Saturated Fat - Prime Fuel

"Palmitic acid is the fatty acid that your liver manufactures from sugars. In fact, the only fat humans evolved to burn for fuel directly is saturated fat. All other fats we trans-saturate first, and then burn. It would seem strange then given the complexity of the human body that we evolved to preferentially make saturated fats over polyunsaturates, unless we prefer saturated fat because it is more stable and hence less prone to oxidation.
The canard that saturated fats, "clog your arteries," is just that, bogus. The medical establishment has never believed this since they knew full well plaques form inside the arterial wall, not on the surface. Why this idea was allowed to percolate through the public, I do not know.
http://entropyproduction.blogspot.com/2009/02/all-medical-science-is-wrong-within-95.html

Study Evaluates Low Carb Impact on Renal Function

"This study provides preliminary evidence that long-term weight loss with a very-low-carbohydrate diet does not adversely affect renal function compared with a high-carbohydrate diet in obese individuals with normal renal function."
http://www.adajournal.org/article/S0002-8223(09)02086-0/abstract


In other words, the conjecture that low carb diets are damaging to the kidneys was not supported during this one year study.

Wheat Prescription

Reposted in its entirety:The world according to the Wheat Foods Council and the Whole Grains Council

You might get a kick out of what the Wheat Foods Council and the Whole Grains Council recommend for a sample meal plan:

Breakfast: Whole grain raisin toast

Lunch: Sandwich on whole grain
Snack: Rye bread crackers
Dinner: Whole grain pasta with your favorite sauce

Breakfast: Whole grain waffles 

Lunch: Hamburger on whole grain bun

Snack: Graham crackers

Dinner: Whole grain homemade pizza on whole grain pita crust

Remember Morgon Spurlock's documentary movie, Super Size Me? (If you haven't already seen it, Super Size Me is viewable for free on Hulu.) Spurlock conducts a self-inflicted 30-day experiment of eating at McDonald's fast food restaurants every day. In short, the results on Spurlock's weight and health are disastrous. 

How about Wheat Belly: The Movie? We would chronicle our star through a 30-day course of meals served up by the Wheat Foods and Whole Grains Councils, all featuring wonderful wheat products in every meal. We could measure blood sugar, triglycerides, LDL, small LDL, weight, etc. 

WHS - Seed Oil Hypothesis

Concise, important post about why we don't want to eat seed oils.  Fits the general model of not necessary for health, suspect due to their novelty in the human diet, and some data supporting the hypothesis that these oils have a high, negative impact.

The hard part is - they're everywhere and hard to avoid.
http://wholehealthsource.blogspot.com/2010/04/do-seed-oils-cause-multi-generational.html

As per the usual, with Whole Health Source, there's as much to chew on in the comments about the article as there is in the article itself - a benefit of a well established blog with very bright commenters.

Classic Quotes, Twain

Whenever you find yourself on the side of the majority, it is time to reform (or pause and reflect).
- Notebook, 1904
http://www.twainquotes.com/Majority.html

More Taubes - Saturated Fat and Science of Diet

Taubes quoted in Tierney's blog, discussing saturated fat, cholesterol, and the science of diet:

"all the relevant diet trials done in the last decade — randomized controlled trials comparing Atkins-like low-carb diets to AHA low-fat, calorie-restricted diets — of which there are now more than half a dozen, have observed the same result., In each one, LDL on the two diets was a virtual wash and cholesterol profiles (total/HDL) showed greater improvement on the Atkins diet. When the trial looked at blood pressure, that improved significantly on the higher fat, lower carb diet. In this Israeli study, they looked at markers of inflammation — same story.

What we have to keep in mind here is that nutrition is a science (or at least should be) and science is about generating hypotheses, making predictions from our hypotheses, and then seeing if they hold true. The relevant hypothesis here — i.e., what we’ve believed for the past 30-odd years — is that saturated fat causes heart disease by elevating either total cholesterol or LDL cholesterol, specifically. So our prediction is that the diet with the higher saturated fat content will have a relatively deleterious effect on cholesterol. We do the test; we repeat it a half dozen times in different populations. Each time it fails to confirm our prediction. So maybe the hypothesis is wrong. That seems like a reasonable conclusion. No one is proving anything here — as some of your respondents like to decry — we’re just looking at the evidence and trying to decide which hypotheses it supports and which it tends to refute.

The knee-jerk response — as exemplified by quite a few respondents — is to assume that sometime in the not-too-distant past, maybe the 1960s or 1970s, before this low-fat dogma set in, such trials, or far better trials, were done and found the opposite — that the higher the saturated fat in the diet, the lower the cholesterol and the better the cholesterol profile. Or the higher the saturated fat, the greater the mortality. But that’s simply not the case, as I point out in my book. In fact, I’ve been criticized (by Gina Kolata, among others) for going on and on in the book about all the different studies. But I did so precisely because I didn’t want to be accused of cherry picking the data. (I was anyway, but that’s just the nature of this business.) When Ancel Keys, for instance, reported in the 1950s reported that saturated fats raised total cholesterol, which they did in his studies, he based it on comparisons of butter fat to polyunsaturated oils in studies that lasted only two to nine weeks. (He also reported, curiously enough, that the saturated fats had no significant effect on LDL.)

These latest trials just happen to be the best data we have on the long-term effects of saturated fat in the diet, and the best data we have says that more saturated fat is better than less. It may be true that if we lowered saturated fat further — say to 7 % of all calories as the American Heart Association is now recommending — or total fat down to 10 percent, as Dean Ornish argues, or raised saturated fat to 20 percent of calories, as Keys did, that we’d see a different result, but that’s just another hypothesis. The trials haven’t been done to test it. It’s also hard to imagine why a small decrease in saturated fat would be deleterious, but a larger decrease would be beneficial.

