Tag Archives: diet

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

Posted on August 27, 2012 | 17 comments

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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adipose, horcrux of metabolism

Posted on August 13, 2012 | 1 comment

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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the bang for your exercise bucks

Posted on August 6, 2012 | Leave a comment

Exercise causes weight loss when it’s accompanied by diet…  but then again, so does art lessons.  a continuation of “Exercise alone won’t cut it”

Effect of an energy-restrictive diet, with or without exercise, on lean tissue mass, resting metabolic rate, cardiovascular risk factors, and bone in overweight postmenopausal women (Svendsen et al., 1993)

Svendsen divided postmenopausal women in their mid-fifties into three groups for 12 weeks: 1) diet; 2) diet + exercise; and 3) none of the above (a weight-maintenance control, kudos!).  Dieters went from eating 1800 to 1000 kcal/d of a high protein low fat diet.  The exercise consisted of 1.5 hours of aerobic and resistance training 3x per week.  The results, in a nutshell: dieting was effective (they lost weight).  Exercising was effective (fitness improved).  So how much additional benefit did exercise provide? Not much.  The diet alone group lost 21 pounds, while the diet + exercise group lost 23 pounds.  Is that worth 4.5 hours of high intensity exercise?  Body composition was mildly improved by the addition of exercise, as body fat percent declined 19% with diet + exercise and only 14% with diet alone.  But 4.5 hours of high intensity exercise is a LOT of work; and resting metabolic rate declined the most in the exercise group.  To its credit, exercise improved fitness considerably, which bodes well for quality of life, but just to keep it straight, diet alone reduced body weight by 21 pounds; exercise took off an additional 2 pounds… BUT as it turns out, those additional two pounds were probably also from diet, as the exercisers reduced food intake by an additional 57 kcal/d.  This doesn’t sound like much, but over the course of 12 weeks it adds up to 4788 kcal (that’s over a pound of fat mass).  In other words, exercise didn’t contribute to the weight loss.  The Laws of Energy Balance can be cruel.

Resistance training does not contribute to improving the metabolic profile after a 6-month weight loss program in overweight and obese postmenopausal women (Brochu et al., 2009)

Study design was similar to Svendsen’s (postmenopausal women, mid-fifties, etc.), with the exceptions that the diet was less strict and the exercise was resistance training, not aerobic (e.g., treadmill).  Dieting worked (both groups lost weight).  Exercising worked (they got significantly stronger).  So how much additional benefit did exercise provide?  You guessed it: not much.  The diet alone group lost 11 pounds; diet + exercisers lost 13 pounds.  3 sessions of high intensity exercise per week for 6 months led to 2 additional pounds of weight loss.  Unlike Svendsen’s exercisers, however, those two hard-earned pounds were probably due to the exercise, as metabolic rate and food intake declined to the same extent in both groups.  6 months of high intensity weight training for two pounds?  The Laws of Energy Balance: merciless.

Effect of diet and exercise, alone or combined, on weight and body composition in overweight-to-obese postmenopausal women (Foster-Schubert et al., 2012)

Saved the best for last: this study included both a weight maintenance control AND an “exercise only” group.  Kudos, Dr Foster-Schubert.  Study design was similar to Brochu’s and Svendsen’s: 12 months; moderate to high intensity aerobic exercise 3-5x per week, yada yada yada.  Dieting worked (the diet alone and diet + exercise groups lost weight).  Exercising worked (the exercise alone and diet + exercise groups got fitter).  So how much additional benefit did exercise provide?  Fail.  The dieters lost 16 pounds while the diet + exercise group lost 20 pounds.  The exercisers lost 4 pounds.  From those numbers, it might appear as though weight loss from exercise contributed mathematically to diet (4 + 16 = 20).  NOPE.  The exercisers cheated, by dieting :/
Exercisers reduced food intake by 185 kcal/d which amounts to a whopping 66600 kcal over the course of a year.  Theoretically, this could’ve amounted to a loss of over 15 pounds of fat mass.  But it didn’t.  Exercise caused a great enough reduction in metabolic rate to dwindle a 20 pound fat loss all the way down 4 pounds.  Exercise made them 16 pounds slothier.  And what about the diet + exercise group; they lost the most weight so surely exercise had to have added something to it?  NOPE, not here either.  They reduced their food intake more than any other group. The Laws of Energy Balance scoff at exercise.

