3 ms·

In biology a single causation is almost always wrong, especially in correlation between such distant phenomena - neurotransmitter and conditioned behavior. Well

In biology a single causation is almost always wrong, especially in correlation between such distant phenomena - neurotransmitter and conditioned behavior. Well, excess of serotonin could lead to "anxiety" and physical discomfort from a slightest external pressure, as it seems to be with Asperger's, but it is a mere correlation, if correct at all, not a causation. Socially conditioned behavior is way more subtle and complicated phenomena than mere neurochemistry.

_delirium 11y ago
Yes, the paper [1] is fairly careful to point out that this is studying a neurotransmitter pathway's association with social anxiety disorder, which might be useful information in later establishing etiology, but doesn't do so on its own. Their causal hypothesis is actually (if I'm reading it correctly) the reverse of the direction people are assuming from the headline: [other physical features of] social anxiety disorder may cause excessive serotonin production, which may in turn produce additional symptoms, rather than excessive serotonin production being the root cause. That is, unusual upregulation of some pathways involving serotinin sits more towards the end of a causal chain than at its beginning. (Some of these causal chains are more like feedback loops, though, which makes it extra difficult to sort out what constitutes a root cause.) From the paper: > Although we cannot test causal effects in the present study, we speculate that, because raphe nuclei serotonin 1A autoreceptors exert inhibitory feedback on serotonin synthesis and firing, downregulation of inhibitory raphe serotonin 1A autoreceptors previously reported in social anxiety and panic disorder leads to increased serotonin synthesis, and augmented reuptake may be a compensatory mechanism. [1] http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711 http://archpsyc.jamanetwork.com/article.aspx?articleid=23197...

_delirium 11y ago

Yes, the paper [1] is fairly careful to point out that this is studying a neurotransmitter pathway's association with social anxiety disorder, which might be useful information in later establishing etiology, but doesn't do so on its own. Their causal hypothesis is actually (if I'm reading it correctly) the reverse of the direction people are assuming from the headline: [other physical features of] social anxiety disorder may cause excessive serotonin production, which may in turn produce additional symptoms, rather than excessive serotonin production being the root cause. That is, unusual upregulation of some pathways involving serotinin sits more towards the end of a causal chain than at its beginning. (Some of these causal chains are more like feedback loops, though, which makes it extra difficult to sort out what constitutes a root cause.) From the paper: > Although we cannot test causal effects in the present study, we speculate that, because raphe nuclei serotonin 1A autoreceptors exert inhibitory feedback on serotonin synthesis and firing, downregulation of inhibitory raphe serotonin 1A autoreceptors previously reported in social anxiety and panic disorder leads to increased serotonin synthesis, and augmented reuptake may be a compensatory mechanism. [1] http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711 http://archpsyc.jamanetwork.com/article.aspx?articleid=23197...