19 ms·

Individuals with social phobia have too much serotonin

171 points by forloop 11y ago

hndude 11y ago
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. 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.
- ajarmst 11y ago
  One thing that has become increasingly clear is that the simplistic "too much x" or "too little y" theory of Mental illness as a "neurotransmitter imbalance" is flawed to the point of uselessness. Neurotransmitters certainly do mediate synapse growth and activity, but the brain is a complex adaptive organ, and it will adapt to modifications to neurotransmitter levels. This is why antidepressnts become less effective and require stronger doses, and why their sudden withdrawal leads to the massive exacerbation of symptoms. The problem isn't simply that patients "go off their meds". The problem is that meds stop working, and withdrawing them leaves the poor patient with a brain that was adapted to their presence suddenly unable to cope. The meds make the organic problem worse, but it dorsn't show until you withdraw them. We're still basically at the witch-doctor stage of "try it and see" with most if these drugs, with nothing like a proper pathology model or functional description of how the meds work to even do proper long-term studies.
  - ajarmst 11y ago
    Full disclosure: there is pretty good evidence that some of these drugs (like SNRIs) are effective for short-term mitigation of symptoms, although not a great deal above active placebo. Some other therapies are very promising, particularly Cognitive Therapy and a guided Mindfulness program (although study quality on the latter is suspect. DO NOT MODIFY YOUR MEDICATION WITHOUT THE ADVICE AND MONITORING OF A MEDICAL PROFESSIONAL FAMILIAR WITH YOUR CASE.
  - Dylan16807 11y ago
    >the witch-doctor stage of "try it and see" Welcome to differential diagnosis? If that's with-doctor stage then witch-doctor shouldn't be an insult. Understanding mechanism is very useful but not critical. If I had to choose I'd rather have a reliable way to measure mental health in a patient.
  - sramsay 11y ago
    I have often wondered if the adaptive nature of the brain is what's confusing things. In other words, if someone is suffering the systems of major depression or bipolar disorder, and you "shock" that system with a change in brain chemistry, you're going to get change, and that often the change is enough to snap people out of whatever depressive/manic rut they're in. Problem is, that's not a cure.
henderson101 11y ago
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. The human brain is wonderful. 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.
- plausibility 11y ago
  I've had a similar experience. Taking SSRIs (Sertraline, initially 50mg/daily, now 100mg/daily) for social phobia and depression. They definitely helped increase my baseline for positive feelings (i.e., I don't spend as many days curled up in bed feeling hopeless), but it's true that it brings down other aspects of life. Decreased sexual function, loss of emotion in other areas, stuff like that. I wonder whether serotonin is really the magic trick to increasing moods or whether it's just a stop-gap solution that works well enough for most.
  - pja 11y ago
    I wonder whether serotonin is really the magic trick to increasing moods or whether it's just a stop-gap solution that works well enough for most. You’ll find a stack of articles on this topic in amongst the others at http://slatestarcodex.com/ http://slatestarcodex.com/ Maybe start with http://slatestarcodex.com/2014/07/07/ssris-much-more-than-you-wanted-to-know/ http://slatestarcodex.com/2014/07/07/ssris-much-more-than-yo... ?
- 11y ago
digital-rubber 11y ago
When people use cocaine for example, and the levels of serotonin in the brain increase and people become more social. (unless they mix it with alcohol, but that's another issue) Or is there some parabolic effect; then again, too much of something, is never good, we all know that, hence the words 'too much'
sunnyelements 11y ago
dont mess with hardware if you can fix it in software 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 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 manage your attention wisely 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 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
dschiptsov 11y ago
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...
deepnet 11y ago
excitement and anxiety are the same state just differing perception. it is more about imagined outcomes this is exciting and will work out well I feel safe this is exciting and i may come to emotional or physical harm the excitement is the same so long as you don't fear fear itself, that is a feedback loop.
- RivieraKid 11y ago
  Definitely not, it's not the same mental state, one is pleasant the other one not.
  - deepnet 11y ago
    There is no disagreement, that is what I said. Mental state is perception, and this can change from one moment to the next but the excitement/ fear being a hormonal state takes time to subside.
    - Dylan16807 11y ago
      You can use excitement as a broad category that includes good and bad, but there are definitely different hormonal mixes, some that are pleasant and some that are painful, and the difference is not perception.
      - deleted 11y ago
        [deleted]
      - deepnet 11y ago
