The Insulin Paradox

One of the more difficult things to sort out from the enormous amount of information out there is the actual effect, if any, of dietary composition on resulting body composition.  This is complicated from the get-go by many rodent studies that are done on reproductively mature animals that are still growing.  How to compare this to humans who cease growing vertically once they reach adulthood?  Next we have to sort through the studies that are done, and the implications of them, in the context of weight loss/underfeeding vs. those in the context of weight gain/overfeeding.  Clearly there are compensatory mechanisms at play in both situations that are drastically different.  Lastly, and here's where we probably have the least amount of information, and practically nothing in humans, what role does one's dietary composition have on their body composition over the long haul for a "normal" weight stable adult?    Verifiable science basically fails us on this last point, and we're left mostly to the "wolves" of the diet/fitness industry -- e.g. body builders,  trainers and nutritionists for elite athletes, etc. -- for their anecdotal reports.  I don't mean to disparage these folks with the term wolves (hence the quotes), but we can never separate the reports from the reality when there's money on the line in a world where ads are required to include "results not typical" disclaimers.  While I'm not saying all of these folks, or even a majority, are of the 2am infomercial variety, the claims remain largely unverifiable.  It would sure be cool if there was a privacy-sparing way to collect verifiable body composition, dietary and activity data for a large population of free-living humans, eh?

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Exercise v. Diet for Weight Loss

In recent months, mainly sparked by Mr. Exercise Only Makes You Hungry's appearance on the Dr. Oz show, there seems to have been some renewed interest in the LC community in the role of exercise for weight loss.  Most studies show little effect of exercise only, but, as the authors of this study I'm about to share state,  "these conclusions are drawn from studies in which individual energy intake and expenditure were not rigorously controlled or accurately measured" .  When it has been controlled, the calorie deficits created through exercise alone were not sufficient to produce significant weight loss.

Reduction in Obesity and Related Comorbid Conditions after Diet-Induced Weight Loss or Exercise-Induced Weight Loss in Men

This study was done in weight stable (6+ months prior to study) obese (BMI >27) men with waist circumferences over 100 cm (~39").    The men were sedentary, non-smokers, non-light drinkers, and had normal lipids and glucose tolerance.

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Diet, Cardio, Resistance Training & Insulin

Thanks to Mirrorball for "putting a bug in my ear" regarding the impact of exercise on insulin levels.  The basic thought being that if Taubes' theory that lowering insulin makes you lose weight, then exercise should be very effective, especially if you couple it with carbohydrate restriction.  Because, if you "overeat" protein and fat calories those don't impact body weight right?

So I found this study:

Effects of Aerobic or Resistance Exercise and/or Diet on Glucose Tolerance and Plasma Insulin Levels in Obese Men 

Basically they took three groups of men averaging 40-47 years of age, ~100kg weight, ~32 BMI and did 3 interventions: 

1. DO = diet only
2. DA = diet + aerobic exercise
3. DR = diet + resistance exercise

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Of Mice & (Wo)Men: When's the last time you saw an 5'4" 130 pound fat woman?

I'm always amused when a rodent study that seemingly counters the calorie-based theories on obesity comes down the pike.  In predictable fashion, someone in the LC webosphere will pick up on it and use it as an example to counter calorie-based theories on weight/obesity.   A recent example of this is brought to us by low carbers' favorite comedian edutainer, Tom Naughton:  Fat Mice & The Laws of Thermodynamics that referenced the following study:  Mild calorie Restriction Induces Fat Accumulation in Female c57BL/6J Mice.  

Now Tom starts out misrepresenting things by picturing a fat mouse, likely an ob/ob.  This study actually involved females of the strain pictured below:

Kind of a cute little critter, no?   The study was also conducted in the context of calorie restriction and it's demonstrated increase in longevity of mice.  They are not a mutant strain genetically predisposed to obesity.

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More on Water Weight & Insulin

There's an interesting related conversation on this topic going on over at Paul Jaminet's site:

Water Weight: Does It Change When Changing Diets? Does It Matter?

