Category Archives: Energy balance

Candy in disguise II, Op. 87

Posted on July 7, 2012 | 4 comments

Rundown on a few new protein bars, pro’s & con’s, etc.

Perfectly Simple by ZonePerfect
The catch: 3 new bars with 10 or fewer ingredients.  All are gluten-free and have 10 grams of protein.

as the number of ingredients increases, so does the sugar

Sweeteners:
Peanut Crunch: “invert evaporated cane juice”
Toasted Coconut: “invert dried cane syrup”
Cranberry Almond: “date paste”

It takes more sugar in the form of “date paste” (Cranberry Almond, 19 g sugar) to compensate for the lack of “invert evaporated cane juice” (Peanut Crunch, 14 g sugar) or “invert dried cane syrup” (Toasted Coconut, 16 g sugar).  Invert sugar is basically table sugar (sucrose) that has been broken down into glucose & fructose.  1) It’s sweeter, which is why you need less of it; and 2) it’s essentially identical to high fructose corn syrup = used in everything from candy and crackers to cigarettes and soda.  Not good.

Active X Energy Bar
Kosher, organic, but not gluten-free.

Pro’s: less sugar and more fiber than ZonePerfect’s Perfectly Simple. 

These bars rely on the sweetener brown rice syrup which is primarily glucose (significantly less fructose than invert sugar), but it’s complimented with agave (significantly more fructose than invert sugar)… end result?  Organic high fructose corn syrup (a polished turd).

Good2Go bars

High protein, moderate sugar, and preservative-free.

These bars are sweetened with honey, brown rice syrup, invert sugar, and a little coconut sugar.  These bars have more protein and less sugar than both Perfectly Simple and ActiveX.

Last but not least, my personal favorite in the “coolness” department: Chapul.

Pro #1: they owned it!  “sugar” actually appears in the list of ingredients.

Pro #2: while it’s only 6 grams of protein, you’ll never guess where it comes from… crickets!  Yes crickets.  Baked, then ground into a fine powder.

Con: the most sugar and least protein of all.

To put this all into perspective: relative to the nutritional profile of Quest protein bars, these noobs pale in comparison.

Conclusion: candy in disguise.  just sayin’.

calories proper

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Missing: 300 kilocalories

Posted on July 4, 2012 | 9 comments

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

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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ORIGIN vs. pre-diabetes, Op. 83

Posted on June 24, 2012 | 1 comment

Sanofi, one of the world’s largest pharmaceutical companies, just released results from its ORIGIN trial.

Basal insulin and cardiovascular and other outcomes in dysglycemia (2012 NEJM)

The goal was to see if nightly insulin injections could prevent pre-diabetics  from becoming real diabetics.  ORIGIN was monstrous: >12000 participants, 40 countries, 6 years, etc.  FYI the subjects included in this study, mostly pre-diabetics, are not usually candidates for insulin injections (diet and lifestyle modification seem to work OK for this group).  If ORIGIN showed a positive result, then the number of patients to receive this treatment, and therefore the number of prescriptions written for Sanofi’s Insulin Glargine, would increase dramatically =  $anofi 🙂

IMHO, Sanofi is hunting for a new bunch of people to whom they can market their same old drug.  (Not a good practice.)  To stay alive in the fiercely competitive pharmaceutical industry, companies have to either invent new drugs to treat old diseases or invent new diseases that use old drugs.  In this case, they are saying that pre-diabetes, or “dysglycemia,” should be a new indication for insulin.  Pre-diabetes is not a new disease, but insulin was never warranted (Rx = diet and lifestyle modification).

I have no financial disclosures to report (but I’m open to offers).  Of moral disclosures, on the other hand, I’ve got but one.  Insulin injections are fraught with side effects and should be reserved for people who need them.  I don’t believe these people need them.

divide and conquer

After 6 long years of insulin injections (or standard care in the control group), the researchers tested for diabetes.  Lo and behold, diabetes was present in 35% of controls and 30% of the insulin-treated group; i.e., insulin-treated patients had a 20% lower chance of developing diabetes (odds ratio [OR] of 0.80, p = 0.05).  Apparently, insulin prevents diabetes.

