Tag Archives: Atkins

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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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)

[if you follow the advice, that is, at least to some degree] Continue reading

These nutters ate only meat for a year. Place your bets!

Who defines “moderation,” anyway?  An homage to pioneering nutrition research III, Op. 100.  Keep an open mind!  (and remember these words: “no clinical evidence of vitamin deficiency was noted.”)

MY LIFE WITH THE ESKIMO (Stefansson, 1913)

The effects on human beings of a twelve months’ exclusive meat diet (Lieb, 1929)

Prolonged meat diets with a study of kidney function and ketosis (McClellan and Du Bois, 1930)

Vilhjalmur Stefansson traveled with Eskimos in the Arctic for 9 years and lived almost exclusively on meat.  Then he and a fellow expeditioner (Andersen) decided to recapitulate this in a well-controlled, albeit warmer (New York), laboratory setting so they could document the metabolic insanity that ensued. At the time, the Eskimo diet was moderate protein, very high fat, yet they had no heart or kidney problems, were glucose tolerant, and exhibited no signs of ketoacidosis.  So the scientists said: “why not?”  (they were really hoping this apparent healthiness wasn’t due to the frigid Arctic temperatures.)

The studies describe the Central Plains’ Indians who subsisted almost entirely of buffalo meat, which they called the “staff of life,” and South American tribes which eat solely beef and water, then go on to say [sic]: “All of these races are noted for their endurance of exertion and hardships.”  They cite two tribes of Eskimos:  Greenlanders, who ate the typical diet (described above) and showed no signs of rickets or scurvey; and the Labradors, who had both diseases but ate more potatoes, flour, and cereals.  While traversing the Arctic, Andersen developed scurvy at a time when he was eating canned foods and very little meat; this was immediately cured by with raw meat :/

Food for thought: this diet is seriously deficient in vitamin C by today’s standards, but they exhibited NO symptoms.  Perhaps vitamin requirements vary based on the background diet?  Maybe our vitamin C requirement is increased by a Western diet (>50% carbs and lots of vegetable oils).  just sayin’

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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

Missing: 300 kilocalories

or
Weight-loss maintenance, part II (as promised)

Effects of dietary composition on energy expenditure during weight-loss maintenance (Ebbeling et al., 2012)

A three-way crossover study!  Excellent study design.  In brief, the participants lost 30 pounds in 12 weeks on a pseudo-Zone diet (the official version) consisting of 45% carbs, 30% fat, and 25% protein, then switched to one of 3 “weight-loss maintenance” diets for 4 weeks.  (FTR “weight-loss maintenance” cannot even be remotely assessed in 4 weeks, but what the heck, it was a THREE-WAY CROSSOVER.)

To put the issue to bed before it is even raised, the volunteers were given professionally prepared food for about half a year and paid ~$2,500 if they stuck to the plan.  They STUCK to the plan.

or more simply: 

The diets were classified by the authors as high glycemic load (high carb low fat), low glycemic index (e.g., Mediterranean Diet), & low carb (e.g., Atkins Diet).

These “glycemic” indices in general are primarily determined by the carb & fat contents.  A low carb diet will always have a low glycemic index and low glycemic load, and the opposite is true for a low fat high carb diet.  Any high glycemic index food turns into a low glycemic index meal when it’s combined with other foods (like we normally eat).  The only way to make a strictly high GI diet is with low fat; the easiest way to make a low GI diet is with low carb.

The major outcome measurements dealt with energy expenditure, with the premise being that preservation of metabolic rate after weight loss should improve “weight-loss maintenance.”

Resting energy expenditure (REE) is measured by indirect calorimetry.  It’s the amount of calories that a total couch potato would burn daily and is usually determined by body composition (more muscle = higher REE).  While body composition was similar in each group, REE was modestly higher in subjects on the low carb diet.

