Tag Archives: body composition

The current state of affairs in nutri-Twitter

Rant.

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1) It’s almost as if you’re either:

a red meat-eating 110% keto-advocate

or

you think red meat and a ketogenic diet is harmful.

 

If you don’t say the diet is magical, the zealots will try to trick you into, or outright accuse you of saying it’s harmful.

Further,

 

2. And the protein/kidney debate re-surfaced again recently. To be clear: no studies have shown direct harmful effects of protein on kidney function. The studies cited by KDOQI are observational and on end-stage renal disease. Not mild kidney disease or slightly impaired renal function. If I had ESRD, I’d rather play it safe and not enroll in one of Jose Antonio’s high protein diet studies (~4.4 g/kg lol).

I’m pro-LC and HP but not anti-LF. Humans have thrived on a wide variety of diets over time regardless of macronutrient composition. Food quality seems more important in this context.

3. If ketones are muscle-sparing, then…

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CARBOTOXICITY [screaming face emoji]

Noxious Effects of Exaggerated Carbohydrate Intake (Kroemer et al., 2018)

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This blog post is about the above mentioned article. Disclaimer (qualm #1): it is very pro-low carb and refused to include any neutral or negative points about low carb. For example, had it been within the scope of the article, the authors may have said despite excluding the majority of carbohydrate-containing foods, low carb diets actually aren’t restrictive at all. In other words, this is not an unbiased review article.

 

 

Qualm #2: the authors say people have long-recognized the problems of lipid excess and it even has a name, “lipotoxicity.” But these revolutionaries thought the problems of carbohydrate excess need to be recognized so they coined the term “carbotoxicity.” Are we to believe these dorks never heard of “glucotoxicity” even though it was coined before lipotoxicity even was?!

The review is about the molecular, cellular, and neuroendocrine mechanisms that link a prolonged energy surplus to disease and accelerated aging. It doesn’t really distinguish how the energy surplus is established, specifically, but every now and then they throw out there “carbz.” Ignoring that, there are actually some pretty good points.

The history of dietary carbs had three major, transformative steps. The first was the transition from hunter-gatherers to agriculture which shifted the carbs from fruits, seeds, tubers, nuts, roots, and bulbs to a range of cereals (in Europe), rice (in Asia), corn (in Mesoamerica), and potatoes (in South America). And in Weston Price fashion, this was associated with an increase in dental cavities (probably more cause than correlation here).

Acarbose blocks carb digestion, D-glucosamine blocks glycolysis.

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Low carb diet. NAFLD.

An integrated understanding of the rapid metabolic benefits of a carbohydrate-restricted diet on hepatic steatosis in humans (Mardinoglu et al., 2018)

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Critique and analysis.

They did two very small (n=10 & n=7) 2-week long studies of low carb, high protein. Carb/fat/protein was 4/72/24 compared to 20/42/18 at baseline. There was no control group, so the results were compared to baseline.

 

 

Lots of pro’s and con’s on this one… but for that, head over to Patreon! Five bucks a month for full access and there are many other options. It’s ad-free and you can cancel if it sucks 🙂

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Start paying attention to REV-ERB alpha

Hey team, remember when I was making wild predictions about REV-ERB alpha?

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“Food for thought: an endogenous ligand of Rev-erb is heme (the iron-binding element in red blood cells). Heme is degraded into bilirubin.  Elevated levels of bilirubin cause jaundice. A treatment of neonatal jaundice is exposure to blue light. Blue light is a major regulator of circadian rhythms and Rev-erb is an executive-level player in this game. The primary mechanisms of blue light appear unrelated in these two models (melanopsin activation vs. bilirubin photoisomerization), but seem intertwined, because heme activates Rev-erb.  Cool.” (From HERE)

and statements:

“Pharmaceutical-grade circadian augmentation = unwittingly better-timed meals? Improved body composition? …they were eating more and moving less. … One possible mechanistic explanation comes from mice lacking Rev-erb in skeletal muscle (Woldt et al., 2013). Mitochondrial biogenesis was impaired and exercise tolerance was reduced in these mice. Spontaneous physical activity was lower; thus, it stands to reason that Rev-erb agonism may improve skeletal muscle mitochondrial function. This isn’t entirely consistent with the drug study, but pretty close.” (From HERE)

 

REV-ERB is really really good for skeletal muscle.

Beta-hydroxybutyrate inhibits activation of the NLRP3 inflammasome.

 

 

Well, so does REV-ERB alpha! In a new study, knocking down REV-ERB alpha jacked up NLRP3 and pharmacologically enhancing it attenuated NLRP3 (Pourcet et al., 2017). The consequence of this in REV-ERB KO mice injected with LPS was hyper-inflation. No bueno. Mice given the commercially-available REV-ERB alpha agonist “Stenabolic” were protected.