Or not.

Exhibit A.  There’s a caveat to these diabetes rates.  The subjects were tested for diabetes at the end of the study.  Anyone who didn’t have it was re-tested a few weeks later; only those who didn’t have it were re-tested a few weeks later (during which time they received no treatment).  The researchers claim they were trying to assess the “durability of diabetes prevention.”  Here’s the rub:  25% of the patients on insulin tested positive for diabetes at the end of the study.  A few weeks later (during which time they weren’t being treated) some of the people who initially tested negative for diabetes (insulin obviously must have been protecting them), now tested positive, increasing the total to 30%.  This must have happened because they were no longer protected by insulin!  Err, no.  Diabetes in the control group, the group who was deprived of insulin from the start, went from 31% to 35% during the same exact time period.  It’s not “durability of diabetes prevention,” it’s experimental bias: by only RE-testing people who were initially negative, the total could only stay the same (if there were no false negatives) or go up (if there were false negatives).  The fact that it went up in both groups could simply mean that the re-test either: 1) detected diabetes in some people who falsely tested negative the first time around; and/or 2) generated some new false positives.  To correct for this, they should have also re-tested anyone who tested positive for diabetes.  *The importance of this difference is described below.

Exhibit B.  Disclaimer: statistics are the bane of my existence.  

The rate of disease was rather high in both groups (>>10%); if you calculated the  “relative risk (RR)” instead of “odds ratio (OR),” you’d get 0.857. An RR of 0.857 is not as pretty as an OR of 0.80 (lower is better).  Their “OR of 0.80” was barely statistically significant (p = 0.05); I’d be willing to bet that an “RR of 0.857” would not have been so lucky… so why did they choose to publish the OR?  OK, no suspense necessary:  I think if this measurement turned out non-significant, then the entire study would’ve been a waste of time and a LOT of money.  And they would have no shot at an entirely new market for their same old drug.  *This is precisely why proper diabetes diagnoses and statistical analyses were so critical in this study.  To be clear: this is going to come down to a numbers game, and the numbers don’t support a new indication for insulin in pre-diabetics.  But fuzzy math and biased testing makes this appear as though it is a debatable conclusion.

Moving on.

HbA1c, a marker of long-term glucose control was 6.4% at baseline in both groups.  Insulin therapy lowered this to 6.3% (not exactly something to write home about) while it drifted to 6.5% in controls.  This insignificant effect of insulin on HbA1c didn’t come cheap, however.  The insulin treated group experienced a huge number of severe hypoglycemic episodes:

Not surprisingly, the severity of hypoglycemia was totally downplayed in Sanofi’s press release despite it being the most robust and statistically significant finding in the entire study.

People in the insulin-treated group got a little heavier (by about 5 pounds), and surprisingly, the control group lost a little weight (about a pound).  I say “surprisingly” because this population is expected to be weight stable or gaining weight.

Lastly, fortunately, there was no difference in mortality.  This is not unexpected because the intervention was mild and the patients were relatively healthy (i.e., not people who need nightly insulin injections).  When a more intensive insulin intervention was tested on frank diabetics, the study was halted because too many people died.  Enter: The ACCORD study.

Effects of intensive glucose lowering in type 2 diabetes (circa 2008)

Intensive insulin therapy lowered HbA1c waay more in ACCORD than mild insulin therapy did in ORIGIN: 

but it also lowered lifespan: 

In conclusion:  YES, high blood glucose is the culprit, and YES, it needs to be lowered.  But NO, insulin injections are not the answer.  If you have lactose intolerance, you stop eating lactose.  These people have glucose intolerance; they need to stop eating glucose.

calories proper

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Non-sequiter nutrition II, a sugar-thought experiment

Posted on June 20, 2012 | 1 comment

The average western diet contains about 50 grams of fructose from a variety of sources ranging from beneficial fibrous fruits to the more insidious sugar-sweetened beverages, soda and juice.  50 grams of fructose.   2 1/2 cans of Coca-Cola.

