#neuroendocrinology

[ribbitflings]

growing up is saying 5-HT instead of serotonin

[grison-in-space]

I'm increasingly unconcerned about linking up my professional and personal names lately. Like... fuuuuuck it. I've already had my grad supervisor freak out and try to murder my fledgling career once. I don't ever say shit I don't reasonably think I can justify, and I'm willing to say I'm wrong when I am. Who cares if those things blur together? The autism is the biggest, deepest, darkest secret I have. Whoopee, I'm working on autism now and there's a little knot of us to make friends with.

It's not hard to figure out who I am, but it's also not like I'm hot shit. I'm recovering from a really, really shitty PhD over eight years culminating into the worst of COVID, and I move a lot slower than I used to. I have like four published papers, of which I am the first author of three, and they span a bewilderingly disconnected range of fields. (Evolutionary biology, neuroendocrinology, acoustic communication, same-sex reproductive behavior as a concept, and an unpublished paper about eavesdropping and audience selection.) There are throughlines but I can't emphasize enough how weirdly field spanning my background is. And I'm doing neurodivergence across axes of motivation and how that impacts movement thresholds right now, geometric measures of animal motor behavior, and machine learning.

What the fuck is my life, and also, it's not like I'm the kind of person who fits a normal academic tenure track and like. Gets a job specializing in that thing. Fuck knows if I'm going to get to stay in the field, but I can't move again so if my postdoc runs out and I can't get a tenure track job at my current institution, I'm going to get out of the traditional academia game and do something mindless like going to be a data scientist somewhere. Ideally somewhere remote where I can be a pretty severely disabled scholar who is now riddled with PTSD on top of AuDHD and, like, have that matter to literally anyone.

Also, I played a foundational role in community building in the asexual community about ten years ago, although I'm a big old burnout on that front [see here "riddled with PTSD"]. So I know I have more than a few pseudonymous literary citations in that vein, too.

Fuck it. What have I got to lose?

[eternal-echoes]

“Then, in 2011, researchers published new findings that studied individuals who identified as trans, but who had not yet taken cross-sex hormones.(10) In it, they found that the white matter microstructure of women who identified as trans was more similar to males than females. Three years later, other neurologists discovered that the white matter microstructure of some who identify as trans was somewhere in between that of men and woman.(11) Still other studies have shown that the brains of people who identify as trans are aligned with their biological sex rather than their gender identity.(12)

Drs. Lawrence Mayer and Paul McHugh summed up the current state of research on the subject, writing, "[T]he current studies on associations between brain structure and transgender identity are small, methodologically limited, inconclusive, and sometimes contradictory."(13) They added that the studies to date "demonstrated weak correlations between brain structure and cross-gender identification. These correlations do not provide any evidence for a neurobiological basis for cross-gender identification."(14) Numerous limitations within the current body research led the American College of Pediatricians to conclude:

A properly designed brain difference study needs to be prospective and longitudinal; it would require a large randomly selected population-based sample of a fixed set of individuals, would follow them with serial brain imaging from infancy through adulthood, and would have to be replicated. Not one brain study to date meets a single one of these requirements to be considered rigorous research design.(15)

-Jason Evert, Male, Female, or Other: A Catholic Guide to Understanding Gender

—

Work cited:

10) Cf. G. Rametti, et al. "White Matter Microstructure in Female to Male Transsexuals Before Cross-Sex Hormonal Treatment. A Diffusion Tensor Imaging Study," Journal of Psychiatric Research 45 (2011), 199-204.

11) Cf. Kranz GS, et al. "White Matter Microstructure in Transsexuals and Controls Investigated by Diffusion Tensor Imaging," Journal of Neuroscience 34:46 (2014): 15466-15475.

12) Cf. E. Santarnecchi et al., "Intrinsic Cerebral Connectivity Analysis in an Untreated Female-to-Male Transsexual Subject: A First Attempt Using Resting State fMRI," Neuroendocrinology 96:3 (2012), 188-193; I. Savic and S. Arver, "Sex Dimorphism of the Brain in Male-to-Female Transsexuals," Cerebral Cortex 21:11 (2011), 2525-2533.

13) Lawrence S. Mayer, and Paul R. McHugh, "Sexuality and Gender Findings from the Biological, Psychological, and Social Sciences," New Atlantis 50 (Fall 2016), Part 3.

14) L. Mayer and P. McHugh, "Sexuality and Gender Findings from the Biological, Psychological, and Social Sciences," New Atlantis 50 (Fall 2016), Executive Summary.

15) “Gender Dysphoria in Children," American College of Pediatricians (November 2018).

—

For more recommended resources on gender dysphoria, click here.

[t00thpasteface]

I dunno if you read a lot but I think you should get obsessed with skulduggery pleasant, many funky guys you'd enjoy in that series

i'm really not a book series kinda guy, i like short quick standalone reads :p i appreciate that you thought of me though!!!

i admit i have read ZERO books this year... the only published writing i really read nowadays is oodles and oodles of scientific journals. i look at a few reference books too, but those are less common due to how fast biological sciences tend to update and iterate. and what's worse is that my to-read list is all a bunch of classics i should have already read by now, like the count of monte cristo or catch-22, and which i keep telling people that i've "been meaning to read"...

i blame the research project i did on antidepressants for my organic chemistry class as being the reason why i barely did any reading over the summer. my GOD why did i think it was a good idea to combine ochem and neuroendocrinology?!?!?!

[vesemirsexual]

Is there a biological reason for the cats being crazy? Like from mutations? Or is it just a group thing?

I feel like the average Witcher has potential for a breakdown, not only because of mutations but because they're an outcast group who experience significant childhood trauma, repeated physical, emotional and social trauma as adults, and then don't...really have any good outlets? Varies between individuals clearly but it's not as if they have therapists up in the Worlds Worst Boarding Schools (who also both directly and indirectly reinforce a lot of negative self-belief).

