“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.

  1. James Pott says:

    Thank you for a clear and concise review. Especially thank you for your sense of humor,even though some of this is just ‘toe-curdling’. Of course it is good to know that you won’t be the only one who will say: “Something about this bothers me”

  2. Ben Fury says:

    Yes, it is important that science be separated from politics. Otherwise we end up with a lamentable lack of logic like our elected officials:

    “Don’t confuse me with the facts. I’ve got a closed mind.”
    Representative Earl Fredrick Landgrebe, R-Ind., upon being told of the “smoking gun” Watergate tape, 1974.

    President Nixon resigned the next day.

    Be well,
    Ben Fury
    Better Size Me

    • rdfeinman says:

      In the end, many of them turned on Nixon and feigned shock that he was a crook (and as, Jackie Mason said, “such a good crook. Every day something different was missing from the White House). Of course, they did not have the option to pretend that they thought of it first although we did see a certain amount of slouching towards impeachment.

      The nutrition world needs a Special Prosecutor.

      • rdfeinman says:

        Actually, this is meant to be in answer to James Pott: Thanks for the comment. I think, following on Ben Fury’s comments that people see through this. I think most congressman just stood back and let Nixon hang himself. I think most people see the JAMA paper for what it is: a last ditch effort to save an outmoded and futile approach to nutrition. The key thing that I didn’t mention is that there’s no mechanism here. There’s no talk of insulin. The paper is supposed to be about protein but there’s no discussion of all the work on signaling by leucine, of the mTOR pathway. It’s pure old phenomenology. It’s all as somebody described high school science projects: “I poured salt on it and it died.”

  3. David Brown says:

    I wonder why so little attention is paid to gut microbial profiles and activity in trying to explain the results of overfeeding studies. Surely, with more than 4 pounds of intestinal critters feeding and multiplying, a lot of heat energy is released into the body that contributes to temperature regulation. Changes in macro nutrient proportions and micronutrient concentrations would necessarily affect reproduction patterns and fermentation efficiency. For example:

    “Recent research has shown that gut microbes control or influence nutrient supply to the human host, the development of mature intestinal cells and blood vessels, the stimulation and maturation of the immune system, and blood levels of lipids such as cholesterol. They are, therefore, intimately involved in the bodily functions that tend to be out of kilter in modern society: metabolism, cardiovascular processes and defense against disease. Many researchers are coming to view such diseases as manifestations of imbalance in the ecology of the microbes inhabiting the human body. If further evidence bears this out, medicine is about to undergo a profound paradigm shift, and medical treatment could regularly involve kindness to microbes.”

    “Gut bacteria play a role in obesity, which affects about a third of American adults. The gut bacteria populations of the obese are less diverse than those of normal-weight people. Researchers have found that children whose fecal bacteria are composed more of Staphylococcus aureus than Bifidobacteria at birth are more likely to become overweight later in life. Interestingly, one study found that the microbiota of obese adults were very different from the bacteria populations of both normal-weight people and obese people who had had gastric bypass surgery. Researchers from Arizona State University and the Mayo Clinic noted that in obese people, there appeared to be a cooperative relationship between hydrogen-producing bacteria and the one archaean resident of the human gut, a hydrogen-consuming, methane-producing organism. The archaean partner makes fermentation of indigestible polysaccharides (which are complex carbohydrates) more efficient, and the extra fermentation products are converted to fat by the intestines. It appears that obese people’s gut microbes are just too good at their jobs.”

    In trying to explain how the real world works, scientists need to look at the whole picture.

    • rdfeinman says:

      I think people are starting to pay attention to this but it’s not really my field and I have some fear that it will be compromised by the lipophobes. An interesting study in Nature looked at the genetics of bacteria affected by fat or fiber. Surely, fiber (the indigestible carbohydrate you mention) is not the only active component in the gut from dietary carbohydrate. Or is it? It is not my field but anecdotally, many people can tell from gut reaction about how much carbohydrate they’re eating.

  4. Margaretrc says:

    Yeah, something about this bothers me, too. Big time. Thanks for a great analysis that actually makes sense. As usual.

    • rdfeinman says:

      Many are bothered. Two things are required. We need a hearing, conference, investigation in which all sides are heard and there is a truly independent panel (not people whose grants are funded by organizations on whose study section their friends sit — possibly inevitable when you have a pervasive orthodoxy with that controls all the political and administrative aspects of the problem). The other thing we need is an experiment in which everybody agrees on what we are doing and what they outcome is, as I had described in my email to George Bray. The offer stands. I and my colleagues are willing to cooperate with Pennington or anybody else to define and carry out the experiment. You can write to the authors and ask if they will play (be sure to copy me) and you can write to the NIH and ask whether they can help.