It’s also true that I don’t think that LDL is a particularly meaningful predictor of heart disease risk, and I think total cholesterol is meaningless (based on the evidence that I recount in the book). But the point is that the AHA and the National Cholesterol Education Program and the authorities at the National Heart, Lung and Blood Institute do think LDL is meaningful, and that’s the basis by which they have always recommended low-saturated-fat diets. They also think that total cholesterol/HDL is the single best predictor of heart disease risk, so by their assessment, more saturated fat is better than less. I think the best predictors of risk regarding cholesterol profiles are HDL and the size and density of the LDL particles themselves, and maybe measurements of a protein known as ApoB (the protein component of the LDL particle itself) — and the existing diet trials in those cases also suggest that saturated fats are at worst harmless and perhaps even beneficial.

Last point, the funding. It’s true that the study was financed by the Atkins Foundation, but to assume that the researchers went out and falsified their findings or twisted their observations to satisfy the source of funding is naive. Regrettably, the only institutions that will finance clinical trials, for the most part, are those that stand to gain from the results. That’s why the pharmaceutical industry finances drug trials. It would be nice if the government financed all these trials, but they don’t. So it’s up to the Atkins Foundation and any other organizations that might hold similar beliefs. In this case, the Atkins-funded diet trial observed the exact same results as similar NIH-funded diet trials.

Worth noting here is that the NIH has also spent $5 million recently for a large (300+ subjects, two-year-long) Atkins vs. AHA low-fat diet trial. This is a larger and longer version of a pilot trial that observed results similar to the Israeli trial. To my knowledge, it’s the largest diet/weight trial the NIH has ever funded. The principal investigator was Gary Foster of Temple University, currently the president of the Obesity Society, which is to obesity these days what the American Heart Association is to heart disease. In February of 2007, Dr. Foster told me the researchers had “completed the final 2 year assessments on most but not all” of their subjects. This week he told me that a paper on the results is “in the peer review process” and that “journal policies prevent me from saying more than that.” It would be nice to see those results, and we can only hope they’ll be published soon."

http://tierneylab.blogs.nytimes.com/2008/07/24/the-fat-fight-goes-on/

Dr. Davis on T3 Supplementation Rx

T3 for accelerating weight loss  (excerpts follow)

Thyroid health, in general, is extremely important for weight control, since even subtle low thyroid hormone levels can result in weight gain. The first step in achieving thyroid health is to be sure you are obtaining sufficient iodine. (See Iodine deficiency is real and Healthy people are the most iodine deficient) But, after iodine replacement has been undertaken, the next step is to consider your T3 status.

I've seen T3 ignite weight loss or boost someone out of a weight loss "plateau" many times.

Endocrinologists cringe at this notion of using T3. They claim that you will develop atrial fibrillation (an abnormal heart rhythm) and osteoporosis by doing this. I have yet to see this happen. 

T3 added to other weight reducing efforts, such as wheat elimination and exercise, accelerates the weight loss effect considerably. 5 lbs lost will likely be more like 8 to 10 lbs lost; 10 lbs lost will likely be more like 15 to 20 lbs, etc.

The tough part: Finding a prescriber for your T3.

Review of a Critique, Conclusion

(continued from yesterday) Mr. BS has good reason to at least attempt to be high handed with GCBC.  GCBC is an elemental attack on the quality of work of the entire field of nutrition for the last forty years.  If Taubes is right, a very large number of people in government and in the “leaders” of the nutrition field are being told, effectively, “you guys have wasted the last 40 years of your professional lives and have been upstaged by a journalist.”  In fact, that is what has happened, in my humble as ever opinion.  This is how Taubes describes it in his rebuttal to one such field leader (link below): 

“Finally, I would like to identify one potential conflict of interest on Bray's part that he neglected to mention. In the 1970s, as I discuss in GCBC, the hormonal/enzymatic regulation of fat tissue was deemed irrelevant to the cause, cure and prevention of human obesity. I identify Bray as one of two individuals most responsible for this dubious accomplishment, and 'for effectively removing the [century-old] concept of the fattening carbohydrate from the nutritional canon . . .' (GCBC, p. 417). Thus, Bray's critique of GCBC may be as much a defense of his own career as it is an unbiased assessment of the book.” 

Even worse, if Taubes is right, the folks who were doing what they thought was best for the people of this nation, actually have done incalculable harm in recommending consumption of high carbohydrate and low fat over the last 30 to 40 years.  At the very least, it is clear that those recommendations were not based on good science, and at the worst, they’ve killed and damaged as many or more people as the cigarette industry, and used the United States Government to do so. 

The prestigious nutrition journals that Mr. BS is so proud to have been published in, and his entire profession, is diminished in significance if Taubes is right.  They’ve been advocating, for as long as I’ve been aware, a diet loaded in carbohydrate, including such nonsense as ‘healthy whole grains’, low fat dairy, bananas, oatmeal, breakfast cereals, and potatoes while avoiding saturated fat.  They have confidently stated, without scientific proof, that the way towards better health is by eating more high density carbohydrates as a way of avoiding fat.  We’ve been told by this “profession” that high protein will damage our kidneys, but they’ve made this pronouncement with no scientific evidence to back it up.  If they got anything right, it was to avoid transfats (which ironically only came into vogue after the saturated fat witch hunts began).  How eager do you think Mr. BS and his profession will be to embrace it if the proof is forthcoming of just how badly they’ve missed the mark? 

