High protein diet: UNLEASH THE TABOO

At first, this article reads like a sarcastic blog post or something (Kalantar-Zadeh et al., 2019).

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[their words in italics; my commentary is not]

How often have you been told to eat more protein and less carbohydrates to stay healthy?

Uhmmm, never?

This is not an emerging food culture but rather a prevailing dogma in our society.

What society is that?!

Physicians, dietitians and other health care professionals tell us constantly about the advantages of a high-protein diet (HPD), such as losing weight rapidly, burning calories, diminishing appetite, preventing obesity, managing metabolic syndrome and treating diabetes. 

Which physicians!

This contemporary creed has gone so far that we feel continuously pressured to eat more protein and less carbohydrates, including even less fruits and vegetables. 

Am I taking crazy pills?

We feel compelled to eat only the meat patty of the sandwich and leave behind the bun when eating in front of others, otherwise we may lose credibility among friends and peers. 

Yes, crazy pills.

If somebody dares to recommend a ‘low-protein diet’ (LPD) or, even worse, to imply that ‘HPD may cause harm’, then it would be considered a serious aberration to health and a taboo.

This is some seriously emotionally charged stuff. TABOO! And as I read on, it became clear…….

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These pork rinds are the bomb 🙂

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Testing the carb-insulin model (CIM) in mice

or, the biggest mouse study that’s ever been done (Hu, Speakman, et al., 2019)

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Background rant: 20 years ago I thought I had a firm understanding of CIM. 10 years ago things got a little dicey here and there. Since then, the goalposts have been shifted so far and so frequently it’s a mess… we’ve come a long way from Atkins (for better or worse)

I disavow.

That said, regardless of where the goalposts were set, everyone should bookmark this study. They varied every macronutrient in nearly every possible way and took a variety of metabolic assessments (insulin sensitivity, body weight, food intake, etc.).

So whether or not their study tested the CIM to which you subscribe, there is still a ton of information here. My comments are mainly on CIM here lol

Speakman’s CIM is broken down into 5 somewhat overlapping parts.

  1. Increased dietary carbs increases fasting insulin which decreases fasting glucose

-In the context of any CIM, the postprandial state seems more relevant here; as in, ‘carbs increase insulin which reduces glucose and you get fat storage from the insulin and hangry from the hypo.’

These pork rinds are the bomb 🙂

2. Carbs and insulin induce de novo lipogenesis which makes you fat

-My only qualms here are: DNL is quantitatively more of a liver thing, and anyway, most of the fat that gets stored came straight from the diet, not DNL.

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Sunlight, reptile bulbs, and NO

Ultraviolet radiation suppresses obesity and symptoms of metabolic syndrome independently of vitamin D in mice fed a high-fat diet (Geldenhuys et al., 2014)

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Sunlight > vitamin D supps. It is known.

Brief review of vitamin D synthesis: TEAMWORK!

In brief: cholesterol -> 7-dehydrocholesterol in skin; sunlight (UV radiation) converts that into D3 which goes to liver on DBP and is made into 25(OH)-D3. That then goes to kidneys and is transformed into the active form, 1,25(OH)2-D3. What’s not shown in that graphic is when you have enough D, it’s instead converted into an inactive 24,25(OH)2-D3. This prevents toxicity from sunlight D.

Hypervitaminosis D (from supps) is rare but unpleasant.

Seasonally, in some extreme latitudes, fancy UV lamps &/or [speculatively] much cheaper reptile bulbs may supplement sunlight. And it’s not just vitamin D!

This study showed sunlight also increases nitric oxide in the skin, which has effects beyond the D… may also be supplemented with NO-inducing skin creams (also speculative), if applied to the right spots…

Big tie-in with our beloved brown adipose tissue.

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Cold Thermogenesis RELOADED

A lot of cool studies about brown adipose tissue (BAT) lately; here’s the rundown.

