts.  The bottom line will be that there is flaw in grand principles like “Random controlled trials are the gold standard.” “Observational studies are only good for generating hypotheses,”  “Metabolic Ward Studies are the gold standard.” Science doesn’t run on such arbitrary rules.

The Office of Research Integrity is hosting a conference on the Quest for Research Excellence and, for the first time, there is session that directly confronts policy and The Crises in Nutrition. The Speakers will delineate the problem — the two worlds of establishment nutrition and the major challenge of low carbohydrate diets, the growing problems of childhood obesity and our failure to deal with it, the confusion in the popular press on scientific issues, and finally, the voice of the patient, the failure to listen to the people who are dissatisfied with official guidelines and who have found workable solutions themselves. Three specific goals are recommended: 1) open hearings in which all researchers are represented, 2) funding research in which all people in low carbohydrate research work with others and finally, 3) a new oversight agency from NSF or Office of Research and Technology Policy.

The three goals may be a useful crystallizing point for moving forward. What can you do?

  1. Contact your elected officials and copy one of the authors from the conference. Use the Abstracts below as a basis for your own version of what needs to be done. The three goals can be more narrowly focussed for your own interests.
  2. Encourage local media to cover the meeting. Information is at http://ori.hhs.gov and the speakers can be contacted directly.
  3. Publicize your version of the three goals on your blog, your facebook page or other social media.

2011 Office of Research Integrity Conference Washington DC

Quest for Research Excellence, March 15, 2012.

Session on Crisis in Nutrition.

Chair: Richard David Feinman Contact Information: feinman@mac.com (917) 554-7794

Introduction and Abstracts.

The interest in nutrition for general health and for the prevention and treatment of disease is probably greater than at any time in history. A fairly large research community has grown up to provide information on the subject but the excellence of the results and their ability to inform the general public is highly questionable. The prospect for the future quality of research is similarly discouraging. This session focusses on a crisis in nutrition: the confusion in the public’s mind and the lack of accountability of official agencies and their failure to consider minority points of view. Four areas are considered in this session: the need to consider work that has been done on carbohydrate restriction (the major alternative to current recommendations), the limitations of current media representations of research, the problem of childhood obesity, and finally, the failure to listen to the patients who have not been well served by current ideas and who have discovered alternatives for themselves. The public, athrough forums and comments to blogs and other social media, have expressed substantial dissatisfaction with the current state of medical nutrition.

Three approaches are suggested as first steps for resolving the current crises:

  1. First, we need hearings to be held by congress or HHS in which all major researchers in nutrition are represented. We have to have everybody in the game. The USDA guidelines committee, the American Health Association nutrition panels have to meet with their critics. In particular, researchers in dietary carbohydrate restriction should be able to meet and discuss issues with their critics. This is what the government can do. Better than taxation or other punitive measures, they can bring out the information. The NIH or congress should hold meaningful hearings where all sides are heard.
  1. Second, we need to fund a study in which researchers in dietary carbohydrate restriction and critics of such diets cooperate to design a long-term comparison of CRD and low-fat diets, Mediterranean diets or whatever. The groups agree on methods of procedure, make-up of the diets, how compliance will be effected, and what parameters will be measured. They “write the paper first, leaving room for the data,” that is, they agree in advance on what the possible outcomes are and what conclusions could be drawn from them. In this way, the public and other scientists will have a sense that the issues have adequately been addressed and the results reliably evaluated.
  1. Finally, what’s needed is the creation of a new oversight organization, possibly under the auspices of the National Science Foundation or the Office of Science and Technology Policy in which scientists with no personal stake in nutrition, assess bias in grant awards and publications. The scientific principles involved in nutrition are neither so technical nor so profound that accomplished scientists from other fields cannot evaluate them. Such organizations might make recommendations (or indicate the limitations in existing knowledge that prevent making recommendations) after hearing all credentialed experts.

In the end, we have to say whether there is really a problem or not. Is their really an epidemic of obesity and overweight? Is there a crisis in the incidence of diabetes, or not? Are our health problems, the rising cost, the patient suffering, real? If they’re real, we have to use everything we have. We have to have real science and we can’t continue with one expert committee after another making recommendations but taking no responsibility for outcomes and refusing to show any willingness to confront their critics.

