6 ms·

Are the authors ignorant of the renin-angiotensin-aldosterone system? Vasopressin reduces altruistic behavior in empathetic people. Cortisol clasically raises v

Are the authors ignorant of the renin-angiotensin-aldosterone system? Vasopressin reduces altruistic behavior in empathetic people. Cortisol clasically raises vasopressin. Autism is characterized by low regulatory APVR2 (vasopressin receptor 2) function, leading to high baseline vasopressin and issues staying hydrated

cinntaile 4y ago
If you research something specific, it doesn't necessarily mean you're oblivious to other things. They might just be outside of the scope of your research.
- Khelavaster 4y ago
  Exactly. Problematic when "lurking variables" with strong correlated effects (like vasopressin activity in this study) are of scope.
thomas536 4y ago
Re hydration Do you have any good reading on that link? Searched just now and there's a lot to wade through to find a good article
- tomatowurst 4y ago
  does he mean the body doesn't hydrate properly, or produce saliva? or water bottles?
  - chownie 4y ago
    Maybe lack of a thirst urge, which would match my autistic experience.
  - Khelavaster 4y ago
    I mean that the body most won't respond to signals to reabsorb water from the bladder because of weak QVPR2 activity. AVPR2 only shows up (significantly) in the kidneys. It pumps water back from the bladder to the bloodstream. AVPR1 and AVPR3 show up in the brain (and drive/control any hormonal response tied to water availability/quality/safety-to-access. Including territorial mammals marking territory.) Vasopressin is actually a mirror-image of oxytocin, with a few hundred million years of divergent mutations. Unique to mammals. That's why mammals are the only vertebrates that independently, separately, regulate water and ions. (Thus, sweating, lactation, crying, uncalcified placenta vs egg, etc.) So the brain keeps pumping out vasopressin (in response to dehydration-induced corticotropin-releasing factor). This leads to water "running right through". And high baseline vasopressin levels that go even higher with dehydration. Less commonly, especially for men, the body overreacts to vasopressin. Excessive vasopressin 2 receptor efficacy or transcription leads to low baseline vasopressin. Low vasopressin 'magnifies' any oxytocin activity. Leads to "human-hyperstimulated" autism and high innate trust in unfearful situations. Also often leads to low territory/spatial mapping capacity. This is what we're talking about.
- Khelavaster 4y ago
  A. Research dates back to the 90s. Thousands of researchers have added their perspectives. B. Look at what vasopressin does, in humans and other mammals. C. Consider that Vasopressin Receptor 2, is right by the X pseudoautosomal region, so is mutated 15x-20x more frequently. Compare how often you've seen other pseudoautosomal differences in people with Vasopressin transcription differences. Or just start searching for random genes from around the pseudoautosomal region + autism. Transcription differences in one pseudoautosomal gene are so closely tied to differences in others, you see a very unusually high number of correlations between autism-uninvolved genes and autism. (Just as so many genes around TNF-alpha/6p21.3 are spuriously tied to autoinflammatory issues; major histocompatibility complex issues; tenascin-X-tied disorders including Ehlers-Danlos; and 17-hydroxysteroid-dehydrogenase-8 variance [which deactivates androgens+estrogens, and synthesizes moderate estradiol]. Or how so many genes near the adjacent corticotropin-releasing-hormone-receptor-1 (CRHR1) and Tau protein (MAPT), in the same area as DNA-repair-gene breast-cancer-associated1 (BRCA1), are spuriously tied to irrecoverable oxidative cell damage and neurodegeneration.) C...Some very important pseudoautosomal genes include the final stage of melatonin synthesis (ASMT & ASMTL); antiviral and anti-small-pathogen signal receptors, for interleukin 9 and interleukin 3; SPRY3 lymphoid-to-myeloid switch granulocyte-macrophage colony stimulating factor (GM-CSF); cytokine-like-receptor 2 (CLRF); glycogenin 2 (starting-point for muscle fibers); steroid sulfatase (activates androgens, estrogens, progestogens); sex receptor Y and protocadherin-11-Y (PCDH11Y) in men [causing heritable father-to-daughter changes in protocadherin-11-X and near-adhacent androgen receptor]. D. Also, check out the research from the last head of the Kinsey Institute. They hired her for that vasopressin+oxytocin triggers pair-bonding, and monogamy in monogamous mammals. e.g. "Oxytocin and Vasopressin Circuits in Context of Love and Fear", from the 'Vasopressin System in Behavior' edition of Frontiers in Neuroendocrinology: https://www.frontiersin.org/articles/10.3389/fendo.2017.00356/full https://www.frontiersin.org/articles/10.3389/fendo.2017.0035... "Opposite effects of oxytocin and vasopressin on the emotional expression of the fear response" https://www.sciencedirect.com/science/article/abs/pii/S0079612308004184 https://www.sciencedirect.com/science/article/abs/pii/S00796... Dune's Fremen are stellar thought-experiments of vasopressin-driven folks who feel strong oxytocin boosts in their own homes/territory.
JamesBarney 4y ago
If they had high levels of baseline vasopressin, shouldn't this make it easier to stay hydrated because it increase the amount of fluid reabsorbed by the kidneys?
- whatshisface 4y ago
  Not if the high levels were an incomplete response to very low receptor performance. Biochemical signaling pathways are a mixture of negative-feedback systems that do not assume anything about the sensitivities of each receptor (because in a pure feedback system the signal would be amplified until it activated the receptor sufficiently) and "level-interpreting" (I don't know the actual term) systems where each concentration communicates a specific semaphore-like claim and if the downstream receptor does not match the sender, it will get the message wrong. One simple case where the second phenomenon arises is when the production of the signalling compound is prevented, by the finite ability of the cell to make it, from rising to the levels that would agonize the downstream receptor enough to achieve whatever the cell was going for.
  - JamesBarney 4y ago
    That makes sense.

cinntaile 4y ago

If you research something specific, it doesn't necessarily mean you're oblivious to other things. They might just be outside of the scope of your research.