Taubes puts it like this (GCBC page 450) commenting on the “no assumptions” nature of two researchers Taubes admires:

“This is how functioning science works.  Outstanding questions are identified or hypotheses proposed; experimental tests are then established either to answer the question to refute the hypotheses, regardless of how obviously true they might appear to be.  If assertions are made without the empirical evidence to defend them, they are vigorously rebuked.  In science, as Merton noted, progress is made only by first establishing whether one’s predecessors have erred or “Have stopped before tracking down the implications of their result or have passed over in their work what is there to be seen by the fresh eye of another.”  Each new claim to knowledge therefore, has to be picked apart and appraised.  Its shortcomings have to be established unequivocally before we can know what questions remain to be asked, and so what answers to seek – what we know is really so and what we don’t.  “This unending exchange of critical judgment,” Merton wrote, “of praise and punishment, is developed in science to a degree that makes the monitoring of children’s behavior by their parents seem little more than child’s play.” 

The institutionalized vigilance, “this unending exchange of critical judgment,” is nowhere to be found the study of nutrition, chronic disease, and obesity, and it hasn’t been for decades.  For this reason, it is difficult to use the term “scientist” to describe those individuals who work in these disciplines, and, indeed, I have actively avoided doing so in this book.  It’s simply debatable, at best, whether what these individuals have practiced for the past fifty years, and whether the culture they have created as a result, can reasonably be described as science, as most working scientists or philosophers of science would typically characterize it.  Individuals in these disciplines think of themselves as scientists; they use the terminology of science in their work, and they certainly borrow the authority of science to communicate their beliefs to the general public, but “the results of their enterprise,” as Thomas Kuhn, author of the The Structure of Scientific Revolutions, might have put it, “do not add up to science as we know it.” 

 

We live in interesting times.  Information that would not have been available to the vast majority of us is but a few keyboard clicks away.  Unburdened by professional indoctrination, we have the benefit of wanting to believe what is true about diet and health, regardless of who the truth may embarrass, and we have the chance to test it out for ourselves, on ourselves.  How to do that?  Eat meat and vegetables, nuts and seeds, some fruit, little starch, no sugar and no wheat.  Supplement with fish oil and gel cap vitamin D.  Get your lipids tested, insulin levels too if you can, and note that your TG to HDL ratio will be less than 3.5.  Then consider yourself a victor in the diet wars, and live long and well.

Another critique of GCBC may be found here: http://www.proteinpower.com/drmike/wp-content/uploads/2008/07/bray-review-of-gcbc.pdf

Dr. Mike Eades’ and Gary Taubes’ Response to Dr. Brey: http://www.proteinpower.com/drmike/wp-content/uploads/2008/07/taubes-response-to-bray-ob-reviews.pdf

Dr. Mike Eades’ additional response: http://www.proteinpower.com/drmike/weight-loss/more-braying-from-bray/

Review of a Critique, Part 4

Mr. BS then moves on to another topic – Taubes’ hypothesis that, as Mr. BS writes it – well, he writes it about three different ways, and finally he comes pretty close:  “(Taubes’) claim is that positive energy balance is a result of accumulating excess fat, not the other way around.”  He again does the “predictions resulting from this hypothesis” routine, but his understanding of Taubes’ points is insufficient, so again his test predictions are not valid.  Mr. BS is fully wedded to the “body fat accumulation results from eating too much” model, and he cannot think through the implications of Taubes’ hypotheses, the most relevant two of which are as follows:

5. Obesity is a disorder of excess fat accumulation, not overeating, and not sedentary behavior.

6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

In other words, as previously mentioned, Taubes’ focus is on causality.  The energy balance equation does not say anything about causality (but tons of folks have assumed that it does).  What they assume is “fat people get fat because they eat too much and work/exercise too little.”  This of course has never been proved, as most who believe it to be never thought to question it.  Note that this belief is rooted in a moral conviction that obesity results from human frailty.  Stated another way, the belief that obesity is a simple matter of people being too gluttonous and too lazy is a moral judgment – and thus serves the bias of any who wish to feel virtuous because they are not fat.  The question for those of us who would rather understand than judge the growing phenomenon of deteriorating health associated with increasing obesity is:  what has caused a larger and growing percentage of our fellow citizens to grow obese in the last 30 to 40 years?  It strikes me as unlikely on its face that the answer is “people are getting more lazy and more gluttonous”, particularly when viewed alongside the statistically significant increase in the number of people who are working out for the sole purpose of being leaner and more healthy.

How could it be true that fat accumulation causes hunger and thus more eating (increased intake of food energy), as well as a lower activity level (decreased expenditure of energy)?  The key is the work of insulin.  If carbohydrate intake is excessive, which means (by definition) it drives blood glucose towards a toxic glucose concentration level, resulting in an insulin secretion (the body’s natural defense for toxic glucose levels), blood glucose levels are reduced.  Muscles and organs can absorb some glucose at the cellular level, but most of the excess glucose will be converted to triglycerides and stored as fat.  Further, the consistent excess intake of carbohydrates will result in an increased baseline level of insulin – whatever that is for each individual.  High insulin levels prevent the body from liberating fat to make it available for use.  In effect the body fueled with excess carbohydrate is starving within a couple of hours of eating.  That is to say, just as in a starving body cannot get energy to its cells, so it is with the body we’ve described above.  There is energy in the body as stored fat – but at the cellular level, it may as well be in the next county. 