bollocks

So there you have it.  Trying to lose weight via exercise alone is like bringing a cup of water to a forest fire.  It is too easily compensated for by reductions in metabolic rate.  In studies spanning the course of 20 years, exercise has consistently failed to contribute to weight loss.  Exercisers lost weight if and only if they dieted.  Diet + exercise might be as effective as diet + art lessons or diet + Facebook, although the latter two are less likely to make you slothier.  Exercise will make you better, and maybe even happier, just not skinnier.

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skinny is the new fat, Op. 95

Posted on August 3, 2012 | 3 comments

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.

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Yo-yo dieting revisited, a thought experiment

Posted on July 29, 2012 | Leave a comment

If at first you do not succeed, try, try again.  Opus 94.

Yo-yo dieting is “probably” not good, but giving up is worse IMO.  I say “probably” because obesity researchers have empirically tested just about every single weight loss intervention except this one.  Furthermore, you’d be hard pressed to find an obese population who’d agree to undergo an intensive weight loss regimen, only to intentionally regain the weight.  Rinse.  Repeat.  The study would be a nightmare to design from a philosophical perspective, and psychological torture to the volunteers.  But what if they did?  Would they end up with more fat mass?  Less?  Right back to where they began?

Changes in energy expenditure resulting from altered body weight (Leibel, Rosenbaum, and Hirsch, 1995)

Maybe you don’t recognize the study by name, but you have definitely heard about their key finding: weight loss causes a decline in metabolic rate which makes further weight loss or simply maintaining more difficult.  The other finding was that the opposite also occurs: during weight gain, metabolic rate increases to drive weight back down to its starting point.

bollocks

All-in-all this was a great experiment and it has a lot of street cred; nobody including myself has ever had anything really bad to say about it.  In brief, volunteers were fed either: 1) the maximally tolerated amount of self-selected foods (~6500 kcal!) until they gained 10% of their body weight; or 2) 800 kcal of a liquid formula (40% fat, 45% carbs, and 15% protein) until they lost 10% of their body weight.  

When lean subjects gain 10% of their initial body weight, 80.1% of it is fat mass.  In obese subjects, however, only 58% is fat mass.  Thus, obese people gain more muscle and less fat than lean people during weight gain (e.g., the holidays).  After a 10% weight loss, 64% of the weight is fat mass in lean subjects while a whopping 84% is fat mass in obese subjects.  Thus, obese people lose more fat and less muscle than lean people during weight loss (e.g., New Year’s resolutions).

Here goes nothing:
Take a 100 kg (220 pounds) obese person who has 50 kg fat mass (50% body fat) and a 70 kg (154 pounds) lean person with 14 kg fat mass (20% body fat). After 10% weight loss, body weight declines by 10 kg in the obese subject and 7 kg in the lean subject.  83.6% of the weight lost (~8 kg) is fat mass in the obese subject and 63.7% (~4 kg) is fat mass in the lean subject:

After 10% weight regain, body weight increases 9 kg in the obese subject and 6 kg in the lean subject.  60% of the weight gained (5 kg) is fat mass in the obese subject and 80% (5 kg) is fat mass in the lean subject:

Rinse.  Repeat:

Encore!:

By the end of 3 complete yo-yo cycles, the obese person is down 3 kg body weight, but more importantly their fat mass has declined by 9 kg, from 50% to 42% of their body weight (winner!).  The unfortunate lean subject, however, despite being 2 kg lighter, now has an additional 2 kg of fat mass; in other words, they lost weight but got fattier (20% body fat to start out, 23% by the end).

