okay, so the long and the short of it is real long and also fairly identifying with respect to my career, so this is all going under cut.
during my phd, I got really interested in condition-dependence for sexual signaling. people frame this thing as an index of good genes, but I was really skeptical of the idea that genetic quality was necessarily all that strong a signal to perpetuate female choice. there's just too much randomness in individual experience for that to be all that strong a signal. I thought that condition dependence made more sense as, basically, a great way to partition resources depending on how much you have overall--kind of like a luxury good vs. a basic staple.
so I spent a lot of time thinking about how bodies self-assess their overall resource levels, which is how I got into metabolic signaling. The thing about metabolism and self-perception of overall energetic resources is that carbohydrate metabolism and fatty acid metabolism exist as.... not totally parallel systems, but they more or less act along their own pathways. So I did a bunch of work poking at carbohydrate and adipose metabolism blockers to try to get at self-perception of resource levels without modifying actual resource levels. That's how I got into the whole thing. Blockers didn't work super well for me, in part because most of them hadn't been touched in like thirty or forty years and in part because bodies use a whole bunch of indices to determine resource levels. So I moved on to poking at endogenous resource availability signals.
I specifically did some work with leptin, which was a much-bandied about "cure for obesity" when it was initially discovered about thirty years ago as a 'satiety hormone.' Unfortunately, beyond a certain threshold point, adding more leptin to the system doesn't stop feeding behavior/motivation/whatever, so the weight loss industry more or less dropped it as a focus. Most of the work with leptin research focuses on it in terms of this "threshold" above which it doesn't change feeding behavior.
Except that if you artificially manipulate leptin to increase leptin levels on a free-feeding animal, I found that you get more investment in social behavior/sexual signaling than if you just inject saline. And I found all kinds of systems leptin has a finger in the pie for: depression, bone density, reproductive investment, and especially immune challenge. Ah, Greg Demas over at University of Indiana has done some incredibly fascinating work on leptin and broader adipose signaling, more people should read his shit. Especially the stuff with hamsters, which have some interesting modifications that allow them to basically treat their hoards in the same ways that other animals handle fat depositions. No idea how, but it's wildly cool.
Fat is generally distributed in specific pads, especially in rodents--humans tend to sort of distribute ours through some of our muscle tissue in addition to our own fat pads--and it has both cis-acting and trans-acting hormonal functions as an endocrine organ in its own right. That's right: adipose tissue produces endocrine signals that the body needs in order to understand what its overall resource capacity is. Some of these signals are clearly cis-acting: for example, if you remove the epididymal fat pad that hangs out near the testis from a rodent, that testicle will no longer be able to produce sperm until and unless the fat pad regenerates (which it will do if you leave a tiny bit left). It does not help to have the same fat pad available subcutaneously under the back--it's not about how much fat the animal has--it's about how much of that fat pad is available right by that testis.
The thing about metabolic signaling and the hypothalamus more generally is that our endogenous hormones often regulate a whole bunch of systems at once. Take glucocorticoids--that's cortisol in humans--which psych and pure behavior folks tend to gloss as "stress hormones." In fact these are also wildly important hormones that control our insulin production, which is why perpetually elevated levels of same will slowly kill your insulin receptors and result in metabolic dysfunction. (Well, at high levels--at shorter levels, if you're stressed out all the time, maybe it's better to not move as much and retain more body fat, forage a bit less. After all, moving around is a great way to get noticed by something that thinks you're delicious.)
The other thing about metabolism, digestion, and motivation to eat or forage is that most things are pretty cheap, metabolically speaking. The harder I looked at costs of these elaborated sexual traits, the more I found that those costs tended to be the result of other actors in the ecological space: being overheard or perceived either by other members of your species that you didn't want to perceive your signal, or else being eaten by a predator. Most of these signals are actually not that metabolically expensive in terms of actually producing tissues or organs or displays.
So it occurred to me a long time ago that "calories in, calories out" is probably a pretty bad index of how an animal chooses to maintain its resources on an ongoing basis. Extra adipose tissue has obvious costs to haul around, and if resources are abundant, why bother? Studies like the Vermont Prison Overfeeding Study (in which prisoners were asked to gain 25% of body fat, maintain it for 10 weeks, and then try and lose it again--and did so very easily) and Leibold, Rosenbaum, and Hirsch 1995 (which found that people 10% under their normal set point burned energy much more slowly, and people 10% above that set point burned energy much faster--even when measuring just plain resting metabolic rate) convinced me that it was probably more tricky than that.
uh, this is already quite long so I will leave it at that, but basically:
-we also know that the secretions of satiation-inducing hormones like ghrelin change based on how we expect to feel after consuming a food: foods labeled 'diet' that we have learned to associate with unsatisfying experiences result in less ghrelin secretion, even as compared to the same food item with a different label
-orexin, like leptin and the glucocorticoids, is clearly connected to not only sleep and satiety but also to stress response and pain signaling
I forget if I had anything else to say, but here's everything I got off the dome.
2087
kianamaiart
vaporwave
izzy806
stormborns
gummygunk
