Gluconeogenic precursors on LCHF

Metabolic advantage (MA): theoretical boost in energy expenditure induced by a diet. Some studies show it exists, others don’t. In any case, ask any keto proponent about MA and they’ll surely say something like, “if it exists, gluconeogenesis (GNG) may be one of the main drivers.”

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I can get behind that because GNG is an energetically expensive process and is likely increased when you’re not eating carbs. Ie, keto.

Disclaimer: this may be another demonstration of how nutritional ketosis isn’t muscle sparing.

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[sorry for the poor image quality, here’s the source for a better version]

This brings us to the relevance of substrate. In general, the main gluconeogenic substrates are glycerol (from adipose), lactate (from glucose metabolism), and amino acids (eg, alanine & glutamine from skeletal muscle).

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If we’re doing more GNG, we need more GNG substrate/precursors.

Lactate: the contribution of lactate to GNG doesn’t even budge during prolonged starvation, in a #context when we’re trying to do anything & everything to preserve GNG precursors… boring.

Next up: glycerol, then amino acids (it’s good!).

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Protein & sarcopenia

Unless otherwise requested, this will be my last post on protein for a while. I promise. Maybe.

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Came upon another review that went over some of the nuances of different protein sources, amino acid profiles, etc., and lean mass (Gorissen and Witard, 2018).

While I don’t think this really matters that much, most people on Earth get their protein 60% from plants, 40% from animals. Flip those values for the Americas and Europe.

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Wrt protein: I think quantity from diverse sources is more important than shooting for some specific amino acid score. It’s more practical and less guesswork, imo.

  • Sarcopenia sucks (P<0.05). It’s one of the leading causes of reduced quality of life.
  • Anabolic resistance: dietary protein intake usually stimulates muscle protein synthesis. This is reduced in inflammation and aging. There are a few steps to get around this.
  • Protein balance is muscle protein synthesis (MPS) AND muscle protein breakdown (MPB). The authors acknowledged this in the intro (YAY!), but the whole review focused on the former.
  • In general, it is thought that dietary protein supports MPS while insulin blunts MPB (over-simplified).

As detailed below, strategies to augment muscle protein synthesis (MPS) to the anabolic effects of dietary protein:

  • increase the dose (moar protein) — added protein provides more substrate to support MPS. Protein-induced insulin secretion helps blunt MPB
  • exercise can sensitize skeletal muscle to the anabolic effects of protein
  • seafood/DHA may have a similar sensitizing effect (2 or 3 studies support this)
  • cheat code LEUCINE (supported by many studies) – the gymbroni’s got this one right. It’s why whey, soy, and lean chicken are go-to’s: most leucine per calorie. Steak, nuts, and eggs have it too, but much less per calorie.

#context

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do you need animal-based protein?

Protein combining. Complementary foods. Whatever you want to call it.

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for example, corn lacks lysine but has plenty methionine whereas the opposite is true for beans, so succotash gives you a complete spectrum of essential amino acids. Or rice & soy. The former more common in the Americas, the latter in Asia. It pops up in many cultures around the world.

in practice, however, not very relevant

and it probably doesn’t even apply to anyone with an internet connection. I’ve yet to come upon Disease X which prevents one from eating all but a single food item. There are some inherited metabolic disorders which require you to restrict 1 or more amino acids, for example, but that’s like taking a diet from 100 to 95, not 100 to 5 as would be with “Disease X”

further, if you eat enough rice (and nothing else), you can get enough essential amino acids to fulfill your protein requirements. You will be hugely nutrient-deficient, but at least you’ll have those aminos

What about an egg white? It has a great [probably perfect] ratio of amino acids, but you’d still be deficient unless you ate a lot of them — not too unlike the example with rice 🙂

fewer carbs & calories to get the same amount of high biological value (BV) protein with the egg white than rice, sure, but that’s a topic for another day

Enter: vProtein

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In the beginning it was “IAA” — YES or NO? does a food have enough indispensable amino acids YES or NO. Binary.