        I agree and I am certain that everyone's experiences vary. For instance some people enjoy things they consider frightening - others hate it. My suggestion is that there is not a direct causal link between a higher or lower level of seratonin and a mental state called anxiety. The same bodily state can enjoin one to flight or fight. Attitude, history, personality, self-belief and training can alter ones attitude to the same hormonal situation. Changing the way one thinks about things can be very effective. I do not mean to trivialise such a change, this can require professional help, such as congitive behavioral therapy. I posit there is not a one-to-one correlation between seratonin level and a mental state ( fright or excite ) but that other factors confound it. Perhaps this is why these studies have come to seemingly contradictory ideas about seratonin levels and mental states ? Links between the chemistry of the brain and distinct mental states seems less well established than proponents of the 'chemical-imbalance' school of therapy maintain.
martijn_himself 11y ago
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. Does anybody have any tips/ suggestions how to deal with this?
- DanBC 11y ago
  Cognitive Behaviour Therapy - a short course of between 6 to 14 hours (one hour per week). Find a reputable therapist (in England you'd look for BACP). Or meditation and mindfulness would probably help. You may find sleep hygiene helps, but if you're not having trouble the rest of the time it might not. http://www.nhs.uk/Conditions/Insomnia/Pages/Treatment.aspx http://www.nhs.uk/Conditions/Insomnia/Pages/Treatment.aspx For rare events, not trying to cure insomnia, consider zopiclone (or any of the Z drugs). You'd take one before the event; you'd get a good night sleep; you avoid the addiction problems that are risked if you take it every night. (Obviously I'm not a doctor and this isn't medical advice).
  - superplussed 11y ago
    I have had exactly the same issue, and have used a meditative technique that I learned in Nepal to help with sleeping: Count from 27 to 1 with each inhalation. If you miss a number, ie between 15 and 14 you lost your focus and thought about something else, and missed the count, start over. My experience is that generally I will fall asleep before I get to 1, and on extreme cases it will take going from 27 to 1 more than once, but it always ends with sleep. The only difficulty I have now is being disciplined enough to not think "I got this" and try to sleep without the technique. Often what happens when I think that is I toss and turn for 3 hours before I just give in to the technique and finally fall asleep.
- bayesianhorse 11y ago
  Sleep deprivation is one of the most reliable and strong antidepressants, but also one of the least practical. Some clinics actually make patients stay awake for a period of time. I don't recommend "self-medicating" on purpose, though... In many case this makes everything worse.
spacko 11y ago
Taking half a litre blood from somebody suffering hypertension obviously solves that problem ... ... so great - now we have the solution to social phobia! </irony>
tvm 11y ago
Being a person diagnosed with social phobia I thought that myself many years ago. All the SSRIs and SRNIs actually made whole thing worse.
- glasz 11y ago
  honest question: is that phobia a real problem for you? or did somebody tell you it is?
  - tvm 11y ago
    Honest answer: Yes a serious problem. Two years ago I've had panic attack in the elevator and I was just technically unable to go into office where I worked (I've had a good job and I was content there). Doing ordinary things like groceries, etc. was terribly hard. Went through brain CT, EMG and some other tests and after some months psychiatrist gave me F40.2 (social phobia) stamp. Went through various medications that made things much worse (yeah, all these medications actually tried to retain serotonin in the brain). Rivotril and other drugs that actually "disable" the brain work, but they aren't the solution. Being extremely tired also works, but it is not very practical. It's rather debilitating illness and my life went to hell.
    - glasz 11y ago
      thanks. crazy situation. don't get me wrong, i'm just naive, but would using headphones (listening to music), not looking at people and closing the eyes in the elevator work?
      - tvm 11y ago
        Well, it's more complicated than that. Your hand will start to tremble uncontrollably when someone looks at you. Your face will blush, your legs will start to shake. You might eventually go and vomit. Elevator filled with people is of course extreme case. But I was in the elevator alone. I just couldn't open the doors of the office, take a sit in my corner and greet all these great guys that I've worked with for many years. I'm not sure what caused that. I've actually acted as a project manager in my early twenties and everything was fine (I could handle meetings and all that idiocy just fine). Then it all went downhill and I can't tell if the onset of these symptoms was gradual (and I was just simply ignoring them) or if they appeared suddenly.
bayesianhorse 11y ago
The paradox being that SSRIs have been shown to be beneficial for social phobia ...
- devdoomari 11y ago
