Hmmm.. having been on an SSRI (at the time I was depressed) and suffering from a mild to middling social anxiety disorder (which stems from a chronic childhood one which lessened as I reached my mid 20's), for me SSRI's made me feel indestructible and fearless. But they also made me feel like I had no emotions at all and removed sexual desire and affected pleasure, so I stopped taking them and instead dealt with the causes of my depression. I still get bouts, but I have a mechanism in place to handle the symptoms and they mostly dissipate. That coupled with an ability to separate/compartmentalise personal and work life (as in, they just don't cross over in my mind), a lot of the stress I feel is only in the parts of my day when I am in the section of my life that I'm having issues with.<p>The human brain is wonderful.<p>So in short - I don't think I fully believe what they have found. I think the problem is that the extra Serotonin papers over the cracks well enough to work for most people. So, maybe my experience is just due to the fact it made me relax and that was the reason for my issues in the first place? Who know, I'm not a doctor. All I know is that more Serotonin felt better than less at the time.
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.
>> Previous studies have led researchers to believe that individuals with social anxiety disorder or social phobia have too low levels of the neurotransmitter serotonin. A new study, however, shows that the situation is exactly the opposite.<p>It's stuff like this that is destroying the reputation of science in general. I know it's one thing to "lead to believe" and another to "show that", and perhaps that's what happened here. But every time the accepted explanation does a 180 science dies a little bit. I don't mean the big changes like relativity, but the blatant reversals. Fatty food is bad - no it's good. Carbs are great - no they're not. Drugs pulled from the market that had been "tested".<p>I think a lot of cases are not really reversals, but misunderstandings or incorrect interpretations of results that later get clarified. Not sure what the answer is.
I really think we're dealing with some very complicated biochemistry here. I have never seen a single psych drug, the PI sheet for which did not begin, "The exact mechanism of action is unknown" (or words to that effect). And that includes very old drugs like Lithium.<p>Obviously, these drugs can provide relief for people suffering from various kinds of mental disorders. Most of them target serotonin, norepinephrine, dopamine, and a laundry list of receptors. Yet it still amazes me that no one can seem to draw a clear line between these chemical interventions and relief from symptoms.<p>Given all that, every piece evidence becomes <i>potentially</i> significant. But it also means a long, long slog through inferential statistics, patient self-reports, placebo effects, and targeted studies like this one that may fail to account for a thousand other factors.<p>I'm not a biochemist, but I think I would find this work both fascinating and very frustrating.
I find this hard to believe when considering raves and MDMA.<p>If anything people with too much serotonin and a social phobia probably do not have enough serotonin receptors, and the extra serotonin is the body compensating.
dont mess with hardware if you can fix it in software<p>that study is an example of a horribe broad brush approach that gets pursued because its a low hanging fruit. physcial quantities are easier to objectively measure and present and subsequently selling tanglible pills is more marketable and controllable<p>you can influence your neurotransmitters, endocrine system, and behaviour with thoughts and habits, for example: fantasize porn, your passion projects, see what people see when they see you, first person view in a roller coaster, check out youtube climbing scaling radio towers and skyscrapers, etc.. duh just about any engaging movie or book<p>manage your attention wisely<p>social phobia/anxiety arises from habitual limited perspective misinterpreting the environment. in some situations fear is appropriate healthy and helpful, the key solution is to notice the difference objectively<p>see yourself, your surroundings, other people, from an external reference/point of view, see through from outside the building, from the roof, maybe perched on top of a lamp post, birds eye view, whatever, use your illusion
I've spent lots of time studying neurotransmitters and their relationship with various mental illnesses and amino acids. It has been my understanding for a while now (from the book 'The Mood Cure' by Julia Ross) that too much of a neurotransmitter can have the same symptoms as too little. That book also seemed to indicate that dopamine and serotonin have an antagonistic relationship with each other, so too little (or too much?) serotonin can cause an excess of dopamine, which can lead to all kinds of anxiety, including potentially social phobia.<p>I've been considering buying books on endocrinology/neurobiology to further study these phenomena, if anyone with more knowledge/experience could enlighten me on this I'd really appreciate it.
That is not too surprising. On the one hand serotonine not only acts as a neurotransmitter, but has a mechanical function controlling blood-pressure and a multitude of other things as well.
(See this comment: <a href="https://news.ycombinator.com/item?id=9476594" rel="nofollow">https://news.ycombinator.com/item?id=9476594</a>)<p>Easier triggered bodily alertness in unpleasant situations probably creates a feedback-loop which shuts off rational thinking (frontal cortex) further -> anxiety.<p>On the other hand, I think a good metaphor for it's complex role as a neurotransmitter is "bandwidth". If your serotonine-levels are too low, some regions in your brain have trouble communicating with each other. Hence when your amygdala starts sending out signals of imminence, your rational prefrontal cortex might be able to think "No need to be afraid.", but it's not able to properly communicate that back. The other way around works too: the signals of imminence might not arrive clearly ("I didn't even realize I was afraid"), so you can't act properly.<p>If serotonine-levels are too high, this communication and loops might work TOO well. Imagine a "weak non-specific signal" from a confused (lack of a better word) amygdala that starts off a thought, which in turn throws the amygdala into a feedback-loop that you can't get out off. In that situation it would have been easier if the weak signal would have been dismissed in the first place.
social phobia = psychiatric disorder, in case i can't speak in public? do i have to speak in public? i'd be very careful with that kind of judgement. in general, having experience with how "modern medicine" and society in general handle such proclaimed "problems", psychology is a great deal of bullshit.<p>i myself don't like masses of people. i embrace this preference. and i love it. most amassment of people aren't even useful.<p>to everybody who's eating chemicals because some say you don't fit in: STOP IT. tell <i>them</i> to fit in. don't sell yourself and everybody like you to pharmaceuticals and others.<p>btw: did they actually disable copying of text (on iOS) on this site?