Then there was the PDCAAS — protein digestibility-corrected amino acid score — which combined IAA with BV and rated foods on a scale of 0-1. Better, but still overall uninformative.

What I like more than both, and what is far more interesting/educational, is vProtein. Someone did all the hard work for you…

Maximize high BV protein, minimize amino acid excesses* & deficiencies.

AND GIVE SPECIFIC FOOD COMBINATION EXAMPLES <- 100x more valuable than getting a YES or NO based on IAA or a PDCAAS of 0-1

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Protein is the last thing that will make you gain weight

A randomized 3-way crossover study indicates that high-protein feeding induces de novo lipogenesis in healthy humans (Charidemou et al., 2019)

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First it was protein will kill your kidneys and bone, then it kicked you out of ketosis or was converted straight to glucose. Now, not only does it stimulate de novo lipogenesis (DNL), but it is the amino acids themselves that are literally converted to fat.

Do the biochemical pathways exist? Sure. More so on paper because I doubt very much of the fat stored in your body literally came from protein. I can see if you increased protein enough to drive a big energy surplus, then some more dietary fat would get stored as body fat and you might see increased DNL, but even some older protein overfeeding studies show this doesn’t really happen that much*

*it’s tricky to define the magnitude of a surplus if expenditure keeps going up; with protein, the surplus on paper is usually overestimated

Which brings us to today’s study. Great study design (3-way crossover), single meal prepared & provided to the participants. Small sample size. Weird nutritional controls, although I suspect this decision was more practical than scientific. The high fat diet was very high fat and the high protein diet was… higher than control, but if I were designing this study trying to show ‘protein -> DNL -> fat,’ I’d’ve gone with more than 40g.

I don’t even care that the added protein came from soy, which is high in glutamate, similar to beef, and slightly less insulinogenic than whey.

Indeed, this study was very nuanced…


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Circadian rhythms and exercise — re-setting the clock in metabolic disease

Maybe the title isn’t as clever as “Watch the clock, not the scale” or “Clocking in, working out” but this review was pretty good (Gabriel and Zierath, 2019).

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1- I’m a big fan of activity. Walking, hiking, frequent breaks from sitting, and lifting weights are among the things I do daily (and advocate).

2- The elephant in the room (for me at least): exercise timing and the diurnal variation in human performance.

Remember back when researchers would put people on a ketogenic diet for a few days, take some measurements of physical performance, then conclude keto sucks for athletes? But then we learned about ketoadaptation and now know that 3 weeks is the minimum.

It’s happening again, but this time with exercise timing. Take two random people — athletes, old or young, male or female (it’s been tested in all of these populations) — and take some measurements of physical performance in the morning or afternoon, wait a couple days, then measure in the reverse condition.

Same thing every time: performance is greater in the afternoon.

BUT if you train a group consistently in the morning, performance in the morning improves and there’s no longer a diurnal difference. Interestingly, this doesn’t happen to a group that’s trained in the afternoon; they’ll still perform worse in the morning (eg, Chtourou and Souissi, 2012).

There are many implications, nuances, and caveats to this…

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Palmitoylethanolamide. What now?

Palmitoylethanolamide (PEA, not to be confused with phenylethylamine).

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It does all the things in mice (alleviates pain, inflammation, anxiety, etc.), but now that it is widely available in supplement form, what is the evidence in humans?

It’s specific targets are largely unknown. PPARa? Endocannabinoid system? CB1? Others?

[doesn’t look like much, does it]

A few case studies and a clinic that pushes it HERE. Most start with 300 – 600 mg once or twice a day.

Histamine intolerance?

Remember when people used to joke about marijuana for eye health? Well, that might be partially true and argues for either: 1) a common endocannabinoid target of PEA and something in marijuana; or 2) cannabis has an extensive & complicated profile of bioactive compounds and PEA has nothing to do with the cannabinoid system (Costagliola et al., 2014 & Pescosolido et al., 2011).

More studies have been published on pain & inflammation (below)

Is anyone gonna try PEA? Let me know.