There’s a common set of reactions in a starving body.  The core temp will decrease as the body starts looking for ways to conserve.  Starving people move around less. They feel, generally, more hungry.  So the notional body we’ve described above will result in human that will eat what’s available but will likely otherwise be conserving energy in ways that are not conscious. 

In summary, the driver for the accumulation of more fat for this person is the de facto deprivation of energy by the natural cycle that results from excess carbohydrate intake. 

This is not to say that no one on the planet is a gluttonous, lazy slob.  What I believe, and what Taubes’ work points to, is that gluttony and laziness are not likely drivers of population wide changes in body fat percentage.  It also seems unlikely that kids started to develop type II diabetes all of sudden, at the exact same time that the ‘authorities’ began to obsess over fat consumption (resulting in parents and governments feeding their kids a higher carbohydrate diet), because they became gluttonous and lazy.  If anyone chooses to believe that fat people are morally deficient, that’s their choice of course.  The only thing that leaves is the question of which meds to treat them with because, as the last 30 years have proved, the “eat less workout more” advice is not working (and for obvious reasons once the CH is understood).  My experiment in high carbohydrate land made me significantly fatter despite acute attention to my intake and while working out six days a week, sometimes twice per day, doing resistance training, cardio and martial arts.

In the end, Mr. BS’s piece includes an admission that he’s all wrong, but doesn’t realize it.  I quote: “There is strong evidence that diets high in refined carbohydrate, and the ingestion of sweet and palatable foods, cause disruptions in appetite regulation.  This then leads to overeating.” 

Then we are treated to Mr. BS’s closing shot: “Those of you who think Taubes is without bias, keep in mind that he has built a career around the CH.”  First off, anyone who thinks anyone is without bias is either immature or ignorant or both.  That’s why humanity benefits from the scientific method, the guiding principle of which is do not trust humans (especially other scientists).  But secondarily, Mr. Taubes was a highly regarded science journalist long before he started publishing the material that was eventually encapsulated in GCBC.  If anything, his work of late has put him into great conflict with a majority of the scientists and many doctors who care about this topic.  And that brings me to a reasonable segue to the close of this review, which I hope you'll join me for tomorrow.

Deadly Quartet

http://archinte.ama-assn.org/cgi/content/abstract/149/7/1514
Does obesity cause hypertension, hypertriglyceridemia, glucose intolerance, and hyperinsulinemia?

Or does hyperinsulinemia cause the rest?  If you control the hyperinsulinemia, you affect the others, suggesting a causal relationship.

How do you control hyperinsulinemia?  Carb restriction.  Eat meat and vegetables, nuts and seeds, some fruit little starch and no sugar.

Review of a Critique, Part 3

(continued) Mr. BS’s fourth test prediction – “Fat overfeeding, without additional carbohydrate, should not result in weight gain since insulin secretion is not increased” - is also invalid.  If one is consuming too much carbohydrate, and is also “fat overfeeding”, the CH would predict additional weight gain.  This is because, as previously discussed, excessive carbohydrate intake results in high levels of insulin secretion, and insulin signals storage of both blood sugar as fat, and of fatty acids in the blood as stored fat.  Insulin also shuts off the body’s ability to liberate stored fat (acts as a master hormone, limiting the effect of the 7 or so hormones that can release stored fat).  In other words, the results Mr. BS reports are consistent with the CH.  Further, synthesis of body fat requires glucose.  With low levels of glucose due to carbohydrate restriction (100g/day maximum), fat synthesis is impeded.  A more accurate test prediction derived from the CH would be as follows:  “Fat overfeeding in the absence of excessive carbohydrate intake will result in a lesser increase in body fat than an isocaloric combination of fat overfeeding and excessive carbohydrate intake.”  Higher levels of fatty acids in the blood from high fat intake, absent high insulin levels, do not require that the fatty acids be converted to stored body fat.  Should there be a need, there’s nothing to prevent fat liberation for oxidation.  GCBC cites studies which indicate that fatty acids are moving in and out of adipose tissue more or less constantly in a normal human.  If, however, carbohydrate intake is excessive, both glucose and fatty acids will be trapped in storage – in other words, in additional adipose tissue.

After his simulated but invalid duel with the CH through his initial four test predictions, Mr. BS posits additional objections he has to the CH.  First, he states that insulin has a hunger reducing effect on the brain, and uses this fact as a refutation that high insulin levels could result in hunger. In other words, he’s suggesting that this one influence – insulin’s appetite suppressive quality – is the main or most significant factor on human hunger.  This is a stunning over-simplification of human hunger, which depends on any number of factors, not all of which are clearly understood.  But as regards insulin, first and foremost, the function of insulin is to protect the brain and nervous system from toxic levels of glucose.  The appetite suppressive effect of insulin may be real, if all other things are equal, but I doubt there’s a one of us that has not noticed being hungry 2-3 hours after a high sugar and/or high carbohydrate meal.  This post-eating hunger cycle is generated after high glucose levels force an insulin response, which results in conversion of glucose to storage, resulting in low glucose levels.  What the insulin levels are at which points in the cycle is not known to me to any level of precision, but I believe that insulin is “consumed” as it does its job of getting glucose out of the blood and into the tissues.  The post eating hunger cycle - “excessive carbohydrate consumption drives high glucose drives insulin response resulting in low glucose and increased hunger” - is characteristic of folks who eat high carbohydrate diets, and most recognize the cycle when they hear it described. 