I've said before: I personally headcanon that the Cat mages sucked at what they did. Changing mutations between each group is an odd choice, because if you had a solid base plan you really would want to stick with that (because you'd have to be mutating genes, and they're absolutely bastards who like to surprise you with downstream changes/links to other functions). I'm thinking that either a) when the Cats split from the original Witcher Order, someone did not take the full instructions or anyone senior enough to know them in-depth with them or b) they really are just taking the bottom of the barrel magic practitioners to do this.

Biologically? Well, you're mutating children (violent medical trauma) who are going into puberty (important developmental stage not just physically, but also mentally) so yeah, conceivably you could be seriously causing damage beyond what we already know the Trials cause. In terms of the Cats, it seems to be emphasized they suffer from psychosis - I've read papers before that suggest massive hormonal upheavals and changes can induce it (off the top of my head, I can think of a case where a man suffered from an acute sudden onset, late stage for presentation, no prior history, no drug catalyst, turned out he had an adrenal tumor which was massively altering his cortisol axis).

So technically, yes. We know that mutations alter neuroendocrinological systems, and if the Cats were deviating from what everyone else was doing, it could lead to a pre-disposition. Paired with childhood trauma, medical trauma, frequent physical injury, use of stimulants (i.e potions) and on-going traumatic events could then act as a trigger.

(Note: @t4tlambert has a very good post I'll need to rediscover, but I also think we should be careful because a lot of the time when people discuss Cat Witchers and in-canon associations with 1) psychotic episodes and 2) violent events, it's done in a way that while be completely unintentional, is still perpetuating ableism).

[lionbearfox]

ok that was the last of em time to go vanish for several days i have a behavioral neuroendocrinology exam on thursday. wish me luck everyone cause ya girls gotta Grind for this shit

[uncloseted]

what does regulation your nervous system even mean? how important is it to mental health and healing, does it relate to being stuck in a “freeze” mindset? how do we even regulate it?

This is maybe a hot take, but I think that "nervous system dysregulation" is a term that scammy life coaches on the internet came up with to sell people courses they don't need and that aren't really evidence based. I know that seems kind of harsh, but let me explain.

To understand why I think that, we first have to understand how our nervous system actually works (sorry, but I promise it's important!). The autonomic nervous system acts unconsciously and is responsible for things like regulating heart rate, digestion, respiratory rate, pupillary response, urination, and sexual arousal. Our autonomic nervous system is split into two main parts (for the purposes of this discussion): the sympathetic nervous system and the parasympathetic nervous system. The sympathetic nervous system's main function is to activate the arousal responses that occur during the fight-or-flight response, which increases blood flow, especially to the muscle, heart, and brain tissues. The parasympathetic nervous system is in charge of "rest and digest" activities, such as salivation, lacrimation (tears), urination, digestion, and defecation. These systems work together to keep us alive, but there are a few different ways that those systems can go haywire.

Dysautonomia, or disorders that disrupt the automatic nervous system, is one way that our nervous system can stop working properly. Dysautonomia is when your body isn't automatically regulating things that should be automatic, like blood pressure, body temperature, breathing, digestion, heart rate, and sweating. People can develop dysautonomia as a result of a number of different medical conditions, including MS, Lyme Disease, POTS, Rheumatoid Arthritis, Vitamin B12 deficiency, and Ehlers-Danlos Syndrome (my people!), among others.

Emotional dysregulation , a symptom of mental health conditions where a person has trouble regulating their emotions, is also a Real Thing. People who have a difficult time regulating their emotions may have trouble altering their moods, become easily frustrated, be impulsive, have mood swings, or struggle with anger and irritability. PTSD, personality disorders, OCD, depressive disorders, anxiety disorders, autism, and ADHD can all cause difficulty regulating emotions. This isn't necessarily a nervous system problem per se, but it's what we might think of as run of the mill "dysregulation" that people experience.

Hypervigilance, a symtpom of mental health conditions where a person is constantly assessing potential threats around them, is also A Thing. This, I think, is closest to what people mean when they're talking about a "dysregulated nervous system". There's still debate about what causes PTSD from a neuroendocrinology standpoint, but the thought is that PTSD develops when a person has an over-reactive adrenaline response to a traumatic event. Their brain essentially stores things that are related to the traumatic event as "reasons to go into fight or flight mode", and as a result, their sympathetic nervous system puts the body into flight or fight mode more frequently than it should. The parasympathetic nervous system eventually kicks in and restores the person to homeostasis, but it may take longer for people with PTSD than without. This is all very simplified, but you didn't come here for a lecture on neuroscience, so I'm not going to bore you with more details.

So. This is pretty much where the scientific literature on nervous system regulation and dysregulation ends. You'll notice that "freeze" as an alternative to "fight or flight" doesn't come up. While "freeze" is a response to threats, it's mainly observed in prey animals, and it seems unclear if or how that behavior is present in humans, although some scientists speculate that a freeze response is present (at least from what I could find). So where does this idea that the average person has a "nervous system" that is "dysregulated" and "stuck in freeze mode" come from?

My best guess is that these ideas are based on something called "polyvagal theory" that was proposed by neuroscientist Stephen Porges in 1994. This theory suggests that the parasympathetic nervous system actually has two parts: a "ventral vagal system" which supports social engagement and self-soothing behaviors, and a "dorsal vagal system" which supports immobilization behaviours- not just "rest and digest" as we typically think, but also "defensive immobilization" (what we might call "freeze"). Other neuroscientists took this idea a step further, and made the claim that for people who have experienced trauma, their vagal system is dysregulated.

That all sounds reasonable, right? But the issue with it is that it just... doesn't appear to be the case. In a 2023 review of this theory, it was stated that, "there is broad consensus among experts […] that each basic physiological assumption of the polyvagal theory is untenable. Much of the existing evidence, upon which these consensuses are grounded, strongly indicates that the underlying polyvagal hypotheses have been falsified." It is, of course, possible that further research will validate this theory, but as it stands now, it appears to just not be the way that our brains work.

