Tag Archives: body composition

Coffee and cigars, the breakfast of champions

Or more specifically, caffeine and nicotine… or really just nicotine.  Today is about the lesser of two evils: nicotine, Mother Nature’s little helper (the other evil being cigarettes [not coffee]).  This curious little molecule is an anti-inflammatory memory boosting appetite suppressant.  If it didn’t screw with the reward mechanisms in your brain, it’d be a vitamin. Part 1.  Cigarettes, nicotine, and metabolic function Exhibit A: Activation of the cholinergic anti-inflammatory pathway ameliorates obesity-induced inflammation and insulin resistance  (Wang et al., 2011) translation: “nicotine is good for mice.” Continue reading

Exenatide and tapeworms, Op. 116

The great Dr. Schoeller can polish a turd like no other.  Dale Schoeller’s claim to fame is his extensive work on one of the best ways to measure total energy expenditure in free-living individuals: doubly-labeled water.  In doubly-labeled water, subjects drink stable isotope-labeled water; instead of hydrogen + oxygen = H20, the stable isotope-labeled water is deuterium + oxygen-18 = D218O.  Deuterium is excreted just like hydrogen, in water as urine & sweat.  Oxygen-18 is excreted just like oxygen, in water and carbon dioxide.  So the subjects lose deuterium & oxygen-18 in water at equal rates, but only oxygen-18 in carbon dioxide; so this technique basically measures carbon dioxide production, which is proportional to energy expenditure.  Clever. 

Being that Schoeller practically invented the technique, his interpretation of these total energy expenditure data are not flawed, but that’s not where he went astray.

Alterations in energy balance following exenatide administration (Bradley et al., 2012)

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Metabolic rate per se

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Admittedly, the effect of diet on metabolic rate is small (i.e. statistically non-significant in most cases), but its incredible consistency across space and time suggest it could be true.  And given the difficulty of maintaining a reduced body weight after dieting, it might even be important.  The following studies are examples of widely differing subject populations in various metabolic conditions; yet the effects of diet on metabolic rate exhibit a phenomenal degree of similarity.

disclaimer: I don’t know what’s more important – metabolic rate per se, the diet behind it, or the resulting hormonal adaptations.  All of the diets that are associated with a higher metabolic rate are also predicted to result in lower insulin levels and higher fat oxidation.  Thus, we are left with a triumvirate of diet, hormonal milieu, and energy expenditure… all of which are important for body composition and quality of life.

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[ketogenic] elite artistic gymnasts

Before you say anything, “elite artistic gymnasts” could probably beat you in a race running backwards.  (with you running forwards.)  They are elite athletes.  And given a sufficient keto-adaptation period, they perform better sans carbs.

Ketogenic diet does not affect strength performance in elite artistic gymnasts  (Paoli et al., 2012)

This study looked at body composition and various performance measures before and after 30 days of a very low carbohydrate ketogenic diet (“VLCKD,” < 25 grams of carbohydrate per day) or a normal diet (“WD,” > 250 grams of carbs per day).  25 grams of carbs is very very low, less than Atkins and Kwasniewski.  On the other hand, 41% protein is pretty high.

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Missing: 300 kcal… AGAIN!

Or, the curious perils of crappy sleep, part II: calorie-thieving gnomes.

In part I of the Crappy Sleep series, we discussed, among other things, the malevolent metabolic effects of the most utterly abnormal sleep structure (28-hour days, 6.5 hours of sleep per night [~5.6 hours / 24 hours], and dim lighting during the days).  In this study, the sleep was disrupted to a physiologically relevant degree for two weeks: 8.5 vs. 5.5 hours per night; in a cross-over study.

In part I of Missing calories, we discussed the effects of 3 different diets on metabolic rate after weight loss.  In this study, energy balance was assessed during 2 different sleep regimens in dieters in a CROSS-OVER STUDY.  If you haven’t guessed it, I believe a well-designed and executed cross-over study is superior, necessary, and essential for most metabolism-related studies.

Insufficient sleep undermines dietary efforts to reduce adiposity   (Nedeltcheva et al., 2010)

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BPA

Though they won’t kill you [instantly], environmental and dietary xenoestrogens warrant a bit of attention, especially considering their theoretical mechanism of action is, among other things, augmenting insulin secretion.  This is of particular importance given the growing body of evidence of a causal role for insulin hypersecretion in the obesity epidemic (see Barbara Corkey’s 2011 Banting Lecture for an overview).

And this is the SECOND time this year BPA has made headlines.