Mr. BS’s next criticism of the CH is:  “Another thing the carbohydrate hypothesis cannot explain is why there are many lean people who eat moderate to high carbohydrate diets (even people who do not have high daily expenditures).”  First off, the CH as described in GCBC does not assert that all individuals will fatten if they eat a high carbohydrate diet.  Therefore, in no way does it have to explain the phenomenon of the “high carbohydrate skinny dude” to be valid.   That said, even a rudimentary understanding of the topic would lead one to believe that in sensitivity to food intake, or carbohydrate intake, a human population will demonstrate a bell shaped distribution.  That is, some will be able to eat big piles of nearly anything and seemingly never fatten (in shape, these people are often what has been described as ectomorphs – tall, thin, shoulders often smaller than hips, and with ‘stringy’ muscles vice dense or puffy muscles).  Ectomorphs could be said to often be less insulin sensitive than average.  Others, the ones at the other end of the bell shaped curve for insulin sensitivity, are frequently endomorphs; large in the pelvis, soft in appearance as they tend to have more subcutaneous fat, and frequently, they seem to fatten on food that others would starve on.  To invalidate the CH, one would need to show that a test population failed to fatten when on a diet consisting of excess carbohydrate when compared to an isocaloric, low carbohydrate diet.  In other words, there is a very simple explanation for the skinny people we all know who can eat a ton but never get fat – they are relatively insensitive to insulin (not to be confused with pathological insulin resistance). 

Tomorrow we'll hit the last points of Mr. BS's critique.

Fasting Boosts Chemo Effect

"Fasting for two days protects healthy cells against chemotherapy, according to a study appearing online the week of Mar. 31 in PNAS Early Edition. Mice given a high dose of chemotherapy after fasting continued to thrive. The same dose killed half the normally fed mice and caused lasting weight and energy loss in the survivors." http://www.physorg.com/news126202490.html

OK, only a mouse study, but it is consistent with the idea that cancer seems to get an inordinate survival benefit from high blood glucose levels, and is more sensitive to the action of insuling and insulin like growth factor than are normal tissues. If this is one of the cancer cell's main competitive advantages, we may be 'evening the playing field' such that our normal cells can out duel the cancer.

Review of a Critique, Part 2

(Continued)
Mr. BS proposes four predictions he derives from his understanding of the CH.  Naturally, if a prediction follows from a hypothesis, and that prediction can be falsified by known data, the hypothesis may be considered falsified.  For example, if I hypothesize that the sun comes up because I wake up, I could predict that if I did not wake up, the sun would not rise.  I can then falsify my hypothesis by noting that the sun has risen many times when I slept.  However, this kind of science is only as good as the participant’s understanding of the hypothesis in question.  Since Mr. BS appears not to understand the CH, then it should come as no surprise that his suggested test predictions are inadequate tests of the CH (a more objective test of a hypothesis is of course an intervention study, and such is proposed for the CH in some detail in GCBC on page 466 of the paperback version).

Having established these straw man predictions, based on an incomplete or incorrect understanding of the CH, Mr. BS proceeds to knock down all four.  The question is whether his test predictions are valid – do they really test the CH?   

Mr. BS’s first test prediction: if the CH is true, then the following should be observed:  “An inverse relationship between carbohydrate intake and body fat loss during food restriction, independent of energy intake.”

His first test prediction would be more accurately stated as follows: 

“Carbohydrate intake resulting in chronically high blood sugars and insulin levels should result in increased body fat accumulation when compared with an isocaloric diet composed of a macronutrient skew which does not generate chronically high blood sugars and insulin levels.”  Interestingly, Taubes suggests in one article that he thinks 100g/day or less is a ballpark number for a safe amount of daily carbohydrate consumption.  The uncited study (or studies) that Mr. BS says he refers to in his prediction falsification effort supports Taubes:  “I only observed an independent effect of carbohydrate intake at very low (italics mine) carbohydrate levels (<100g/day).”

Nutritionists on the whole seem to think that the minimum carbohydrate intake per day should be a level that I would consider "high" - 200 grams or more in order to ensure the brain gets enough glucose from ingested carbs, and to ensure that adequate calories can be ingested without overconsumption of protein (typical conjecture is that “too much is bad for the kidneys”) or fat (in line with the now conventional wisdom that “too much causes obesity and CVD”).  Those who use carbohydrate restriction with clients, however, would not call 100g/day a “very low intake level.”  Folks like the Drs. Eades or Dr. Atkins target 50-100g/day as normal carbohydrate intake.  In short, Mr. BS’s bias as a traditionally trained nutritionist is on display in his analysis.

Test prediction number 2 is, if the CH is true, then one should observe:

“A positive association between insulin levels and body weight gain.”

Mr. BS’s second test prediction is close to a Taubes hypothesis:  “8. Insulin is the primary regulator of fat storage. When insulin levels are elevated - either chronically or after a meal – we accumulate fat in our fat tissue. When insulin levels fall, we release fat from our fat tissue and use it for fuel.”  Mr. BS’s prediction refutation is invalid because he does not cite studies, and without being able to examine the studies he uses to refute the hypotheses prediction, we cannot know if they say what he interprets them to say.  Testing this hypothesis will take a carefully designed study.  If such a study has been done, I wish Mr. BS had cited it so I could examine it.