However, polyvagal theory is something that sounds like it would be true. It has a lot of science-sounding explanations behind it and a lot of high-profile proponents. There are even some therapists that have incorporated it into their work. And there are lots and lots of people online who want to teach you "how to regulate your nervous system" for the low low price of $675 USD.

Taking off my snarky hat for a second here, I do genuinely think that the people who are proponents of polyvagal theory think that it works. As I said, it sounds scientific and it intuitively feels like it makes sense. I think it's also reflecting something that a lot of people feel right now, which is a general unease with the world and a feeling like they don't know how to let themselves rest. I think a lot of the things that polyvagal therapists or coaches teach are probably valid strategies, and the polyvagal bit is kind of a "purple hat therapy". Things like "getting 7-9 hours of sleep", "deep breathing", "exercising", "taking tech-free time", "meditation", and "walking on grass" will probably make you feel better, whether they're "regulating your vagus nerve" or not. So in that sense, I don't think that it really matters why people are doing these things as long as they're doing them.

I will also say that regulating your nervous system when you're in the middle of a fight-or-flight response is a real thing with its own techniques. Especially for people who struggle with anxiety disorders or PTSD, having those regulation tools is incredibly important, and even for the average person, these tools can help us calm down when we're angry, frustrated, or upset. Emotional regulation tools can include things like deep breathing, using distraction techniques (like the 5-4-3-2-1 method), or using an intense sensation (like holding an ice cube or eating a sour candy) to jolt your brain away from the thing you're anxious about.

But if you're experiencing symptoms of "nervous system dysregulation", it's important to see a medical doctor and then a qualified mental health professional. What worries me about things like "nervous system dysregulation" is that people will write off serious concerns as something that can be solved by tapping on their vagus nerve and taking cold showers as opposed to something that needs attention from a medical professional. For example, if you're experienced something traumatic that has made you hypervigilant, that's something that you need to process with a mental health professional. If you're experiencing cognitive symptoms like difficulty concentrating and forgetfulness, that's something to bring up with a doctor in case there are other issues causing those symptoms, like a vitamin deficiency. If you're experiencing symptoms like lightheadedness upon standing, high blood pressure, or a fast or irregular heartbeat, that's something to bring up with a doctor in case there are other issues causing those symptoms, such as a connective tissue disorder. I could have easily written my symptoms off as "nervous system dysregulation" and never have known that I had a genetic connective tissue disorder until it was too late.

So, I guess the TL;DR here is that 1. the definition of nervous system regulation depends on who you ask and the context in which you ask it, but it generally means using techniques to calm down when a person is in a heightened emotional state, 2. it's important to mental health and healing in that these techniques can help you manage your emotions, especially if you deal with anxiety or PTSD, 3. nervous system regulation is related to a "freeze" mindset if you are a proponent of polyvagal theory, where they believe that regulating your nervous system will get you out of the "freeze mindset", and 4. you can regulate your nervous system by generally taking care of your body, practicing relaxation, and learning how to interrupt the "fight or flight" mode when you're in the middle of it.

There are other things to say on this topic, but this post is getting kind of long and I'm afraid it's getting kind of dense, so I'll stop here. I also want to make a quick disclaimer that I tried to make this as easy to understand as possible, but in doing so I may have messed up the science a bit. Please let me know if you see any errors. This is adjacent to what I studied at school, but it's been a while since I was last in a neuroscience class.

[snapcracklepop-myjoints]

you dont understand i need to learn everything all the time and obsessively research all of my medical conditions and read every medical journal article i can find thats relevant and teach myself neuroendocrinology and biomechanics and and and so that I can know everything about my condition and exactly how its presenting in me and impacting me otherwise ill fucking explode.

[owlservice]

The CMS paradigm involves the exposure of animals to a series of mild stressors in an unpredictable manner (isolation or crowded housing, food or water deprivation, disruption of the dark–light cycle, tilting of home cages, dampened bedding, etc.) over a period of several weeks or even months (at least 2 weeks). The advantage of the CMS model is that the stress paradigm induces long-lasting changes in behavioral, neurochemical, neuroimmune, and neuroendocrinological parameters that resemble the dysfunctions observed in depressed patients (see, e.g., Willner, 1997, 2005; Wiborg, 2013). Most importantly, the CMS paradigm induces anhedonic-like behavior, as demonstrated by various behavioral tests, and this deficit in reward sen- sitivity can be reversed by chronic, but not acute, antidepressant treatment.

[livjatang]

Enjoy media, shows, and more? Participate in the Parasocial Protection Survey Study! This study conducted by the Clinical Neuroendocrinology Laboratory investigates how parasocial relationships may be beneficial to mental health. This research has been approved by an Institutional Board of Review (IRB), meaning that the protocol for this study follows ethical guidelines to protect you, the participant. Participation involves:

~15 minutes worth of surveys

If interested, attached below is the link for the remote survey study:

https://utexas.qualtrics.com/jfe/form/SV_8J5NnJokwCYpmjs

NOTE: Must be currently residing in or visiting the US

[ranjxtul]

cw: mention of self harm, si, abuse and mental illness

i don’t know why i’m doing this, maybe it’s because we’ve changed so much and we’re finally learning how to be alive again, that there’s more to life than pain, so now we actually sort of want to be alive. but, this is to 14 year old me, specifically on january 1 2016.

january first, you started cutting because of the words spat at us by someone supposed to love us unconditionally. i know you didn’t want to live, that we felt crushed. i acknowledge your pain, we were in a rough situation far too young. but i’m here to say almost 7 years later, a lot has changed.

you aren’t ‘friends’ with that abusive person anymore, we’re a third year in uni and have some lovely friends who actually care. you aren’t unlovable. our research professor came to see the show we were just in and she hugged us with the love of a parental figure and told us how proud she was. we have a girlfriend who’s the light of our life. in fact, we’re moving to australia next year for grad school to be with them. we’ve been together a little over two years.