50 grams x 4 kcal/g = 200 kcal

200 kcal / 2,000 kcal = 10%

10% of your calories are provided by fructose

Even the very high end of fructose intake rarely exceeds ~85 grams, which is still < 20%.  My point?   This is nowhere near the 60% used in mouse diet studies.  Disclaimer: I think fructose causes leptin resistance because of data from such studies.  60% fructose is the fructose that causes leptin resistance and increased susceptibility to obesity.  What does this say about “normal” levels of fructose intake?  Toxic doses cause leptin resistance and obesity susceptibility in mice, well, because they’re toxic, and fructose toxicity just so happens to manifest like that (in mice).   60% is toxic.  15 cans of Coca-Cola per day (depending on who’s counting); but is it relevant?

39 grams of sugar, roughly half of which is fructose

In mouse studies, toxic doses are used for practical reasons- it’s cheap.  The animals can be rendered leptin resistant, glucose intolerant, and susceptible to obesity within a few months of feeding this expensive purified synthetic diet.  This probably (probably) takes over 100 times longer in humans simply because it’s nearly impossible for humans to ingest mouse-toxic-levels of fructose.

1. If the dose was based on body weight (like a drug; e.g., mg/kg or mpk):

60% fructose x 12 kcal/d = 7.2 kcal.  Divided by 4 kcal/g = 1.8 grams per day.

1.8 grams for a 40 g mouse = 45 g/kg.  For a 70 kg (154 lb) human = 3,150 grams of fructose or roughly 12,600 kcal.  I.e., 150 cans of soda or about a week’s worth of calories.  In other words, you’d have to eat a hypercaloric fructose-only diet for months.

2. If the dose was based on calories:

60% fructose x 2,000 kcal/d = 300 grams = 15 cans of soda or doughnuts per day.   News flash: that’s gross, but it won’t kill you.

fructose: still not as dangerous as playing in traffic

How about just lowering your lifetime sugar exposure.  39 grams of sugar is worse than 0.01 grams of stevia or sucralose.  Anyone remember “water?”  Even if you believe “a calorie is a calorie,” exclusively, it’s still really hard to burn off 39 grams of sugar.  Try running 2 miles.  Skinny kids might do this automatically after drinking a can of soda or eating a doughnut.  Not most adults.

Don’t play in traffic either.

calories proper

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XL soda ban, Op. 80

Posted on June 8, 2012 | 1 comment

People have been warned about the dangers of excess sugar consumption, but compared to the anti-smoking campaign, the recent proposal to ban XL soda’s is like bringing a cup of water to a forest fire.

In an ideal world, a proper health initiative designed to provide people (kids too) with good nutrition information would work. The new proposal takes a different route: it bans the sale of soda’s larger than 16 ounces (but you can still buy 2-12 ouncers).  I see two possible outcomes: 1) someone who would’ve bought one 24 ouncer of soda might settle for 16 ounces; 2) the one in a million customer who wanted 24 ounces will walk away with two 12 ounce sodas instead.  Win-win, right?  In the first case, the toxic sugar burden is lessened by a third.  In the second, a potentially valuable lesson on “serving size” will be on display.   Serving size 2.0, in 3-D, spelling-it-out for all to see.

It might actually work.  From a nutritional perspective, 90 grams of highly bioavailable sugar (HFCS) is a biological disaster.  Pound for pound, there aren’t many worse things you can consume… it’s the anti-thesis of “moderation.”  Regardless of your stance on the calorie debate, no one can argue that 90 grams of sugar all-at-once is more detrimental than it’s caloric content would imply.  Even for skinny people (metabolic obesity?).  It’s worse than dietary fat, and  might be THEE cause of leptin resistance.