Crisis in nutrition: I. Research Integrity and the Challenge of Carbohydrate Restriction.

Author: Richard David Feinman.

Objective: Research integrity extends beyond falsification of data and explicit misconduct. We assessed the extent to which established majority opinion recommending dietary fat and saturated fat reduction has failed to cite contradictory evidence, accepted undocumented conclusions and marginalized contributions of alternative points of view, specifically the role of dietary carbohydrate restriction, the major challenge to current recommendations..

Main points: Government and private health agencies have long recommended a reduction in dietary fat, particularly saturated fat, in the treatment or prevention of cardiovascular disease, obesity and diabetes. While there are many disclaimers, low-fat in some form remains the standard nutritional recommendation. Alternative strategies based on control of insulin fluctuations via carbohydrate restriction, while widely used by many in the community, have been discouraged if not actually attacked. This has contributed to a “two worlds” system that has increased confusion among scientists and the public. While there are many exceptions and some emerging acceptance of carbohydrate restriction — which frequently fails to cite earlier work — there is a perception of a majority opinion with pervasive control of the scientific infrastructure: editorial boards, study sections and health agency administration. Examples will be given of undocumented negative statements about low-carbohydrate diets, misrepresentation of data and extensive failure to cite relevant papers from the literature. Most troubling is the tendency to accept some of the conclusions previously demonstrated in low-carbohydrate research without, again, giving appropriate citations to that research. This has led a significant part of the population to distrust official recommendations and medical science.

There is a need to re-evaluate published data on carbohydrate restriction and to guarantee adequate peer review of future manuscripts and grant applications on macronutrient composition of the diet. More generally, better communication and cooperation between researchers and physicians with different opinions can only benefit science and society, a society that is admittedly not making good progress on obesity, diabetes and metabolic syndrome.

Conclusions & Recommendations:

Recommendations for better integration of different points of view include government-sponsored meetings where all scientific approaches can present their own opinions and address critics, representation on study sections and editorial boards of people with experience in carbohydrate restriction-insulin control diets and long term comparative trials that include PIs with experience and understanding of the role of the glucose-insulin axis in obesity, diabetes and metabolic syndrome. Agreement in advance between the “two worlds” as to the expected outcomes and interpretations would provide most benefit for the public and scientist-community interactions. Given the pervasiveness of the problem, in the end, intervention of new oversight agencies, e.g. from NSF or Office of Science and Technology, may be needed

Figure 1. Comparison of low-carbohydrate diets to low-GI diets and high cereal diets.

Crisis in nutrition: II. The popular media and research publications  

Author: Richard David Feinman.

Objective: The public relies on popular media for description of nutrition research. A major interest is the controversy over macronutrient composition of the diet and particularly the role carbohydrate-restriction, the major challenge to official recommendations. The goal is to assess the extent to which statements to the media and especially press releases from authors, author institutions and journals accurately represent the results of reported research. To determine the extent to which personal bias influences and is taken as fact by the media.

Main points: Authors of research papers should sensibly have great freedom in describing the implications of their research to the media, but it is important that the public be aware of when that opinion does or does not follow directly from the publication. Two examples are given. In one, an animal study (Foo, et al. Proc Natl Acad Sci USA 2009, 106: 15418-15423), the accompanying press release implied that it was motivated by observations of patients in a hospital which were not described, were unsubstantiated and would have been purely anecdotal. In a second example, a press release stated that carbohydrate-restricted diets (CRDs) were not included in a comparative study because of their low compliance (Sacks, et al. N Engl J Med 2009, 360: 859-873. No data were given to support this assertion and it is, in fact not true — CRDs have, on average, better compliance than other dietary interventions. The study concluded that the macronutrient composition of the diet was not important even though, as implemented, dietary intake was the same for the groups studied and, again, the CRD was not included in the study. It seems likely that that this would have an inhibiting effect on the willingness of individuals to choose a CRD, an outcome that was not justified by the published research.