  5. George Henderson says:

    I’ve had a crash course in microbiota recently, the influence of some “probiotic factors” on the gut dendritic cells lessening Th17 (a very pro-inflammatory cell type which is increased in chronic -itis syndromes and type 2 diabetes) and switching differentiation to T regulatory cells, which promote immune tolerance (sometimes being granted the serenity to accept those things we can’t change is better for us immunologically too). This stops production by B-cells of ineffective low-avidity or outdated antibodies, which helps to get rid of circulating immune complexes and improves Th1 immunity. It also means the B cells and complement system are better able to meet the next acute threat.
    I do agree this is the kind of science that can be hijacked by lipophobes. I don’t think probiotics alone are going to fix diabetes in anyone, but I do think that of the minority who are not helped much by low-carb, quite a few will find that probiotics (and other “diabetes vaccines”) when added to low carb will help.

    On the calorie system, do you think that the fact that the 4:4:9 ratio for carb, protein, and fat uses rounded figures, which are themselves averages of rather variable scores (the calory value of individual amino acids, or fats of different types, varies quite a lot) introduces much room for error, especially where two different types of food are measured? Or is this controlled for in some way (say by always making two identical meals, waiting to see how much of the first gets eaten, then burning that amount of the second meal in a calorie-measuring machine).
    Also, is burning all poohs and wees in the same machine an important part of any metabolic advantage study? (presumably the job of the lowliest intern). Dried dung is quite a good fuel source…

    • rdfeinman says:

      Interesting story on microbiota. On calories, I think there is lots of variability right from the start. The 4 kcal is, in fact an approximation and depends on amino acids, etc. but the main fallacy of a calorie-is-a-calorie lies in not understanding that the calorie goes with the reaction, not with the material. The 4 kcal are not IN the carbohydrate, they are the heat of complete oxidation. The reason energy balance is found most of the time, is that when comparing similar individuals, the other metabolic processes may be similar and cancel out and oxidation may be the major effect but there is a lot of variation.
      The bottom line is that a meaningful experiment has big changes. Volek’s experiments show big effects which, whatever the limitations of diet records, tell you what’s going on. What is good about Bray’s paper is that it shows individual effects and they are not all that different for any conditions. So, when you want to say that there is no difference in fat storage, you have to have an experimental protocol that is set up to show big differences. Carbohydrate has the largest effects. By keeping that constant, all the variability that you mention comes into play. Also, you have to check each parameter to find out whether it is the raw data or “corrected” for things that you might not want to correct for.
      This is a general rule. The extremely small changes in relative risk found in all those epidemiologic studies would be laughable if you got to see the spread in the individual data and if they were not being used as a tool for keeping people obese and diabetic. (Did I overstate the case?)

  6. greensleeves says:

    I’m confused. I’ve never met any low-carb person who denied that “calories count.” No one says an average sedentary Joe can eat 6,000 calories a day and not gain weight.

    The whole idea that you have “to prove calories count because low-carbers deny it” is plain false. Rather, it seems the low-carb community says “calories count, but for most people, a low-carb diet makes it unnecessary to actually bother to count them.”

    I think the hassle of tracking calorie amounts and weighing food is really a barrier to most weight loss plans, and big reason compliance and adherence is so low with most diets.

    Reading blogs suggests to me that most low-carbers do track with fair accuracy – but since it’s not drilled into them as a “must” they feel less overwhelmed by it. And that lack of “must” actually increases their compliance. Humans are just irrational that way.

    • rdfeinman says:

      Well, one of my arguments with Gary Taubes has always been that that GCBC implies that calories don’t count and that has given the lipophobes a point of attack. But, of course, the press release from JAMA is disingenuous. If the work was really done because of challenges by low-carbers (or even high-proteiners, whoever that is; Layman, Paddon-Jones and other workers are only suggesting that low protein is a problem), they would have cited that work and, in fact, Layman and others show the value of substituting protein for carbohydrate but you can do something. Remember, you paid for it.

      1. Layman DK, Baum JI: Dietary protein impact on glycemic control during weight loss. J Nutr 2004, 134(4):968S-973S.
      2. Layman DK, Boileau RA, Erickson DJ, Painter JE, Shiue H, Sather C, Christou DD: A reduced ratio of dietary carbohydrate to protein improves body composition and blood lipid profiles during weight loss in adult women. J Nutr 2003, 133(2):411-417.
      3. Layman DK, Shiue H, Sather C, Erickson DJ, Baum J: Increased dietary protein modifies glucose and insulin homeostasis in adult women during weight loss. J Nutr 2003, 133(2):405-410.

      • I find the sort of paper being discussed is quite annoying, because they could have designed it properly, so I could know whether or not calories count and so whether or not I’m doing myself a favour or a disservice by counting calories on top of my generally successful low-carb diet.

        By designing the experiment as they did, they just wasted my tax money to come up with a non result.

        One fairly expensive, properly designed intervention study could explore the corners and middle of the 4D space that is macronutrient ratios and total volume/calories. Then we would know. Paying for studies like Dr Bray’s is just getting in the way of that.