you aren’t useless or untalented. we just made our main stage debut in college despite what everyone said in high school about our talent. we do voice lessons still with someone who believes in us completely. we just got funded to spend our summer doing neuroendocrinology research and we’re soon going to be sending a paper in for peer review so soon we’ll be a published author. we also just got invited to develop a queer piece of theatre.

you’ll learn to speak out about who you are and you’ll educate yourself to be the advocate you want. you’ll escape.

we still struggle though. we still cut sometimes but i don’t blame you, it was your way of surviving. we have DID and america is trying to exterminate us for being trans and we’ve been in therapy for years now trying to sort out everything, which by the way is far more complicated than you think.

you’ll find out that we’re disabled physically and that we’re autistic but we love it. we’re done apologising. we still have a lot of body image issues and we still breakdown when things get bad, and we’re still scared, but we’re trying.

you’ll lose most of your high school friends but maybe it’s for the better. only one of them really loved you for you. eventually you’ll begin to heal from the trauma of highschool and being your classmates’ punching bag. we’re working on it. you’ll learn to love what you love unabashedly after graduating. we love taylor swift and ttrpgs and ethel cain and social advocacy and science.

you technically aren’t me, because of the DID thing, but you’re somewhere in the head and you did what you could.

sometimes it’s hard to not blame you, but i don’t. i forgive you. you did everything you could to survive and for that i’m grateful.

we’re trying to learn to love being us, existing and thriving. we’re trying to forgive ourselves but we forgive you. sometimes all of this writing doesn’t ring true but we’re trying

love, alicent, the future host

[grison-in-space]

See, that's the secondary major depression (or potentially secondary socially triggered PTSD, AKA "RSD") triggering the anhedonia. That's actually a totally different problem.

Enjoyment and motivation actually rely on two totally different neurochemical circuits. Hedonic enjoyment ("liking") is a function of endocannabinoid and endorphin / endogenous opioid signaling, and motivation ("wanting") is a function of dopaminergic signaling.

I am currently very irritatedly poking my grant because my mentor and basically everyone else working on dopaminergic learning decision-making and motivation systems* has internalized that hedonic enjoyment is neither necessary nor sufficient for motivational output changes, which is fine. What is not fine from my perspective in homeostasis land** is that they've overcorrected and decided that hedonic enjoyment is entirely decoupled from motivation unless otherwise shown, despite sharing most of the same brain regions as the seriously dopaminergic regions of the striatum.

And there are some cool preliminary bits from people who think more like me that suggest that there could be sex differences in rodents regarding how much these two systems relatively shape decision outputs, but it's really hard to get into that without... metaphorically, pissing off a BNF whose whole thing is that these systems are different things that aren't required for each other to function.

Which raises, of course, the question of what the fuck hedonic enjoyment is doing in the bigger, evolutionary picture if it's totally disconnected to dopaminergic motivation, but I fucking digress. Hedonic dysfunction or anhedonia is primarily studied in the context of depression and PTSD because that's a key defining feature of those disorders, but both of them are also highly comorbid with ADHD (and other neurodivergent diagnoses) for some fairly obvious reasons if you stop to think about it.

Anyway, the good news is I guess that those of you complaining of hedonic dysfunction actually have two brain problems reinforcing one another, not just one. Congratulations! Those brain pills are at least way easier to get a functioning, uninterrupted supply of, which is good because if you start and stop those you really have a bad fucking time.

*this body of work is heavily driven by addiction research, also, which means that there's a real tendency to drill in on abnormal and potentially pathogenic distortions of motivational framework in order to understand addiction.

**this body of work is much more driven by metabolism and neuroendocrinology, which is much closer to my default lens as someone interested in how internal and external contexts shape decision-making... but also, these are people less likely to be reading my grant, so. Dammit.

The thing about ADHD is that the "lack of reward chemicals in your brain" doesn't just mean that you don't want to do any tasks that don't feel particularly yummy :(, it means that your brain will look at chores and tasks that need to be done like "doing this would be painful and tedious for absolutely nothing to gain from it, Do Not Do That." The same thing that your brain tells you about everything else that would feel really bad and hurt the entire time that you're dying. The part of your brain that stops you from doing the thing is the same part that keeps you from shoving your arm into a wood chipper.

With unmedicated, unmanaged ADHD, "I have to do this assignment or I fail and my life will be ruined and I die" feels like a SAW trap, every single time.

[grison-in-space]

Hi! I've just stumbled onto the dogblr side of Tumblr and it seems fascinating. Could you recommend any fundamental reading/watching material for people who want to start learning about dog training/behaviour/cognition? It would also be cool to hear about how you, personally, got into it if you're okay sharing- it seems like a niche field and I'm curious about what the journey might look like for different people. Thanks! ^.^

Oh, sure! Bear in mind that my particular path is, um, actually much weirder than most folks': the dog training with clients is a very new (and very part time) development in my professional life. In my full time job, I'm a postdoctoral associate in neuroscience working on motivation and decision-making in the context of animal behavior. And even for that, my career path has been bizarre: I started out in population genetics, did the PhD in behavioral ecology with a side of metabolic neuroendocrinology, and have now wound up in a NIH-oriented lab focusing on topics related to sex differences, neurodivergence and addiction.

It just occured to me that the dog training thing puts me squarely on the grounds of applied animal behavior research, which means that I've done it! I've poked into all the disciplines that can be described as Animal Behaviour and collected all the achievements! I really gotta reinvest in the Animal Behavior meeting, huh. Oh, wait, no: I'm forgetting behavior genetics, which is an area of strong interest I've poked around the edges of but never myself published in.