  What if those with social phobia are creating those serotonins to counter-act other social-phobia-causing stuff? IMHO, this article really shouldn't say serotonin causes social phobia based on 'social-phobiacs have lots of serotonin'
  - klibertp 11y ago
    Yeah, it remains me of how masturbation was thought to lead to severe mental illness based on the fact that severely mentally ill patients tended to masturbate...
glasz 11y ago
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. i myself don't like masses of people. i embrace this preference. and i love it. most amassment of people aren't even useful. to everybody who's eating chemicals because some say you don't fit in: STOP IT. tell them to fit in. don't sell yourself and everybody like you to pharmaceuticals and others. btw: did they actually disable copying of text (on iOS) on this site?
- xiaq 11y ago
  No, an important aspect of mental diagnosis is that the patient is actively troubled by the problem but is unable to change on his own; otherwise it is more of personality. If you just hate socializing, you don't have social phobia. If you sincerely believe that washing your hands every ten minutes make you cleaner and do so, you don't have OCD. Psychologists are not as eager to judge as you might imagine.
  - don_draper 11y ago
    I'll bet a lot of people take these drugs not because they have to but want to. They want to look the part for work, or talk to the hot chick in the bar.
- Dylan16807 11y ago
  When an irrational fear prevents you from doing something, that's basically a definition of psychiatric disorder. It doesn't matter if you have no great desire to do it in the first place. If someone thinks an activity isn't useful then that can mitigate a phobia, but it's orthogonal to the actual existence or not of a phobia. Nobody is judging you for your preferences. "won't" and "can't" are different things. So if you're calling the overuse of chemicals bullshit, fine. But don't call a clear diagnosis bullshit.
- jerf 11y ago
  The article was certainly a bit casual with its terms, but as a human being, you shouldn't be generally nervous about mere socialization with others. You may be specifically nervous, if you need to impress the others, or if you're in a foreign land for the first time, but you should not generally be nervous about all social interaction. If you are, you have a problem. It may not be something that we should necessarily throw medication at, we've all got problems of one sort or another, the benefits of medication may not outweigh the costs, but it is a problem. Nervousness is different than boredom, lack of desire, or lack of seeking it out. I can cover those bases quite well. I often don't want to socialize. But I'm not fearful of it, I just find it boring in most groups. On the other hand, "public speaking", as in, getting up in front of a crowd and making any sort of speech, well, I've heard multiple people who make a living doing it that they never actually stop being nervous about it before hand. They learn how to get through it, but they're always nervous. Heck, I daresay such nerves are rational, really. That would seem to be a different category of issue.
snarfy 11y ago
I find this hard to believe when considering raves and MDMA. 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.
- ska 11y ago
  With most biological systems, it's a pretty safe bet that things are more complicated than that.
  - zyb09 11y ago
    With the limited ways we're able to study brain disorders at the moment, it feels to me like we're trying to debug an user level application by looking at the signals that pass through the system bus.
    - jerf 11y ago
      I have often pondered the question of how much we'd know about biology today if biologists had the same tools we did. Can you imagine the progress we could make if we could freeze a cell, set watchpoints on any molecules we wanted, step forward and backward at any time increment we chose, run arbitrary queries, make arbitrary changes to the running cell in an arbitrary tree of possibilities, and do this on any cell we liked? A competent biochemist team could probably discover more in a week, and with greater confidence, then the they would in their entire lives the conventional way.
anti-shill 11y ago
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. Fool me once...
mpg33 11y ago
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.
phkahler 11y ago
>> 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. 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". 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.
- sjtrny 11y ago
  Drugs are in a totally different category than peer reviewed articles. They go through rigorous testing that works the vast majority of the time to weed out unsuitable drugs. On the other hand peer review (having been through it a few times) is extremely sloppy and reviewers do not do due diligence. Often the reviewers can't even if they wanted to (no raw data released etc) and they have to blindly accept the authors claims. I don't think science dies a little bit each time a dissenting or contradictory result is published. In fact it is a good thing. We need more people to try and reproduce others work. But at the moment we have is a problem of scale. In other words it only looks bad when there are two different conclusions. We need many more reproductions to come to a clear answer.
  - TallGuyShort 11y ago
