Tag Archives: energy expenditure

Discordant insulin sensitivity on a high protein diet

So, we have another “high protein” weight loss study (Smith et al., 2016).  Or really, a “low (0.8 g/kg) vs. moderate (1.2 g/kg) protein weight loss study.”  In brief, it took ’em about 6 months to lose 10% of their starting body weight, then were given 4 weeks of weight stability before “after” measurements were taken.

Important: this was not a contest to see who would lose more weight; they kept going and adjusting food intake until both groups lost 10%.  Not really ad lib, but otherwise a good study design imo.  The intervention was relatively weak (eg, protein 0.8 vs. 1.2 g/kg), but on the plus side, that’s realistic and very “do-able.”  If you’re interested in super-high protein diets (3-4 g/kg), check out research by Jose Antonio.

 




 

Big yet not unexpected finding: the low protein group lost about twice as much muscle than the normal protein group.

 

fat-free-mass

 

The isocaloric normal protein group lost more fat and less muscle than the low protein group.

But then everyone freaked out because the low protein group experienced a significant improvement in muscle/liver insulin sensitivity whereas the normal protein group didn’t:

 

glucose-rate-of-disappearance

 

-The headlines were hilarious, like, “high protein makes weight loss not work anymore.”

-Then some critics jumped the shark and blamed it on “liquid calories,” because whey protein shakes are totes non-Paleo, and #JERF.

-TBH, I found more interesting the changes in adipose insulin sensitivity

The normal protein group had the most insulin sensitive adipose of all groups… yet they lost more fat mass despite eating just as much or even slightly more than the other groups.

 

adipose-insulin-sensitivity

 

Does this mean they’re doomed to regain the weight?  I don’t think so, as high dietary protein is one of the strongest predictors of weight loss success long-term.

HERESY!  the low protein group had: 1) lower basal insulin than the normal protein group; 2) lower adipose insulin sensitivity; 3) ate less (NS); yet lost less fat mass.

 




 

In other words, the normal protein group had higher basal insulin, more insulin sensitive adipose tissue, and slightly higher food intake (NS).  According to the insulin model, they should’ve lost less fat mass than the low protein group, but they didn’t.

Is this another chink in the armor of the insulin model?

The truth seems to be: people lose weight on both LC and LF diets by giving up junk food.  On LC, this is accomplished by giving up carbs; on LF, this is accomplished by switching to better carbs.  Some people adhere better to one diet or the other.  Maybe insulin sensitivity has something to do with it.

Insulin from high protein: not bad?
Insulin from good carbs: not bad?
Junk food: no bueno.
So maybe just maybe it’s not just ze insulin…

 




 

Back to the protein…

This was not sorcery; it’s been seen before in a variety of different paradigms: dietary protein has a profound impact on nutrient partitioning.

Yes, even when it’s liquid calorie insulinogenic whey protein isolate bro-shakes.

Yes, even when it’s not crazy-high levels of protein…  seriously, 1.2 g/kg is not “high”

 

+ + +  +   +     +     +        +             +                     +

Past blog posts on [the non-sorcery of] dietary protein:

Holiday feasts, the freshman 15, and damage control

Dietary protein, ketosis, and appetite control.

Nutrient Partitioning: …a *very* high protein diet.

Protein “requirements,” carbs, and nutrient partitioning

Cyclical ketosis, glycogen depletion, and nutrient partitioning

Meal frequency, intermittent fasting, and dietary protein

Muscle growth sans carbs

+ + +  +   +     +     +        +             +                     +

For full access to all articles and much more (or if you just like what I do and want to support it), become a Patron! It’s three bucks a month and there are many other options. Sign up soon because there are only a limited number of spots left at the $3 level. It’s ad-free and you can cancel if it sucks ????

Also, I’m open to suggestions, so please don’t hesitate to leave a comment or contact me directly at drlagakos@gmail.com.

Affiliate discounts: if you’re still looking for a pair of hot blue blockers, Carbonshade  is offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERETrueDark is running a pretty big sale HEREIf you have no idea what I’m talking about, read this then this.