Mr. BS’s third prediction is, if the CH is true, then it should be true that “Fructose, a carbohydrate that generates very little change in blood sugar and very little insulin secretion, should result in less fat gain than glucose."  Mr. BS does not clarify what he means by fructose, nor does he cite the studies he claims falsify his (invalid) prediction.  Most likely he means high fructose corn syrup.  More importantly, Mr. BS’s third test prediction (as shown above) isn’t valid.  A valid prediction based on the CH would be:  “Fructose accelerates the fat storage signaling of excessive carbohydrate intake by increasing insulin resistance, which reduces the ability of non-adipose tissue to respond to insulin signals, therefore requiring that adipose tissue take up a greater portion of excess blood sugars.”  This prediction is validated to at least some degree by the non-cited study result Mr. BS refers to.

Tomorrow, we'll look at the fourth test prediction, and a few additional items covered in Mr. BS's post.

Review of a Critique of GCBC, Carbohydrate Hypothesis, Part 1

I found a critique by a fellow that takes issue with Gary Taubes and his ‘carbohydrate hypothesis’ (CH).  Taubes’ summation of the CH is presented in his book Good Calories, Bad Calories (GCBC).  I’ve read that book about four times because I want to understand it – and I think it is that important.  This author, (http://www.thebsdetective.com/2009/10/bullshitter-of-day-oct-7th-gary-taubes.html), Mr. BS, sees it differently.  I’ll use several posts to review Mr. BS’s critique.

Taubes’ hypotheses from GCBC are here: http://fireofthegodsfitness.blogspot.com/2010/03/tubs-of-taubes.html

Gary Taubes does not claim authorship of the CH, because as he reports in his book the CH was the conventional wisdom for the better part of the last 150 years.  The idea that eating fat makes one fat is a relatively new idea – a low fat, high carbohydrate diet is a fad diet. 

Mr. BS lists as his credentials a master’s degree in nutrition, and he points out in a “confident” style he’s been published in ‘prestigious’ professional journals.  There’s an implied arrogance in the very title of his post – who’s he to award “bullshitter of the day” status to others?  He also utilizes some language that strikes me as fairly pretentious, such as: “Taubes is a journalist (not a scientist).”  Why does he think this is a significant distinction?  Another choice quote: “I am going to approach the carbohydrate hypothesis as a true scientist should approach it.”  This implies he knows true science, whereas Gary Taubes does not.  One can only get away with this sort of pompous attitude if they are very, very good at what they do.

To be forthright about my bias, I see Gary Taubes as a noteworthy scientist (not to be confused with an in the lab researcher), and I believe his impact on health and nutrition will be historic and positive.  Credentials rarely impress me.  What most impresses me is clear thought, intellectual integrity and a well presented case.  What follows is an effort to use Mr. BS’s criticism to highlight some of the more useful insights one can gain from GCBC.

For the purpose of this series of posts, the definition of healthy carbohydrate intake is “less than 100g/day of non-starchy vegetables.”  “Excess carbohydrate intake” will be the term used to describe a an intake of carbohydrate that would increase blood glucose levels to a dangerous level unless controlled by insulin secretion.  Practically, what that means is eating too much grain, potatoes, corn, rice, sugar (or one of the other plant foods high in glycemic load) or processed foods which are typically loaded with both sugar and fat.

Mr. BS starts by illustrating, at best, an imprecise understanding of the CH.  The essential part of Taubes’ message in GCBC relates to causality and the impact of causality in understanding the energy balance equation and applying it to human metabolism.  His primary point on this topic is that while the energy balance equation is not the least bit in question (it is after all the First Law of Thermodynamics), the application of this law to human obesity is not particularly useful because it does not give any insight into causality. Or, as a physicist puts it:

“Applying the 1st Law to living organisms is Proof by Tautology. Yes, 1 + 1 = 2, but this tells us absolutely nothing about the underlying mechanics. The 1st Law does not (I repeat N-O-T) tell us whether you store excess energy in the form of fat, or bleed it off into the atmosphere by dilating blood vessels next to the skin, sweating, etc. To do so would require an accounting of entropy.”

(http://entropyproduction.blogspot.com/2009/02/all-medical-science-is-wrong-within-95.html - this post is worth reading in its entirety):

Mr. BS states: “Taubes blames carbohydrate, not increased food intake, for the epidemic of obesity in this country.”  More accurately stated, Taubes believes:

6. Consuming excess calories does not cause us to grow fatter, any more than it causes a child to grow taller. Expending more energy than we consume does not lead to long-term weight loss; it leads to hunger.

7. Fattening and obesity are caused by an imbalance- a disequilibrium – in the hormonal regulation of adipose tissue and fat metabolism. Fat synthesis and storage exceed the mobilization of fat from the adipose tissue and its subsequent oxidation. We become leaner when the hormonal regulation of the fat tissue reverses this balance.

In GCBC Taubes points out that using government stats for estimates, it appears that carbohydrate consumption has increased since the 1970s, while fat consumption has been stable.  But the CH does not require that we know that there is or is not increased energy consumption in our fattening population.  The important issue is causality.  The consumption of excess carbohydrate causes storage of energy as adipose tissue, and/or a reduction of expenditure of energy by the body.  How?  I’ll explain further, as we work through Mr. BS’s critique tomorrow.

Primal Blueprint

This is a good read. I have not read Mark's book, and know for a fact I won't believe everything he advocates.  However, I also have no doubt that anyone that follows this plan will live well.  This program is at least a cousin of CrossFit.