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More and more, with more sophisticated techniques, scientists are discovering we have more BAT than previously believed. And they all have theories on how it works and if it can be manipulated to make us healthier.

Activated BAT secretes a lot of stuff:

Exercise increases circulating 12,13-diHOME in humans (old, young, male, female, sedentary, active) (Stanford et al., 2018).

In mice, too, and surgical removal of BAT abolishes this effect. Dosing them with 12,13-diHOME increases fatty acid uptake and oxidation in skeletal muscle.

BOOM

Cold exposure induces the enzyme 12-LOX in BAT which synthesizes lipid mediators that improve glucose tolerance (Leiria et al., 2019).

Cold exposure in this #context is a few degrees above your shivering threshold. It’s NOT an ice bath — it’s shorts & a t-shirt in 50(ish) degrees F (10 C).

The good news: if you dislike exercise or find cold exposure unpleasant, there are other ways, eg, beta-3 adrenergic receptor agonism and some nutrients that can be obtained via diet.

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“Fats for thoughts”

An update on brain fatty acid metabolism (Romano et al., 2017)

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This was an interesting review, although it got off to a rocky start by stating: “glucose is the preferred energy substrate of the brain.”

My opinion is that “preferred energy substrate” is a weird concept in this context. When glucose declines and ketones increase, ketones will be used. Are they preferred now?

I’m not saying either are preferred. Just making note of this.

Given the title of the article, I was expecting a lot on DHA/fish oils but there was a good deal on ketones.

Yes, the brain definitely uses ketones; this is particularly important during starvation and it comes in handy during hypoglycemia.

it’s likely that you can avoid going into a coma during hypoglycemia if there are a lot of ketones around. Brain doesn’t use a lot of fatty acids, probably, to reduce the risk of hypoxia and/or oxidative stress (the former because FA oxidation is slow).

-> exercise is probably the number one “anti-aging” agent (good for everything but cognitive health in particular)

-> exercise & ketones -> +brain-derived neurotrophic factor (BDNF)

^^^I rather like BDNF and humbly suggest this may lean toward ketones being more “preferred”

Coconut oil may be helpful in this context.

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Diabetes Education to Lower Insulin, Sugars, and Hunger (the DELISH study)

Interesting lipid findings from the DELISH study (Mason et al., 2019).

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The nefarious “sdLDL” — whether you’re a believer or not in any cholesterol hypothesis relating to health, most agree that if LDL levels predict disease, it’s the small dense ones that do it best.

DELISH was a good study. Not a super-intensive double-blind randomized crossover study of keto vs. SAD, but rather a moderately ketogenic (> 0.3 mM bHB), “cut out the sugar & processed foods” intervention.

It worked.

The participants cut their carb intake in half but maintained baseline fibre intake suggesting indeed, they were cutting out processed carbs, not non-starchy ones, green leafys, berries, etc.

In the intro, it is mentioned that sometimes, LDL-C increases on a ketogenic diet. This has more to do with the specific foods than the macro’s or process of ketogenesis, and that was a general theme of this paper.

Indeed, this one had to do with red meat…. ooooohhh

If you’re interested to see how it played out, head over to Patreon! Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 

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The totality of evidence favors some manner of eTRF: 6 vs. 3 vs. 2 meals/d

Two studies. one compared 6 vs. 3 meals per day (Jakubowicz et al., 2019); the other 6 vs. 2 (Kahleova et al., 2014).

BOTH eTRF!!!!! Finally.

Tl;dr #1: with regard to body composition, 3 protein-containing meals/d seems to be the sweet spot. Muscle likes frequent feedings, but no additional benefit is seen beyond 3x/d.

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Tl;dr #2: If you’re gonna IF, the totality of evidence favors some manner of eTRF.

According to the data, the traditional 3 meal/d eTRF is great, less hunger, more satiating, etc. Or is you want to be like some anti-aging guru and skip dinner a few times/wk & go to bed hungry for that hormetic response or something, there are data supporting that too.