20% off some delish stocks and broths from Kettle and Fire HERE

If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS.

calories proper

 

Become a Patron!

 

 

Save

Save

Save

Save

Save

Save

Save

Save

Save

Share

Long-term fat adaptation

Recent comments about FASTER have upgraded this study to “the only long-term study on fat-adaptation.”  Needless to say, I disagree.  Again.

Side note: FASTER had no randomization or intervention (ie, confounded by selection bias, among others); they basically recruited long-term low carb & high carb ultra-endurance runners and measured the stuffings out of ’em.

Ultimately, they showed a very high maximal fat oxidation rate in low carb ultra-runners, 1.5 grams per minute.  This is important because MAXIMAL HUMAN FAT BURNING CAPACITY

 

TROGDOR the BURNiNATOR

 

In previous studies on SAD (Standard Athletic Diet haha), maximal fat oxidation at similar VO2max% has been reported to be much lower, <1 g/min (eg, Hetlid et al., 2015 and Volek et al., 2016).

 

Continue reading

Share

Gypped by GIP

Dr. Johnson’s recent paper is nothing short of a monster.  They did a TON of experiments.  Here, I only want to focus on one aspect.

The insulin-obesity hypothesis in a nutshell (very oversimplified): more insulin = more fat mass and vice versa.

I know I know, it was mice fed standard rodent chow, but also included models relevant to human biology like reduced insulin and caloric restriction, which may reflect certain aspects of ketogenic diets and intermittent fasting… and some of the results actually do reflect what happens to humans.  Some.

 

Continue reading

Share

Keto-Crossfit

Study: a handful of average-bodied Crossfitters in their mid-30’s were recruited and told to either: 1) keep doing what they’re doing; or 2) go full keto.  Crossfit 4x/week.   Strength testing before and after 6 weeks (Gregory et al., 2017).

I’ll start with the best part: KETOADAPTATION IS A REAL TRUE THING THAT WORKS (P<0.05).  Otherwise, this group’s performance would’ve plummeted.  It is known.

The performance test was time to complete a 500-meter row, 40 body weight squats, 30 abdominal mat sit-ups, 20 hand release pushups, and 10 pull-ups.

Tl;dr: both groups knocked about a half a minute off their time!

The key here is duration: 6 weeks of ketogenic dieting is adequate to restore performance back to baseline.  <3 weeks is not.

 

performance

 

Here’s the downside (sort of):

 

body comp

Basically, the keto group dropped carbs and failed to compensate by upping other calories.  I know I know, spontaneous ad lib appetite reduction, but this is a study on PHYSICAL PERFORMANCE.

 




 

And in further support of “muscle growth sans carbs,” keto dieters upped protein by 15% and this still wasn’t enough to compensate for the reduction in carbs/insulin: they still lost a bit of lean mass (NS).  Imagine if they hadn’t increased the brotein? yikes

 

food

 

so basically, they lost body fat because CICO and retained lean mass because exercise and protein haha jk

 

Admittedly, it was cool to see the body comp changes, but we know fat loss eventually plateaus and people start eating maintenance calories again (maybe a bit more if Ebbeling can be believed).  And this is where they remain for the rest of their lives (hopefully).  So at 6 weeks, they were still losing weight, nowhere near where they’re going to be for the rest of their lives, but THAT’s where I’d like to see performance testing (ie, at a stable body weight).  Don’t get me wrong, I hate myself in advance for making this critique: the researchers should’ve pushed more calories in the keto dieters bc this is a confounder in a study on PHYSICAL PERFORMANCE…  but this doesn’t really matter in the big scheme of things because Blackburn’s group did that and showed the results were the same haha

 

 

On another note, I don’t think people should expect an additional performance boost from being more ketoadapted (or more fat-adapted or whatever), primarily because whether the study is 3 weeks or 6, performance never really gets better than baseline in experienced athletes.  With more advanced training techniques, sure (and I think this is common), but not more keto- or fat-adaptation.

