Category Archives: insulin

[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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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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Why diets fail, Op. 106

Correction: diets don’t fail, dieters do.  And don’t take that the wrong way; adhering to a restrictive diet is one of the most difficult tasks for ANYone; thus, the obesity epidemic.  Some recent insights into diet-induced weight loss success, or lack thereof, have shed a new light on why some dieters adhere and others don’t.

In Insulin resistance, I discussed how insulin sensitivity may influence how well someone responds to a diet.  In brief, insulin resistant obese people do much better on low carb than low fat in a closely controlled clinical setting.  If you’re one of the lucky few insulin sensitive obese people, then simply reducing calories works.  Unfortunately, however, most obese are insulin resistant.

When it comes to devising a weight loss strategy, I’m willing to cut every corner and use every trick in the book to achieve success.  Data in this new analysis came from Chris Gardner’s notorious A to Z study, where patients were given diet books and told to have at it.  It was the weakest intervention in the history of diet studies, but it is exactly what everyone who wants to lose weight does.  And just like in Gardner’s study, most people fail.

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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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The easy diet diet II

Full disclosure.  IMHO, with regard to obesity and weight loss diets, low carb is a little bit better, most of the time.  It’s not such a huge difference that it’s ridiculously obvious, and in situations where low carb proper is too impractical, it might just be more important to focus on eliminating as many empty calories as possible.  Because as discussed in the Easy diet diet, Op. 72, you don’t have to go militant zero carb; simply “low carb seems to work pretty well.

In type 2 diabetes, randomization to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss (Gulbrand et al., 2012)

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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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Adipose, Horcrux of Metabolism

Part II.  The importance of the ability to un-store fat: implications for resistance exercise and muscle function in humans.

Adipose triglyceride lipase contributes to cancer-associated cachexia  (Das et al., 2011)

Mice and humans with certain types of cancer lose a lot of weight, a condition known as cachexia.  Besides causing a major decline in quality of life, this usually predicts mortality.  But tumor-burdened ATGLko mice exhibit none of this (closed bar = control; open bar = mice with tumors):

Unfortunately, much of this weight is type II muscle (left), while type I muscle is largely spared (right).  ATGLko mice are immune to muscle loss.

Type II muscle is white, burns sugar, and flexes fast and strong (that’s why I said “unfortunately,” above).  Type I muscle is red, burns fat, and flexes slow and weak.

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adipose, horcrux of metabolism

You wanna burn fat?  ATGL (Adipocyte Triacylglycerol Lipase) is your man.  ATGL is responsible for breaking down fat, a necessary precondition for fat burning.  Mice lacking ATGL accumulate tons of fat: 20x more in the heart, 10x more in testis, 3x more in skeletal muscles, 2x more in the GI tract, etc., etc.  Not surprisingly, they’re overweight.

Part 1.  The importance of the ability to un-store fat: appetite, body composition, and insulin.

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skinny is the new fat, Op. 95

I’ve been known to rave about the phenomenon of metabolically obese normal weight (MONW), or fat skinny people.  In brief, this population exhibits insulin resistance, metabolic syndrome, hypertension… all things usually associated with obesity… but they’re lean.   In fat skinny people, I wrote about two epidemiological studies on markedly different populations (Americans and Koreans); these two peoples have virtually nothing in common (culture, foods, genetics, etc.).  Despite these differences, there was a strong similarity in the macronutrients associated with metabolic dysregulation in otherwise lean individuals (aka fat skinny people): in the first study, high carb and low protein diets were the major culprits, with a smaller contribution of low fat.  In the second study, high carb and low fat were at fault (protein intake wasn’t analyzed).

A new study that is about to hit the presses didn’t intend to say anything about fat skinny people, but they weren’t counting on ME.

Body mass index, diabetes, hypertension, and short-term mortality: a population-based observational study, 2000-2006 (Jerant and Franks, 2012)

This study included over 50,000 people aged 18-90.  Between the years 2000 and 2005 about 3% died, which was statistically just enough to ask “why?”  In brief, they compared body weight, blood pressure, smoking, and diabetes with mortality risk.  

In each BMI category, the square is higher than the circle.  DM = diabetes (the squares).  Diabetes increases mortality risk independent of BMI.  Now just focusing on the squares; as you move from left to right, body weight is increasing but mortality risk in diabetics is decreasing.  A 150 pound diabetic has a higher mortality risk than a 200 pound diabetic, who has a higher mortality risk than a 250 pound diabetic.  Huh?

Perhaps the lean diabetics are fat skinny people, the elusive MONW?  If so, according to the research discussed HERE, their diet might have made them that way.  The lean diabetics (aka fat skinny people aka MONW aka NOD [non-obese diabetics]) eat less protein, more carbs, and less fat.  This might be a reach, but collectively (1 + 2 + 3) these data imply a poor diet might be worse than obesity for diabetics.

disclaimer: this is not true in most circumstances, i.e., skinny people can usually whatever they want.  There are skinny diabetics, but they are significantly rarer than obese diabetics.  In other words, most type II diabetics are obese, the lean ones just eat a crappier diet. You might be wondering: “how are they skinny if they eat so poorly?”  My guess is that they just haven’t eaten enough of it [yet]; it’s rare to stay lean on a “crappier diet.”