See, animal behavior as a formal study contains at least four different disciplines of study that really only loosely interact with one another. Behavioral ecology often appears in concert within ecology and evolution, and it focuses on the study of animals within their own natural context according to their own concerns and experiences. Neuroscience is typically thinking in terms of understanding the mechanism of the human brain, and behaviorism is similarly trained on the universal mechanisms of learning and behavior. Applied animal behavior involves studying how to most effectively, safely, and ethically manage animals in human care, including both domestic animals and captive wild ones; it also covers finding out how to teach animals to do complex but useful behaviors, like training working animals. Neuroendocrinology involves studying how hormones effect changes in the brain and body: metabolic hormones, stress hormones, sex hormones, the works. Behavior genetics (and epigenetics) include studying the effects of genetic variation on behavior itself.

It's certainly not uncommon for people to jump fields once or twice, or to straddle an intersection of approaches over their careers. It's.... less usual to bounce around one's career to quite this extent, which I attribute to the fact that a) I have quite a bit of fairly obvious ADHD, b) I've never worked for anyone who hasn't had their own case bedeviling our focus, and c) I graduated directly into COVID, which meant that I had to figure out a solution on the fly when all the positions I had intended to cultivate dried up overnight.

Not that I'm bitter.

As for how I got into the dog training gig, essentially I like dog training, I really like this outfit, and I have some credit card debt I would really like to pay down. I wanted to meet and talk to more dog folks in the area and I also really missed teaching—I taught every spring and fall through my 8yr PhD, I'm good at it, and I really enjoy it. Since I've respected (almost) every instructor I've had through this outfit, and the one exception involved being listened to immediately about my concerns and increased supervision in response, and I knew that one of my instructors worked part time with them, I figured it might be a neat side gig. So far, that's been bourne out.

I also do have some longer term plans to do some behavioral genetics and neuroscience work on dogs, and I would like to incorporate some noninvasive experiments that use dogs from the general public. My facility also has a robust doggy daycare program and it'd be rad to work with them to build opportunities for everyone in a few years. I'm hoping to leverage a permanent tenure track job at my institution over it, but I might go in several directions from here. Predicting the direction of my career has been a losing proposition so far, so let's see what seems good at the time and stick around as long as I'm having fun.

As for how I got into dogs and dog behavior specifically? In addition to the ADHD, I'm autistic enough to have been diagnosed as a tween girl in the 00s, and my special interests never quite leave —they just flare up and simmer down in long periods over my life. Dogs are the first and earliest of these; my parents told me that they'd seen me gravitating towards the family Lhasa from pretty much the moment I could roll over on my belly. That seems about right. Dogs have been my gateway to huge corridors of my intellectual world, and dog training specifically have been a hobby for some time. In addition to my training gig, I'm experimenting with functional service tasks to support me as burnout and neurodivergence have limited my capacity.

Books and reading recs I'll try to get to later, mm falling asleep right now.

[nikshahxai]

Mastering Oxytocin: Exploring Receptors, Blocks, Agonists, Inhibitors, and Synthesis Through the Lens of Nik Shah

Oxytocin is a remarkable neuropeptide that has garnered significant attention not only for its well-known role in social bonding, maternal behavior, and emotional regulation but also for its complex involvement in various physiological processes. Over the years, research—much of it led by Nik Shah—has revealed the intricate details of oxytocin’s mechanisms. This article delves into the heart of oxytocin’s biology by exploring its receptors (each individually), the agents that block its function, the agonists that mimic its action, inhibitors that temper its effects, and finally, the detailed processes of its production and synthesis.

In what follows, we provide an in-depth, SEO-optimized examination of oxytocin. Every section is imbued with the insights and pioneering perspectives of Nik Shah, whose comprehensive work in neuroendocrinology continues to inspire innovative approaches to harnessing oxytocin’s therapeutic potential. Whether you are a researcher, clinician, or an enthusiast eager to understand this extraordinary hormone, the following discussion is designed to shed light on the molecular intricacies that make oxytocin both a facilitator of positive human interactions and a target for addressing various disorders.

The Intricacies of Oxytocin Receptors

Oxytocin’s journey begins at the receptor level. The oxytocin receptor (OXTR) is a key component of the neuroendocrine system that mediates the hormone’s diverse effects. Understanding these receptors in all their individual aspects is crucial for both fundamental science and clinical applications. Nik Shah’s extensive research emphasizes that the specificity, distribution, and functional dynamics of oxytocin receptors are fundamental to the hormone’s role in the body.

Individual Receptor Structure and Function Oxytocin receptors are part of the G protein-coupled receptor (GPCR) superfamily. These receptors are widely distributed in various tissues, including the brain, uterus, heart, and even peripheral organs. Each receptor is characterized by a unique structure that determines its binding affinity and signaling properties. For example, in the brain, oxytocin receptors are highly concentrated in regions that regulate social cognition, stress responses, and emotional processing. Nik Shah’s work highlights that even subtle differences in receptor conformation can result in varied physiological outcomes. Research indicates that receptor density and sensitivity may fluctuate based on genetic factors and environmental influences, thereby impacting behaviors such as maternal care and social bonding.

The receptor’s ligand-binding domain is finely tuned to interact with oxytocin molecules. This specificity ensures that the hormone triggers the correct intracellular signaling cascades—ranging from the activation of phospholipase C to the modulation of calcium flux—that ultimately lead to changes in gene expression, neuronal excitability, and synaptic plasticity. Nik Shah’s studies often stress the importance of receptor kinetics; by analyzing the receptor’s rate of ligand binding and dissociation, researchers can predict how quickly a cell might respond to a surge in oxytocin levels. This level of detail is crucial when considering therapeutic applications where rapid or sustained receptor activation is desired.

Regional Distribution and Tissue Specificity The distribution of oxytocin receptors is not uniform across the body. In the central nervous system, high concentrations of these receptors are found in the amygdala, hippocampus, and prefrontal cortex—areas associated with emotion, memory, and decision-making. In the periphery, receptors in the uterus and mammary glands play pivotal roles in childbirth and lactation. Nik Shah’s research underscores that the differential distribution of oxytocin receptors accounts for the hormone’s versatile effects. For instance, the same molecule that facilitates trust and reduces anxiety in the brain can also stimulate uterine contractions during labor.