I’m geeking out about REV-ERB alpha & SR9009. And fwiw, I don’t think anything will actually fully replace the benefits from actual physical activity and/or exercise, although it’s very hard for some people; eg, COPD, CHD, etc. In those populations, if they can’t exercise enough to really improve their condition, something like this might help. But I’m sure perfectly healthy people are going to try it. If you do, let us know in the comments!

For more about this fascinating research and how it can work for you (or if you just like what I do and want to support it), head over to Patreon! Five bucks a month gets you full access and there are many other options.

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UPDATED Affiliate links: 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 HERE.
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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

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Regulation of Circadian Behavior and Metabolism by Synthetic Rev-erb Agonists (Solt et al., 2013)

Rev-erb alpha modulates skeletal muscle oxidative capacity by regulating mitochondrial biogenesis and autophagy (Woldt et al., 2013)

SERcadian Rhythms

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Need vs. Optimization: Omnivores & Carnivores.

Humans are omnivores but does that mean we need to eat plants AND animals?

To address this, we first need to ask 2 questions:
1) need for what?
2) need vs. optimization?

STORY TIME

Scientists were determining the amino acid requirements of cats by feeding them semi-synthetic diets with various levels of each amino acid, one at a time. Tedious. A lot of cats x a lot of amino acids x a lot of levels of each amino acid = a lot of work. What made it even more difficult (and equally more interesting) was that they didn’t know what they were looking for — this was long before we knew what we know now about biology.

Tyrosine

Funny thing, when they got to tyrosine: below a certain level and their black cats started turning red! At an even lower level, certain neuroloogical abnormalities set in. So, how much tyrosine do cats need? Enough to maintain their beautiful black coats? I think we can all agree that the level which induced neurological abnormalities was too low. What about fur color?

 

What if female cats prefer males with beautiful black coats? So the males have a better chance at reproducing if their diet is at the higher level of tyrosine. I’d say fur color is pretty important in this #context! [how ya like ‘dem apples]

Need vs. Optimization

Note: this occurred over the course of weeks-to-months, not hours-to-days.

Note (2): unlike humans, cats are obligate carnivores. Real, actual, carnivores.

 

 

Arginine

Below a certain level of arginine and the cats looked dizzy, wobbled around, and some of them died.

Not weeks-to-months. Hours-to-days. This is what it’s like to be a carnivore. They NEED to eat meat or die rapidly (this is one of the few examples of an acute nutritional deficiency causing severe toxicity in the entire animal kingdom).

Cats have an inability to downregulate protein degradation and need arginine to dispose of the nitrogens via urea cycle. Humans just reduce burning proteins when protein intake is low.

 

 

Part 2Lobsters are omnivores and arginine is weird.

Lobster tail is rich in arginine (this might be what gives it a bit of a sweet-like flavor). If lobsters are fed an arginine-deficient diet, they go cannibal and eat other lobsters’ tails!

What does this say about lobster arginine requirements?

Need vs. optimization: they’re perfectly healthy, but is preventing cannibalism a “need?”

. .  .   .     .        .             .                     .

 

 

So, I ask again: Humans are omnivores but does that mean we need to eat plants and animals?

One retrospective study showed stroke victims who had consumed blueberries the day before showed significantly less cognitive decline post-stroke than those who hadn’t. Blueberries. Not green tea, blackberries, or dark chocolate. Blueberries. Do humans need to eat blueberries?

What if this was confirmed in a double-blind RCT? Is preventing post-stroke cognitive decline a need or an optimization?

Which is more important to you?

I didn’t have it in me to put this behind a paywall because while I think the answer is getting simpler & simpler (eg, SunlightHunger-Free Diet[s] and DietFitshot Blue-Blockers, etc.), fad diets are getting weirder & weirder. Just eat like an adult.

That’s all for now!

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Is gluconeogenesis demand-driven? answer: it depends (#context strikes again!)

Context #1. The easiest way to explain gluconeogenesis (GNG) is how it relates to starvation. If you’re not eating food, your brain still needs a steady supply of fuel. Mostly glucose at first (ketones come later), but since you’re not eating anything, glucose comes from hepatic GNG (huge potential supply*) or glycogenolysis (limited supply). *One of the precursors for GNG, glycerol, comes from stored fat (which you’ll die of something else before you run out of stored fat bc GNG).

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In this case, it is mostly true that GNG is demand-driven.

 

If you’re interested in this, more HERE.

 

Context #2. Protein (which also contains GNG precursors) doesn’t acutely increase glucose. But you might think protein does convert to glucose via GNG but protein also induces a splash of insulin which is why blood glucose doesn’t rise. Read this blog post at least up to the awesome Fromentin study: “8% of the blood glucose produced under optimal gluconeogenic conditions came from dietary protein.” But also check out the Conn & Newburgh studies. And Gannon.

 

 

This is usually the reason recreational keto dieters say they can be high protein, which either ends up looking like PSMF or it’s probably not very ketogenic (which doesn’t really matter in this #context; protein is restricted in therapeutic ketogenic diets).