For those not familiar with the Perfect Health diet, one component is to get ~400 cal in "safe starches" -- around 100g.  For those transitioning to their diet from a low carb diet, some have experienced a not-unexpected weight gain.  I've added some thoughts to the comments there and -- can't be sure and some is just a hunch -- but I think any weight bounce is probably more carb associated, predominantly glycogen repletion.  It may well be due to replenishing other "carb" molecules with their associated water as well.  My guess is that for the most part these changes show up on the scale more than in dimensions.  That was my experience during the almost 3 years of my "low carb cheating" plan.  I can't know for sure for the first year and a half or so of that, because I never weighed, but I didn't gain size during my cheats (pants still fit fine) and later after I weighed I sometimes saw a few pound gain, but again this didn't effect the fit of the skinny-jeans much if at all.  

However my current interest/focus is building on this recent post of mine:

Insulin, Weight Loss & Water Weight

In that post I referenced two studies that I'll repeat link to here:

Changes in abdominal subcutaneous fat water content with rapid weight loss and long-term weight maintenance in abdominally obese men and women - This one discusses how following rapid weight loss and improvement in insulin sensitivity of the fat tissue, fat mass increases due to increased associated water resulting from improved blood flow.

Disparate Hydration  in Adipose and Lean Tissue Require a New Model for Body Water Distribution in Man.  This one discusses various models of determining total body water content, and the contribution of adipose tissue often ignored for lean populations.  It also discusses the extra and intracellular distribution of water in adipose tissue and lean tissue.

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GCBC Reference Check ~ Part I of ? ~ Metabolic Adaptability & Energy Balance

Ever since I discovered that Taubes had actually cited the 2003 Reshef et.al. paper in GCBC, I've been intrigued by what many of his other references ACTUALLY said.    In that regard, I've picked up a few of these older text books by various authors and experts cited by Taubes in the book.

One such expert is Keith Frayn, who I've dubbed "the English guy" as Taubes previously described him.  I've been sharing some of his more scholarly contributions (e.g. peer review journal articles), and have more to come on that front.  None of these made it into GCBC, however.  I'll leave it to you, my readers, to decide for yourselves what this says about the quality of Taubes' research on the topic.

But this post is looking at the words of Keith Frayn that Taubes DID include in GCBC.  

Chapter 17 of GCBC opens as follows:

Before World War II, the proposition that obesity was caused by overeating - the positive-caloric-balance hypothesis - was one of sever competing hypotheses to explain the condition.  After Hilde Bruch reported that obese children ate immoderately, and Louis Newburgh insisted that a perverted appetite was the fundamental cause of obesity, the positive-caloric-balance hypothesis became the conventional wisdom, and the treatment of obesity, as Jean Mayer observed, became the provenance of psychiatrists, psychologists, and moralists whose primary goal was to rectify our dietary misbehavior.   Any attempt to dispute the accepted wisdom was treated, as it still is, as an attempt to absolve the obese and overweight of the necessity to exercise and restrain their appetites, or to sell something, and often both.

This conviction that positive caloric balance causes weight gain is founded on the belief that this proposition is an incontrovertible implication of the first law of thermodynamics.  "The fact remains that no matter what people eat, it is calories that ultimately count," as Jane Brody explained in the New York Times.  "Eat more calories than your body uses and you will gain weight.  Eat fewer calories and you will lose weight.  The body, which is after all nothing more than a biochemical machine, knows no other arithmetic."

For fifty years, clinicians, nutritionists, researchers, and public health officials have used this logic as the starting point for virtually every discussion of obesity.  Anyone who challenges this view is seen as willfully disregarding a scientific truth.  "Let me state," said the Columbia University physiologist John Taggart in his introduction to an obesity symposium in the early 1950s, "that we have implicit faith in the validity of the first law of thermodynamics,"  "A calorie is a calorie," and "Calories in equals calories out," and that's that.

But it isn't.  This faith in the laws of thermodynamics is founded on two misinterpretations of thermodynamic law, and not in the law itself.  When these misconceptions are corrected, they alter our perceptions of weight regulation and the forces at work.

Taubes then goes into his spiel about how 50 years of "bad obesity research" was spawned based on the notion that overeating and sedentary behavior cause obesity rather than the other way around.  This is but one of many contradictions in this book and his lectures.  On the one hand he makes claims that calories don't count (e.g. his analysis of Shai), while on the other hand, acknowledging that they do, but that thousands of obesity researchers are simply misguided as to the cause.  On the one hand he claims that the obese eat less than the lean, yet in this section of the book he goes on to describe how it is the fat accumulation that drives the obese to eat more.  