    The problem is that things go from being talked about as a statistical correlation with a probability of error, to being a "link", to being the thing people base their diets and other philosophies on. The anti-vaccine movement resulted in a lot of people touting science as the reason you should trust vaccines, conveniently ignoring the fact that it appears to have started from a phony scientific study. The fact that the phrase "a new study ... has found exactly the opposite" can be published by serious researchers is exactly why we shouldn't be going around proposing that people be legally forced to inject themselves with things because they're considered scientifically illiterate. As Scott Adams said in his piece on the subject, "Science isn’t about being right every time, or even most of the time. It is about being more right over time and fixing what it got wrong." [1] That should be kept in mind by people who are publishing, reporting on, and reading these studies. [1] http://blog.dilbert.com/post/109880240641/sciences-biggest-fail#ixzz3dWKWf6k5 http://blog.dilbert.com/post/109880240641/sciences-biggest-f...
jcroll 11y ago
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.
sramsay 11y ago
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. 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. Given all that, every piece evidence becomes potentially 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. I'm not a biochemist, but I think I would find this work both fascinating and very frustrating.
- PaulHoule 11y ago
  Note there are at least 14 known serotonin receptors: https://en.wikipedia.org/wiki/5-HT_receptor https://en.wikipedia.org/wiki/5-HT_receptor and this is responsible for the rich pharmacology of serotonin-affecting drugs such as the SSRIs, hallucinogens such as LSD, and MDMA which delivers an entirely different experience, atypical antipsychotics, antimigraine drugs, anti-emetic drugs such as Ondansetron, etc. It doesn't matter "how much" serotonin you have as where it is. Note that serotonogenic drugs have radically different modes of actions such as agonist, antagonist, partial agonist as well as the reuptake inhibitors, and that many serotonin receptors are actually autoreceptors on the other side of the junction which suppress the production of serotonin at the terminals. Personally I think of the SSRI drugs as "antineurotics" and what they seem to do is help me keep compensated under stress. That is, rather than going to pieces, I stay rational under provocation. This might be why Scientology hates SSRIs so much, because it really does seem to make your "reactive mind" much weaker.
  - sramsay 11y ago
    Right. I think that's why we get into the "let's try this" mode with doctors, which has been mentioned in this thread. That can be frustrating for patients, but "sertonergic drug" (or effect) is a hugely broad category, and we don't have any way to know in advance which part of what thing needs to be affected in what way -- or even if it's serotonin that's the problem! I hear what you say about "reactive mind." I've never heard it put that way, but man does that capture depression/mania and a whole host of other brain cooties.
tomstokes 11y ago
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. 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." 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. 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. This is another good study to have, but it's important to not be too quick to think that this contradicts our current understandings. [1] http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711 http://archpsyc.jamanetwork.com/article.aspx?articleid=23197... [2] http://www.ncbi.nlm.nih.gov/pubmed/22791197 http://www.ncbi.nlm.nih.gov/pubmed/22791197
don_draper 11y ago
Everyone is different and there is no single elixir to solve all problems, but meditation helped me greatly.
j_baker 11y ago
> 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. 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?
ksenzee 11y ago
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. [1] https://www.psychologytoday.com/blog/mad-in-america/201011/new-rat-study-ssris-markedly-deplete-brain-serotonin https://www.psychologytoday.com/blog/mad-in-america/201011/n...
- eivarv 11y ago
  Isn't it more that we don't understand why it works (i.e. what kind of connection serotonin has with these mental illnesses) rather than the mechanism of action itself, which is believed to be serotonin staying longer in the synaptic cleft by way of inhibiting reuptake, leading to repeated stimulation of the post-synaptic receptors? I was under the impression that SSRI's were specifically designed to target the serotonin system.
tremols 11y ago
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. 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.
bspates 11y ago
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.
_bdog 11y ago
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: https://news.ycombinator.com/item?id=9476594 https://news.ycombinator.com/item?id=9476594) Easier triggered bodily alertness in unpleasant situations probably creates a feedback-loop which shuts off rational thinking (frontal cortex) further -> anxiety. 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. 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.