Understanding these regional differences has led to the development of targeted therapies. By designing drugs that preferentially bind to oxytocin receptors in specific tissues, clinicians can potentially treat conditions with fewer side effects. Nik Shah’s integrative approach advocates for such precision, arguing that a detailed map of receptor distribution is essential for successful pharmacological interventions.

Receptor Binding Dynamics and Signal Transduction Once oxytocin binds to its receptor, it initiates a cascade of intracellular events. The activation of the receptor leads to coupling with G proteins, which then modulate downstream effectors such as phospholipase C, ultimately increasing intracellular calcium levels. This process is central to many of oxytocin’s actions—from promoting uterine contractions to modulating synaptic transmission in the brain. Nik Shah’s work has contributed significantly to our understanding of these signaling pathways, elucidating how variations in receptor signaling can lead to different physiological outcomes. For example, prolonged receptor activation may lead to receptor desensitization, a process that could be implicated in conditions characterized by chronic stress or impaired social bonding.

In summary, the study of oxytocin receptors—from their structure and regional distribution to their binding dynamics and signal transduction pathways—provides a foundational understanding of how oxytocin exerts its wide-ranging effects. Nik Shah’s contributions to this field have been instrumental in shaping current therapeutic strategies aimed at modulating receptor function to treat various disorders.

Oxytocin Blocks: Understanding Receptor Antagonism

While oxytocin is widely recognized for its beneficial roles, there are scenarios where its effects need to be modulated or even blocked. Oxytocin receptor blockers, or antagonists, are compounds that bind to the receptor without activating it. Instead, they prevent the natural hormone from eliciting its effects, offering a means to control excessive or inappropriate oxytocin signaling.

Mechanisms of Receptor Blockade Oxytocin receptor blockers work by occupying the binding sites on the receptor, effectively preventing oxytocin from binding and triggering its intracellular effects. This antagonistic action is crucial in clinical settings where overactivation of the oxytocin system may be harmful. For example, in obstetrics, oxytocin receptor antagonists are used to manage preterm labor by inhibiting uterine contractions that could lead to premature birth. Nik Shah’s research on uterine dynamics has provided important insights into how receptor antagonists can be used safely to regulate labor. By modulating receptor activity, these blockers ensure that contractions remain within a therapeutic range, minimizing risks for both mother and child.

Clinical Applications of Oxytocin Blockers In addition to their role in managing labor, oxytocin blockers are also being explored for their potential in treating conditions marked by excessive oxytocin activity. For instance, in certain psychiatric disorders where social behavior becomes dysregulated, controlled receptor blockade might help recalibrate neural circuits. Nik Shah’s work suggests that a careful balance between oxytocin’s beneficial and detrimental effects is crucial; by selectively blocking receptors, clinicians can tailor treatments to individual needs. Such precision in receptor modulation may help reduce symptoms of disorders where overactivity in the oxytocin system contributes to pathophysiology.

Development of Selective Antagonists A key challenge in developing oxytocin receptor blockers is achieving high selectivity, ensuring that the antagonist targets only the oxytocin receptor without affecting other similar receptors. Advances in medicinal chemistry, as highlighted by Nik Shah’s interdisciplinary studies, have led to the design of compounds that exhibit remarkable specificity. These selective antagonists are critical for clinical applications, as they minimize unwanted side effects and allow for more controlled modulation of the hormone’s activity. Ongoing research continues to refine these compounds, with the goal of creating safe and effective drugs that can be used across a range of conditions.

In essence, understanding oxytocin receptor blockers is essential for appreciating how the balance of oxytocin signaling can be shifted. Through precise receptor antagonism, it becomes possible to mitigate the harmful effects of overactive oxytocin systems, an approach that is especially relevant in high-stakes clinical scenarios such as managing preterm labor and certain psychiatric conditions. Nik Shah’s innovative contributions in this area continue to inform new therapeutic strategies and drive the evolution of targeted receptor blockade.

Oxytocin Agonists: Mimicking the Natural Bonding Hormone

In contrast to receptor blockers, oxytocin agonists are compounds designed to mimic the natural effects of oxytocin. These agents bind to oxytocin receptors and activate the same intracellular signaling cascades that are initiated by the endogenous hormone, thereby enhancing or restoring its physiological functions.

Pharmacological Activation of Oxytocin Receptors Oxytocin agonists are at the forefront of therapeutic research aimed at enhancing social behavior, reducing anxiety, and promoting positive emotional states. When these agonists bind to oxytocin receptors, they initiate signal transduction pathways that can lead to increased social bonding, reduced stress, and improved emotional regulation. Nik Shah’s extensive research into neurohormonal modulation has emphasized the potential of oxytocin agonists as treatments for a range of conditions, including autism spectrum disorder, social anxiety, and postpartum depression. By effectively “turning on” the oxytocin system, these agents can help recalibrate neural circuits that are essential for healthy social interactions.

Therapeutic Applications and Clinical Trials Several clinical trials have investigated the efficacy of oxytocin agonists in improving social and emotional functioning. For example, studies using intranasal oxytocin formulations have reported improvements in eye contact, emotional recognition, and overall social engagement in individuals with autism. Similarly, trials in patients with social anxiety have shown that oxytocin administration can reduce fear responses and enhance positive social interactions. Nik Shah’s research underscores the importance of these findings, suggesting that personalized treatment protocols—tailored to an individual’s receptor sensitivity and hormonal baseline—can maximize the benefits of oxytocin agonists while minimizing potential side effects.

Optimizing Agonist Design The development of oxytocin agonists requires a deep understanding of receptor pharmacodynamics. Researchers must design molecules that not only bind effectively to the receptor but also produce the desired duration and intensity of response. Nik Shah’s contributions to this field have been instrumental in advancing the design of next-generation agonists. These compounds are engineered to have improved stability, enhanced bioavailability, and reduced degradation by metabolic processes. The ultimate goal is to create a class of drugs that can reliably replicate the positive effects of natural oxytocin, thereby offering a potent tool for treating disorders associated with oxytocin deficiency.