This isn’t a TPMC original, but this graph of soda, diabetes, and obesity is just about as compelling as epidemiology can be:

 

douse those sugar cubes with artificial flavors, colors, and preservatives, and we’re good to go

If the ban goes into effect and actually impacts sales, will there be a backlash? more food company lobbying?  increased government subsidies (reduced HFCS consumption -> more taxpayer dollars used to cover the losses)?  Who knows.  If it teaches people a lesson about serving size or empty calories it might be worth it.

calories proper

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Resveratrol, energy balance, and another reason to distrust health journalism, Op. 79

Posted on June 2, 2012 | 2 comments


The great red wine compound “resveratrol,” at it again.  Disclaimer: 150 mg of resveratrol per day is too low and 30 days is too short to detect anything close to what was seen in the infamous resveratrol mouse study (Baur et al., 2006 Nature), which showed resveratrol to be the best drug ever on the planet.

This study, on the other hand, utilized the highest quality study design and was published in a great journal, but was a flop.   And the media got it wrong too:  “Resveratrol holds key to reducing obesity and associated risks.”  No, it doesn’t.

Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humans (Timmers et al., 2011 Cell Metabolism)

The study design was pristine.  Kudos.

Sample size too small (n=11) and study duration too short (30 days), but it was a randomized, double-blind, placebo-controlled, crossover study.  And although this type of drug study does not require such a thorough assessment of compliance (a pill count would’ve sufficed), the authors tested blood levels of resveratrol and its metabolites… cool.

On the docket: resVida, DSM Nutritional Products, Ltd.

Divide and conquer

The table above shows baseline characteristics in placebo and treatment groups, but this is peculiar because although the study was randomized (which is confirmed by the high degree of similarity between the two groups), it was also a crossover.

Brief review of my Prelude to a Crossover series (I  & II):

phase 1) half the subjects get drug and half gets placebo

phase 2) both groups get nothing for a washout period

phase 3) everybody switches and gets the other treatment

There are technically two baseline periods (before phase 1 and before phase 2), and all the subjects are in both.  As such, there is only one set of baseline values, so I’m not sure what the data in the above chart actually reflect.  Is this a mistake? or are these data only representative of one of the treatment sessions (which would be an egregious insult to the prestigious crossover design).

In any case, the subjects were all clinically obese, ~100 kg (220 pounds), BMI > 30, body fat > 25%, but otherwise metabolically healthy (fasting glucose levels of < 100 mg/dL).

But here’s where it starts going from technically flawed to weird:

Insulin levels may have been statistically significantly lower after resveratrol compared to placebo, but not after considering baseline insulin was ~15-16 mU in both groups.

insulin proper

The authors noted that after treatment, insulin levels were 14% lower in resveratrol compared to placebo (green circle).  BUT whatever was in that placebo pill was almost twice as good!  The placebo reduced insulin levels by 27% (red circle)!  (take THAT!)  I’m glad the authors reported these data instead of burying them, but they illustrate yet another flaw.

150 mg resveratrol (10-15 bottles of red wine) for a 220 pound person = 1.5 mg/kg; 200x less than what Baur gave his mice (300 mg/kg). Interestingly, however, this produced plasma levels of resveratrol almost 3x higher (180 vs. 65 ng/mL). I have no idea how this happened, but the benefits and lack of toxicity [at such a low dose] bode well for recreational resveratrol supplementation.

As mentioned above, resveratrol was totally safe, but how to interpret this is unclear.  Our options are: 1) good; 2) meaningless; or 3) simply not bad (which I suppose is kind-of-like #2).  It could be interpreted as meaningless because resveratrol, the anti-aging drug, is meant to be taken for a very VERY long time (i.e., forever).  This study proved that resveratrol was safe when taken for 30 days which is considerably shorter than forever.

Furthermore, the dose was phenomenally low, ~150 mg/d, so anything other than “totally safe” would be a huge red flag.

Does resveratrol in fact mimic calorie restriction, as stated in the title?  During calorie restriction, food intake declines (by definition), metabolic rate and insulin levels also decline, but free fatty acids and fat oxidation increases.  In the resveratrol group metabolic rate and insulin declined (recall however that the placebo was pretty impressive also in this regard), but free fatty acids and fat oxidation decreased.  Although proper calorie restriction trials in humans haven’t happened yet, some of these  effects don’t jive.  A decline in metabolic rate will reduce the amount of fat burned.  But relative fat oxidation also declined, leading to what could be a profound reduction in fat burning… coupled with no change in food intake (noted by the authors) this will result in increased fat mass.  Energy Balance 101- no ifs, ands, or buts.  This study was far too short-term to detect a meaningful increase in fat mass, but if these preliminary findings are true (and my interpretation of the data are correct), then this drug might just make you fat.