Conclusions & recommendations: Practices should be evaluated and guidelines should be generated by academic societies, scientific journals and the popular media as to what constitutes appropriate press description of published research. Reasonable principle are that only those specific conclusions that derive directly from the publication. The generally accepted idea that authors make clear what is their personal opinion and what is the product of research should be the norm.

Biography: Richard David Feinman, PhD in Chemistry (University of Oregon) is Professor of Cell Biology at SUNY Downstate Medical Center. His current area of research is nutritional biochemistry and biochemical education especially as it relates to macronutrients and bioenergetics. He is founder of the Nutrition & Metabolism Society and former co-editor-in-chief of the journal Nutrition & Metabolism.

Figure 2. The world according to Reuters. Low-fat is good. It’s bad. It’s not as bad as we thought. Wait! Eat more fruits and vegetables. “The low-dat diet craze?” Is that what it’s been? Is?

Crisis in nutrition: III. Childhood Obesity: Prevention and Intervention 

Author: Wendy Knapp Pogozelski, Dept of Chemistry, SUNY Geneseo, Geneseo, NY 14454.

Objective: Almost one-third of American children aged 2-11 qualify as obese or overweight, with obesity-related diseases such as type 2 diabetes greatly on the rise in this population. Despite the labeling of the crisis as “epidemic,” funding to study childhood obesity has been limited and restricted to the traditional intervention strategies (to reduce calories, to reduce dietary fat and to exercise more) despite the fact that these efforts have been largely unsuccessful. The time has come for frank assessment of foundational beliefs about a) the causes of obesity in children and b) effective prevention and intervention strategies. This talk will discuss assumptions that are barriers to research and will compare results from traditional calorie-restriction programs with results from programs that have emphasized carbohydrate control and insulin reduction.

Main points: The current generation of children is predicted to be the first to experience a lower life expectancy than that of its parents. Children across the world are experiencing unparalleled rates of obesity, heart disease and type 2 diabetes. Relatively little formal research has addressed the causes of childhood obesity, perhaps due to an assumption that the problem is already understood. Despite reluctance to use children as subjects in studies that depart from the traditional “eat less and exercise more” philosophies, it has been noted that the current efforts, dietary recommendations, educational programs and mandates of school lunch programs could be characterized as experiments. These experiments, like the numerous interventions based on traditional strategies, have had poor results but it has been very difficult to implement or fund those approaches that focus on carbohydrate control despite demonstrable success in this area. We will examine typical meals given in schools and at home, compare data from various obesity interventions and discuss causes of obesity on a molecular level

Conclusions & recommendations: The crisis warrants policy change. 1) Funding for childhood obesity should be increased. 2) A broader range of methods and principal investigators should be instituted, with greater accountability required of funded investigators. 3) The USDA nutritional recommendations, a “one size fits all” guide for school meal programs should be reevaluated and reformulated to take into account all strategies for obesity prevention and intervention. 4) Education for physicians, dietitians and health care professionals, as well as the general public, should be altered to include an understanding of the most positive results in obesity prevention.

Biography: Wendy Pogozelski, PhD in Chemistry (Johns Hopkins University) is Professor of Chemistry at SUNY Geneseo. Her research has been in radiation effects, DNA damage, and DNA computing. Current efforts are directed toward biochemical-based nutrition education for health professionals, educators and the general public. In addition to developing teaching materials that incorporate nutrition research, Dr. Pogozelski writes and lectures on diabetes and works with local and national organizations to improve nutrition education.

Figure 3. Before and After from James Bailes’s No More Fat Kids

Crisis in nutrition: IV. Vox Populi

Authors: Tom Naughton, Jimmy Moore, Laura Dolson

Objective: Blogs and other social media provide insights into how the public views the current state of nutrition science and the official dietary recommendations. We ask what can be learned from online discussions among people who dispute and distrust the official recommendations.