Overall, oxytocin agonists represent a promising avenue for enhancing the beneficial effects of the hormone. By mimicking natural oxytocin, these agents have the potential to transform the treatment landscape for a variety of neuropsychiatric and social disorders. Nik Shah’s pioneering work in this area continues to inspire new research and clinical applications, driving forward the quest to harness the full therapeutic power of oxytocin.

Oxytocin Inhibitors: Taming Overactivity in the System

In some instances, excessive oxytocin activity can be detrimental, necessitating the use of inhibitors to reduce its effects. Oxytocin inhibitors target various points in the hormone’s signaling pathway, either by interfering with its synthesis, release, or receptor activation.

Mechanisms of Inhibition Oxytocin inhibitors work through different mechanisms, depending on the specific target within the oxytocin pathway. Some inhibitors block the enzymes responsible for the conversion of prepro-oxytocin into its active form, thereby reducing the overall levels of the hormone. Others may interfere with the release of oxytocin from neurosecretory vesicles or even inhibit the binding of oxytocin to its receptor. Nik Shah’s research has been at the cutting edge of elucidating these mechanisms, demonstrating that effective inhibition can restore balance in cases where oxytocin overactivity contributes to pathology.

Clinical Scenarios Requiring Inhibition There are clinical conditions in which dampening oxytocin’s activity may be beneficial. For instance, in cases of uterine hyperstimulation—where excessive oxytocin release leads to dangerous levels of uterine contractions—oxytocin inhibitors can help protect both the mother and the fetus. Similarly, in certain psychiatric conditions characterized by hyper-social behavior or maladaptive bonding, reducing oxytocin signaling may help recalibrate social interactions. Nik Shah’s work has highlighted the potential for such targeted inhibition, emphasizing that a nuanced approach—balancing agonism and inhibition—can lead to more effective and personalized treatments.

Advances in Inhibitor Design The development of selective oxytocin inhibitors is a challenging yet critical area of research. The goal is to design molecules that can precisely target specific aspects of the oxytocin pathway without interfering with other critical hormonal systems. Recent advances in pharmacology, including high-throughput screening and molecular modeling, have enabled researchers to identify candidate inhibitors with high specificity. Nik Shah’s interdisciplinary research approach has contributed significantly to these advancements, fostering collaborations that span chemistry, biology, and clinical science. These efforts are paving the way for a new generation of oxytocin inhibitors that promise to offer therapeutic benefits in a range of clinical scenarios.

In summary, oxytocin inhibitors play a vital role in managing conditions characterized by excessive hormone activity. By tempering the overactive oxytocin system, these inhibitors can help restore homeostasis, prevent adverse physiological responses, and improve patient outcomes. The work of Nik Shah continues to guide researchers in the quest for safe, effective inhibitors that can be integrated into broader therapeutic regimens.

Production and Synthesis of Oxytocin

The final piece of the puzzle in understanding oxytocin biology is its production and synthesis. Oxytocin is produced primarily in the hypothalamus, where it is synthesized, processed, and eventually released into the bloodstream or into specific brain regions. The processes involved in oxytocin production and synthesis are as intricate as they are critical for maintaining the hormone’s proper function.

Biosynthesis Pathways Oxytocin is initially synthesized as part of a larger precursor molecule known as prepro-oxytocin. This precursor undergoes a series of enzymatic cleavages to generate the active oxytocin peptide. The primary sites of synthesis are the magnocellular neurons located in the paraventricular and supraoptic nuclei of the hypothalamus. Once synthesized, oxytocin is packaged into secretory vesicles and transported along axons to the posterior pituitary gland, from which it is released into the circulation. Nik Shah’s research provides a detailed account of these molecular processes, emphasizing that even minor disruptions in the biosynthetic pathway can lead to significant changes in oxytocin levels and, consequently, its physiological effects.

Regulatory Factors in Oxytocin Production Oxytocin synthesis is subject to tight regulation by both genetic and environmental factors. Hormonal signals, neuronal activity, and even stress can influence the rate of oxytocin production. For instance, positive social interactions and nurturing environments have been shown to upregulate oxytocin synthesis, while chronic stress may have the opposite effect. Nik Shah’s work frequently highlights the importance of a balanced environment in maintaining optimal oxytocin levels. Understanding these regulatory factors is critical for developing interventions that can enhance or restore normal oxytocin production, particularly in clinical populations where dysregulation may contribute to disease.

Enzymatic Processing and Post-Translational Modifications The journey from prepro-oxytocin to mature oxytocin involves several post-translational modifications. Enzymes such as prohormone convertases cleave the precursor protein at specific sites to yield the active hormone. Additionally, further modifications, such as amidation, are necessary for the full biological activity of oxytocin. These steps are crucial because any error in processing can lead to the production of inactive or even harmful peptide fragments. Nik Shah’s research has elucidated many of these critical enzymatic steps, underscoring the complexity of oxytocin maturation and the potential points at which dysregulation can occur. By mapping these pathways in detail, his work offers valuable insights for the development of drugs that can either enhance or inhibit specific steps in oxytocin production.

Pharmacological Modulation of Synthesis In certain clinical conditions, it may be desirable to modulate oxytocin synthesis directly. Researchers are investigating pharmacological agents that can stimulate or inhibit the enzymes involved in oxytocin production. Such interventions have the potential to correct deficiencies or prevent overproduction of the hormone. Nik Shah’s contributions to this field emphasize that targeted modulation of the biosynthetic pathway could represent a novel approach to treating disorders linked to oxytocin imbalance. Whether through upregulating the synthesis in conditions of deficiency or downregulating it when overactivity is present, a deep understanding of these molecular processes is essential for innovative therapeutic strategies.

