Tag Archives: body composition

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”

 

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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

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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.

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Circadian arrhythmia in different types of obesity

This study was pretty interesting.

Three groups of women:

1) normal weight

2) gynoid obesity (stores more fat in hips & butt), defined by WC/HC < 0.85

3) android obesity (stores more fat in belly, which is rare in women), defined by WC/HC > 0.85

 

First, we get confirmation that insulin sensitivity (IS) is better in morning than evening.  But then we get these interesting glucose tolerance curves:

 

circadian-glucose-tolerance

 

Fat stored in your hips & butt is thought to be healthier than that stored in your belly region.  This is confirmed here.  Gynoid obesity, while exhibiting an attenuated AM/PM difference, was able to restore euglycemia by the end of the experiment at both time points.  Ie, gynoid obesity selectively improved IS in the evening.

 




 

Android obesity, which is more nefarious than gynoid (also confirmed here), had a similar though not as robust effect in the evening but deteriorated IS in the morning.

One potential interpretation: it’s better to have a little extra fat stored in your hips and butt than to be lean or have belly fat.  However, I have a qualm with that interpretation.  Healthy people show a robust circadian difference in glucose tolerance.  Just as insulin resistance (IR) is an accepted physiological phenomenon observed in some ketogenic dieters, I view this circadian difference, also, as physiological.

 

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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.

 

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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

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Hey CICO, I’m playing by your rules.

Brief background: the notorious Ebbeling study of 2012 showed an apparent metabolic advantage of a ketogenic diet.  After losing some weight, participants were assigned to low fat (LF), low GI, or ketogenic diets.  As expected, energy expenditure (EE) declined in all groups after weight loss.

 

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Insulin resistance is a spectrum

The history of low fat diets is riddled with crappy low fat food-like products.

Food quality matters.

Free full article on Patreon! <- link

Take a group of obese people and assess insulin sensitivity however you like: some researchers demand nothing less than a hyperinsulinemic-euglycemic clamp (Gold Standard), others are OK with insulin levels during an oral glucose tolerance test.

Next, divide the people up based on this — there are a few ways you can do it.  You can: take the top half vs. the bottom half (a method which includes everyone); take the top third vs. bottom third (excluding the middle third); take the top quarter vs. bottom quarter (excluding the middle 50%), etc.

THIS MATTERS because in referencing this topic, many people claim most obese are insulin resistant.  They may be more insulin resistant than lean people, but even within obese people, there’s a spectrum, and the spectrum matters in this #context.

 

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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.

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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.

 

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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

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Muscle growth sans carbs

1.  net muscle growth = synthesis – breakdown

2.  need =/= optimization

3.  #context

 

muscle sans carbs

 

I’m totally cool with keto, honestly!  but still don’t really like seeing stuff like the above graphic and people interpreting it to mean “KETO IS MUSCLE-SPARING.”

 

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