171 points by forloop 11y ago

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. 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.

ajarmst 11y ago
One thing that has become increasingly clear is that the simplistic "too much x" or "too little y" theory of Mental illness as a "neurotransmitter imbalance" is flawed to the point of uselessness. Neurotransmitters certainly do mediate synapse growth and activity, but the brain is a complex adaptive organ, and it will adapt to modifications to neurotransmitter levels. This is why antidepressnts become less effective and require stronger doses, and why their sudden withdrawal leads to the massive exacerbation of symptoms. The problem isn't simply that patients "go off their meds". The problem is that meds stop working, and withdrawing them leaves the poor patient with a brain that was adapted to their presence suddenly unable to cope. The meds make the organic problem worse, but it dorsn't show until you withdraw them. We're still basically at the witch-doctor stage of "try it and see" with most if these drugs, with nothing like a proper pathology model or functional description of how the meds work to even do proper long-term studies.
- ajarmst 11y ago
  Full disclosure: there is pretty good evidence that some of these drugs (like SNRIs) are effective for short-term mitigation of symptoms, although not a great deal above active placebo. Some other therapies are very promising, particularly Cognitive Therapy and a guided Mindfulness program (although study quality on the latter is suspect. DO NOT MODIFY YOUR MEDICATION WITHOUT THE ADVICE AND MONITORING OF A MEDICAL PROFESSIONAL FAMILIAR WITH YOUR CASE.
- Dylan16807 11y ago
  >the witch-doctor stage of "try it and see" Welcome to differential diagnosis? If that's with-doctor stage then witch-doctor shouldn't be an insult. Understanding mechanism is very useful but not critical. If I had to choose I'd rather have a reliable way to measure mental health in a patient.
- sramsay 11y ago
  I have often wondered if the adaptive nature of the brain is what's confusing things. In other words, if someone is suffering the systems of major depression or bipolar disorder, and you "shock" that system with a change in brain chemistry, you're going to get change, and that often the change is enough to snap people out of whatever depressive/manic rut they're in. Problem is, that's not a cure.

henderson101 11y ago

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. The human brain is wonderful. 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.

plausibility 11y ago
I've had a similar experience. Taking SSRIs (Sertraline, initially 50mg/daily, now 100mg/daily) for social phobia and depression. They definitely helped increase my baseline for positive feelings (i.e., I don't spend as many days curled up in bed feeling hopeless), but it's true that it brings down other aspects of life. Decreased sexual function, loss of emotion in other areas, stuff like that. I wonder whether serotonin is really the magic trick to increasing moods or whether it's just a stop-gap solution that works well enough for most.
- pja 11y ago
  I wonder whether serotonin is really the magic trick to increasing moods or whether it's just a stop-gap solution that works well enough for most. You’ll find a stack of articles on this topic in amongst the others at http://slatestarcodex.com/ http://slatestarcodex.com/ Maybe start with http://slatestarcodex.com/2014/07/07/ssris-much-more-than-you-wanted-to-know/ http://slatestarcodex.com/2014/07/07/ssris-much-more-than-yo... ?
11y ago

digital-rubber 11y ago

When people use cocaine for example, and the levels of serotonin in the brain increase and people become more social. (unless they mix it with alcohol, but that's another issue) Or is there some parabolic effect; then again, too much of something, is never good, we all know that, hence the words 'too much'

sunnyelements 11y ago

dont mess with hardware if you can fix it in software 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 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 manage your attention wisely 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 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

dschiptsov 11y ago

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...

deepnet 11y ago

excitement and anxiety are the same state just differing perception. it is more about imagined outcomes this is exciting and will work out well I feel safe this is exciting and i may come to emotional or physical harm the excitement is the same so long as you don't fear fear itself, that is a feedback loop.