RQ (respiratory quotient) measures the relative amount of fat and carbs you’re burning: 0.7 = fat oxidation; 1.0 = carb oxidation.  It is determined by diet (eat more carbs, burn more carbs), body composition (have more body fat, burn more body fat), and exercise intensity (marathons burn fat; sprints burn carbs).  The higher carb oxidation on the low fat diet and higher fat oxidation on the low carb diet likely reflect the respective dietary compositions.

 

 

Total energy expenditure (TEE) is exactly what its name implies.  It’s the total amount of calories you burn in a day.  If your body weight is stable, then this is also approximately how many calories you’re eating.  This result is actually pretty interesting.  TEE on the low carb diet was over 300 kcal higher relative to the low fat diet.  This is probably at least partially due to the higher protein content of the diet (30% vs. 20% of total calories or 150 vs. 100 grams per day).  TEE of the intermediate low GI diet was in between low fat and low carb diets (2937 kcal/d), so TEE increased as carb intake declined and fat intake increased across all 3 diet groups.  Follow the blue boxes in the figure below to see the averages, and since this was a THREE-WAY CROSSOVER (!), you can follow the lines to see how each person fared individually:

300 kcal is equivalent to an hour of exercise, yet subjects on low carb weren’t exercising more (although the slowly-losing-his-wits-Dr Bray suggested otherwise in an editorial, arguing that the increased TEE/REE ratio meant increased physical activity, despite the actual data, which showed if anything, slightly lower total and moderate-vigorous intensity physical activity in the low carb group).

Burning an additional 300 kcal per day is like losing over 2 pounds of fat per month by doing exactly nothing.  BUT

to be clear (e.g., disclaimer, mea culpa, evidence of heresy, etc.):

  1. all participants in the study ate the same amount of calories
  2. low carbers burned over 300 more calories per day compared to low fat dieters
  3. body composition  and body weight were similar between the groups

300 calories per day is a LOT of calories, why didn’t it impact weight loss?

This seemingly paradoxical conclusion suggests energy intake is the primary determinant of weight loss, independent of energy expenditure and diet composition.  It is either a violation of The Laws of Energy Balance, experimental error, or evidence of dark magic.

Moving on,

the authors were quick to note urinary cortisol (an anti-inflammatory and stress hormone) and CRP (a marker of systemic inflammation) were highest on low carb, and this could cause insulin resistance.  However, I’d note 2 things: 1) CRP declined in ALL groups relative to baseline, but the reduction was less in low carbers compared to the other groups; and 2) CRP was low and within the normal range in all subjects throughout the entire study. But most importantly, hepatic and peripheral insulin sensitivity improved most in low carbers, in whom CRP and cortisol was the highest.

Similar to the Jakubowicz study (dessert for breakfast), the Ebbeling study was interesting but not groundbreaking; nothing to write home about.  Both showed modest benefits for low carb over low fat.  The news media haven’t feasted on these studies yet, but when they do, however, I’m sure they’ll disagree.  “Weight-loss maintenance” is a riddle wrapped in a mystery inside an enigma, not a simple question to be elucidated by a mere 4-week diet study, even if it’s a three-way crossover.  even if it has dark magic.

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Don’t eat doughnuts for breakfast, Op. 85

or
Weight-loss maintenance, part 1

“Weight-loss maintenance” is a critical part in the battle against obesity because losing weight is much easier and significantly more successful than keeping it off.  The difference lies predominantly in duration: a few months of dieting to lose weight vs. keeping it off for the rest of your life.  Two diet studies on the topic were recently published, and while neither study really addressed the issue proper, some interesting points can be gleaned from both.

Study #1

Meal timing and composition influence ghrelin levels, appetite scores and weight loss maintenance in overweight and obese adults (Jakubowicz et al., 2012)

16 weeks of weight loss followed by 16 weeks of “weight-loss maintenance.”