      • rdfeinman says:

        Less expensive than the study you describe, would be to seriously analyze the studies that have been done, an example of which is in the post and others to follow. There are two aspects to counting calories. First, is it a good strategy for weight loss and we’ve done innumerable experiments showing that it is not generally useful. If only calories count, and all of the apparent differences between diets of different macronutrient composition were due to experimental error, we would expect a 50:50 distribution of which diet does better. In fact, low-carbohydrate diets almost always do better, sometimes there is a draw. Nutritionists consider that in a draw, low-fat wins which I think used to be true of some games or sporting events: in a draw, the champion keeps his title.

        As for your tax dollars, you can write to your congressperson or to Secretary Kathleen Sibelius or sites at HHS. The Surgeon General is Regina Benjamin. There is no reason not to suggest the kind of experiment you and I have in mind. If you do write, please send me a copy; we are collecting letters to the government.

  7. Bill says:

    Well said Dr. Feinman, great post. Dr. Bray’s stance is similarly transparent in his first report of POUNDS LOST, and especially in the more recently published follow-up!

    • rdfeinman says:

      The second reference concludes “Participants lost more fat than lean mass after consumption of all diets, with no differences in changes in body composition, abdominal fat, or hepatic fat between assigned macronutrient amounts.” Isn’t that the opposite of the conclusion from the JAMA paper? What’s transparent is that they really don’t care about the data as long as they can conclude with the party line. Very sad.

      • Bill says:

        Yes! that is the exact line which caught my attention. Very sad indeed.

      • rdfeinman says:

        You might consider sending a letter to the editor since the two reports are in conflict with the PNAS paper.

        In addition, the widely cited Sacks, et al. further shows disregard of any sense of consistency. Says “By 2 years, weight loss remained similar in those who were assigned to a diet with 15% protein and those assigned to a diet with 25% protein” (My emphasis), “assigned to a diet” is the key variable for them but, in practice the diets were all the same. And, of course, the brilliant observation that “attendance was strongly associated with weight loss,” analogous to saying that if you are a hitter, who’s pitching is less important than whether you actually show up at the ballpark.

        In fact, attendance was associated with greater protein intake in distinction to their “CONCLUSIONS: Reduced-calorie diets result in clinically meaningful weight loss regardless of which macronutrients they emphasize.”

        “All-seeing heaven, what a world is this!”

  8. George Henderson says:

    A sedentary Joe could try to eat 6,000 calories a day from fat and protein and not gain weight at the point where appetite ceased. The same Joe would gain weight on carbohydrate and protein because more of the 6,000 would get eaten, as well as (or as part of) the fattening effect of carbohydrate. And this is why low-carbers generally have no need to count calories, calories don’t “count”.
    I have late-medieval food tables showing over 7,000 calories per diem being consumed in some scandanavian courts (in Capitalism and Material life 1400-1800 by Paul Braudel). Even allowing for error, waste and ration fraud (and alcohol is only included up to 10% of calories), this is pretty remarkable.

    Perhaps there is a schism in dietary science between the phenomenologists and the mechanists.
    The phenomenologists collect and interpret fresh data in ways influenced by discussion and uptake of their interpretations of past phenomenological data, whereas the mechanists collect and interpret data in ways influenced by their growing understanding of the mechanisms involved.

    • rdfeinman says:

      I agree. The way I put it is that medicine is big on a top-down approach whereas biochemical perspective is bottom-up. All of which is fine if you understand that mechanism is primary and if it doesn’t play out experimentally, you have to show that, but then, in nutrition, the Venn diagram shows increasingly small union of medicine and science.

  9. George Henderson says:

    What’s especially interesting here is that they seem to be saying that SAFA lowers VLDL and TG, except at higher intakes of carbohydrate. Not a straight trade-off between carbs and fat for VLDL-TG levels as you might expect, but a beneficial physiological effect of SFA alone?

    Lipid Insights. 2011 Aug 23;2011(4):7-15.
    Dietary Carbohydrate Modifies the Inverse Association Between Saturated Fat Intake and Cholesterol on Very Low-Density Lipoproteins.
    Wood AC, Kabagambe EK, Borecki IB, Tiwari HK, Ordovas JM, Arnett DK.
    SourceDepartment of Epidemiology, University of Alabama at Birmingham, School of Public Health, Birmingham, AL 35294, USA.

    We aimed to investigate the relationship between dietary saturated fat on fasting triglyceride (TG) and cholesterol levels, and any mediation of this relationship by dietary carbohydrate intake. Men and women in the NHLBI Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) study (n = 1036, mean age ± SD = 49 ± 16 y) were included. Mixed linear models were run with saturated fat as a predictor variable and fasting TG, very low density lipoprotein cholesterol (VLDL-C), low density cholesterol (LDL-C) and high density cholesterol (HDL-C) as separate outcome variables. Subsequent models were run which included dietary carbohydrate as a predictor variable, and an interaction term between saturated fat and carbohydrate. All models controlled for age, sex, BMI, blood pressure and dietary covariates. In models that included only saturated fat as a predictor, saturated fat did not show significant associations with fasting lipids. When carbohydrate intake and an interaction term between carbohydrates and saturated fat intake was included, carbohydrate intake did not associate with lipids, but there was an inverse relationship between saturated fat intake and VLDL-C (P = 0.01) with a significant interaction (P = 0.01) between saturated fat and carbohydrate with regard to fasting VLDL-C concentrations. Similar results were observed for fasting TG levels. We conclude that, when controlling for carbohydrate intake, higher saturated fat was associated with lower VLDL-C and TGs. This was not the case at higher intakes of carbohydrate. This has important implications for dietary advice aimed at reducing TG and VLDL-C levels.