For full access to all articles and much more (or if you just like what I do and want to support it), become a Patron! It’s three bucks a month and there are many other options. Sign up soon because there are only a limited number of spots left at the $3 level. It’s ad-free and you can cancel if it sucks ????

Also, I’m open to suggestions, so please don’t hesitate to leave a comment or contact me directly at drlagakos@gmail.com.

Affiliate discounts: if you’re still looking for a pair of hot blue blockers, Carbonshade  is offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HERETrueDark is running a pretty big sale HEREIf you have no idea what I’m talking about, read this then this.

20% off some delish stocks and broths from Kettle and Fire HERE

If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS.

 

calories proper

Become a Patron!

 

 

Share

Rodent keto studies

Next time someone says VLC/keto is harmful or at least not helpful for fat loss because of a new rodent study, they’ll probably be wrong.

BOOKMARK THIS ONE GUYS.

Rodent studies on ketogenic diets or exogenous ketones are valuable and interesting in a variety of #contexts, although I’d argue that regulation of fat mass isn’t really one of ’em.

For starters, rodents aren’t particularly ketogenic – it’s rare to see ketones >1 after an overnight fast even in long-term ketoadapted mice.  Also, many rodents gain weight until they die, whereas humans plateau and stay relatively weight-stable for their entire lives (at least historically, and I’m not talking about yo-yo dieting).

Skeletal muscle, on the other hand, seems more similarly regulated: keto isn’t muscle-sparing in either specie… most people, perhaps unwittingly, increase protein intake on keto, and THIS spares muscle (N.B. this is simply to spare muscle, whereas in non-keto dieters, it’s not uncommon to see increased muscle in the #context of high protein).  That’s because carbs are more anabolic than fat.  QED.

There’s just a fundamental difference in the way fat mass and appetite is regulated between the species.  There are many similarities, which is why these studies are still valuable, but fat mass isn’t one of ‘em.

 

Continue reading

Share

AMYLIN

Brief background reading: amylin (according to Wikipedia)

 

In a study by Hollander on type II diabetics, the synthetic amylin analog pramlintide was tested (Hollander et al., 2003).  In this year-long RCT, over 600 patients were treated with placebo or up to 120 ug pramlintide BID (twice per day).  On average, these subjects were obese (BMI 34), diabetic for ~12 years, and had an HbA1c of 9.1%.  After one year, HbA1c declined 0.62% and they lost about 1.4 kg… not very impressive.

 

But it’s not all bad news; after viewing those relatively negative results (3 lb weight loss over the course of 1 year), another group of researchers led by Louis Aronne and Christian Weyer believed amylin had yet to be tested proper.  So they designed a better study; it was shorter, used higher doses of pramlintide, and they enrolled obese yet non-diabetic patients (Aronne et al., 2007).  They opted for higher doses of pramlintide (240 ug TID [three times per day]) because in dose-escalation studies, the incidence and severity of adverse drug reactions was consistently low at all doses tested.

 

They chose to study obese-er subjects (BMI 38, compared to 34 in the Hollander study) because obese subjects lose fat more readily than lean people, so if the study is designed to measure fat loss, then it is better to select a population of subjects where more fat loss is predicted.  They selected non-diabetic subjects for a similar reason; diabetics must regularly inject insulin which promotes the accumulation of fat mass — this could counteract any fat reducing effects of pramlintide.
In other words, it was a more powerful and better designed study.

 

After 16 weeks, pramlintide-treated subjects lost an average of 3.6 kg (~8 lbs), or about half a pound per week.  30% of patients lost over 15 pounds (1 lb/wk)!  Importantly, the weight loss didn’t appear to have reached a plateau by week 16, so it would have most likely continued along a similar trajectory had the study been longer.  There were no side effects, and a battery of psychological evaluations showed that the patients receiving pramlintide felt it was easier to control their appetite and BW, they didn’t mind the daily injections, and overall well-being increased.  At the very least, these evaluations meant the subjects weren’t losing weight because of nausea or malaise.  In fact, it was quite the opposite.