I have more to say on some of the ensuing discussion on the direction of causality when I procure some other references, but for now let's fast forward a bit.  Taubes goes on to describe metabolic adaptation, regulation and homeostasis.  The implication he makes in this discussion is that human metabolism is extremely varied and adaptable.  Yes, there are differences due to hormonal levels (e.g. hypothyroidism is a basic example), and different macronutrients elicit different thermogenic effects, but there are limits.  Hormonal signals can downregulate metabolism, lower body temp, etc.  But there's only so far this can go ... or we die!  By the same token, overfeeding studies have demonstrated time and again that whatever signalling and adaptations (futile cycling) may occur in response cannot prevent considerable weight gain.   Taubes basically implies that no matter what we may do consciously to (a) maintain caloric balance, (b) induce positive caloric balance, or (c) induce a caloric deficit, our bodies will adapt, entirely beyond our control, to restore some pre-programmed homeostasis.  (Of course eating carbs throws all of this exquisite regulation out the window because they "singularly" induce an insulin response and cause net fat accumulation regardless of the caloric state).  In any case, I believe Taubes takes this adaptability to his usual extremes.  If our bodies were this adaptable, then almost nobody would get obese (surely there would be no reason for the uptick as the genetically lean would still be wasting away those ~300 cal/day extra they ate, no?).   But also, nobody could ever lose weight by any means, even low carb.    Yes, our bodies do adapt.  Insulin resistance is one such adaptation as is the inevitability of decreases in basal metabolic rate that accompany caloric restriction (on LC too), etc.  

So, here's the whole of Taubes' quotation of Keith Frayn (including the entirety of the paragraph for some context):

Among researchers who study malnutrition, as opposed to those whose specialty is obesity, these compensatory effects to caloric deprivation are taken for granted, as is the fact that hormones regulate this process.  "Changes in ... hormones such as insulin and glucagon (*87) play an important role in this metabolic response to energy restriction," explains Prakash Shetty ... "These physiological changes may be considered as metabolic adaptations which occur in a previously well-nourished individual and are aimed at increasing the 'metabolic efficiency' and fuel supply of the tissues at a time of energy deficit."  We should not be surprised that "dieting is difficult", as Keith Frayn of Oxford University says in his 1996 textbook, Metabolic Regulation, "It is a fight against mechanisms which have evolved over many millions of years precisely to minimize its effects ....  As food in take drops, the level of thyroid hormone fals and metabolic rate is lowered.  Food intake has to be reduced yet further to drop below the level of energy expenditure .  Hunger mechanisms, including the feeling of an empty stomach, lead us to search for food ... ."

IN ALL OF THE PAGES AND REFERENCES AND WHATNOT IN THIS DEFINITIVE WORK, THIS IS THE ONLY MENTION OF FRAYN'S WORK????

OK, I'll quiet back down now and address this text and what it has to say.

First, I'll note two things:  

1. Frayn says dieting is difficult, not impossible.  IOW, if we are able to override these adaptive mechanisms for long enough, we can and will lose weight.  It's not fair that likely we'll have to continue to do so for a period of time if not all eternity, but Frayn does NOT say, as Taubes implies, that the adaptation is so considerable as to negate any efforts of caloric restriction.  At some point, almost all dieters will have to confront this reality.  (Yeah, I know, it's NOT FAIR!!!!!)
2. Frayn acknowledges what many many low carbers discover somewhere down the line:  That food intake must be further restricted if we're to move beyond just a reduced girth.  When one considers the caloric deficits we LC'ers are in during our rapid initial losses (personally, I probably lost 85-90% of my weight rather steadily in the first 10 months, I'm now ~40 months into this journey), this "efficiency based" adaptation is likely greater for us than for the "slow but steady" formulaic reduced calorie plan.

The Frayn quote comes from Chapter 10 of Metabolic Regulation entitled Energy balance and body weight regulation.  

The chapter begins with a discussion of Energy Balance including the equation:  Energy intake (food) = Energy expended (heat, work, biosynthesis) + Energy stored.  

On an hourly basis, the energy intake and energy expenditure may not match each other at all... Therefore it is necessary to have short-term storage compounds, such as glycogen and triacylglycerol, which can buffer these mismatches.  In the longer term -- over a period  of months or years -- the glycogen stores, which have a finite and fairly small capacity ..., cannot buffer mismatches between intake and expenditure.  The stores of triacylglycerol in adipose tissue are our long-term buffer.  In other words, if energy intake exceeds expenditure consistently, triacylglycerol accumulates in adipose tissue, which accords with common observation.