    PMID: 21912485 [PubMed] PMCID: PMC3170517Free PMC Article

  10. Re: working with Mr. Bray.

    When I was a scientist, I noticed that there are two completely separate types of scientists: one which exhibits curiosity and the other one which does not. I doubt if your offer to Mr. Bray will ever be accepted because you most likely belong to those two different groups. There is no common ground whatsoever.
    I wrote a more in-depth series of articles about that phenomenon in a much broader scope. Begin with this link, and this is the whole series. (Warning – this is not a politically correct subject!) .

  11. George Henderson says:

    Nostracism, you mentioned earlier, quoting Einstein. From Nos = we, us, our, I believe. If ostracism is us excluding someone by shutting them out, nostracism is us sidelining them by inviting ouselves in.
    “we found that E=MC2”. Especially while implying, but not demostrating, that all the rest of the general theory of relativity is still fatally flawed. This allows us to own the equation even more than Einstein does, as he doesn’t fully understand its true importance.
    And so it goes…

    • rdfeinman says:

      Einstein meant that Hilbert was making it common property, that is, not giving Einstein credit. E=mc^2, however, is from Special Relativity. The argument is over the field equations from General Relativity which David Lindley, the science writer, says is easier to understand than Special Relativity. I think he meant the results are more intuitive. On the other hand, Einstein said Special Relativity is not hard to understand: we only have to change our concept of time.

  12. George Henderson says:

    Sorry, the book is by Fernand Braudel, 1967. 7212 calories reconstructed from menus in Pavia, for 1613-1614. Of course there may have been waste, but it certainly tells us what they thought of portion size in those days! Yet how much obesity was there among the wealthy in Pavia, 1613-1614?

    Can I be the first(?) to say, an empty calorie is an empty calorie – NOT! Surely because of the repetitive nature of Beta-oxidation reactions, amongst other factors, metabolism of SFA involves fewer enzymes and less number and variety of co-enzymes per calorie than glycolysis. Carbohydrate can squander thiamine and ascorbate, and brings in nothing, while fat increases delivery of 4 fat-soluble vitamins (and only squanders sodium?).

    • rdfeinman says:

      I am not sure what you are referring too but even George Bray now admits that a calorie is not a calorie although I am not sure about your example. Vitamins are re-cycled so, in theory, don’t enter into the energy equation.

  13. George Henderson says:

    There’s an extra hypothesis that obesity is partly due to burning “empty calories” from refined carbohydrate or fat, resulting in micronutrient deficiency. (or rather, vitamins and minerals in a refined diet not being sufficient for proper regulation as well as oxidation). It could be determined whether carbohydrate and fat are in fact equal in this regard (I guess not for a number of reasons). The “empty calorie” theory is part of the justification for lumping sugar and fat together in public health misinformation.

    This brilliant exchange about cholesterol comes from the 1970s series “A Bit Of Fry And Laurie”
    Hugh Laurie is the patient and Stephen Fry is the GP, who has just prescribed cigarette smoking for Laurie’s lung problem:

    Hugh I suppose you’re going to tell me that cholesterol isn’t bad for you next.

    Stephen What’s cholesterol?

    Hugh It’s … well, you know –

    Stephen Yes I know perfectly well what it is, but I don’t suppose you’d so much as heard of it until a few years ago. You’d die without the stuff.

    Hugh Yes but too much is bad for you.

    Stephen Well of course too much is bad for you, that’s what “too much” means you blithering twat. If you had too much water it would be bad for you, wouldn’t it? “Too much” precisely means that quantity which is excessive, that’s what it means. Could you ever say “too much water is good for you”? I mean if it’s too much it’s too much. Too much of anything is too much. Obviously. Jesus.

    Hugh But I thought the balance of informed medical opinion held that –

    Stephen You thought, you thought. You didn’t think, did you?

    The full text and video link is here: http://abitoffryandlaurie.co.uk/sketches/doctor_tobacco

    • rdfeinman says:

      Very funny routine although the ADA nutritional guidelines have substantially compromised the impact of parody.”of course empty calories cause deficiency. That’s why they’r called empty. “Empty” precisely means that quantity which is not there….”