In brief, the weight loss was accomplished by one of two hypocaloric (1400 kcal/d) isocaloric pseudo-Dukan Diets (higher protein & lower fat than Atkins)

The catch:  Breakfast for the people in HCPb (High Carbohydrate and Protein breakfast)  had twice the calories, 6x the carbs, and half more protein than LCb (Low Carb breakfast).  This was compensated, calorically, by a much smaller dinner.  In other words, they ate like a King for breakfast, a Prince for lunch, and a Pauper for dinner… with the added bonus of a “sweet food… chocolate, cookies, cake, ice cream, chocolate mousse or donuts.”  For breakfast.

People in both groups lost roughly similar amounts of weight in the weight loss phase:

During the first 16 weeks (weight loss phase), a strict 1400 kcal diet was implemented.  During the second 16 weeks (“weight-loss maintenance” phase), macronutrient composition was supposed to be kept similar, but subjects were “free to eat as motivated by hunger or cravings.”  Critique #1a: this study would’ve greatly benefitted by food intake questionnaires to know more accurately what these people were eating; the importance of this becomes more apparent soon.

At three times throughout the study (baseline, week 16, and week 32), a “Breakfast meal challenge” was administered to assess Hunger, Hatiety, and Food Cravings.  Unfortunately, however, the “Breakfast meal challenge” was administered… after… breakfast.  HCPb binged on a high calorie 3-course meal which included dessert while LCb nibbled on a lite breakfast… And the researchers needed a 100-millimeter Visual Analog Scale and 28-item Food Craving Inventory Questionnaire to figure out who would be hungrier afterwords?  Really?

Divide and conquer

Table 2.  There were no major differences between the groups, and between those who completed or didn’t complete the study except for weight loss in those who withdrew.  Apparently, people who didn’t lose any weight on the hypocaloric weight loss diet decided to quit (was it the diet or the dieter that didn’t work? [sorry, no offense]).  In any case, this would’ve introduced a systematic bias except the non-weight-losers were similar in both diet groups.  But Hunger & Satiety was also similar between completers and dropouts… I wonder why…  i.e., the diet was working for those who were losing weight, because Hunger was low and Satiety high; in the dropouts who didn’t lose weight, Hunger was low and Satiety high because they were eating more (which is why they didn’t lose weight).  IOW: “not hungry -> eat less -> lose weight -> complete the study” vs. “eat more -> not hungry -> don’t lose weight -> dropout of the study.”  People are “not hungry” in both groups, but for different reasons.

Critique 1b: this is another place where a food intake questionnaires would come in handy.

During the weight loss phase, LCb lost a little bit more weight and became a little bit more insulin sensitive than HCPb, which is interesting only because the macronutrients were so similar.  Thus, it may have been an effect of “meal-size-timing.”  In other words, don’t eat like a King for breakfast, a Prince for lunch, and a Pauper for dinner.

Ghrelin, a hunger hormone, was significantly higher in LCb and this actually correlated very well with measured Hunger levels (unlike leptin, the far more popular anti-hunger hormone, discussed in depth HERE).  And insulin, a theorized yet controversial hunger hormone, did not: insulin was lower at week 16 while Hunger was 2x higher; and insulin was 2x higher at week 32 compared to week 16 while Hunger was the same at those time points (Table 3).  Thus, for those interested (which is admittedly probably only me), neither leptin nor insulin correlate with Hunger levels; but this study showed that ghrelin does.  Furthermore, similar to those leptin data mentioned above, Hunger was not correlated with weight loss (which is kind-of-fascinating).

The second half of the study (“weight-loss maintenance”) was complete bollocks and made no sense whatsoever (you’ll see it on the evening news).  What you can conclude from this study, however: people following the moderately higher protein and lower carb pseudo-Dukan Diet (LCb) lost modestly more weight during the first 16 weeks than those following the more traditional higher carb version (HCPb).  BOTH diets were “high protein” and “low carb,” and people in BOTH groups lost a lot of weight (~30 pounds in 4 months).  The media hasn’t had their way this study [yet], but when they do, I’m sure the they’ll disagree.

Don’t eat doughnuts for breakfast, you heard it here first.

 

calories proper