> Based on previous studies, it was believed that individuals with social phobia had too little serotonin and that SSRIs increased the amount of available serotonin. In a new study published in the scientific journal JAMA Psychiatry, researchers from the Department of Psychology at Uppsala University show that individuals with social phobia make too much serotonin.<p>Hold on a sec. What exactly did this study do differently? If the previous studies showed one thing, why should we suddenly believe this study that says it's all false?
I don't usually have any problems with social events- I just don't sleep the night before, so I am exhausted on the day.<p>Does anybody have any tips/ suggestions how to deal with this?
That's very interesting, especially combined with data showing that SSRIs in fact decrease brain serotonin over the long term [1]. We truly do not understand the mechanism of action for these drugs.<p>[1] <a href="https://www.psychologytoday.com/blog/mad-in-america/201011/new-rat-study-ssris-markedly-deplete-brain-serotonin" rel="nofollow">https://www.psychologytoday.com/blog/mad-in-america/201011/n...</a>
Is low serotonin the cause of social phobia? or is social phobia the cause of low serotonin?. The evident power of mind over body is an uncomfortable truth for a few industries.<p>So we need some sort of cause & effect algebra so that fallacious and faulty reasoning doesn't get smuggled in the name of science, otherwise science is just some form of social control exploiting the power - highjacked from religion - of an alleged ownership over the truth.
Almost 10 years ago I read a study that attributed (not too much or too little serotonin), but sending the wrong serotonin allele types for various social situations. This correlated to genetic predispositions to both social anxiety and certain forms of autism. It seems odd these later studies seem to be focusing on a far more general use case of whether more or less serotonin in general is a cause.
ssri's have done more harm than good for me. I simply feel numbed out...have little emotion and a poor memory. It basically kills the emotion -> memory feedback loop that you need to learn and grow. In my experience I felt more stuck on the drug than off them.
They don't even know what serotonin does. Every antidepressants action mechanism is just a shot in the dark, trial and error and it's questionable whether any of them work at all. Yes Tom Cruise is right on this one.
excitement and anxiety are the same state just differing perception.<p>it is more about imagined outcomes<p>this is exciting and will work out well I feel safe<p>this is exciting and i may come to emotional or physical harm<p>the excitement is the same<p>so long as you don't fear fear itself, that is a feedback loop.
This is a good study, but it's important to understand that the study results [1] don't really contradict much of our current understanding of serotonin-related antidepressant activity. If you read through the actual study, you'll see that the authors aren't disagreeing with SSRI activity but rather attempting to gather more insight into the accepted anxiolytic activity of SSRIs.<p>Neurotransmitter reductionism is one of the more difficult pop-neuropsychiatry concepts to shake, because it's so tempting to think of neurotransmitters like serotonin in the same way we've come to think of more basic biomarkers like cholesterol levels or other hormone levels. Neurotransmitter function is several orders of magnitude more complex, and can't simply be summarized as "too much" or "too little."<p>For example, neurotransmitter signaling is often divided in to two components: Tonic and phasic release. Tonic signaling is lower frequency (think closer to DC current for a very crude analogy), while phasic release is higher frequency (think more along the lines of AC current). The balance of tonic vs phasic signaling often has a massive influence on the actual outcome of the signaling. SSRIs are frequently (and wrongly) thought of as generically "increasing serotonin levels" when what they're really doing is altering serotonin dynamics in the synaptic cleft. Inhibiting the serotonin reuptake pump causes the serotonin to stick around longer in the synaptic cleft, which (again, roughly speaking) slows the serotonin dynamics down a bit and moves toward tonic, rather than phasic, signaling. It's not difficult to find studies showing relationships between serotonin tonic and phasic signaling, SSRIs, and stress adaptation differences. See [2] for the first example I found in a quick search.<p>Another very important component of serotonin signaling are 5-HT1A autoreceptors located on presynaptic terminals. These are part of the feedback loop regulating serotonin release. Briefly, 5-HT1A autoreceptors bind serotonin in the synaptic cleft and apply negative feedback to serotonin release. More serotonin in the synaptic cleft results in more 5-HT1A autoreceptor activation, which will in turn slow serotonin release. SSRIs will increase extracellular serotonin area under the curve, which will result in additional 5-HT1A activation and altered serotonin release dynamics. This system will ultimately re-regulate to some other set-point after several weeks, which is theorized to be part of the reason for the therapeutic lag in SSRI treatment, and also thought to explain why SSRIs often initially cause more anxiety by acutely increasing serotonin levels before the system re-regulates. 5-HT1A autoreceptor modulation is also the theorized mechanism of action of anti-anxiety medications like Buspirone, and 5-HT1A modulation is a property of two of the most recent anti-depressant medications Vortioxetine and Vilazadone.<p>This is another good study to have, but it's important to not be too quick to think that this contradicts our current understandings.<p>[1] <a href="http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711" rel="nofollow">http://archpsyc.jamanetwork.com/article.aspx?articleid=23197...</a><p>[2] <a href="http://www.ncbi.nlm.nih.gov/pubmed/22791197" rel="nofollow">http://www.ncbi.nlm.nih.gov/pubmed/22791197</a>
and once again medical science thinks it knows all, and the healthcare industry will of course prescribe powerful medications for a price that will undoubtedly cure us of our ills.<p>Fool me once...
Taking half a litre blood from somebody suffering hypertension obviously solves that problem ...<p>... so great - now we have the solution to social phobia!<p></irony>