  14. majkinetor says:

    @ George Henderson

    There’s an extra hypothesis that obesity is partly due to burning “empty calories” from refined carbohydrate or fat, resulting in micronutrient deficiency
    I suspect that many unresponsive obese patients have micro nutrient deficiencies. Carnitine, choline, C, Mg, D, and so on. After all, all different fat pathways must work in order for it to be burned, not only the one that promote lipolysis and some different in order to utilize nutrients from food (bile for instance, much needed for high fat diet)

    We know that in paleolithic times micronutrient input was amazingly many times over what we have now – http://goo.gl/MtTYN http://goo.gl/OY9Oz – and we also know that primates have larger input http://goo.gl/BByrG and we also have experimental support with obese humans:

    Effects of multivitamin and mineral supplementation on adiposity, energy expenditure and lipid profiles in obese Chinese women
    A total of 87 subjects completed the study. After 26 weeks, compared with the placebo group, the MMS group had significantly lower BW, BMI, FM, TC and LDL-C, significantly higher REE and HDL-C, as well as a borderline significant trend of lower RQ (P=0.053) and WC (P=0.071). The calcium group also had significantly higher HDL-C and lower LDL-C levels compared with the placebo group.

    Anyway, if you have more links about the topic I would appreciate any info.

    • rdfeinman says:

      I don’t know about the relative micronutrient abundance in paleolithic times although I will try to follow up on your article. As for supplementation in Chinese women, I don’t have access to the original article which is absolutely necessary given the number of nutritional papers that find effects that are of statistical significance but of limited practical significance.

      • George Henderson says:

        Try this http://www.ncbi.nlm.nih.gov/pubmed/17109595
        which tends to support the “inadequate for regulation and metabolism” empty calorie hypothesis.
        There is a third version; that we eat to consume replacement values of protein, minerals, micronutrients, before calories, so will consume extra calories if food is not supplying these.
        All three versions have supporting evidence, but all tend to become largely irrelevant once macronutrient balance is improved on a meat-based diet.
        When I ate veges I believed very much in orthomolecular medicine, now that I eat meat I think John Yudkin was right about vitamins.
        Another contingent phenomenon?
        However, would I have ever reined in my sugar intake enough to go low-carb in the first place without chromium, biotin, Mg, etc?
        Possibly not.

      • rdfeinman says:

        Are you sure this is the right study. This is about chromium and vitamins and the results in the abstract don’t sound too good.

  15. David Brown says:

    Regarding protein and micro nutrient deficiencies, low intake of supportive nutrition would likely curtail gut microbe activity or distort gut microbe profile. In addition, a healthy gut microbe profile seems to helps with weight control. http://www.docstoc.com/docs/30525645/Dieting-with-Microbes-Using-Probiotics-for-Weight-Loss—My-Experience

  16. George Henderson says:

    Slouching towards low-carb part XXXIV: the Protein Leverage Hypothesis, a class 3 “empty calorie” theory which fits in with this post and Bray’s study in concept, only under the command of behavioural psychologists this time…

    Obes Rev. 2005 May;6(2):133-42.
    Obesity: the protein leverage hypothesis.
    Simpson SJ, Raubenheimer D.
    SourceDepartment of Zoology and University Museum of Natural History, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. stephen.simpson@zoo.ox.ac.uk

    The obesity epidemic is among the greatest public health challenges facing the modern world. Regarding dietary causes, most emphasis has been on changing patterns of fat and carbohydrate consumption. In contrast, the role of protein has largely been ignored, because (i) it typically comprises only approximately 15% of dietary energy, and (ii) protein intake has remained near constant within and across populations throughout the development of the obesity epidemic. We show that, paradoxically, these are precisely the two conditions that potentially provide protein with the leverage both to drive the obesity epidemic through its effects on food intake, and perhaps to assuage it. We formalize this hypothesis in a mathematical model. Some supporting epidemiological, experimental and animal data are presented, and predictions are made for future testing.

    This hypothesis has recently been revived in New Zealand and a correspondence is taking place in the Letters column of the NZ Listener, which ignores fat satiety and insulin etc., yet obviously slouches .

    Raubenheimer writes in this week (in an otherwise intelligent analysis of the research which you would surely approve; I regret that it isn’t yet available digitally and is too long to copy by hand) about how we evolved to eat a high-protein, low-fat, low carbohydrate diet.
    Whatever you say Professor.
    tell that to the mammoths….

    Here is the original article about the PLH

    • rdfeinman says:

      I am not sure what the ideas is. There is, contrary to the abstract, a good deal about effect of protein. Layman’s group, in particular, has described effects of replacing carbohydrate with protein. Carbohydrate restriction is inherently tied to protein intake since the need for gluconeogenesis increases the demand on protein. And, because protein has the highest costs in terms of thermic effect of feeding and other processing, it is undoubtedly a key part of metabolic advantage. This was the point of our first papers on the subject: Feinman RD, Fine EJ: Thermodynamics and Metabolic Advantage of Weight Loss Diets. Metabolic Syndrome and Related Disorders 2003, 1:209-219, and 1. Feinman RD, Fine EJ: “A Calorie is a calorie” violates the second law of thermodynamics. Nutrition Journal 2004, 3(9), the latter available without subscription at http://www.nutritionj.com/content/pdf/1475-2891-3-9.pdf.