 

Continue reading

Share

Tissue-specific fatty acid oxidation

Does it matter where fatty acids are oxidized, liver or skeletal muscle?  Of course, they’re oxidized in both tissues (quantitatively much more in the latter), but relative increases in one or the other show interesting effects on appetite and the regulation of fat mass [in rodents].

Warning: a lot of speculation in this post.

A LOT.

It’s known that LC diets induce a spontaneous decline in appetite in obese insulin resistant patients.  Precisely HOW this happens isn’t exactly known:  the Taubes model?  improved leptin signaling?  probably a little bit of both, other mechanisms, and possibly this one:

 

Exhibit A. Oxfenicine

 

oxfenicine

Continue reading

Share

“Insulin Dynamics”

This one has a bit for everyone.

 

Relationship of Insulin Dynamics to Body Composition and Resting Energy Expenditure Following Weight Loss (Hron et al., 2015)

 

I think study was actually done a few years ago, originally published here (blogged about here), and re-analyzed through the eyes of Chris Gardner.  I think. (But it doesn’t really matter as the study design appears to be identical.)

 

Experiment: give someone an oral glucose tolerance test (75 grams glucose) and measure insulin 30 minutes later.  Some people secrete more insulin than others (a marker of insulin resistance); these people also have a lower metabolic rate after weight loss = increased propensity for weight regain.  However, if these people follow a low carbohydrate diet, then the reduction in metabolic rate is attenuated.  Some people who don’t secrete a lot of insulin after a glucose load may do better in the long-run with a lower fat diet.

 

Continue reading

Share

Hall et al., THE FIRST SIX DAYS (update)

Some people say the study design was rigged to favor the Low Fat diet (LF), which is dirty business but not exactly criminal; sometimes, this happens in science.

The claims go something like this: baseline diet was so high in carbs that they were locked into making unreasonable adjustments to formulate isocaloric low fat and low carb diets; eg, fat was too low in the low fat diet and carbs weren’t low enough in the low carb diet.

The biggest finding was “Fat Imbalance,” which favored LF.  Here’s why I don’t think the baseline diet mattered very much.

Tl;dr: drastically cutting fat intake (LF diet) is much more effective than upregulating fat oxidation (LC diet) to create a large Fat Imbalance in an acute setting, ie, THE FIRST SIX DAYS.

 

Continue reading

Share

Meal frequency, intermittent fasting, and dietary protein

Dietary protein “requirements” are some of the most context-dependent nutrient levels to decipher, and depend largely on energy balance and even meal frequency.

An objective look at intermittent fasting (Alan Aragon, 2007)

Meal frequency and energy balance (Lyle McDonald, 2008)

New study: “Increased meal frequency attenuates fat-free mass losses and some markers of health status with a portion-controlled weight loss diet” (Alencar et al., 2015)

This wasn’t well-received in social media because bro-science & many low carb advocates say grazing is no longer in vogue — “it’s much better/healthier/whatever to eat once or twice daily, because intermittent fasting and all that jazz” …however, this may be problematic when it comes to meeting overall protein needs, which is particularly important when you’re losing weight.

 

 

The study: 2 vs. 6 meals per day, crossover.

Conclusion: “On average, fat-free mass (FFM) decreased by -3.3% following the 2 meals/d condition and, on average, and increased by 1.2% following the 6 meals/d condition (P<.05).

 

fat-free mass

 

In other words, 6 meals per day was better for body composition than 2 meals per day.  But context is everything, and this hypothesis has been tested from a variety of different angles, so what does it mean?

The relevant context here: 1) big energy deficit (1200 kcal/d for obese women is a pretty low calorie intake); and 2) “adequateTM” protein intake (75 g/d).

The standard dogma says that in the context of an adequate protein hypocaloric diet, meal frequency matters a LOT, whereas with high protein, it doesn’t matter as much.  Theory being that with an “adequate” (read: too low?) overall protein intake, the fasting periods are simply too long with only two meals per day; you need either: 1) higher protein intake; 2) increased meal frequency; or 3) more calories (ie, smaller energy deficit).

