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When Grasshoppers Go Biblical: Serotonin Causes Locusts To Swarm

  1. I wonder if that's why some cyberbullies suddenly get so nasty sometimes. Sometimes they are in group, so cowardly, it's awful. The worst is the passive-aggressiveness, when they don't even want to take responsibility for their behavior. See that everywhere, and it's no surprise with what people put in their bodies.

    Some anti-serotonin substances increase my aggression but it's reactive. Makes me less docile.
  2. I don't remember if this has been posted before, but I do know Haidut talked about this on a podcast with Danny Roddy. Regardless, it's worthy of bringing back up.
  3. Seratonin causing them to be gregarious, more social and stronger? Am I missing something here?
  4. *crickets*
  5. So it seems like serotonin has a social status-seeking response? At least in locusts and lobsters
  6. Could someone with a scientific bent talk a little more about this please. I’m finding myself a bit confused and at odds with what the studies seems to be implying, and what the general consensus is on here about seratonin.
    Thanks guys.
  7. What are you missing? Excess Serotonin turn peaceful grasshoppers into swarming, angry, murderous destructive locusts that will destroy everything in their path, including each other. The article describing this destructive, murderous gang as "more social" and "gregarious" is disingenuous, at the very least.
  8. Is that not beneficial? Furthering the line of the grasshopper species is pretty good for grasshoppers. And outcompeting intraspecial males is good for the male ones.

    Just take a look at human pre-bronze age history. There were a couple of very lucky guys living on the planet 50k years ago, as virtually all men today are descended from them.
  9. Why only men? All women today are descended from them too then.
  10. Because men can father thousands of sons, but women can only mother ~30 daughters.

    To be clear, I'm refering to Y DNA haplogroups here, not autosomal DNA.
  11. It is only "beneficial" for survival and only under very stressful circumstances, by killing off everybody else that competes for limited resources. It is is not at all beneficial for health, and even if those males end up reproducing more their offspring will be in worse health than their fathers. In times of relative abudance, the "locust" phenotype has been shown to be highly avoided by females and can quickly lead to elimination of that specific overstressed gene pool. So, not exactly a good mating strategy. Btw, the only reason those locust males managed to reproduce to start with is because they either killed off all other males so the females had no other option, or because the males forced copulation.
    Also, just because scarcity happens every once in a while naturally does not mean we should artificially reproduce the phenotype that it engenders (locust) by prescribing serotonergic drugs or creating artificial scarcity so people can maul each other over food or whatever other resource has been made scarce. Contrary to popular opinion, evolutionary complexity and intelligence regresses under stress and progresses under abundance. A "locust" is not going to come up with a way to fly to the stars, but a "grasshopper" might. Stressed = dumb, plain and simple. Do you think that is truly beneficial?
    Leisure And Desire Required For Intelligence, Knowledge And Progress
  12. Well I don't disagree with anything you've said. But the fact remains that resources are finite, and certain realities real, and in many cases across space and time, some individuals don't have the option of leisurely living.

    This more or less mirrors the rough phenomenon of r/k selection (you can argue to what extent this is genetic, it doesn't really matter). But there's a reason yellow jackets are so successful, while paper wasps are less so, and mud daubers almost impossible to encounter.

    I view it as a degenerated state of existence, but just as thermodynamic heat death will win in the end, the degenerated/dominance oriented/aggressive will always be the majority within the small privileged pocket of life (which is already a rarity).
  13. By all means, as I said in my post as well, in times of scarcity it probably pays off to be a powerful, brutal, formidable, adversary. All I am saying is that we should not be aiming to artificially reproduce scarcity (if there is none naturally) just to stimulate that competitive, brutish behavior on purpose as if it would lead to something good. While it may be very good for short term survival eventually it leads to reverse evolution and potentially even a die-off event (in the human version things World War, civil war, disease epidemic, etc).
    If there is natural scarcity, then so be it. But to reproduce it (and its serotonergic phenotype) artificially is pathological behavior, at least to me. That's what the SSRI drugs do.
  14. I agree. I was referring to the inevitable reality of animal life and human civilization.
  15. and that phenotype is going to see scarcity (zero sum; a finite pie) where there is none--like a self-fulfilling prophesy--attrits his/her environment and desecrates anything good right before them.
  16. Very true.
  17. So, if I got these articles correctly, it must be very similar mechanism as caloric restriction?
    Chronic food restriction in young rats results in depression- and anxiety-like behaviors with decreased expression of serotonin reuptake transporter
    [Edit: Fixed link, was wrong article]
    SERT slows down through whatever mechanism, including possible 5-HT1x autoreceptor downregulation.