RivieraKid 11y ago
Definitely not, it's not the same mental state, one is pleasant the other one not.
- deepnet 11y ago
  There is no disagreement, that is what I said. Mental state is perception, and this can change from one moment to the next but the excitement/ fear being a hormonal state takes time to subside.
  - Dylan16807 11y ago
    You can use excitement as a broad category that includes good and bad, but there are definitely different hormonal mixes, some that are pleasant and some that are painful, and the difference is not perception.
    - deleted 11y ago
      [deleted]
    - deepnet 11y ago
      I agree and I am certain that everyone's experiences vary. For instance some people enjoy things they consider frightening - others hate it. My suggestion is that there is not a direct causal link between a higher or lower level of seratonin and a mental state called anxiety. The same bodily state can enjoin one to flight or fight. Attitude, history, personality, self-belief and training can alter ones attitude to the same hormonal situation. Changing the way one thinks about things can be very effective. I do not mean to trivialise such a change, this can require professional help, such as congitive behavioral therapy. I posit there is not a one-to-one correlation between seratonin level and a mental state ( fright or excite ) but that other factors confound it. Perhaps this is why these studies have come to seemingly contradictory ideas about seratonin levels and mental states ? Links between the chemistry of the brain and distinct mental states seems less well established than proponents of the 'chemical-imbalance' school of therapy maintain.

martijn_himself 11y ago

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. Does anybody have any tips/ suggestions how to deal with this?

DanBC 11y ago
Cognitive Behaviour Therapy - a short course of between 6 to 14 hours (one hour per week). Find a reputable therapist (in England you'd look for BACP). Or meditation and mindfulness would probably help. You may find sleep hygiene helps, but if you're not having trouble the rest of the time it might not. http://www.nhs.uk/Conditions/Insomnia/Pages/Treatment.aspx http://www.nhs.uk/Conditions/Insomnia/Pages/Treatment.aspx For rare events, not trying to cure insomnia, consider zopiclone (or any of the Z drugs). You'd take one before the event; you'd get a good night sleep; you avoid the addiction problems that are risked if you take it every night. (Obviously I'm not a doctor and this isn't medical advice).
- superplussed 11y ago
  I have had exactly the same issue, and have used a meditative technique that I learned in Nepal to help with sleeping: Count from 27 to 1 with each inhalation. If you miss a number, ie between 15 and 14 you lost your focus and thought about something else, and missed the count, start over. My experience is that generally I will fall asleep before I get to 1, and on extreme cases it will take going from 27 to 1 more than once, but it always ends with sleep. The only difficulty I have now is being disciplined enough to not think "I got this" and try to sleep without the technique. Often what happens when I think that is I toss and turn for 3 hours before I just give in to the technique and finally fall asleep.
bayesianhorse 11y ago
Sleep deprivation is one of the most reliable and strong antidepressants, but also one of the least practical. Some clinics actually make patients stay awake for a period of time. I don't recommend "self-medicating" on purpose, though... In many case this makes everything worse.

spacko 11y ago

Taking half a litre blood from somebody suffering hypertension obviously solves that problem ... ... so great - now we have the solution to social phobia! </irony>

tvm 11y ago

Being a person diagnosed with social phobia I thought that myself many years ago. All the SSRIs and SRNIs actually made whole thing worse.

glasz 11y ago
honest question: is that phobia a real problem for you? or did somebody tell you it is?
- tvm 11y ago
  Honest answer: Yes a serious problem. Two years ago I've had panic attack in the elevator and I was just technically unable to go into office where I worked (I've had a good job and I was content there). Doing ordinary things like groceries, etc. was terribly hard. Went through brain CT, EMG and some other tests and after some months psychiatrist gave me F40.2 (social phobia) stamp. Went through various medications that made things much worse (yeah, all these medications actually tried to retain serotonin in the brain). Rivotril and other drugs that actually "disable" the brain work, but they aren't the solution. Being extremely tired also works, but it is not very practical. It's rather debilitating illness and my life went to hell.
  - glasz 11y ago
    thanks. crazy situation. don't get me wrong, i'm just naive, but would using headphones (listening to music), not looking at people and closing the eyes in the elevator work?
    - tvm 11y ago
      Well, it's more complicated than that. Your hand will start to tremble uncontrollably when someone looks at you. Your face will blush, your legs will start to shake. You might eventually go and vomit. Elevator filled with people is of course extreme case. But I was in the elevator alone. I just couldn't open the doors of the office, take a sit in my corner and greet all these great guys that I've worked with for many years. I'm not sure what caused that. I've actually acted as a project manager in my early twenties and everything was fine (I could handle meetings and all that idiocy just fine). Then it all went downhill and I can't tell if the onset of these symptoms was gradual (and I was just simply ignoring them) or if they appeared suddenly.