Main points: A growing share of the population no longer trusts the dietary advice offered by private and government health agencies. They believe the supposed benefits of the low-fat, grain-based diets promoted by those agencies are not based on solid science and that benefits of low-carbohydrate diets have been deliberately squelched. The following is typical of comments the authors (whose websites draw a combined 1.5 million visitors monthly) receive daily:

“The medical and pharmaceutical companies have no interest in us becoming healthy through nutrition. It is in their financial interest to keep us where we are so they can sell us medications.”

Similar distrust of the government’s dietary recommendations has been expressed by doctors and academics. The following comments, left by a physician on one of the authors’ blogs, are not unusual:

“You and Denise Minger should collaborate on a book about the shoddy analysis put out by hacks like the Dietary Guidelines Advisory Committee.”

“Sometimes I wonder if people making these statements even took a basic course in biochemistry and physiology.”

Many patients have given up on their health care professionals and turn to Internet sites for advice they trust. This is particularly true of people with diabetes who find that a low-fat, high-carbohydrate diet is not helping them control their blood glucose. As one woman wrote about her experience with a diabetes center:

“I was so frustrated, I quit going to the center for check ups.”

The data suggest a serious problem in science-community interactions which needs to be

explored.

Conclusions & recommendations: Our findings document a large number of such cases pointing to the need for public hearings and or conference. The community is not well served by an establishment that refuses to address its critics from within the general population as well as health professionals.

Figure 4. Some comments from the Active Low-Carber Forums (140, 660 members on March 12, 2012).

Biographies:

Tom Naughton is a former writer for a health magazine, a contributor to the Encylopedia Britannica’s Health and Medical Annual, a documentary filmmaker, and popular blogger who specializes in health and nutrition issues.

Jimmy Moore’s top-rated “Livin’ La Vida Low-Carb” blog has drawn more than 6 million visitors since 2005. His podcast show, “The Livin’ La Vida Low-Carb Show with Jimmy Moore” has featured interviews with hundreds of respected doctors and researcher. He has also authored two books.

Laura Dolson, MS is a writer and cancer support provider at Mediconsult.com, and hastaught health and nutrition classes at a junior high charter school in California. Her About.com nutrition website draws hundreds of thousands of visitors monthly.


(Answers to last week’s organic puzzler at the end of this post).

One of the more remarkable results from Jeff Volek’s laboratory in the past few years was the demonstration that when the blood of volunteers was assayed for saturated fatty acids (SFA), those subjects who had been on a very low-carbohydrate diet had lower levels than those on an isocaloric low-fat diet. This, despite the fact that the low-carbohydrate diet had three times the amount of saturated fat as the low-fat diet. How is this possible? What happened to the saturated fat in the low-carbohydrate diet? Well, that’s what metabolism does. The saturated fat in the low-carbohydrate arm was oxidized while (the real impact of the study) the low-fat arm is making new saturated fatty acid. Volek’s former student Cassandra Forsythe extended the idea by showing how, even under eucaloric conditions (no weight loss) dietary fat has relatively small impact on plasma fat.

The essential point of what I now call the Volek-Westman principle — we should be speaking of basic principles because the idea is more important than specific diets where it is impossible to get any agreement on definitions — the principle is that carbohydrate, directly or indirectly through insulin and other hormones, controls what happens to ingested (or stored) fatty acids. The motto of the Nutrition & Metabolism Society is: “A high fat diet in the presence of carbohydrate is different than a high fat diet in the presence of low carbohydrate.” Widely attributed to me, it is almost certainly something I once said although it has been said by others and the studies from Volek’s lab give you the most telling evidence.

The question is critical. Whereas the scientific evidence now establishes that dietary saturated fat has no effect on cardiovascular disease, obesity or anything else, plasma saturated fatty acids can be a cellular signal and if you study the effect of dietary saturated fatty acids under conditions where carbohydrate is high and/or in rodents where plasma fat better correlates with dietary fat, then you will confuse plasma fat with dietary fat. An important study identified potential cellular elements in control of gene transcription that bear on lipid metabolism.

So, it is important to know about plasma saturated fatty acids. First, recall that strictly speaking there are only saturated fatty acids (SFA) — this is explained in detail in an earlier post.  What is called saturated fats simply mean those fats that have a high percentage of SFAs — things that we identify as “saturated fats,” like butter, are usually only 50 % saturated fatty acids (coconut oil is probably the only fat that is almost entirely saturated fatty acids but because they are medium chain length, they are usually considered a special case).