To be clear, this study has never been done.  But Leibel, Rosenbaum, and Hirsch’s data are impeccable so any flaws in this hypothesis don’t stem from there.  The lean subjects in their study were 154 pounds; clearly not a population in dire need of weight loss.  Perhaps yo-yo dieting got a bad rap from skinny people trying to get skinner, who instead got fattier and told everyone else to give up if dieting didn’t work the first time.  I’m not against pharmacotherapy or bariatric surgery for those in whom diet has failed, but saying “I’m not against” it is a far cry from saying “I’m for it.”  Furthermore, given the results from this thought experiment, among other things, I’m definitely saying “try, try again.”

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Exercise-induced hunger attenuates exercise-induced energy deficit

Posted on July 26, 2012 | Leave a comment

and what we can’t learn from rodent studies.

Mandatory pre-reading: Exercise alone won’t cut it

It’s difficult to conduct experiments on energy balance in humans because they’re we’re all so diverse.  This is one reason why researchers use animal models; diet, exercise, and even genetic background can be rigorously controlled to a degree unimaginable in humans.  Despite all of this, however, exercise studies involving rodents are consistently inconsistent and inherently flawed.  They are not applicable to weight loss or energy balance in humans.  “Attention nutrition researchers, stop doing them.”

Exhibit A.  Cafeteria diet-induced insulin resistance is not associated with decreased insulin signaling or AMPK activity and is alleviated by physical training in rats (Brandt et al., 2010)

Three groups of rats: 1) chow-fed controls; 2) cafeteria-junk-food-diet; and 3) cafeteria-junk-food-diet + exercise.  The exercise was high intensity and consisting of swimming 5x per week with a tiny dumbbell attached to their tail (equal to 2% of their body weight).

In these lucky rats, exercise completely blunted weight gain, but did so, at least in part, via reduced food intake.  Exercise-induced anorexia might reflect the unnatural-ness of a rat subjected to a rigorous exercise protocol; it’s stressful for them.  Exercising rats are not happy thinking they’re doing something good for themselves; they’re trying to not drown.  And while exercise corrected their body weight, it failed to normalize fasting insulin (above) and glucose tolerance (which may also confirm they are stressed out):

Needless to say, in humans, it’s the exact opposite.  With exercise, food intake increases, body weight stays the same (usually), and insulin sensitivity is superbly enhanced.  But to further drive home the point that these studies should not be conducted with rodents, it’s not even consistently “the exact opposite.”

Exhibit B.  Effects of food pattern change and physical exercise on cafeteria diet-induced obesity in female rats (Goularte et al., 2012)

In this somewhat more complicated study, cafeteria diet-fed rats: 1) went on a diet; 2) started an exercise regimen; or 3)  both. 

In contrast to Brandt’s findings, exercise increased food intake and failed to reduce body weight (similar to unlucky subject number 9).  However, in agreement with Brandt, exercise failed to normalize insulin (above) and glucose tolerance:

One of the greatest metabolic benefits of exercise in humans, i.e., restoration of insulin sensitivity, is not reproduced in 2 rodent studies.

Unfortunately, the hypothesis that exercising rats is just like torturing rats was actually tested.

Exhibit C.  Effects of epinephrine, stress, and exercise on insulin secretion by the rat (Wright and Malaisse, 1968)Swimming had an effect on glucose and insulin that was strikingly similar to receiving foot shocks (i.e., electrocution).

And last but not least, to bring it around full circle, here’s how it is supposed to look:

Exhibits D, E, and F.  A 12-week aerobic exercise program reduces hepatic fat accumulation and insulin resistance in obese, Hispanic adolescents (van der Heijden et al., 2012)

Exercise protocol: cycling.  10 minutes warm-up, 30 minutes at 70% VO2peak (HR > 140 bpm), 10 minutes cooldown.  Only TWICE per week.

1) VO2peak significantly improved, confirming that this seemingly puny exercise routine had a real physiological impact.

2) Neither body weight nor fat mass declined, suggesting this was truly “exercise alone.”  I.e., they weren’t dieting.

3) HOMA-IR, a measure of insulin resistance, declined.

1+2+3 = exercise improves insulin sensitivity.

Effects of aerobic versus resistance exercise without caloric restriction on abdominal fat, intrahepatic lipid, and insulin sensitivity in obese adolescent boys (Lee et al., 2012)

Above: body weight didn’t change, confirming this was “exercise alone.”
Below: insulin sensitivity improved in both exercise groups.