  17. George Henderson says:

    I will copy part of Proff. David Raubenheimer’s letter here; I think he is referring to Bray (but I missed the middle part of this correspondence so I’m not sure).
    Don’t think he’s necessarily a psychologist any more… PLH is a hypothesis about protein influencing eating behaviour.
    BTW, I consider Jennifer Bowden, the NZ Listener “nutritionist”, to be a public menace. She advises that children be switched to low-fat milk at age 2, that coconut fat be avoided, and similar inanities. She still looks up to Ancel Keyes and believes implicitly in the lipid hypothesis, food pyramid, etc. Her idea of a healthy diet seems to be the standard modern chimera; mostly whole-grains, fruits and veges, some lean protein, a little monounsaturated fat and PUFA from vegetable oil and fish.

    Here goes:
    “Several lines of evidence support PLH. First it has been shown in three experimental studies that under controlled conditions, reducing the proportion of protein in the foods of humans results in an increase in energy intake. In the most recent study,…a decrease from 15% to 10% protein resulted in a 12% increase in energy intake…Second, our analysis of 23 previously published studies (meta-analysis) shows a similar association between dietary protein and energy intake.
    [NOTE: I wonder if D. Raubenheimer et al. could be persuaded to re-analyse the same data to check whether fats and type of fat, especially at low carbohydrate intakes, are also associated with energy intake, and whether this is synergistic with the PLH effect – GDH]
    Third, the large diogenes study showed that outside of the experimental laboratory, high protein foods were associated with the long-term success of weight loss programmes.
    Fourth…[the NHNES study] has shown the rise of obseity in the US is associated with a reduction in the % of protein in the national diet [other evidence shows the appetite for protein is particularly strong]… evidence that humans evolved (and are therefore resumably adpated to) diets high in protein relative to carbohydrate and fat.
    [NOTE: is this meant to convey “high in protein relative… compared to today’s SAD”, which would be right, or “high in protein relative…as proportion of energy”, a diet which would be unlikely to sustain any primate species for long? – GDH]
    Rather than expand on the supporting evidence, I will briefly consider the study presented by Scott as evidence against the PLH. The participants in that study were deliberately overfed to a fixed energy intake of diets with either 5%, 15% or 25% of protein. The question asked was whether the composition (% protein) …had any effect on obesity – i.e., a psysiological question.
    Since PLH is a hypothesis abut the effect of dietary protein on energy intake (behaviour), a study in which … intake is … fixed cannot be taken as a test of the hypothesis. But it is worth considering… whether low-protein diets (at fixed enerhy intakes) are associated with adverse or favourable physiological responses
    Scott suggests the best outcome was associated with the low protein, because the experimental group on the 5% protein diet put on less weight that those who had 15% or 25% dietary protein. What she fails to point out is that the difference in weight gain was due to poor lean (muscle) growth on the low-protein diets…In fact the high-protein diet was associated with a greater ability to get rid of the excess energy that was eaten, and a trend towards low-protein subjects accumulating more fat.
    Studies have therefore associated low-protein diets with increased energy intake, reduced ability to get rid of energy excesses, and reduced lean growth. There is no doubt obesity has complex causes and the final word is not in; but in the meantime I will not be putting my money on low-protein diets as the solution to the obesity epidemic.

    David Raubenheimer
    (Belmont, Auckland)

    Letters to the Editor
    February 4-10 (it’s a highbrow TV guide) 2012

    Perhaps the final word was “insulin”, wich has nowhere appeared in this discussion to date.
    Raubenheimer nonetheless talks sense, I think.

  18. George Henderson says:

    Unfortunately the meta-study seems not to be published online. This is an example of Prof. Raubenheimer’s work.

    Geometric analysis of macronutrient selection in the adult domestic cat, Felis catus
    November 23, 2010.

    Adrian K. Hewson-Hughes1,*,
    Victoria L. Hewson-Hughes1,
    Andrew T. Miller1,
    Simon R. Hall1,
    Stephen J. Simpson2 and
    David Raubenheimer3

    We report feeding studies on adult domestic cats designed to disentangle the complex interactions among dietary protein, fat and
    carbohydrate in the control of intake. Using geometric techniques that combine mixture triangles and intake plots from the
    geometric framework, we: (1) demonstrate that cats balance their macronutrient intake, (2) estimate the composition of the target
    balance and (3) reveal the priorities given to different macronutrients under dietary conditions where the target is unachievable.
    Our analysis indicates that cats have a ceiling for carbohydrate intake, which limits ingestion and constrains them to deficits in
    protein and fat intake (relative to their target) on high-carbohydrate foods. Finally, we reanalyse data from a previous experiment
    that claimed that kittens failed to regulate protein intake, and show that, in fact, they did. These results not only add to the
    growing appreciation that carnivores, like herbivores and omnivores, regulate macronutrient intake, they also have important
    implications for designing feeding regimens for companion animals.

  19. George Henderson says:

    Regarding the chromium-biotin study, I may not have selected the best example of these, as I haven’t been paying as much attention to micronutrient research since becoming a carnivore. I note that the subjects were medicated for diabetes. I can certainly testify that the effect on sugar craving is remarkable, but it’s possible that this just creates a window of opportunity to improve the diet, and that, if you just “covered carbohydrate with chromium” and went on with your SAD life, the eventual outcome wouldn’t be much better than if you “covered carbohydrate with insulin” as fools suggest.