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Cannabinoids and sleep

I was not looking forward to writing this, in part, due to my love-hate relationship with cannabinoids: on one hand, they show potential in many difficult-to-treat conditions; on the other hand, some psychiatric risks and this (CB receptor activation is diabetogenic).

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Further, don’t underestimate the complexity of cannabis plants and the endocannabinoid signaling system.

The cannabinoids (Babson et al., 2017):

-THC, the main psychoactive component of cannabis (also in drug form as Nabilone)

-CBD, a non-psychoactive component of cannabis

-Dronabinol, a highly purified synthetic (-)-trans-D9-THC. It’s actually 2-3x weaker than Nabilone (which is a further testament to the complexity of this system, imo).

Nabiximols (Sativex), a roughly 1:1 combination of THC & CBD.

To be clear, the main therapeutic use of cannabinoids is anti-emetic (prevents vomiting) & appetite-stimulation in some conditions (eg, cancer, HIV). The more interesting part, imo, is some of the human studies (discussed below) on people with difficult-to-treat conditions, who also sleep poorly, where any improvement in sleep quality inevitably improves their condition.

This article is specifically on sleep. I’ll do follow-ups on anxiety and maybe inflammation if you’re interested. Let me know!

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Circadian rhythms, time-restricted feeding, and healthy aging

Circadian rhythms optimize physiology and health by temporally coordinating cellular function, tissue function, and behavior” (Manoogian & Panda, 2017).

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These rhythms dampen with age and metabolic dysfunction. Part of the age factor is caused by a natural decline in eyesight as we age and that deteriorates our ability to entrain the master clock with light.

Light/dark & feeding/fasting (and even exercise [before 4pm]) are our tools.

Even I’ll admit 2-3 meals a day with no snacking seems optimal for most people and a good pattern for optimizing protein utilization. Want to mix in some intermittent fasting? eTRF seems like the strongest contender but my interpretation of the evidence is somewhat less strict than what appears in the literature — eg, I don’t think you need a kcal % distribution of 50/30/20 or need to have dinner at 3pm. Just shifting away from a late eating pattern seems sufficient.

A lot of things started going downhill after the invention of artificial lighting — we no longer have the automatic light/dark cycle.

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Ketogenic diet: glucose, lipids, and inflammation

Glucose and lipid homeostasis and inflammation in humans following an isocaloric ketogenic diet (Rosenbaum et al., 2019)

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-Rosenbaum & Leibel come out of retirement? These scientists did some of great pioneering work on the biology of leptin in weight gain/loss.

-I don’t know how much Kevin Hall contributed to this study but he’s been working HARD lately!

4 weeks of a baseline diet (15% protein, 50% carb, 35% fat) -> no washout? -> 4 weeks of a ketogenic diet (15% protein, 5% carb, 80% fat)

Following each diet period, a ketogenic & conventional meal tolerance was done:

Diet breakdown, sample menu, and my analysis below:

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A bigger dinner decreases parasympathetic activity leading to less restorative sleep

Clunky title, I know. The study was comparing two different kcal distributions on autonomic nervous system activity and sleep (Tada et al., 2018).

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There were two conditions in this randomized crossover trial: breakfast/lunch/dinner calories either as 1:2:1 (the low-energy dinner group [LED] or 1:1:2 (the high-energy dinner group [HED]).

Then they were monitored overnight to assess autonomic nervous system activity and sleep.

What was the point of this study? The next step in the scientific method! Researchers have noticed correlations between dietary intake (meal size, not timing) and restorative/non-restorative sleep. So now they want to test if meal size directly influences sleep.

The authors extended the conclusions slightly beyond what the study was designed to test, imo. They previously noticed bigger dinners & poorer sleep during the luteal phase in women and this correlated with progesterone. But in this study they didn’t include the right controls to test that: luteal phase vs. follicular phase [and optionally, vs. men or postmenopausal women].

That said, I’m sure sex hormones definitely play a role here, it just wasn’t clearly teased out in this study.

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