In Volek’s study, 40 overweight subjects were randomly assigned either to a carbohydrate-restricted diet (abbreviated CRD; %CHO:fat:protein = 12:59:28) or to a low fat diet, (LFD; %CHO:fat:protein = 56:24:20). The group was unusual in that they were all overweight would be characterized as having metabolic syndrome, in particular they all had, atherogenic dyslipidemia, which is the term given to a poor lipid profile (high triacylglycerol (TAG), low HDL-C, high small-dense LDL (so-called pattern B)). Metabolic syndrome (MetS) is the predisposition to CVD and diabetes and is characterized by the constellation of overweight, atherogenic dyslipidemia and, by now, a dozen other markers.

The paper is one of the more striking for the differences in weight loss between two diet regimens. Although participants were not specifically counseled to reduce calories, there was a reduction in total caloric intake in both two groups. The response in weight loss, however, due to the difference in macronutrient composition, was dramatically different in the two groups. The CRD group (labelled as very low carbohydrate ketogenic diet (VLCKD) in the figure) lost twice as much weight on average as the low-fat controls despite the similar caloric intake. Although there was substantial individual variation, 9 of 20 subjects in the CRD (VLCKD) group lost 10% of their starting weight. more than that lost by any of the subjects in the LFD group. In fact, nobody following the LFD lost as much weight as the average for the low-carbohydrate group and, unlike George Bray’s demonstration of caloric inefficiency, whole body fat mass was where the major differences between the CRD (VLCKD) and LF appeared (5.7 kg vs 3.7 kg). Of significance is the observation that fat mass in the abdominal region decreased more in subjects on the CRD than in subjects following the LFD (-828 g vs -506 g). This is one of the more dramatic effects of carbohydrate restriction on weight loss but many have preceded it and these have been frequently criticized for increasing the amount of saturated fat (whether or not any particular study actually increased saturated fat). Although the original “concern” was that this would lead to increased plasma cholesterol, eventually saturated fat became a generalized villain and, insofar as any science was involved, the effects of plasma saturated fat were assumed to be due to dietary saturated fat. The outcome of Volek’s study was surprising. Surprising because the effect was so clear cut (no statistics needed) and because an underlying mechanism could explain the results.

Saturated Fat

The dietary intake of saturated fat for the people on the VLCKD (36 g/day) was threefold higher than that of the people on the LFD (12 g/day). When the relative proportions of circulating SFAs in the triglyceride and cholesterol ester fractions were determined, they were actually lower in the low carb group. Seventeen of 20 subjects on the CRD (VLCKD) showed a decrease in total saturates (the others had low values at baseline) in comparison to half of the subjects consuming the LFD had a decrease in saturates. When the absolute fasting TAG levels are taken into account (low carbohydrate diets reliably reduce TAB=G), the absolute concentration of total saturates in plasma TAG was reduced by 57% in the low carbohydrate arm compared to 24% reduction in the low fat arm who had, in fact, reduced their saturated fat intake. One of the saturated fatty acids of greatest interest was palmitic acid or, in chemical short-hand, 16:0 (16 means that there are 16 carbons and 0 means there are no double bonds, that is, no unsaturation).

So how could this happen? The low fat group reduced their SFA intake by one-third, yet had more SFA in their blood than the low-carbohydrate group who had actually increased intake. Well, we need to look at the next thing in metabolism.