1. I’m lazy.

Ironically, I spent 25 years of my life pursuing high level fitness and peak health through hard work, discipline, sacrifice and misery. That didn’t work out for me. I’m over it. Now I just want the best results with the least amount of pain, suffering, and sacrifice. I jokingly tell my ex-triathlete buddies, “I’d rather look fit than be fit.” Of course, the irony is that when you actually do what it takes to look fit (eat right, cut the Chronic Cardio, sprint a bit now and then and lift intensely two or three times a week ) you become VERY fit. And healthy. And happy. And more productive. The best part of Primal Blueprint living is that you can get appreciably better results with significantly less time, less effort and less sacrifice. Instead of the old 20-30 hours a week I used to put in training, I now train less than three hours total a week. I try to play the rest of the time.

2. I love good food.

Some people mistakenly think the Primal Blueprint requires giving up eating good food. Nothing could be further from the truth. When I was a college endurance athlete, my buddies nicknamed me “Arnold,” after Arnold Ziffle, the pig on Green Acres. I could eat more than just about anyone in school (including the football linemen). I ate everything and enjoyed it all. But I became a slave to the carbs and to the hunger that they generated every three hours of my life. Later, when I retired and researched the damage I was doing eating grains, sugars,hydrogenated oils and all the other stuff I consumed to fuel my massive cardio efforts, I feared I might have to suffer a lifetime dearth of gustatory delights if I wanted to keep my boyish figure. Never happened. Primal eating reprograms the genes in a way that takes the edge off hunger, while assuring more-than-adequate energy and stable blood glucose levels. Now, I eat as much as I want, whenever I want from a list of fabulously tasty foods. I just avoid eating most things from that other list. Hunger doesn’t drive my life the way it used to. When I sit in a restaurant with a rare 20-ounce rib eye steak, a bowl of butter-sautéed mushrooms and a glass of fine Cabernet in front of me, I never feel sorry for myself that I didn’t order pasta or that I won’t be having the bread or potatoes or rice. And for dessert, if I’m still hungry, I’d really rather have another lamb chop or a bowl of berries than a slice of cardboard cake or mucous-inducing ice cream. Worst case, I can have a small taste of the latter and be satisfied.

3. I like to play.

I spent a fair amount of my life training for grueling endurance contests (marathons, Ironman triathlons, 24-hour relay running events). Only just recently did it occur to me that I NEVER really had fun while I was competing or while I was training. Admittedly, I could sometimes get into “the zone,” but that’s really only a temporary zone of less pain. I did appreciate the valiance of my efforts and certainly felt pride in my accomplishments, but from the time the gun went off until I crossed the finish line, I never once could truthfully say, “Isn’t this fun?”  In contrast, today I plan most of my (minimal) training around being able to participate in fun activities later. And while I don’t necessarily see play as “workout time,” it is most assuredly contributing to my fitness. Primal Blueprint training gives me the functional strength and endurance to jump into an aggressive Ultimate Frisbee game, stand-up paddle and surf for two hours, take a 90-minute trail hike with sprints thrown in, play a round of golf, or snowboard for five days in a row. I stay fit so I can play at stuff I find FUN.

4. I like to sleep.

I used to feel guilty if I slept too much. As if I were missing out on something that might be taking place while the lights were still on somewhere. Now I get at least eight hours every night and embrace the idea that I am NOT wasting time, but am recharging the batteries and will probably live longer as a result. I think most people would prefer to get adequate sleep, but feel like it’s a sign of weakness that they “need” eight or nine hours. It’s not. Sleep is integral to health.

5. I don’t like being sick.

No one does. At the peak of my endurance career, I got colds and flus five to seven times a year. I also had severe seasonal grass pollen allergies. The nature of Chronic Cardio training (all that cortisol) and the obligate high carbohydrate diet (all that sugar) kept my immune system so trashed that anything that was going around was going to take me down with it. And stuff is always going around. The Primal Blueprint works because everything about it is contemplated to support or boost the immune system and not trash it. My allergies have long since disappeared. I rarely get any kind of cold or flu now and, if I do, it’s with no real down time and over quickly. Many people argue that this benefit alone is worth the switch to Primal.

http://www.marksdailyapple.com/10-real-life-reasons-why-the-primal-blueprint-works-for-me/

Primal's Carb Continuum

The linked article is a great summary of a common sense approach to carb consumption - "read and heed."
http://www.marksdailyapple.com/the-primal-carbohydrate-continuum/

Barefoot Running .... Better?

""Most people today think barefoot running is dangerous and hurts," Daniel Lieberman, a professor of human evolutionary biology at Harvard University, said in a prepared statement. "But actually you can run barefoot on the world's hardest surfaces without the slightest discomfort and pain…It might be less injurious than the way some people run in shoes." 

Lieberman and his group used 3-D infrared tracking to record and study the running and strike style of three groups of runners: people who had always run barefoot, people who had always run with shoes, and people who had switched from shoe to shoeless. 

They found that when runners lace up their shmancy sneakers and take off, about 75 to 80 percent land heel-first. Barefoot runners—as Homo sapiens had evolved to be—usually land toward the middle or front of the food. "People who don't wear shoes when they run have an astonishingly different strike," Lieberman said. "
http://www.scientificamerican.com/blog/post.cfm?id=running-barefoot-is-better-research-2010-01-27

Even better than the short article is the video in which they teach you how to run down a gazelle on the African savanna - I have to try that one of these days ...

Sugar Substitutes

... "new research suggests that the body is not so easily fooled, and that sugar substitutes are no key to weight loss — perhaps helping to explain why, despite a plethora of low-calorie food and drink, Americans are heavier than ever.

"The new study, say the scientists, offers stronger evidence that how we eat may depend on automatic, conditioned responses to food that are beyond our control."

