Category Archives: diet

The poor, misunderstood autophagy

Autophagy isn’t a big deal in the way some Internet Bro’s think it is.  Yes, Dr Ohsumi received a Nobel Prize for cracking deeply into this nut, but that in no way means “intermittent fasting is awesome because autophagy.”  Autophagy isn’t awesome like that.

Alternate title: The dark side of autophagy.

For example: Autophagy contributes to muscle wasting in cancer cachexia (Penna et al., 2013)

Cachexia (muscle wasting) is one of the leading contributors to poor quality of life in cancer patients.  Thanks, autophagy.

“Autophagy is the major process for degradation of cellular constituents, its rate being enhanced under stress conditions leading to organelle damage…”

 

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The Hunger-Free Diet(s)

It started out as “lose weight without hunger on LCHF” and went all the way to “effortless fasting on keto.”  Works for some and it might be true, but the same can be said for low fat diets!  The key, I think, in both contexts, is simple: fewer processed & refined foods… something the Paleo movement got right, imo (although I still think many low-calorie sweeteners are way less unhealthy than HFCS & sugar).

The logic:

1) add “good calories” like almonds to your diet and appetite spontaneously compensates by eating less other stuff: energy neutral

2) you don’t compensate for added “bad calories” like sugar-sweetened beverages: positive energy balance

3) remove bad calories from your diet and you don’t compensate by eating more other stuff: negative energy balance

 

Book: Good Calories, Bad Calories

 

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Non sequiter dietary fats

Tl;dr: SFA and DHA

Essential fatty acids?  Well, there’s really only one, DHA, and we really only need a gram or two.  In other words, our entire requirement for dietary fat can be met by about 2% of total calories (plus a few extra grams to accommodate fat-soluble vitamins) (plus DHA is never the sole fat in a food, so you’d be getting a few more grams of other fats, too).  But still, a very low fat diet!  But impractical and probably not very palatable or healthy.

On average, dietary fat comprises about a third of calories, roughly equally divided between SFA, MUFA, and PUFA (slightly less PUFA).

Major sources of SFA are pizza and desserts – no wonder SFA gets a bad rap!

 

cheese-crust-pizza

 

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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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calories proper

 

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Keto myths & facts

:::begin rant:::

Trigger warning?  Maybe.

Disclaimer: I’m pro-LC (P<0.05), but not anti-LF because LF works better than LC for some people.  And with the exception of things like keto for neurological issues, I think macros take a back seat to many other factors.

Myths: carbs cause insulin resistance (IR), diabetes, and metabolic syndrome.  Carbs are intrinsically pathogenic.  If a healthy person eats carbs, eventually they’ll get sick.

And the only prescription is more keto.

cowbell

And of course all of this could’ve been prevented if they keto’d from the get-go.

Proponents of these myths are referring to regular food carbs, not limited to things like Oreo Coolattas (which would be more acceptable, imo).  Taubes, Lustig, Attia, and many others have backed away from their anti-carb positions, yet the new brigade proceeds and has even upped the ante to include starvation.  Because “LC = effortless fasting?”

Does this sound sane?

“No carbs ever,
no food often…
otherwise diabetes.”

oreo-coolatta

no one in their right mind would say lentils & beans cause diabetes

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Circadian rhythms and breast cancer

Over the course of human evolution, diets varied widely over time, seasons, geography, etc., ie, we can obviously thrive on many different dietary patterns… but the light/dark cycle was there the entire time.  Why is this not the most important talking/debating point?  Why do people think humans need one particular diet but can ignore circadian rhythms?

Because everyone’s still fussing about carbz and what we are “designed to eat”

*smh*

see also: “Lights Out!” by T.S. Wiley

 

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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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Alcohol on keto

This article isn’t about alcohol tolerance.  It’s about your liver.

Tl;dr: with a basic knowledge about alcohol metabolism and ketoadaptation, drinking on keto gives me pause.

It might be nothing, but it gives me pause.

Alcohol is metabolized primarily by alcohol dehydrogenase, producing acetaldehyde and reducing equivalents as NADH.  This pathway produces energy.

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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).

 

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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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