Let’s dive in it -> head over to Patreon! Join the community for up-to-date information about a variety of topics in the health & optimizing wellness space. Five bucks a month for access to this and all previous articles. It’s ad-free and you can cancel if it sucks 🙂

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The NAD+ Precursor Wars!

Many camps here! This is getting fun 🙂

Two different supplements: nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Both backed by good science & scientists (one camp is shilling a supplement while the other camp is selling books, which I don’t really care about) (the social media war is, however, hilarious).

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Both precursors appear equally effective in the rodent studies and I expect this to cross over when NMN finally has human studies.

BIG difference that nobody is really talking about is TISSUE SPECIFICITY.

1st problem: commentators were talking about NR/NMN as if it passed from your gullet directly to the liver. NR would be absorbed directly; NMN would be dephosphorylated to NR, absorbed, get re-phosphorylated back to NMN then converted to NAD+.

[insert Slc12a8 image here]

Since NMN and NR cost the same, this doesn’t really matter. Right?

Supp manufacturers just thought that since NMN was one step closer to NAD+, it might make a better precursor. But if it’s converted to NR prior to absorption, who cares?

And if the liver just releases niacinamide (NAM) to the rest of the body, WHO CARES?

THE PLOT THICKENS

This becomes relevant with all the different preparations on the market — intranasal, sublingual, regular oral (NR/NMN), NAD+ directly, and why can’t I just save a ton of money and use NAM instead! Relevant, yes. And interesting. I’ll summarize…

Have you tried any of these? Let us know in the comments 🙂

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Nicotinamide Riboside (NR)

or nicotinamide mononucleotide (NMN)

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There is some banter about which is the better NAD+ precursor, but I don’t think it really matters. They are interconverted in vivo and cost about the same…

NR has been studied in both humans and rodents whereas NMN research is primarily rodents. I’m usually biased toward human studies, but again, I don’t think it matters in this #context.

Why NAD+ ?

Because OMG all of the animal studies! It’s like resveratrol all over again…

oh wait…

But seriously, old mice given either NAD+ precursor look like young mice by nearly every measure. NR and NMN have never been directly compared, but both produce equally positive effects in the various rodent models in which they’ve been tested.

And I’m fairly well-convinced NAD+ levels do decline with age…

Anyone gonna try NR or NMN? Let me know in the comments!

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“Ketogenic diet and skeletal muscle hypertrophy: a frenemy relationship?”

You can say that again!

Hot off the presses (Paoli et al., 2019).

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Good paper. Nice background with information about muscle protein balance, anabolic & catabolic factors, and signaling pathways.

At one point the authors seem to have confused a study on starvation ketosis with nutritional ketosis, but in all fairness they also acknowledged the study showing beta-hydroxybutyrate can inhibit AKT which is important for skeletal muscle hypertrophy (Yamada et al., 2010).

Let’s dive right in to Table 1 which is a summary of human studies on keto & lean mass:

Starting with the study by Wood and colleagues (2010), who studied: a low fat diet, low fat + exercise, keto, and keto + exercise. Everyone lost weight. The low fat group lost significantly more lean mass than any other group. The authors interpreted this to mean keto “had a protective effect on muscle mass.”

LFD+ex, Keto, & Keto+ex all lost the same amount of lean mass although the keto groups were getting 50% more protein.

Another interpretation, one could say that 50% more protein and even resistance exercise weren’t enough to prevent keto-induced muscle loss. They lost just as much lean mass as LFD+ex and Keto.

Jabekk and colleagues compared resistance exercise + usual diet with resistance exercise on keto (Jabekk et al., 2010).

The authors concluded: “a general conservation of muscle mass.”

That’s OK, but the control group gained lean mass! Thus, an alternate interpretation could be that keto blunted muscle gains.

Not acknowledging the control groups, as in Table 1, is a not-so-subtle-way of shifting goal posts imo.

Similar issues in the study by Paoli and colleagues (Paoli et al., 2010)…

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