"What they mean is that like Pavlov's dog, trained to salivate at the sound of a bell, animals are similarly trained to anticipate lots of calories when they taste something sweet — in nature, sweet foods are usually loaded with calories. When an animal eats a saccharin-flavored food with no calories, however — disrupting the sweetness and calorie link — the animal tends to eat more and gain more weight, the new study shows. The study was even able to document at the physiological level that animals given artificial sweeteners responded differently to their food than those eating high-calorie sweetened foods. The sugar-fed rats, for example, showed the expected uptick in core body temperature at mealtime, corresponding to their anticipation of a bolus of calories that they would need to start burning off — a sort of metabolic revving of the energy engines. The saccharin-fed animals, on the other hand, showed no such rise in temperature. "The animals that had the artificial sweetener appear to have a different anticipatory response," says Susan Swithers, a professor of psychological sciences at Purdue University and a co-author of the study. "They don't anticipate as many calories arriving." The net result is a more sluggish metabolism that stores, rather than burns, incoming excess calories."

"Swithers ... says that the study does suggest artificial sweeteners somehow disrupt the body's ability to regulate incoming calories. "It's still a bit of a mystery why they are overeating.""

"Though it's premature to generalize based on animal results that the same phenomena would hold true in people, Swithers says, she notes that other human studies have already shown a similar effect. A University of Texas Health Science Center survey in 2005 found that people who drink diet soft drinks may actually gain weight; in that study, for every can of diet soda people consumed each day, there was a 41% increased risk of being overweight." 

My take - if you have already done some work on what you eat (and are eating predominantly meat, vegetables, nuts and seeds), and are ready to take more steps, eliminate the fake sugar products to see what that gets you.
http://www.time.com/time/health/article/0,8599,1711763,00.html#ixzz0kSYmc4XZ

Dr. Cordain Revises Stance on Sat Fat

BLUF:  "The bottom line is that we do not recommend cutting down saturated fatty acid intake but rather decrease high-glycemic load foods, vegetable oils, refined sugars, grains, legumes and dairy."


Nice bit that follows describing the mechanisms driving formation of atherosclerotic plaques (note: the LDL that oxidizes most easily is the small, dense LDL; the levels of these LDLs are driven higher by high carb consumption):
"Moreover, some studies have suggested that there’s not enough scientific data to support the view that increased total or LDL cholesterol is an independent risk factor for CVD, but rather oxidized LDL. Plaque production is mediated by oxidized LDL but not LDL. Oxidized LDL can produce shedding of the inner layer of the artery namely glycocalix. Then oxidized LDL infiltrates in the intima of the artery. Oxidized LDL is eaten by macrophagues, a process known as phagocytosis, and therefore macrophagues are transformed into foam cells which produce the fibrous cap.

Once the fibrous cap has been produced we need to break it down in order to produce an ischemic event. Lectins and low-grade chronic inflammation are involved in the activation of matrix metalloproteinases which break down the fibrous cap.

In summary, high total cholesterol or LDL levels do not increase CVD risk but rather oxidized LDL. To produce oxidized LDL we need the factors mentioned above. Hence, consumption of saturated fatty acids is not an issue if we control several other factors such as those mentioned before.

Dr. Cordain wrote a book chapter where he shows that saturated fat consumption in ancient hunter-gatherer populations were usually above recommended 10% (American Heart Association) of energy from saturated fats yet non atherogenic."

The bottom line is that we do not recommend cutting down saturated fatty acid intake but rather decrease high-glycemic load foods, vegetable oils, refined sugars, grains, legumes and dairy."

http://thepaleodiet.blogspot.com/2010/03/paleo-diet-q-saturated-fat.html

Grain, the Double Edged Sword

"Consumption of high levels of whole grain cereal products impairs bone metabolism not only by limiting calcium intake, but by indirectly altering vitamin D metabolism. In animal studies it has been long recognized that excessive consumption of cereal grains can induce vitamin D deficiencies in a wide variety of animals [81–83] including primates [84]. Epidemiological studies of populations consuming high levels of unleavened whole grain breads show vitamin D deficiency to be widespread [85–87]. A study of radiolabelled 25-hydroxyvitamin D3 (25(OH)D3) in humans consuming 60 g of wheat bran daily for 30 days clearly demonstrated an enhanced elimination of 25(OH)D3 in the intestinal lumen [88]. The mechanism by which cereal grain consumption influences vitamin D is unclear. Some investigators have suggested that cereal grains may interfere with the enterohepatic circulation of vitamin D or its metabolites [84, 88], whereas others have shown that calcium deficiency in- creases the rate of inactivation of vitamin D in the liver [89]. This effect is mediated by 1,25-dihydroxyvitamin D (1,25(OH)2D) produced in response to secondary hyperparathyroidism, which promotes hepatic conversion of vitamin D to polar inactivation products which are excreted in bile [89]. Consequently, the low Ca/P ratio of cereal grains has the ability to elevate PTH which in turn stimulates increased production of 1,25(OH)2D which causes an acceler- ated loss of 25-hydroxyvitamin D."

http://www.direct-ms.org/pdf/EvolutionPaleolithic/Cereal%20Sword.pdf

So, in case you needed another reason not to eat bread (whole grain or otherwise):

- besides the fact that it has a high calorie to nutrient ratio, and

- rapidly digests into simple sugar and thus drives blood sugars to unhealthy levels resulting in the insulin cascade, and 

- the fact that it has many 'anti-nutrient qualities', and 

- the fact that most bread doesn't taste good enough to eat by itself (how much sugar and/or butter do you slather on your bread to make it desirable?);

Here's another thing we don't need - it interferes with vitamin D utilization.