#BenignDietaryKetosis #BDK

 

 

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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

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Context #3. the mouse doctor is in 🙂

Context #3b. Chronic high protein.

Context #4. Random thoughts on animal foods.

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Poor sleep, “dietary disinhibition,” and weight gain

“Dietary disinhibition”

In school, the concept was taught like this: recruit a bunch of people and tell them it’s for a cookie taste-testing project. Give them a form with a bunch of questions about cookie quality (taste, texture, sweetness, etc.) and a plate of cookies.

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SWITCHAROO!

They aren’t there for a cookie taste-test. It turns out that some people experience “dietary disinhibition” wherein if they eat one cookie, they think something like “well, I’ve blown my diet for the day, so might as well just eat the whole plate of cookies” (actually, I’m pretty sure it’s way more complicated than that, but I learned it in a nutrition class, not a psychology class).

It’s not a lot of people — most would just take a bite and fill out the questionnaire — but it’s been replicated in enough settings that it’s probably a real phenomenon.

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Intermittent fasting is nothingsauce

So Twitter got supermad when I said the human studies on intermittent fasting are not compelling. Not the anecdotes or n=1’s. The actual human studies.
And instead of “not compelling,”
I may have said “nothingsauce.”

Hilarity ensued. I was bombarded with
ALL.
THE.
ANECDOTES.

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Someone was kind enough to send me all the proof that I was wrong. Here are the 5 non-Varady studies, reviewed.

Tl;dr: as long as you’re not eating like a child, “Eating > not eating. QED.”

 

 

Alternate day calorie restriction (ADCR) improves clinical findings and reduces markers of oxidative stress and inflammation in overweight adults with moderate asthma (Johnson et al., 2006)

Study design: n=10, 8 weeks, NO CONTROL GROUP. Every other day they ate 20% of normal and ad lib the other days. This would’ve been much cooler if they included a 40% caloric restriction and weight maintenance (WM) control groups. The former to see if ADCR was superior to a similar reduction in energy intake and the latter because people behave differently when their being observed (regardless of which group they’re in) (few studies include a WM control group).

Result: body weight declined by 8%. Is that worth having nothing but a snack every other day? How about compared to 40% CR? Nothingsauce?

Oh yeah, uric acid increased and BDNF decreased. So, gout, kidney stones, and cognitive deterioration. Yummy nothingsauce.

 

The effects of modified alternate-day fasting diet on weight loss and CAD risk factors in overweight and obese women (Eshghinia et al., 2013)

Study design: similar to the above, and also lacking a control group.

Result: BW declined by 7%.

Critique: same. No control group. Would this have been better than CR or anything else? They basically just say “it’s relatively safe;” but it’s not, really… and some forms of intermittent fasting can have harmful side effects.

 

For the rest of this article (including some LOLZ & facepalming), head over to Patreon! It gets better (or worse, depending on how you look at it): metabolic mayhem, rebound hyperglycemia, some circadian chicanery #eTRF, and much more.

And stay tuned: since BDNF actually declined in the Johnson study, I’m following up with a review of intermittent fasting vs. various aspects of cognition, memory, mood, sleep, etc.

On Patreon, five bucks a month gets you full access. It’s ad-free and you can cancel if it sucks 🙂

UPDATED Affiliate links: 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 HERE.

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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.

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Isocaloric MCT-supplemented ketogenic diet may improve cognition in Alzheimer’s patients

Two-thirds of the time, it works half of the time 🙂

Yes, we all pretend to know the mechanism how ketones may improve cognition in MCI/Alzheimer’s, but we don’t. Nobody does.

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-Preferred fuel? kinda meaningless

-Niacin receptor? if so, where are the studies on niacins or even nicotinamide riboside (the latter is kind of unrelated, but should yield some niacin in vivo) (P.S. blog post on NR in the works).

-Epigenetics? Idk. Of those, I’d say probably all contribute somehow.

Ketogenic Diet Retention and Feasibility Trial #KDRAFT (Taylor et al., 2017)

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I’m not anti-keto, but I’m not anti-science.

The ketogenic diet inhibits mTOR but spares muscle. Wait, wut?

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mTOR is a key mediator of skeletal muscle growth. Primarily via stimulating protein synthesis, although some researchers are even looking for ways to activate it to prevent atrophy (eg, Dyle et al., 2014) (eg, ursolic acid & tomatidine).

Role of skeletal muscle mTOR in mechanical load-induced growth (Goodman et al., 2011)

Signaling pathways mediating muscle mass in aging skeletal muscle: role of mTOR (Sandri et al., 2013)

Mechanisms regulating skeletal muscle growth and atrophy (Schiaffino et al., 2013)

mTOR is necessary for proper satelite cell activity and skeletal muscle regeneration (Zhang et al., 2015)

 

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