So is skinny the new fat?  Being lean with type II diabetes is an indicator of EMPTY CALORIES; it could be riskier for all-cause mortality than obesity in diabetics.

“Attention endocrinologists, diabetologists, and general practitioners: don’t assume diet is not a problem in your skinny diabetics because they are skinny.  Indeed, diet might be THE problem.”

And no, if you’re a skinny diabetic, this DOESN’T mean gaining weight will make you live longer.  it just doesn’t.

 

it just doesn’t.

calories proper

what is our proper “natural” diet?

Figuring out how best to eat, physiological insulin resistance, and an homage to pioneering nutrition research.

Insulin resistance, as we know it today, is associated with poor nutrition, obesity, and the metabolic syndrome.  But it’s FAR more interesting than that.  Indeed, it could even save your life.  At the time when the pioneering studies discussed below were occurring, the researchers had no idea insulin resistance was going to become one of the most important health maladies over the course of the following century.  Furthermore, these somewhat-primitive studies also shed some light, possibly, on how we should be eating.  hint: it might all come down to physiological insulin resistance.

The reduced sensitivity to insulin of rats and mice fed on a carbohydrate-free, excess fat diet (Bainbridge 1925, Journal of Physiology)

Rats were fed either a normal starch-based diet (low fat), or a high butter diet (low carb) for one month, then fasted overnight and injected with a whopping dose of insulin (4 U/kg).  First, take a guess, what do you think happened and why.  Then, click on the table below.

To make a long story short, all the starch-fed rats died while all the butter-fed rats lived.

On a high-fat zero-carb diet, plasma insulin levels are low.  Insulin is low because there no carbs (i.e., it’s supposed to be low).  Under conditions of low insulin, unrestrained adipose tissue lipolysis leads to a mass exodus of fatty acids from adipose tissue.  These fatty acids accumulate in skeletal muscle and liver rendering these tissues insulin resistant.  But this doesn’t matter, because insulin sensitivity is unnecessary when there aren’t any carbs around.  So if that rogue research scientist who’s always trying to jab you with a syringe filled with insulin actually succeeds, you won’t die.  The high-fat diet prevents insulin-induced hypoglycemic death.  This is physiological and absolutely critical insulin resistance.

To determine if this was specific to dairy (butter) or a general effect of a high fat zero carb diet, Bainbridge repeated the experiments with lard.  Lo-and-behold, lard-fed rats were just as fine as those dining on butter.  

To be sure, these studies exhibited a high degree of animal cruelty… but their simplicity is laudable.  And Bainbridge’s findings are not an isolated case.

Studies on the metabolism of animals on a carbohydrate-free diet.  Variations in the sensitivity towards insulin of different species of animals on carbohydrate-free diets (Hynd and Rotter, 1931)

Instead of starch, lard, and butter, Hynd and Rotter used milk and bread, cheese, and casein.  And their findings were essentially identical to Bainbridge’s: mice, rats, or rabbits fed carbohydrate-free diets were insulin resistant and protected against insulin-induced tragedies.

The interesting finding was in kittens, who sadly maintained insulin sensitivity when fed fish (high protein) or cream (high fat).

You’re probably thinking: why would I say any state of heightened insulin sensitivity is “sad?”  WELL, I say “sad” because we’re talking about physiological insulin resistance; a condition when resistance to the hypoglycemic effect of insulin is essential, and lack thereof is incompatible with survival.  To be clear: 1) kittens remain insulin sensitive on high fat and protein diets; and 2) this is OK because there aren’t any rogue research scientists running around trying to jab them with insulin.  While I can’t say for sure, this might have something to do with what kittens are supposed to eat, i.e., their natural diet.  High protein and fat diets won’t make them insulin resistant because unlike rodents, that is their normal diet.  (real mice eat fruits and seeds; laboratory mice eat pelleted rodent chow; cartoon mice eat cheese.)   Lard causes ectopic lipid deposition in insulin sensitive tissues in rodents because they aren’t accustomed to it.  Mice are optimized to eat a high carb diet.  Kittens eat protein and fat, usually in the form of mice.  But when given bread, kittens develop insulin resistance.  There is no bread in mice.

While we shouldn’t base our diet around the possibility of turning a corner and being jabbed with a syringe filled with insulin, perhaps we are simply more similar to kittens.  Hypercaloric diets loaded with sugar, excess carbohydrates, and empty calories cause [pathological] insulin resistance (which could theoretically save your life if a rogue research scientist jabbed you with insulin), whereas the opposite is true for diets high in fat and protein.  This is repeatedly demonstrated in diet intervention studies, most recently in the notorious Ebbeling study (Missing: 300 kilocalories).  When people were assigned to the very low carbohydrate diet, insulin sensitivity was significantly higher than when they were on low fat diets:Soapbox rant: I’m not saying low carb is what we are supposed to eat.  Nor am I saying it is the optimal diet.  IMHO any diet which excludes processed junk food and empty calories is “healthy.”  The Paleo diet isn’t healthy because some nutritionista says it’s what we are supposed to eat; Paleo is healthy for the same reason as Atkins, Zone, South Beach, and a million others: no junk food.

Maybe the diet we’re supposed to eat has nothing to do with the healthiest diet.  Maybe not.  But it probably isn’t bad for you.  just sayin’

calories proper