Is obesity primarily mediated by deficiencies in GABA, GABA transmission and/or GABA reception?
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In other words, are most cases of obesity caused by GABAergic factors, such as:

  • insufficient quantities of the neurotransmitter GABA, or

  • too much reabsorption of GABA, or

  • GABA receptors not responding to GABA?

I am planning to write a paper on this hypothesis (unless someone disproves it in the comments).

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Why haven't I heard of people on benzos losing lots of weight?

Do you intend this in the sense of "GABA plays a leading role in mediating the interaction between [hyperpalatable food / increased food availability / changing food nutrient composition / ...] and obesity" or "obesity is specifically caused by something impacting GABA, and not by the modern diet"?

predictedYES

@jacksonpolack That's a good point. I guess I'm not as much of a warrior for unicausal theories of the obesity epidemic as the Slime Mold Time Mold bloggers are, so I wouldn't go so far as to say that e.g. hyperpalatable food plays no role - but equally, I don't think it plays as big of a role as people seem to think. So I don't really mean either of those things - I mean something closer to "while a bunch of different things may impact GABA, GABA is at the nexus of all the most important causes of obesity" or "At the level of human physiology, GABA is the most important causal factor behind the obesity epidemic".

Hm, why do you think that, if you don't mind giving a summary?

I think there’s more of a story occurring between anxiety and appetitive-motivational-signaling with ghrelin than gaba.

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