Khelavaster 4y ago
Exactly. Problematic when "lurking variables" with strong correlated effects (like vasopressin activity in this study) are of scope.

thomas536 4y ago

Re hydration Do you have any good reading on that link? Searched just now and there's a lot to wade through to find a good article

tomatowurst 4y ago
does he mean the body doesn't hydrate properly, or produce saliva? or water bottles?
- chownie 4y ago
  Maybe lack of a thirst urge, which would match my autistic experience.
- Khelavaster 4y ago
  I mean that the body most won't respond to signals to reabsorb water from the bladder because of weak QVPR2 activity. AVPR2 only shows up (significantly) in the kidneys. It pumps water back from the bladder to the bloodstream. AVPR1 and AVPR3 show up in the brain (and drive/control any hormonal response tied to water availability/quality/safety-to-access. Including territorial mammals marking territory.) Vasopressin is actually a mirror-image of oxytocin, with a few hundred million years of divergent mutations. Unique to mammals. That's why mammals are the only vertebrates that independently, separately, regulate water and ions. (Thus, sweating, lactation, crying, uncalcified placenta vs egg, etc.) So the brain keeps pumping out vasopressin (in response to dehydration-induced corticotropin-releasing factor). This leads to water "running right through". And high baseline vasopressin levels that go even higher with dehydration. Less commonly, especially for men, the body overreacts to vasopressin. Excessive vasopressin 2 receptor efficacy or transcription leads to low baseline vasopressin. Low vasopressin 'magnifies' any oxytocin activity. Leads to "human-hyperstimulated" autism and high innate trust in unfearful situations. Also often leads to low territory/spatial mapping capacity. This is what we're talking about.
Khelavaster 4y ago
A. Research dates back to the 90s. Thousands of researchers have added their perspectives. B. Look at what vasopressin does, in humans and other mammals. C. Consider that Vasopressin Receptor 2, is right by the X pseudoautosomal region, so is mutated 15x-20x more frequently. Compare how often you've seen other pseudoautosomal differences in people with Vasopressin transcription differences. Or just start searching for random genes from around the pseudoautosomal region + autism. Transcription differences in one pseudoautosomal gene are so closely tied to differences in others, you see a very unusually high number of correlations between autism-uninvolved genes and autism. (Just as so many genes around TNF-alpha/6p21.3 are spuriously tied to autoinflammatory issues; major histocompatibility complex issues; tenascin-X-tied disorders including Ehlers-Danlos; and 17-hydroxysteroid-dehydrogenase-8 variance [which deactivates androgens+estrogens, and synthesizes moderate estradiol]. Or how so many genes near the adjacent corticotropin-releasing-hormone-receptor-1 (CRHR1) and Tau protein (MAPT), in the same area as DNA-repair-gene breast-cancer-associated1 (BRCA1), are spuriously tied to irrecoverable oxidative cell damage and neurodegeneration.) C...Some very important pseudoautosomal genes include the final stage of melatonin synthesis (ASMT & ASMTL); antiviral and anti-small-pathogen signal receptors, for interleukin 9 and interleukin 3; SPRY3 lymphoid-to-myeloid switch granulocyte-macrophage colony stimulating factor (GM-CSF); cytokine-like-receptor 2 (CLRF); glycogenin 2 (starting-point for muscle fibers); steroid sulfatase (activates androgens, estrogens, progestogens); sex receptor Y and protocadherin-11-Y (PCDH11Y) in men [causing heritable father-to-daughter changes in protocadherin-11-X and near-adhacent androgen receptor]. D. Also, check out the research from the last head of the Kinsey Institute. They hired her for that vasopressin+oxytocin triggers pair-bonding, and monogamy in monogamous mammals. e.g. "Oxytocin and Vasopressin Circuits in Context of Love and Fear", from the 'Vasopressin System in Behavior' edition of Frontiers in Neuroendocrinology: https://www.frontiersin.org/articles/10.3389/fendo.2017.00356/full https://www.frontiersin.org/articles/10.3389/fendo.2017.0035... "Opposite effects of oxytocin and vasopressin on the emotional expression of the fear response" https://www.sciencedirect.com/science/article/abs/pii/S0079612308004184 https://www.sciencedirect.com/science/article/abs/pii/S00796... Dune's Fremen are stellar thought-experiments of vasopressin-driven folks who feel strong oxytocin boosts in their own homes/territory.

JamesBarney 4y ago

If they had high levels of baseline vasopressin, shouldn't this make it easier to stay hydrated because it increase the amount of fluid reabsorbed by the kidneys?

whatshisface 4y ago
Not if the high levels were an incomplete response to very low receptor performance. Biochemical signaling pathways are a mixture of negative-feedback systems that do not assume anything about the sensitivities of each receptor (because in a pure feedback system the signal would be amplified until it activated the receptor sufficiently) and "level-interpreting" (I don't know the actual term) systems where each concentration communicates a specific semaphore-like claim and if the downstream receptor does not match the sender, it will get the message wrong. One simple case where the second phenomenon arises is when the production of the signalling compound is prevented, by the finite ability of the cell to make it, from rising to the levels that would agonize the downstream receptor enough to achieve whatever the cell was going for.
- JamesBarney 4y ago
  That makes sense.