Oddly enough, they did detect an increase in fat accumulation in skeletal muscle:

(perhaps instead of calling it a calorie restriction-mimetic, the authors should’ve gone with exercise-mimetic, citing the athlete’s paradox (e.g., van Loon and Goodpaster, 2006)

In contrast to the popular antidiabetic drug rosiglitazone, which shifts fat storage from liver (where it causes a host of health maladies), to adipose, where it can be stored safely indefinitely, resveratrol shifted fat storage from liver to skeletal muscle.  This is interesting because while the fat storage capacity of adipose is seemingly unlimited, I doubt the same is true for skeletal muscle, which needs to do a lot of stuff, like flex.

If these findings are true, which I seriously question, then it would be interesting to see what happens to skeletal muscle fat stores after a few months, considering they doubled in only 30 days (this is unbelievable, literally).

The authors try to make the case that the increased muscle fat came from adipose, but until they report body composition data, this is a tough sell.  The elevated fasting free fatty acids support their claim, but the accompaniment of unchanged meal-induced FFA suppression with lower adipose glycerol release don’t; perhaps the missing glycerol is being re-esterified to nascent adipose-derived free fatty acids?  Increased adipose tissue glucose uptake would be supported by the lower glucose levels, but that is already more-than-accounted for by the increased RQ (indicative of increased skeletal muscle glucose oxidation).

There are some mysteries in these findings, and the improper handling of crossover data do not help.  If this paper is true and my interpretation of the energy balance data are correct, resveratrol might just make you fat :/

Unless of course you’re a mouse, in which case it’ll make you better in every quantifiable measure.

calories proper

p.s. I don’t think resveratrol will really make you fat, I think this study elucidates nothing.

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The curious perils of crappy sleep

Posted on May 5, 2012 | 2 comments

Don’t try this at home

Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption (Buxton et al., 2012)

The most utterly abnormal sleep structure was studied- for 3 weeks, the subjects were subjected to: 1) a 28-hour day; 2) 6.5 hours of sleep per night (equivalent to 5.6 hours in a normal 24-hour day); and 3) dim lighting during the days.  This was done to completely destroy circadian rhythms, and accordingly, metabolic calamity ensued: insulin response went down and hyperglycemia went up (compare black to red bars). 

B, baseline; SRCD, sleep-restricted circadian-disrupted; R, recovery period

Other notable findings:

1) sleep-restricted subjects ate 6% more

2) their metabolic rate declined 8%

3) body temperature went down 0.09 degrees

All of these things point to one common endpoint: weight gain.  Indeed, the authors even concluded that sleep restriction and disrupted circadian rhythms should increase the risk of obesity… except for one thing: everyone in the study lost weight (1.7% of initial body weight).

 

…suspense…

 

How, you ask?  during the increased waking hours, physical activity actually went up (a LOT).  This may have been because the researchers didn’t recruit an average lot, or group of subjects who were generally representative of the population at large.  No, this was a highly selective group of “healthy people.”  And what do healthy people do when their awake?  It’s probably what they don’t do that matters.  Healthy people spend less time sitting around (in general).  Had the researchers recruited a group of overweight subjects with their X-Boxes, I imagine the increased food intake would not have been adequately balanced by increased physical activity and they would’ve gained weight.

like this guy

I do NOT recommend sleep restriction for weight loss.  Even though glucose metabolism was completely restored after 10 days of recovery (gray bars in the figure above), lingering signs of metabolic dysregulation were still apparent (scary).

RMR and leptin

Perhaps not necessarily video game junkies, but those who are otherwise at increased risk of developing obesity do tend to move around less during the day if they sleep less at night (in contrast to the very healthy people mentioned above).

