BCAA’s Impact Health And Lifespan Indirectly Via Amino Acid Balance And Appetite

Mito

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“Elevated branched-chain amino acids (BCAAs) are associated with obesity and insulin resistance. How long-term dietary BCAAs impact late-life health and lifespan is unknown. Here, we show that when dietary BCAAs are varied against a fixed, isocaloric macronutrient background, long-term exposure to high BCAA diets leads to hyperphagia, obesity and reduced lifespan. These effects are not due to elevated BCAA per se or hepatic mammalian target of rapamycin activation, but instead are due to a shift in the relative quantity of dietary BCAAs and other amino acids, notably tryptophan and threonine. Increasing the ratio of BCAAs to these amino acids results in hyperphagia and is associated with central serotonin depletion. Preventing hyperphagia by calorie restriction or pair-feeding averts the health costs of a high-BCAA diet. Our data highlight a role for amino acid quality in energy balance and show that health costs of chronic high BCAA intakes need not be due to intrinsic toxicity but instead are a consequence of hyperphagia driven by amino acid imbalance.”

Branched-chain amino acids impact health and lifespan indirectly via amino acid balance and appetite control | Nature Metabolism
 

whit

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Are they supplamenting BCAA or just looking at elevated levels in the blood?

Since when was serotonin suppression a bad thing?
 

CLASH

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I couldnt access the ful study but its looks like a hypothesis as opposed to an actual study. It seems that theyre combining a bunch of assumed positions to create this hypothesis:

Elevated BCAAS lower serotonin-> lowered serotonin increases appetite-> increased appetite means increased calories-> increased calories means obesity (calories in/ calories out)-> increased obesity means increased morbidity and mortality

I think this would be very difficult to prove.

I think @Mito posted it specifically to show you can lower central serotonin using BCAA.
 

whit

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I couldnt access the ful study but its looks like a hypothesis as opposed to an actual study. It seems that theyre combining a bunch of assumed positions to create this hypothesis:

Elevated BCAAS lower serotonin-> lowered serotonin increases appetite-> increased appetite means increased calories-> increased calories means obesity (calories in/ calories out)-> increased obesity means increased morbidity and mortality

I think this would be very difficult to prove.

I think @Mito posted it specifically to show you can lower central serotonin using BCAA.
That's how it seemed.
I think you are correct.
I've found BCAA to be a good tool for recovery.
Thanks for the clarification.
 
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I couldnt access the ful study but its looks like a hypothesis as opposed to an actual study. It seems that theyre combining a bunch of assumed positions to create this hypothesis:

Elevated BCAAS lower serotonin-> lowered serotonin increases appetite-> increased appetite means increased calories-> increased calories means obesity (calories in/ calories out)-> increased obesity means increased morbidity and mortality

I think this would be very difficult to prove.

I think @Mito posted it specifically to show you can lower central serotonin using BCAA.
This has actually been proven to be false by another study that showed that serotonin antagonists such as cyproheptadine increase lifespan by 20-30%. It is well known that serotonin antagonists increase hunger, and I think the increased hunger is a sign of vitality. Indeed, the assumption that eating more leads to weight gain is a necessary( and false) assumption that is needed to build the hypothesis that low serotonin( and, consequently, things that lower it) is bad. Considering that weighing too little is also bad, we have another benefit of lowering serotonin: avoidance of cachexia or tissue wasting.
 

magnesiumania

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Obesity is nothing but blue light toxicity as leptin is a photoreceptor detroyed by fake light. So many metabiloc aspects are linked to your light environment. Like b12 deficiency which is nothing but lack of strong UV that modulate it aswell as folate.
 

Astolfo

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Serotonin depletion > loss of 5ht2c activity > hyperphagia, obesity.

Lorcaserine (5ht2c agonist) is an anti obesity drug.
Prozac, a weak 5ht2c antagonist is associated with increased appetite in some cases. (Not all, because it's also a SSRI)

5ht2c, mainly its active subtypes (mrna) supress hunger. Also positively regulates hps axis, directly! I guess, the study is true. But can we use BCAA as a short-term recovery tool from hyperphagia? (Caused by overedited 5ht2c receptors) (pssd?)

@boris
 

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