BPA. Looks like some kind of medieval weapon or something.

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Soda vs. childhood obesity

What happens if you give skinny kids a can of fully sugared regular soda to drink every day for a year?

What happens if you take the soda away from overweight kids for a year?

The answer to these two questions should be a definitive user’s guide to the question: how bad is soda for my children?   And we got those answers this week.

 

A set of powerful studies were recently published, the likes of which I thought we’d never see.  It’s unethical to assign anyone to start smoking so we can properly study the effects of cigarettes; and before today, I would’ve thought it unethical to assign young children to start drinking fully sugared regular soda.  And not just one or two cans…  over 350.  For the 4 year olds the first study, by the end of the trial they had been on soda for almost a third of their life… during a critical period of development.  Ethics schmethics.  Hopefully this study will never be repeated.

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Insulin resistance

Why it is important and what you can do about it, Op. 105

 

This post was largely inspired by a recent manuscript by Chris Gardner.  He’s an outside-the-box thinker and if you haven’t heard of him, check out this YouTube video: The Battle of the Diets: Is Anyone Winning (At Losing?)

Part I.  

Type II diabetes is the clinical manifestation of insulin resistance.  It is preceded by obesity (except in the cases of MONW & NOD), and caused by poor nutrition.  Markers of insulin resistance are: 1) impaired fasting glucose; 2) impaired glucose tolerance; and 3) elevated HbA1c.  THIS is why it is important: in 2009, Barr and colleagues showed a linear relationship between all three of these risk factors and all-cause mortality in the AusDiab study.  All.  Cause.  Mortality.

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A historical argument against caloric equality

80 years later, a calorie still isn’t a calorie.

Exhibit A.

The treatment of obesity   (Lyon and Dunlop, 1932)

As early as 1932, Lyon and Dunlop recognized that the calories from as little as one slice of bread every day could result in pounds of fat mass gained every year.  For whatever reason, this doesn’t happen to lean people; so they decided to study the effect of different diets on obese subjects in a metabolic ward at the Royal Infirmary.

Their idea of a “diet:” If they could only see how much times have changed!  (this is a hotly debated topic.)

Lyon and Dunlop first tested weight loss vs. total calorie intake.  The diet was roughly 40% carbs, 24% protein, and 36% fat.  Not surprisingly, people fed 800 kcal/d lost more weight than those given 1,000 or 1,200 kcal/d (200 vs. 172 vs. 157 grams of body weight lost per day over the period of 7 – 10 days), confirming that the less you eat, the more weight you lose (duh).  A calorie is a calorie after all, right? …

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Nutrient timing, Op. 101

There is no longer a debate on the value of protein supplements for exercisers.  Now I’d like to make the case for protein timing, or more specifically the value of pre-workout protein supplementation.

Cribb and Hayes (2006) examined the two extremes of protein consumption: immediately before and after working out (“PRE-POST”) vs. 8 hours before and 8 hours after working out (early morning and late evening; “MOR-EVE”).  Each protein shake contained 40 grams protein, 43 grams glucose, and 7 grams creatine.  The subjects were recreational weight lifters, an interesting choice in terms of data interpretation.  I.e., novices are expected to see much greater gains from beginning a new exercise program than experienced exercisers.  Thus, any difference between the groups is expected to be greater.  For example: compare the difference between 5 and 10 to that of 1 and 2.  The relative difference (2x) is the same in both cases, but the absolute difference between 5 and 10 is significantly greater and thus easier to detect.  This stacked the odds against seeing a difference between treatments.  The advantage is that experienced lifters know how to do a high intensity workout, and the results are applicable to people who already exercise.

Notes on the wonders of energy balance:
The protein shakes added ~272 kcal to their total food intake, which caused them to eat less during the rest of the day.  Interestingly, food intake declined by 74 kcal in the PRE-POST group and over twice as much (172 kcal) in MOR-EVE.  Food intake declined in MOR-EVE because the extra calories were just floating around in the bloodstream and thus available to register lots of “excess energy” to the brain.  But the increase in muscle was 2x greater in PRE-POST than MOR-EVE; thus, the extra calories in PRE-POST were immediately invested in laying down new lean mass and therefore weren’t around to signal “excess energy” to the brain.

energy in energy out is bollocks

How the “energy in” is handled is critically important.  With regard to an energy excess, dessert before bedtime is stored as fat but the same amount of calories from protein before exercise are invested into muscle.

A calorie isn’t a calorie because body composition matters.

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