It’s been almost 100 years, why can’t the rats get it right? (by “rats,” I mean scientists who tie weights to rats tails, throw them into a tub of water, and call it “exercise”).

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Exercise alone won’t cut it

Posted on July 23, 2012 | 2 comments

A fundamental reevaluation of the concept of “dieting”

But first, an ode to energy balance:
Diet and exercise, or diet alone,
But “exercise only” does naught but tone.

Exercise is effective for weight loss if and only if it’s accompanied by dieting, not vice versa.  Enter: the best experiment ever.

Exhibit A.  Food intake and body composition in novice athletes during a training period to run a marathon  (Janssen, Graef, and Saris, 1989)

This is, in its most purest form, an isolated “exercise only” intervention.  Volunteers were recruited to train for a marathon; no dietary advice given.  That is a critical point.  In order to test exclusively “exercise only,” you can’t have a group of people who are trying to lose weight via exercise because if weight loss is their goal, watching what they ate would happen automatically and we would not truly have “exercise only.”  This isn’t a diet study; indeed, that’s the point.  Lastly, regardless of the data, it’s hard to say this was an inadequate exercise intervention.  Training for a marathon is no easy task; after 18 months (of “exercise only”), they completed a full marathon in just under 4 hours.  IMHO this confirms they were exercising quite intensely for the entire 18 months.They started this adventure weighing 162 lbs and ended at 157.  If they gained 10 pounds of muscle and lost 15 pounds of fat, then they’d be 5 pounds lighter and I’d be training for a marathon.  But that’s not what happened.  They lost 5 pounds, and only about half of it was fat.

Side note: train for a marathon vs. a calorie non-restricted diet for weight loss?  In the [notorious] Shai study, people assigned to the low carb diet were allowed to eat as much as they wanted as long as it was low carb.  To put things into perspective, after 18 months low carb dieters lost over twice as much weight as the marathon runners, and they weren’t exercising.

Moving on,
5 pounds of weight loss is much less than expected after 18 months of marathon training.  By the end of the study they were running an average of 9 kilometers per day (see the red line in the figure below).

So why didn’t they lose more weight?  In brief, exercise made them hungry, and by the end of the study they were eating an additional 400 kilocalories daily.  I imagine running 9 km burns slightly more than 400 kcal, which is why they lost a few pounds in the process.  Had they been dieting, they would’ve lost a lot more and this study would no longer be a test of “exercise only.”

Exhibit B.  Effect of exercise alone on the weight of obese women (Gwinup, 1975)

In this weight-loss  study, Gwinup claims it is “exercise alone” because it was a group of women who failed to lose weight via dieting and [sic] “were, therefore, most amenable to an attempt to control weight with exercise alone.”  These women had been trying to lose weight for a while, so it’s very likely they were always watching what they ate (unlike the people recruited for the marathon study).  Gwinup’s exercise intervention was simple: walking.  And for some lucky women, it worked.  Take subject number 3, for example: a 37 year old housewife who had been trying to lose weight since she was 20.  By gradually increasing her walking time to just over 2 hours per day, she was able to lose ~ 15 pounds after 18 months.   P.S. that’s not 2 hours including regular daily activities; it’s 2 hours of dedicated exercise time.

lucky subject number 3

But I don’t think this was truly “exercise only.”  It takes about an hour to jog 9 km.  The marathon runners were almost in energy balance ingesting 400 additional kcal suggesting a 9 km jog burns a tad over 400 kcal.

Subject number 3 was walking for two hours (6 km?), yet she lost 15 pounds over the same time period (18 months): 1. her energy deficit was greater than the marathon runners;  2. she lost more weight despite exercising less;  3. the marathon runners were NOT dieting, so “not dieting” results in 5 pounds of weight loss;  4. subject number 3 was exercising less than the marathon runners; if she too was “not dieting,” she could not have lost more weight than the marathon runners;  5. ergo, subject number 3 was not “lucky,” she was dieting.