    I have just watched the wonderful documentary “Lemmy” about the great heavy metal pioneer. I don’t own any Motorhead albums, but this is perhaps the best musician biography I’ve ever seen. Lemmy, at 63, has been diagnosed with diabetes and high blood pressure. After a lifetime diet of amphetamine, Jack Daniels, cigarettes, and oil fried chips (didn’t see him eat anything else). Lemmy is not what I’d call overweight; he has a pot belly and skinny legs. He works out on the bass guitar, doesn’t seem to lack muscle or energy.
    This interests me because the whole insulin resistance leading to diabetes thing clearly can and does exist independent of obesity. DM2 in normal-weight people might be overlooked because of the obesity epidemic.
    Gary Taubes says “whatever makes us fat also makes us sick” – and I think this is true, even if it doesn’t happen to be making us fat.

  20. George Henderson says:

    OK, I get your question, the chromnium-biotin study was not meant to be the Chinese study but just another way of looking at the same effect through clinical testing of two of the most potent micronutrient factors. There are a few of these on PubMed. But I think it possible that, once you have measured the long-term effects of carb restriction, briefer studies showing the arguably similar but much lesser (and harder to sustain, and more expensive) effects of other interventions might no longer seem nearly as impressive.
    They’re just managing a condition they could have been relieving long-term or maybe curing.

  21. George Henderson says:

    Finally, one of my “letters to the editor” on the subject of obesity has been published, in the (new Zealand) Herald on Sunday. Feb 5 2012. A big debate is raging about sugar taxes, fatty and even salty food (which shows the degree of confusion in the public mind). Three professors from Otago wrote in to the Herald on Sunday condemning “energy dense, nutrient poor” food, which is surely an oxymoron.
    My letter was published under the heading

    “Back to Basics”.

    The cure for obesity proposed by Deborah Coddington,
    – eat less, work out and eat a salad – is one that obesity
    researchers have evaluated as ineffective and counter-
    productive. Obesity is a hormonal imbalance. Insulin is
    the hormone that regulates fat storage, appetite and energy.
    One hundred years ago dripping, butter, cheese and cream
    were everyday foods. True obesity was rare. Perhaps we should
    question the mandate we’ve given to trendy nutritionists to
    push their theories that insulin-elevating “complex carbohydrates”
    (read, starchy foods) and unproved novel oils are healthier than
    our traditional diet.

    The unedited letter also contained a reference to Rudyard Kipling’s poem “The Native Born” which praises New Zealand’s “five-meal, meat-fed men”.

    This debate has raged for months and several scientists have contributed, but so far as I know I am the first correspondent or contributor to mention the word “insulin”, or indeed any biochemical mechanism, in the context of the New Zealand obesity debate. This is not a good sign….

  22. Susan M says:

    I haven’t read all the comments foregoing, so forgive me if this was already addressed.

    Gary Taubes noted in Good Calories, Bad Calories (pp. 348-354 in my 2008 paperback edition) that Dr. Pennington clearly elucidated the fat metabolism issue leading to the excess fat storage that we call obesity, and debunked the “calorie is a calorie” notion for fat weight gain. Dr. Pennington, although his argument predated understanding of insulin’s role, was convinced that a defect in fat metabolism created the excess fat storage, and he also took into account gluconeogenesis, retention of lean mass, the hunger consequence of semi-starvation, and the “static” phase of obesity. He used a carbohydrate-restriction diet to effectively treat overweight and obesity associated with heart disease. I find it puzzling that Bray heads a division in the Pennington Biomedical Research Center, and yet so blithely ignores Dr. Pennington’s insights into these issues. Could it be that Bray is more interested in maintaining the political and funding status quo, than in contributing anything substantive to the research literature or effective nutritional recommendations? Or maybe it’s a different Pennington for whom the research center is named?

  23. George Henderson says:

    Freud would probably attribute it to the Oedipus complex. The need to assert one’s own identity by denying one’s parent and standing apart from them.
    Freud himself put an unusual amount of energy into debunking the importance of Shakespeare.

    I’ve been reading a life of Rutherford. Now that is how science should be concieved, and written:

    ” It may be of interest to note, that the experimental results reported in this article lead to experimental proof, if proof is needed, of the correctness of the atomic hypothesis with regard to the discrete structure of matter” (Scientific Weekly Nov 8 1907)

    Proof, if proof is needed.

    Should you ever be in need of a motto, you could latinize that phrase.

    • rdfeinman says:

      In nutrition, proof is not needed. For example, like the dog that didn’t bark in the Sherlock Holmes story, the outstanding thing in Rob Lustig’s viral YouTube is the absence of data. In nutrition, proof is not needed. In fact, it’s generally frowned upon.