In this study, BOTH diets suppressed insulin and induced weight loss, but the increased protein feeding frequency skewed the weight loss to body fat while preserving fat-free mass.   I actually agree with a lot of the bro-science in this case, and also think that 75 grams of protein is not enough in the context of a big energy deficit (if body composition is a goal).




 

Historical precedence?

 

Meal frequency and weight reduction of young women (Finkelstein et al., 1971)

Relevant context:  6 vs. 3 meals per day (3 meals per day may not seem like that many more than 2, but it significantly cuts down on the duration of time spent with no food or protein).

Smaller energy deficit: 1700 kcal/d in overweight patients is less of a deficit than 1200 kcal/d in obese patients.

Higher protein intake: 106 – 115g/d.

Result: nitrogen balance (a surrogate for the maintenance of muscle mass) and fat loss were similar in both groups.  This study fixed two problems in the abovementioned study: 1) 3 meals is better than 2 in the context of an energy deficit; and 2) protein intake was higher.

 

And again here, with 3 vs. 6 meals per day (Cameron et al., 2010), just to make the point that 3 meals per day is better than 2 for preserving lean mass in the context of an energy deficit.

 

The effect of meal frequency and protein concentration on the composition of the weight lost by obese subjects (Garrow et al., 1981)

This study tested the opposite extremes: super-low calorie intake (800 kcal/d), much lower protein intakes (20g – 30g/d), and 1 vs. 5 meals per day.

Result: “a diet with a high-protein concentration, fed as frequent small meals, is associated with better preservation of lean tissue than an isoenergetic diet with lower-protein concentration fed as fewer meals.”

It basically confirmed all of the above.

 

Protein feeding pattern does not affect protein retention in young women (Arnal et al., 2000)

1 vs. 4 meals per day; and 70 grams of protein but no energy deficit (~2000 kcal/d isn’t very hypocaloric for lean young women).  In this study, no effect of meal frequency was seen, likely because 70 grams of protein isn’t inadequate when energy intake isn’t restricted.

 

 

 

1. PROTEIN “NEEDS” ARE HIGHLY CONTEXT-DEPENDENT

2. NEED =/= OPTIMIZATION

3. MEAL FREQUENCY & meal timing and peripheral circadian clocks > “MACRONUTRIENTS”

 

If you’re losing weight (ie, in an energy deficit), then intermittent fasting is cool if protein intake is high (above “adequateTM“)… the bigger the energy deficit, the more protein is necessary to optimize changes in body composition.

 

How much is ‘enough?’  Sorry, can’t give you a gram or even gram per pound of body weight answer… but if you’re losing weight and seeing no discernible effect on body composition (muscle vs. fat mass), then it may be prudent to consider eating more protein-rich foods… and paying more attention to sleep quality (which also greatly impacts nutrient partitioning).

No amount of protein will help you if circadian rhythms aren’t intact!!!

 

 

further reading:

Yes, it’s a high protein diet (Tom Naughton, 2015)

Protein requirements, carbs, and nutrient partitioning

Dietary protein, ketosis, and appetite control 

 

 

For full access to all articles and much more (or if you just like what I do and want to support it), become a Patron! Five bucks a month and there are many other options. It’s ad-free and you can cancel if it sucks 🙂

Also, I’m open to suggestions, so please don’t hesitate to leave a comment or contact me directly at drlagakos@gmail.com.

UPDATED Affiliate links: It’s 2018, join Binance and get some damn cryptoassets or download Honeyminer and get some Bitcoins for free!

Still looking for a pair of hot blue blockers? Carbonshade and TrueDark are offering 15% off with the coupon code LAGAKOS and Spectra479 is offering 15% off HEREIf you have no idea what I’m talking about, read this then this.

20% off some delish stocks and broths from Kettle and Fire HERE

If you want the benefits of  ‘shrooms but don’t like eating them, Real Mushrooms makes great extracts. 10% off with coupon code LAGAKOS. I recommend Lion’s Mane for the brain and Reishi for everything else

Start your OWN Patreon campaign!

Join Earn.com with this link and get paid to answer questions online.

calories proper

 

Become a Patron!

 

Share