Reduced physical activity in adults at risk for type 2 diabetes who curtail their sleep (Booth et al., 2012)

This is not a “very healthy” group of subjects; accordingly, those who slept <6 a night were 27% less physically active and spent over an hour more per day sitting around.  In this study, short sleepers weren’t obese [yet]; but they were predisposed to weight gain.  (even the media seems to agree with this one).

If you DID want to try sleep restriction for weight loss, and even vowed to decrease food intake (in contrast to the highly active subjects in Buxton’s study), the results still might not turn out so good…

Effects of sleep restriction on glucose control and insulin secretion during diet-induced weight loss (Nedeltcheva et al., 2012)

In this study, food intake was intentionally reduced to a similar extent (-10%) in sleep restrictors and non-restrictors, and in agreement with Buxton, metabolic rate declined in sleep restrictors.  And although it was only measured at baseline, physical activity during sleep restriction must have increased because weight loss was similar in both groups.  But here’s the catch:  compared with those who slept 8.5 hours per night, the weight lost by those who slept 5.5 hours per night was primarily fat free mass (which is probably what caused their metabolic rate to go down), whereas it was primarily fat mass in those who got adequate sleep.  This finding alone is reason enough to get a good night’s sleep.

In sum:

Exhibit A, Buxton study: sleep-restricted HEALTHY people ate more but moved around WAY more during sleep restriction = weight loss.

Exhibit B, Booth study: those pre-disposed to obesity moved around LESS during sleep restriction = imminent weight gain.

Exhibit C, Nedeltcheva study: the weight lost by sleep restricted overweight dieters was comprised of muscle mass = not good.

In other words, if you think you’re a healthy person who wouldn’t sit around playing video games in your extra waking hours, or even if you promised not to eat more, the effects of sleep restriction on body composition wouldn’t be pretty (no pun intended).  Maybe you wouldn’t get fatter, but you’d probably get fattier.

 

calories proper

 

 

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Posted in Advanced nutrition, Energy balance, Leptin

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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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Posted in Advanced nutrition, Dietary fat, Energy balance, Protein, Sugar

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Taxes, saturated fat, and HDL, Op. 71

Posted on April 21, 2012 | 4 comments

Since red meat won’t kill you (it will make you stronger), why is taxing saturated fat still up for discussion?  The Danish proposal will add a $1.32 per pound to foods with >2.3% saturated fat; the cost of butter will increase by 30% more and olive oil by 7.1%.  I know, right?  WTF?

Again, I don’t think taxation is the solution, but for the sake of comparison: Arizona’s proposed “fat fee” would cost an extra $50 annually for childless obese patients; Rhode Island’s $0.01/oz of soda; or France’s 3.5% tax on all sugar-sweetened beverages.

Nutritionally speaking, saturated fat should be off the political chopping block; any intervention designed to reduce its consumption will do more harm than good.  In brief, here’s one example of what might happen if it worked, i.e., if dietary saturated fat consumption was reduced:

The effect of replacing dietary saturated fat with polyunsaturated or monounsaturated fat on plasma lipids in free-living young adults (Hodson et al., 2001 EJCN)

Subjects were given a high saturated fat diet and then switched to either a high polyunsaturated fat diet (trial I) or high monounsaturated fat diet (trial II).  In both cases, as seen in the table below, HDL decreased.

 




 

Alternatively, here’s what might happen if dietary saturated fat consumption was increased (in brief):

Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia (Krauss et al., 2006 AJCN)

The bottom two groups in the chart above ate similar diets except monounsaturated fats were replaced by saturated fats in the last group.

As seen in the table below, saturated fat significantly increased HDL.

 

 

So did weight loss, but I’d choose a steak over a stairmaster any day…  (daydream thought bubble: “indeed, ‘adherence’ and ‘compliance’ would be things of the past”)

 

If you believe HDL is important, taxing saturated fat might be a bad idea.  unless you have stock in statins.

 

calories proper

 

 

 

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Posted in Advanced nutrition, Dietary fat, Energy balance, Exercise, Sugar, Uncategorized