The chapter goes on to describe how in most people, this balance is indeed pretty precisely maintained by most people despite the fact that it would seem impossible for us to be able to exactly sense caloric intake to match needs.  Frayn describes how we may be subject to, for example the tightness of one's belt, subconscious signals that alter our behaviors.  The chapter goes on to describe how energy expenditure is calculated and the components of energy expenditure.  There is a graphic on p. 239 that shows basal metabolic rate comprising about 60% of energy expenditure, physical activity about 20%,  diet induced (TEF) about 10% and other factors the remaining 10%.  BMR is highly correlated with fat-free mass.

On p. 240 Section 10.3.2 asks How does obesity develop?

If an individual is overweight or obese, that individual must have been through a period when his/her intake of energy was consistently greater than his/her energy expenditure.  It does not necessarily follow that this is true now; an obese subject may be in energy balance, with a stable weight.  Then we can ask:  if energy intake was greater than energy expenditure, did this arise through (i) an elevated rate of energy intake, compared with people of normal and steady body weight, or (ii) a diminished rate of energy expenditure (again, compared with people of normal and steady body weight)?  The answer may not be the same for all obese subjects.  This question is of interest because if the answer is (ii) -- i.e. diminished energy expenditure -- it implies that the individual will also have a particularly hard job losing excess calories because he/she has a 'biologically' low metabolic rate; it also implies that we might look, in metabolic terms, for the cause of this oddity of metabolism.  

What makes the relatively simple question difficult to answer is that we don't usually get to measure the metabolic rates of obese people before they become so.  And also that long-term energy balance is maintained to a surprising precision of a fraction of a percent, while daily balances are far more variable.  Many, many, folks quite literally wake up one day and realize they are fat and wonder how they got that way.  (As someone who regained 40 or so lbs and gained 60 more over the period of a year or so without binging I can attest to the sort of denial that went on as I seemingly slowly packed the pounds on).  This section goes on to describe the observation that obese have higher levels of EE than lean that can be attributed to higher BMR's correlated with FFM (we don't just gain fat) which would argue against (ii).  The section concludes:

The message from such studies is clear:  for the majority of obese people, the cause of the obesity is not a defect in energy expenditure but a rate of energy intake which is greater than normal.  Of course, if energy expenditure is also lower than normal, perhaps because of lack of physical activity, the situation will be made worse.  The reasons why some people eat more than others are extremely complex and not well understood, and they are outside the scope of this book.

So here is where a follower of Taubes would jump in and say that what he really explains in GCBC is WHY we overeat.  But there is absolutely no evidence in the research Taubes cites to support his notion that energy storage drives excess intake.

Skipping on to Section 10.4  Dieting and metabolic regulation:

Obesity results from an excess of energy intake over expenditure. If the obese or overweight person wants to lose weight, the solution is simple and inarguable: energy expenditure must exceed intake for a suitable length of time. The only alternative is surgery to remove some excess fat.   This message is simple in principle, but extraordinarily difficult to put into practice.  We shall consider why it is difficult, and look at dieting from a metabolic viewpoint.

Remember, Keith Frayn is a TRUE expert in fat metabolism.  It is in Section 10.4.1 Dieting as a battle against adaptation that we find the sole statement attributed to this renowned expert in GCBC.  To refresh:

"dieting is difficult", as Keith Frayn of Oxford University says in his 1996 textbook, Metabolic Regulation, "It is a fight against mechanisms which have evolved over many millions of years precisely to minimize its effects ....  As food in take drops, the level of thyroid hormone fals and metabolic rate is lowered.  Food intake has to be reduced yet further to drop below the level of energy expenditure .  Hunger mechanisms, including the feeling of an empty stomach, lead us to search for food ... ."

This is a typical tactic of Taubes.  Yes, all of this occurs which is why obesity is so difficult to reverse.  But it occurs with LC diets all the same, it is not a rebuke of  "mainstream wisdom" regarding how to achieve weight loss, it is an acknowledgment that once we've accumulated a lot of fat, we are metabolically wired to hold onto it!  The GCBC reader is left thinking Frayn is dissing energy balance based weight loss strategies.  But Frayn has much more to say on this topic as relates to dieting strategies.  Some excerpts:

... A knowledge of metabolism and metabolic regulation enables some common-sense statements about the effects of any particular dietary regimen to be made.  For instance, a diet of grapefruit and bacon is likely to be effective only if its total energy content is suitably low, and if it will be sufficiently satisfying to enable the dieter to eat nothing to supplement it for a suitable length of time.