In the post on An Introduction to Metabolism, we made the generalization that there were roughly two kinds of fuel, glucose and acetyl-CoA (the two carbon derivative of acetic acid). The big principle in metabolism was that you could make acetyl-CoA from glucose, but (with some exceptions) you couldn’t make glucose from acetyl-CoA, or more generally, you can make fat from glucose but you can’t make glucose from fat. How do you make fat from glucose? Part of the picture is making new fatty acids, the process known as De Novo Lipogenesis (DNL) or more accurately de novo fatty acid synthesis. The mechanism then involves successively patching together two carbon acetyl-CoA units until you reach the chain length of 16 carbons, palmitic acid. The first step is formation of a three carbon compound, malonyl-CoA, a process which is under the control of insulin. Malonyl-CoA starts the process of DNL but simultaneously prevents oxidation of any fatty acid since, if you are making it, you don’t want to burn it. This can be further processed, among other things, can be elongated to stearic acid (18:0). So this is a reasonable explanation for the increased saturated fatty acid in the low-fat group: the higher carbohydrate diet has higher insulin levels on average, encouraging diversion of calories into fatty acid synthesis and repressing oxidation. How could this be tested?

It turns out that, in addition to elongation, the palmitic acid can be desaturated to make the unsaturated fatty acid, palmitoleic acid (16:1-n7, 16 carbons, one unsaturation at carbon 7) and the same enzyme that catalyzes this reaction will convert stearic acid (18:0) to the unsaturated fatty acid oleic acid (18:1n-7). The enzyme is named for the second reaction stearoyl desaturase-1 (SCD-1; medical students always hate seeing a “-1” since they know 2 and 3 may will have to be learned although, in this case, they are less important). SCD-1 is a membrane-bound enzyme and it seems that it is not swimming around the cell looking for fatty acids but is, rather, closely tied to DNL, that is, it preferentially de-saturates newly formed palmitic acid to palmitoleic acid.

There is very little palmitoleic acid in the diet so its presence in the blood is an indication of SCD-1 activity. The data show a 31% decrease in palmitoleic acid (16:1n-7) in the blood of subjects on the low-carb arm with little overall change in the average response in the low fat group. Saturated fat, in your blood or on your plate?

Forsythe’s paper extended the work by putting men on two different weight-maintaining low-carbohydrate diets for 6 weeks. One of the diets was designed to be high in SFA (high in dairy fat and eggs), and the other, was designed to be higher in unsaturated fat from both polyunsaturated (PUFA) and monounsaturated (MUFA) fatty acids (high in fish, nuts, omega-3 enriched eggs, and olive oil). The relative percentages of SFA:MUFA: PUFA were, for the SFA-carbohydrate-restricted diet, 31: 21:5, and for the UFA diet, 17:25:15. The results showed that the major changes in plasma SFA and MUFA were in the plasma TAG fraction although probably much less than might be expected given the nearly two-fold difference in dietary saturated fat and, as the authors point out: “the most striking finding was the lack of association between dietary SFA intake and plasma SFA concentrations.”

So although it is widely said that the type of fat is more important than the amount, the type is not particularly important. But, what about the amount? A widely cited paper by Raatz, et al. suggested, as indicated by the title, that ‘‘Total fat intake modifies plasma fatty acid composition in humans”, but the data in the paper shows that differences between high fat and low fat were in fact minimal (figure below).

The bottom line is that distribution of types of fatty acid in plasma is more dependent on the level of carbohydrate then the level or type of fat. Volek and Forsythe give you a good reason to focus on the carbohydrate content of your diet. What about the type of carbohydrate? In other words, is glycemic index important? Is fructose as bad as they say? We will look at that in a future post in which I will conclude that no change in the type of carbohydrate will ever have the same kind of effect as replacing carbohydrate across the board with fat. I’ll prove it.

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Answers to the organic quiz.

“Despite the claims of various diet gurus, excess calorie consumption alone and not the amount of protein in an individual’s diet contributes to the accumulation of unwanted fat….” That’s the tendentious and pretty much inaccurate first line of the press release from JAMA on George Bray’s over-feeding study “Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating.”  “Amount of protein?”  What’s going here?  It hasn’t really been about protein.  Most of us “diet gurus” have claimed that carbohydrate, not protein, in the diet was the key macronutrient in regulating metabolism, consistent with the basic biochemistry of the glucose-insulin axis, or as Dr. Bray described Gary Taubes’s position in a review of Good Calories, Bad Calories:

“The problem is the carbohydrates in the diet, their effect on insulin secretion, and thus the hormonal regulation of homeostasis – the entire harmonic ensemble of the human body.”