Subject number 9, on the other hand, a younger housewife who had only been trying to lose weight for 3 years despite being 7 pounds heavier than subject number 3, was not so “lucky.”

unlucky subject number 9

Subject number 9’s exercise duration was similar (2 hours per day), and for the first half of the study, things were going great, she dropped 10 pounds.  But for the second half of the study, she was gaining it back.  Recruitment inclusion criteria included women who regained weight they lost via diet alone.  So either subject number 9 is biologically resistant to both diet- and exercise-induced weight loss, or she just likes to eat.  To be clear, regarding the second half of subject number 9’s progress: 1. “exercise only;”  2. TWO hours per day;  3.  body weight is steadily increasing.

Exercise worked for subject number 3 because she was dieting; it didn’t for subject number 9 and the marathon runners because they weren’t.

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what is our proper “natural” diet?

Posted on July 18, 2012 | 7 comments

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’

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Posted in Advanced nutrition, Dietary fat, empty calories, Energy balance, Fish, Fructose, insulin, Ketosis, mortality, Protein, Sugar

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Don’t eat doughnuts for breakfast, Op. 85

Posted on July 1, 2012 | Leave a comment

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

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The easy diet diet, Op. 72

Posted on April 26, 2012 | 4 comments

Regular followers of this blog (all 3 of you) know I think positively about carbohydrate-restricted diets.  In randomized controlled intervention studies, low-carb diets are a little better most of the time compared to low calorie and low fat diets (note the italics).  They are healthier and there is probably no end to the benefits of chronically lower insulin levels.  The only relevant disadvantage is that [I thought] such a diet requires too big of a change for most peoples lifestyle…  however, this might not be the case.  In light of some recent [relatively unscientific] findings, that change might not be so big after all.

In one study, Feinman and colleagues (Feinman et al., 2006 Nutrition Journal) surveyed a group of low carb dieters from the “Active Low-Carber Forum” about their diets.  There was no formal subject recruitment or randomization; it was just a bunch of people who were following various low carb diets.  The only requirement was that they were actually following a low carb diet for weight loss.  For starters, there were a LOT of people who lost a LOT of weight: 62% of ~86,000 participants lost at least 30 pounds and kept it off for over a year (I know I know, it’s possible that people who lose a lot of weight are selectively more likely to participate on this particular forum [this study is confounded out the wazoo but still had a few pearls]).

What I found most interesting was what these people said were their biggest dietary changes.  The top 2 were, not surprisingly, avoiding sugar and starch.  Number 3 was drinking more water.  So to sum up the top 3 changes: basic healthy dieting 101; not drastic lifestyle alterations.

Number 4 was the biggie: most people increased their green vegetable intake by over half… not bacon, hot dogs, and red meat… leafy greens.  This is great (just think of all those micronutrients).  They weren’t counting calories or replacing everything in their refrigerator; they were avoiding sugar and eating more leafy greens.

leafy greens: winner

sounds easy, right?  Of course eating more protein and fat also occurred, but it wasn’t a universal requirement: only 5% reported increasing beef, butter, and bacon… instead, people just ate a little more of whatever was most convenient for their lifestyle.

This study changed my view.  These people lost over 30 pounds on low carb and kept it off for over a year without making any huge changes.

Another more recent study (Kirk et al., 2012 Journal of Pediatrics) was a diet intervention study in obese children.  They compared a low carb diet (LC), low glycemic index diet (RGL), and a portion controlled diet (PC).

It’s hard to put kids on a low carb diet.  Indeed, adherence to the low carb diet was horrific, less than 30% at 3 months and down to 20% at 6 months (figure below on the right).  But comparing this to the figure on the left is astonishing.  Despite adherence of only around 25%, low carb dieters had the biggest reduction in body fat.  It’s not until adherence was nil that the kids starting gaining weight back.

weight loss vs. adherence

What does this say about low carb?  it’s the easiest diet in the world, even if you can barely follow it!  25% adherence to a low carb diet resulted in greater fat loss than 80% adherence to the other diets.

You might just be better off half-assing a low carb diet than strictly adhering to any another one-

calories proper

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