... A problem with all special diets is that they cannot be maintained indefinitely.  There is a wealth of research on the effects of dieting, with uniformly depressing results when the study is continued beyond the period of the diet.  Almost all studies of dieting show that there is weight gain when the diet is stopped, and the long-term results of dieting are, for the most part, thoroughly discouraging.  It is not the purpose of this book to recommend diets or exercise regimes, but a few statements can be made, based on sound metabolic principles, about sensible approaches to voluntary regulation of body weight.

... On the energy intake side, it has been shown many times that when special diets are stopped the dieter tends to resume his or her previous diet -- which provided an excessive amount of energy.  The long-term solution has to be to change dietary habits.  Again, years of research have shown that simply trying to eat less of the same things is desperately unsuccessful.  Presumably the body or the brain becomes used to a certain bulk of food, and any less is not satisfying.  So the nature of the diet rather than the amount has to be changed.

I know what you're thinking!  Cut the carbs!!  That's the culprit!!  But Frayn continues:

To the metabolically literate, it is obvious that some foods contain more energy than others in the same bulk; like energy stores in the body, fat-rich foods are more energy-rich, whereas carbohydrate-rich foods contain less energy for the amount of bulk -- especially hydrated bulk, which is what they will be by the time they reach the stomach.  Therefore, the metabolically literate eater consumes a diet relatively high in carbohydrate foods and low in fat-rich foods.  By this means, he or she can actually have a very full stomach and yet not ingest excessive amounts of energy, especially if the carbohydrate is largely in unrefined forms (fruit, vegetables, cereals rather than sugar).  The trick may be to be aware of which foods contain fat:  pastry, biscuits, potato chips and red meat are examples of foods which may be thought of as carbohydrate- or protein-rich, but which actually contain a lot of fat.  This is not just a theoretical argument; a number of studies have shown that body weight is related to the habitual fat content of the diet, with those on lower-fat diets aving, on average, lower body weights. 

However misguided one might consider this advice, it IS the totality of the words of Keith Frayn.  One amongst a few true experts in the field who Taubes acknowledges have corrected him on his misguided G3P theory.  And, let us not forget, someone Taubes readily quotes in GCBC to sort-of "prove" his point that our bodies are supposedly mere bystanders to metabolic adaptations.

I suppose Frayn is just another one of those who have spent their lives in search of misguided theories of obesity this last half century or so.

Changes in Energy Balance and Body Composition at Menopause

Changes in Energy Balance and Body Composition at Menopause: A Controlled Longitudinal Study  (Abstract only unfortunately)

This isn't LC related, but it is weight related.  And ... it's from the "It's Just Not Fair" department :-(

Abstract

Objective: To describe the effects of menopause on resting metabolic rate, body composition, fat distribution, physical activity during leisure time, and fasting insulin levels.

Design: A longitudinal comparison of metabolic changes in women who experienced menopause with changes in age-matched women who did not experience menopause.

Setting: General clinical research center.

Patients: An initial cohort of 35 sedentary healthy premenopausal women (age range, 44 to 48 years). After 6 years of follow-up, 18 women had spontaneously stopped menstruating for at least 12 months and 17 women remained premenopausal. No women received hormone replacement therapy.

Results: Women who experienced menopause lost more fat-free mass than women who remained premenopausal (−3.0 ± 1.1 kg and −0.5 ± 0.5 kg, respectively), had greater decreases in resting metabolic rate (−103 ± 55 kcal/d and −8 ± 17 kcal/d) and physical activity during leisure time (−127 ± 79 kcal/d and 64 ± 60 kcal/d), and had greater increases in fat mass (2.5 ± 2 kg and 1.0 ± 1.5 kg), fasting insulin levels (11 ± 9 pmol/L and −2 ± 5 pmol/L), and waist-to-hip ratios (0.04 ± 0.01 and 0.01 ± 0.01) (P ≤ 0.01 for all comparisons). Menopause did not affect energy intake, fasting glucose levels, or peak oxygen consumption.

Conclusions: Natural menopause is associated with reduced energy expenditure during rest and physical activity, an accelerated loss of fat-free mass, and increased central adiposity and fasting insulin levels. These changes may indicate a worsening cardiovascular and metabolic risk profile.          

If I'm reading this right, there is a combined change in energy expenditure of around 225 cal/day.
Yep ... no fair!!!