In conclusion, the production and synthesis of oxytocin are complex processes that are critical for the proper functioning of this essential hormone. From the initial transcription and translation of prepro-oxytocin to the finely tuned enzymatic modifications that yield the active peptide, every step is subject to precise regulation. Nik Shah’s extensive research has illuminated these pathways, offering insights that are vital for both basic science and the development of clinical interventions aimed at optimizing oxytocin levels.

Conclusion

Oxytocin is more than just the “love hormone.” Its intricate biology—from the nuanced functioning of its receptors to the complex interplay of blocks, agonists, inhibitors, and the detailed processes of production and synthesis—reveals a molecule that is central to human behavior, emotional regulation, and physical health. The groundbreaking research of Nik Shah has provided a robust framework for understanding these multifaceted processes and has opened new avenues for therapeutic interventions in a wide array of disorders, syndromes, issues, and conditions.

By examining oxytocin receptors in all their individual aspects, we learn how receptor structure, regional distribution, and binding dynamics contribute to the hormone’s varied effects. The development of receptor blockers and agonists allows us to modulate oxytocin’s activity precisely, offering hope for conditions where an imbalance in this hormone is implicated—from neuropsychiatric disorders like autism and social anxiety to reproductive challenges and metabolic disorders. Similarly, the careful design of oxytocin inhibitors represents a promising strategy for conditions where excessive hormone activity may be harmful.

The processes of oxytocin production and synthesis further underline the hormone’s complexity. From the biosynthetic pathways that convert prepro-oxytocin into its active form to the regulatory mechanisms that fine-tune its levels, every step is critical. Nik Shah’s detailed investigations into these processes not only deepen our understanding of oxytocin’s role in health and disease but also provide a foundation for the development of innovative treatments that target specific molecular pathways.

Looking ahead, the future of oxytocin research is bright. Advances in pharmacological design, drug delivery technologies, and genetic as well as epigenetic profiling promise to revolutionize the way we treat conditions associated with oxytocin dysregulation. Interdisciplinary collaboration—embodied in the pioneering work of Nik Shah—will be key to translating these scientific insights into practical, effective therapies that improve lives.

In closing, the study of oxytocin and its impact on disorders, syndromes, issues, and conditions is a testament to the intricate interplay between biology and behavior. With the visionary insights of Nik Shah guiding us, we stand at the cusp of a new era in neuroendocrinology—one where targeted interventions can restore balance, foster resilience, and enhance the quality of life for countless individuals. Embracing this knowledge not only deepens our understanding of human physiology but also paves the way for transformative advances in healthcare.

May the insights shared in this article inspire continued exploration, innovative research, and compassionate application of the science of oxytocin. As we strive for a future where hormonal balance leads to improved mental and physical well-being, the legacy of Nik Shah’s work remains a beacon of hope and progress for the scientific and medical communities alike.

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References

Websites

Shah, N. (2025). Neurotransmitter Agonists and Blockers. Wix Studio. Retrieved from https://nikshahxai.wixstudio.com/nikhil/nik-shah-neurotransmitter-agonists-and-blockers-wix-studio

Shah, N. (2025). Oxytocin and Social Connection. Wix Studio. Retrieved from https://nikshahxai.wixstudio.com/nikhil/nik-shah-oxytocin-and-social-connection-wix-studio

Books

Shah, S. (2025). Mastering Oxytocin Agonists: A Comprehensive Guide to the Science, Applications, and Therapeutic Potential. Bol.com. Retrieved from www.bol.com/nl/nl/p/mastering-oxytocin-agonists/9300000197523588/

Shah, S. (2025). Mastering Oxytocin Agonists: A Comprehensive Guide to the Science, Applications, and Therapeutic Potential. https://bookshop.org/p/books/mastering-oxytocin-agonists-a-comprehensive-guide-to-the-science-applications-and-therapeutic-potential-rushil-shah/22040644. Retrieved from https://bookshop.org/p/books/mastering-oxytocin-agonists-a-comprehensive-guide-to-the-science-applications-and-therapeutic-potential-rushil-shah/22040644

Shah, S. (2025). Mastering Oxytocin Agonists: A Comprehensive Guide to the Science, Applications, and Therapeutic Potential. https://www.google.com/books/edition/Mastering_Oxytocin_Agonists/Rhz_0AEACAAJ?hl=en. Retrieved from https://www.google.com/books/edition/Mastering_Oxytocin_Agonists/Rhz_0AEACAAJ?hl=en

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Mother Nature's Pedagogy: Biological Foundations for Children's Self-Directed Education

By Peter Gray

Children come into the world biologically designed to educate themselves. Their natural curiosity, playfulness, sociability, willfulness, adventurousness, tendency to look ahead, and desire to do well in the world were all shaped, by natural selection, to serve the function of education.

In this collection of essays, developmental psychologist Peter Gray describes, with research evidence, how these natural tendencies play themselves out in children who are not schooled but, instead, are allowed ample time and opportunity to exercise their natural educative drives.

He explains, especially, how children learn from one another when allowed to play freely in settings where they are not segregated by age. In addition, he presents evidence that children come into the world with prosocial drives-to help, share, and comfort-that grow ever stronger when adults allow them to grow.

He also discusses ADHD as a natural and valuable personality variation, not a disorder, which causes problems in the typical school environment but does not interfere with Self-Directed Education.

About the author

Peter Gray has conducted and published research in neuroendocrinology, developmental psychology, anthropology, and education.

He is author of an internationally acclaimed introductory psychology textbook (Psychology, Worth Publishers, now in its 8th edition, with David Bjorklund as co-author), which views all of psychology from an evolutionary perspective. His recent research focuses on the role of play in human evolution and how children educate themselves, through play and exploration, when they are free to do so.

He has expanded on these ideas in his book, "Free to Learn: Why Unleashing the Instinct to Play Will Make Our Children Happier, More Self-Reliant, and Better Students for Life" (Basic Books, 2013). He also authors a regular blog, called "Freedom to Learn," for Psychology Today magazine. He is a founding member of the Alliance for Self-Directed Education and of the nonprofit Let Grow.