Tag Archives: calories proper

Intermittent fasting is homeopathy-level #nothingsauce

From all of the published human studies and “n=1’s” I’ve seen on online forums, intermittent fasting is #nothingsauce. Don’t @ me.

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When people lose weight via IF, it’s because of caloric restriction. There’s no metabolic advantage, and if anything, maybe the opposite. Restricting your feeding window to a very short period = metabolic mayhem.

2000 kcals in one sitting?

*smh*

 

 

I believe “early Time-Restricted Feeding” #eTRF showed promise in that recent study because of the “early” part; no so much on the “TRF” part. I believe this, in part, because the large majority of our population suffers from some degree of circadian arrhythmia. Social jet lag, too much artificial light at night, skipping breakfast, etc., etc. An EARLIER feeding window is one way to re-align circadian rhythms.

 

 

It STARTS with Sleep. Wanna improve body comp and make mindlessly better food choices? Fix your circadian rhythms.

Now onto the one of the weirdest, but potentially most revealing human studies on time-restricted feeding…

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The influence of ketones on intermediary metabolism

Two studies: one on infusion of D-b-hydroxybutyrate at three different level producing up to 2 mM at the highest level (Mikkelsen et al., 2014); and one on ingestion of a ketone monoester (R-3-hydroxybutyl-R-3-hydroxybutyrate) producing ~3.2 mM (Myette et al., 2018). Both studies were relatively small (n = 6 and 20, respectively) yet interesting.

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Mikkelsen: mainly justified the use of exogenous ketones in T2DM because of their ability to suppress hyperglycemia and hyperlipidemia. And justified ’em in CNS disorders because adherence is poor in this population and goes downhill with increasing disease severity. They’re anti-ketone salts because: 1) the GI distress and salt load with doses required to get into the 2-3 mM range; and 2) they’re often racemic mixtures of D- and L-b-hydroxybutyrate (“D” is the endogenous one).

 

 

As expected, increasing the infusion dose linearly increased plasma bHB:

Further, as expected, brain uptake increased in parallel to plasma levels:

Interestingly, muscle uptake seemed to become saturated and not increase much further… this may be related to the “muscle-sparing effect of fat-derived fuels,” in other words, muscle is sparing ketones for the brain like it does during late starvation.

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ketones inhibit lipolysis

 

 

 

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Glucose dynamics during prolonged fasts

This is a somewhat complicated level of metabolism. Which tissues are producing what & how much, what are they burning & how much, etc., etc…

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After a few weeks, things begin to level out — we’ll pick it up there. Much of this is from a class I TA’d for in grad school, this book, and all the Cahill studies.

 

 

“The rate of glucose use at this time is around 90-100 g per day [remember, this is starvation, so all of that glucose comes from gluconeogenesis]. Of that, about 40 g is recycled via the Cori and glucose-alanine cycles and the remainder is ‘new’ glucose, ~18 g from glycerol and ~45 g from amino acids.”

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Metabolism of starvation/fasting =/= low carb diet

The Biology of Starvation (intro)

The Biology of Starvation: Renal Gluconeogenesis

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One of the major [obvious] differences in metabolism between fasting and low carb dieting is nitrogen metabolism… because you’re eating protein on a low carb diet, not so much while fasting. During fasting/starvation your body tries to downregulate the urea cycle because you can’t really afford to be ‘wasting’ amino acids/protein. I bet you never thought about the muscle-sparing effect of fat-derived fuels like that!

 

 

“Glucose production in starvation” is important because you need to make all of it and reduce the use of it.

 

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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.

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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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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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Context #3. the mouse doctor is in 🙂

Context #3b. Chronic high protein.

Context #4. Random thoughts on animal foods.

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Light & melatonin: timing is everything

This is kinda like circadian rhythms’ second Nobel Prize. Technically it was LED lights back in 2014, but if you don’t see the connection, I have failed.