Reduction in dietary carbohydrate puts increased demands on protein for gluconeogenesis and other processes but the controlling variable is the carbohydrate. The controversy in nutrition has been largely about fat vs carbohydrate.  Should we be on a low-carbohydrate diet or a low-fat diet?

The quotation in the press release says accurately that “Earlier studies in human beings suggested that diets containing either high or low [levels of] protein are less ‘metabolically efficient’ than diets with normal protein levels.”  Accurate, but written as if metabolic efficiency had always been recognized for its importance in weight loss, as if there had not been a dispute over whether the costs of processing protein were important in energy balance, indeed, written as if Bray and coworkers had not maintained that only calories count in weight gain or loss.  The idea of metabolic advantage, that one diet could be more efficient — more weight gained/calorie — has been largely resisted by the nutritional establishment.  Is this slouching toward Metabolic Advantage? (“Who knows not [the Duke] is dead?  Who knows he is?”)

The debate is also about calories.  Should you cut calories or just cut out carbs?  Is it really “excess calorie consumption” and not the effect of excess carbohydrates ? “A calorie is a calorie” or not. Many of the gurus have gone beyond “claiming” to demonstrating that when carbohydrates are low, weight loss is greater than when carbohydrate is high and that the weight loss on a low-carbohydrate diet is primarily in fat stores rather than lean mass.  In head-to-head comparisons, for however long they are compared, low-carbohydrate diets generally out-perform low-fat diets on other parameters as well, glycemic control, the features of atherogenic dyslipidemia. This has been the major challenge to traditional nutrition and the general approach has been to simply ignore this data and dismiss the researchers with innuendo as above.

In some sense, Bray, et al. answered a question that we weren’t asking, but protein is important if more complicated than carbohydrate and fat. So what did the study find? Bray and coworkers compared three diets of 5 %, 15 % and 25 % protein at an excess of calories, that was nominally the same in each group. The study was a random controlled study and was carried out in a metabolic ward so the results are more accurate than the usual diet study that relies on dietary records.  There is something odd about this study, though, in that if you want to say that only calories are the independent variable, you can’t keep calories constant.  What was actually done was to determine the energy requirements for weight maintenance over a run-in period of 2-3 weeks on a maintenance and then an additional 40 % of calories was added.  So although the calories are constant relative to initial energy expenditure, they are not absolutely the same and this is a study of the effect of varying calories while keeping calories constant. The figure below, re-drawn from Figure 6 of the paper comparing intake of absolute energy to protein intake makes you stop and think.

When you have a small number of subjects, a single outlier can bias the results.  If you remove the single highest point (circled in red), the correlation is likely to get much weaker and the normals and low begin to separate.  In other words, the individual variation (the relative efficiency) is sufficient to make it hard to see the effect of variable energy or, perhaps, as the authors themselves set it up, it is energy normalized for baseline that is the key variable.  Then the authors are right (at least by inspection) that the protein intake does not effect the change in body fat but you have only a single value for the energy. In this case, you cannot say “calories alone account for the increase in fat” (Conclusion in Abstract) because you have only a single point.  If you keep constant the variable (carbohydrate) that is most likely to bring out differences, you shouldn’t be surprised in there are no big differences.

Even taking the conclusions at face value, the authors found, as other diet comparison studies have, that weight loss or, in this over-feeding study, weight gain, was not dependent on calories alone: “a calorie is a calorie” not.  It is likely that this was what the study was originally trying to disprove and the results must have been a disappointment.  The way out was that, in this particular case, the differential weight loss showed up in difference in lean mass, rather than in fat mass as has been found in other studies showing variable efficiency.  Since 5 % is very low protein it is probably not surprising that the diet could not provide enough protein for an increase in lean mass this group.