    I imagine past a certain threshold of SERT inhibition, serotonin build-up in that state (net positive synthesis), and one of the 5-HT2x (or even 5-HT3?) receptors becomes triggered, and then you have swarming?

    It leads me to wonder if maybe avoiding Tryptophan is half-pointless (not counting the Kynurenine pathway) if you simply have enough SERT activity to compensate... is there anywhere where this has been quantified?

    At the same time now I wonder, in starvation, at what stage does tissue Tryptophan become so low as to make serotonin synthesis drop under SERT's clearance rate (effectively preventing swarming)?...

    I could have gotten this wrong, but I can't see what else would make sense
  18. Good point. Usually, sufficient salt in the diet prevents excess serotonin from accumulating. SERT is a sodium dependent protein.
    As far as tissue tryptophan - at least in mammals it never goes too low. It is part of muscle tissue, so as long as the mammal has some muscles left there will be enough tryptophan to synthesize as much serotonin as needed. Not sure how it works in insects but I don't think they run a risk of becoming tryptophan deficient either. Just like us, food availability for them increases SERT activity and reverts them back to normal, civilized creatures.
  19. Thanks for that tidbit about sodium, had completely forgotten about that. (Well also not having disregulated cortisol - fixed the link in my post, mentions it - since acute cortisol increases SERT but chronic compromises it - posted link in another thread [Edit: here])

    I kinda have to take your word on the tissue breakdown... I figured there must be some extreme... i.e. past the point where the organism has any fight left
  20. You could run this experiment: You starve control mice and mice administered p-chrolo-whatever-the-TH-inhibitor-is-again, and you record their activity until they die (Auschwitz for mice... is this evil yet?). The p-chloro mice would die faster (while having more fight in them), but you should still be able to deduce something from their progression...
  21. To clarify, the way I imagine this, is that the SERT-inhibition-triggered buildup may be just the first in one or more food restriction adaption responses that promote increased activity... Because both for locusts swarming and that caloric restriction study, the circumstances don't seem to me to be that extreme. So perhaps past a second point in starvation, something else promotes increased activity?

    Here's one of several possible mechanisms:
    Kynurenic acid is a nutritional cue that enables behavioral plasticity

    Since kynurenine pathway modulates feeding in lower organisms, there could be something similar or derived in higher-level organisms. I figure maybe serotonin is an extra adaptation to the threat of scarcity on top of the kynurenine pathway, for survival of higher organisms? But they may still work in tandem.

    So if you remove serotonergic influence, you're still left with the possibility of lowered kynurenic acid and increased quinolinic acid (the latter only to some extent or possibly caused by B vitamin deficiency?), which should trigger increased desperation and food search...

    So I wonder in parallel, past a further point of deprivation, what exactly happens to serotonin, compared to kynurenine (or other signal)...

    (Also note in that study the "neuropeptide-y-like" pathways (due to low KYNA), not sure how conserved that is in mammals - I still have to read more, always more, and more - but that is possibly a crucial link)
  22. And that brings up another point, which is that the Kynurenine pathway (via TDO) has been thought to account for much more Tryptophan consumption than the serotonin pathways... in part to go toward NAD production... So what if the tissue breakdown Trp all goes toward Kyn/NAD? [Or is it tissue-local enough to bypass this issue?]

    [Edit: Yet another complication: a major TDO inducer in the liver is cortisol, which is clearly going to be high and can only get lower if hormone synthesis dies off - but I don't currently know what happens to that induction if the glucocorticoid receptors becomes insensitive vs sensitive, assuming it does for that - it's probably described somewhere...]