Suggest pre-readings: Melatonin sensitizes the system and LIGHT timing for circadian entrainment

Melatonin plays a pivitol role in circadian entrainment. Literally thousands of papers published about it every year.

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THIS IS WHY YOU NEED BLUE BLOCKERS: A single night light exposure acutely alters hormonal and metabolic responses in healthy participants (Albreiki et al., 2017)

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The Struldbrugs of Luggnag

Intermittent fasting (in mice)

Every-other-day feeding extends lifespan but fails to delay many symptoms of aging in mice.

 

THIS IS BASICALLY THE WORST POSSIBLE OUTCOME

 

The Struldbrugs of Luggnag

 

 

Tl;dr: they’re immortal, but just keep getting older and older and it sucks. It’s basically the exact opposite of what we want, which is something akin to eternal youth.

 

 

This paper was a Giant.

 

Brief background: they were testing a model of intermittent fasting known as EOD, or ad libitum access to food every other day. It’s hard to relate this directly to humans because one mouse day is probably about at least 5 human days… although similar to humans, when chow time comes around, we tend to eat a lot. REFEED MAYHEM.

[rant]
It’s like that dude who takes a pic of 3 big steaks and posts it online, saying “dinner is served, bro” …trying to make it seem like they eat that way normally, ~3x/d, when in reality they’ve been intentionally restricting food intake all day to create a big enough energy deficit to accommodate said steaks… #CICO

P.S. as far as circadian rhythms and dietary protein requirements are concerned, this way of eating isn’t doing you any favors…
[end rant]

 

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Ketosis in an evolutionary context

Humans are unique in their remarkable ability to enter ketosis.  They’re also situated near the top of the food chain.  Coincidence?

During starvation, humans rapidly enter ketosis; they do this better than king penguins, and bears don’t do it at all.

Starvation ketosis

 

Starvation ketosis

Humans maintain a high level of functionality during starvation.  We can still hunt & plan; some would even argue it’s a more finely tuned state, cognitively.  And that’s important, because if we became progressively weaker and slower, chances of acquiring food would rapidly decline.

Perhaps this is why fasting bears just sleep most of the time: no ketones = no bueno..?

Observation: chronic ketosis is relatively rare in nature. This doen’t mean animals evolved a protective  mechanism against ketosis.

 

 

Animals with a low brain/carcass weight ratio (ie, small brain) don’t need it. Babies and children have a higher brain/carcass weight ratio, so they develop ketosis more rapidly than adults. Is this a harmful process? No, more likely an evolutionary adaptation which supports the brain.

ketones age

The brain of newborn babies consumes a huge amount of total daily energy, and nearly half comes from ketones.  A week or so later, even after the carbohydrate content of breast milk increases, they still don’t get “kicked out of ketosis” (Bourneres et al., 1986).  If this were a harmful state, why would Nature have done this?  …and all those anecdotes, like babies learn at incredibly rapid rates… coincidence?  Maybe they’re myths.  Maybe not.




 

Ketosis in the animal kingdom

Imagine a hibernating bear: huge adipose tissue but small brain fuel requirement relative to body size and total energy expenditure.  No ketosis, because brain accounts for less than 5% of total metabolism.  In adult humans, this is around 19-23%, and babies are much higher (eg, Cahill and Veech, 2003Hayes et al., 2012).

 

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Low carb, low glycemic index, or something else entirely

Why Low Carb?

OmniCarb (Sacks et al., 2014)

Study design & results in a nutshell:

5 weeks, low(ish) vs. high carb (40 vs. 58%) with the calorie difference split between protein (23 vs. 16%) and fat (37 vs. 27%).  In other words, the low(ish) carb diet was higher in protein and fat.  And there was 2 versions of each diet —  a high and low glycemic index.  Lots of crossing over; all in all, weak intervention but decent study design & execution.

Aaaand nothingsauce nothingburger.  Goal was insulin sensitivity, not weight loss.

 

glucose and insulin

 

 

 

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