So what are the other diet studies that have found variable efficiency. The reduction in weight found in studies comparing low-carbohydrate diets and low-fat diets not only shows a difference favoring carbohydrate restriction but the improved weight loss is preferentially fat over lean mass. For example, Volek, et al. compared a low fat with a VLCK and the results are as shown below.  In their study, subjects were randomized to one of two hypocaloric diets, a very low-carbohydrate ketogenic (VLCK) diet (carbohydrate <10% of energy) or a low fat (LF) diet and after 8 weeks switched to the other diet. Reported energy was slightly higher during the VLCK but the VLCK group lost more weight and as shown below predominantly in fat, total fat loss, and trunk fat loss for men (despite significantly greater energy intake). The majority of women also responded more favorably to the VLCK diet, especially in terms of trunk fat loss the ratio of trunk fat/total fat was also significantly reduced during the VLCK diet in men and women.  These studies depend on diet recall so are less accurate than the JAMA study but because of the better experimental design, the changes are bigger and with appropriate correction make a less ambiguous case than the JAMA study. The more accurate measurements in the metabolic chamber suggest that individual variation is real and not just due to random error.

So what do we know from Bray, et al.? As described above, there is some ambiguity in what constant energy means. Still, nobody questions that under many conditions, a “calorie is a calorie,” but they actually found that weight gain was different so when metabolic advantage is “claimed” it cannot be dismissed out of hand.  This is different than widely cited studies in the literature that claim macronutrients do not effect weight loss, since if weight gain depends on macronutrient, it is reasonable that weight loss does too.  Similarly, if tissue distribution affects lean mass in this case, then studies where the tissue distribution shows preferential loss of fat can’t be dismissed — again, it is certainly not surprising that a low protein diet will lead to less storage of protein; generally, while it is just as bad a generalization as “a calorie is a calorie,” there is some truth in “you are what you eat.” Also, in the JAMA study, protein was exchanged for fat so a reduction in fat did not have an effect on fat which may or may not be a surprise to many people. Tom Naughton raised a few other questions about Bray, et al. but in the end, the paper reminds me of the joke about the Polish Mafia: they make you an offer you can’t understand.

How to do it.

But  I told George how to do it. A couple of years ago, he and I had a brief correspondence. I made the following proposal. I suggested we could apply for a joint grant and publication to get the answer.  The following is from my email to him in 2008  (I have added some highlights):

 “A modest proposal

 Proponents of carbohydrate-restricted diets (CRD) and critics of such diets cooperate to design a long-term comparison of CRD and low-fat diets.  The groups agree on methods of procedure, make-up of the diets, how compliance will be effected, and what parameters will be measured.

We write the paper first, leaving room for the data, that is, we agree in advance on what the possible outcomes are and what conclusions could be drawn from them.  The final MS can only be edited for language usage. There are no disclaimers, no Monday-morning-quarterbacking, no excuses.

The paper could be submitted while the grant application is being written and would have to be accepted because any objections could be incorporated in the plan.  The grant itself would surely be funded since it incorporates everybody’s specific aims.”

 George hasn’t answered and he obviously has a different approach to the problem but my offer still stands.

In the end, that is what it will take to solve the problem.  Unless we agree on what the question is, how it can be tested and work together to do the experiment, the lipophobes will ignore the low-carbohydrate studies and we will criticize their studies. The real losers, of course, will be the people suffering from obesity and diabetes.  The question everybody always asks me, is why can’t there be a meeting of the minds?  In the current case, why was the JAMA study done?

Why was this study done? 

 Dr Bray discussed the results with news@JAMA via e-mail.

news@JAMA: What are the practical implications of these findings for patients trying to lose weight or for the physicians trying to counsel them?

 Dr Bray: The first practical implication is an old one: calories count. We showed very clearly that the increase in body fat was due to the increased intake of calories and that the amount of protein in the diet did not change it.

 To avoid that slow weight gain that many adults experience in their middle years, people need to watch their weight and increase activity, decrease food intake, or both; changing the diet alone will not do it.”

This sounds like the the same recommendations we’ve had for years.  Writing this, I suddenly realized that, as they say in German: that’s where the dog is buried.  It is about recommendations.  This research is following the recommendations.  It used to be (should be? assume it must be?) that recommendations follow from the research. Now, it’s the other way around.  Committees make recommendations and then research (sometimes by members of the committee) tries to support the recommendations. Something about this bothers me.