      • George Henderson says:

        This amazes me: there are texbooks on biochemistry and physiology that clearly present the data from long series of experiments designed to establish (or prove beyond doubt) the basic pathways of metabolism and hormonal action (and so on). No-one in Med School argues with the textbooks or the classical experimental work behind them.
        But then we get Nutritionists, Dieticians and Public Policy buffs who just ignore all that stuff.
        You get people talking about alkalising foods, for example, who have obviously never even tried the read the chapter on pH regulation in The Physiological Basis of Medical Practice. Now, this chapter is pretty intense, and I don’t pretend to understand it fully myself, but it does seem incompatible with the alkalising foods model that weak acids buffer pH and help to remove surplus H+.

      • rdfeinman says:

        Wait a minute fella’. Are you suggesting that Nutrition is not a scientifically sophisticated field? I mean, like are you one of those guys who think that the field has been taken over by MDs who never studied nutrition and who took one biochemistry course thirty years ago? In any case, I don’t know about alkalizing food. Don’t tell me.

  24. The sentence “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.” doesn’t make sense.

    The maintenance calories varied from subject to subject by a factor of over 2:1. Therefore, the 40% increase varied in calories from subject to subject by a factor of over 2:1. The only things held constant from subject to subject were their protein & carbohydrate intakes.

    • rdfeinman says:

      The sentence means that within the framework of keeping constant energy relative to baseline expenditure, the absolute value of the calories are different. In a sense this is the problem with the whole idea — a calorie for one individual is different than for another individual. I am not sure why I took this paper seriously in the first place. Well, I am sure. ABCNews or someplace asked me to comment on it and, in addition, the tendentious style of the press release about diet gurus was very annoying. This study really doesn’t show anything at all. The stated goal is to measure variation, or lack of variation in weight with diet composition and the conclusion is that weight goes up with calories but is mostly flat as a function of protein. But the two figures show that this is not true. The values are all over the place. To draw a line through it and say that that tells you anything at all is to employ statistics without any thought. When you draw a regression line through a bunch of points you are saying that there is a kind of “true” slope of the line and that random environmental effects introduce fluctuations which have to be smoothed out to see the true value. That’s what you do if you have a chemical reaction and there are slight fluctuations due to slight changes in the temperature in your lab from day to day or something like that. This is not this kind of data. Weight as a function of energy and/or protein (don’t forget that protein contributes to energy) has huge inherent variability. The data really show us nothing at all. The experiment is poor in conception. The individual changes are way too big to say that they are the same (displaced by random error) or the same.

      It was foolish of me to react to the press release and to take this study seriously. The kinds of experiments that do point to the effect of macronutrients show big consistent variation between groups and don’t need much statistics. But the question is about “a calorie is a calorie” which, two years after Bray’s study is hopelessly anachronistic. “A calorie is a calorie” is a sound bite. It’s implication has always been that only calories determines the amount of weight gained or lost. Nobody believes that anymore. Just the different absolute calories that Bray had to use in this experiment shows you that it is not meaningful (and this was a metabolic ward study) and, of course, you can see it in animal studies where you know exactly what they tat. So, is it important for weight loss diets? Well, since it is at least possible, maybe we should design experiments that try to optimize the benefit instead of hopelessly try to show how only calories count. At some point, I will take this post down. It was written two years ago. Those were my salad days when I was green in judgment.

      • Nigel Kinbrum says:

        “This study really doesn’t show anything at all. The stated goal is to measure variation, or lack of variation in weight with diet composition and the conclusion is that weight goes up with calories but is mostly flat as a function of protein. But the two figures show that this is not true. The values are all over the place.”
        I completely disagree. While the regression line has been drawn incorrectly (it should have passed through 0,0), there is a strong positive correlation between additional kcals from fat and increase in fat mass weight. The fact that there is a lot of inter-personal variation doesn’t invalidate that fact.

        With caloric surpluses, there is usually a lot of inter-personal variation, due to their effects on Energy expenditure. Some people are more energetic on a caloric surplus, and increase their TEA & NEAT. Some people are more sluggish on a caloric surplus, and reduce their TEA & NEAT.

        In conclusion, I would suggest that Bray did it right. Using a fixed % above maintenance kcals results in a good variation in kcals above maintenance. Using Fat grams as the extra kcals above maintenance shows that dietary fat can be directly stored as body fat.

        Another interesting fact is that using Fat grams as the extra kcals above maintenance resulted in a reduction in %E from Protein & Carbohydrate. This is the opposite of what happened in the Riera-Crichton study, where an increase in Carbohydrate grams resulted in a reduction in %E from Protein & Fat, leading to the ludicrous conclusion that fat is slimming.

  25. Nigel Kinbrum says:

    Take a look at Figure 6. http://3.bp.blogspot.com/-lP0Sa9kD6ag/U8uOiEw5oCI/AAAAAAAABE8/GlnEWIMrtN4/s1600/Bray+Figure+6.jpg

    Some Definitions:-

    LBM = Lean Body Mass
    FM = Fat Mass = Body Fat

    Weight change = LBM change + FM change

    Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).

    (Maximum weight increase)/(minimum weight increase) = 2.6
    (Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36

    ∴ A calorie *is* a calorie (where weight change is concerned).
    ∴ Insufficient protein can result in loss of LBM (bad).

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