bayesianhorse 11y ago

The paradox being that SSRIs have been shown to be beneficial for social phobia ...

devdoomari 11y ago
What if those with social phobia are creating those serotonins to counter-act other social-phobia-causing stuff? IMHO, this article really shouldn't say serotonin causes social phobia based on 'social-phobiacs have lots of serotonin'
- klibertp 11y ago
  Yeah, it remains me of how masturbation was thought to lead to severe mental illness based on the fact that severely mentally ill patients tended to masturbate...

glasz 11y ago

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. i myself don't like masses of people. i embrace this preference. and i love it. most amassment of people aren't even useful. to everybody who's eating chemicals because some say you don't fit in: STOP IT. tell them to fit in. don't sell yourself and everybody like you to pharmaceuticals and others. btw: did they actually disable copying of text (on iOS) on this site?

xiaq 11y ago
No, an important aspect of mental diagnosis is that the patient is actively troubled by the problem but is unable to change on his own; otherwise it is more of personality. If you just hate socializing, you don't have social phobia. If you sincerely believe that washing your hands every ten minutes make you cleaner and do so, you don't have OCD. Psychologists are not as eager to judge as you might imagine.
- don_draper 11y ago
  I'll bet a lot of people take these drugs not because they have to but want to. They want to look the part for work, or talk to the hot chick in the bar.
Dylan16807 11y ago
When an irrational fear prevents you from doing something, that's basically a definition of psychiatric disorder. It doesn't matter if you have no great desire to do it in the first place. If someone thinks an activity isn't useful then that can mitigate a phobia, but it's orthogonal to the actual existence or not of a phobia. Nobody is judging you for your preferences. "won't" and "can't" are different things. So if you're calling the overuse of chemicals bullshit, fine. But don't call a clear diagnosis bullshit.
jerf 11y ago
The article was certainly a bit casual with its terms, but as a human being, you shouldn't be generally nervous about mere socialization with others. You may be specifically nervous, if you need to impress the others, or if you're in a foreign land for the first time, but you should not generally be nervous about all social interaction. If you are, you have a problem. It may not be something that we should necessarily throw medication at, we've all got problems of one sort or another, the benefits of medication may not outweigh the costs, but it is a problem. Nervousness is different than boredom, lack of desire, or lack of seeking it out. I can cover those bases quite well. I often don't want to socialize. But I'm not fearful of it, I just find it boring in most groups. On the other hand, "public speaking", as in, getting up in front of a crowd and making any sort of speech, well, I've heard multiple people who make a living doing it that they never actually stop being nervous about it before hand. They learn how to get through it, but they're always nervous. Heck, I daresay such nerves are rational, really. That would seem to be a different category of issue.

snarfy 11y ago

I find this hard to believe when considering raves and MDMA. 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.

ska 11y ago
With most biological systems, it's a pretty safe bet that things are more complicated than that.
- zyb09 11y ago
  With the limited ways we're able to study brain disorders at the moment, it feels to me like we're trying to debug an user level application by looking at the signals that pass through the system bus.
  - jerf 11y ago
    I have often pondered the question of how much we'd know about biology today if biologists had the same tools we did. Can you imagine the progress we could make if we could freeze a cell, set watchpoints on any molecules we wanted, step forward and backward at any time increment we chose, run arbitrary queries, make arbitrary changes to the running cell in an arbitrary tree of possibilities, and do this on any cell we liked? A competent biochemist team could probably discover more in a week, and with greater confidence, then the they would in their entire lives the conventional way.

anti-shill 11y ago

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. Fool me once...

mpg33 11y ago

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.

phkahler 11y ago

>> 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. 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". 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.

sjtrny 11y ago
Drugs are in a totally different category than peer reviewed articles. They go through rigorous testing that works the vast majority of the time to weed out unsuitable drugs. On the other hand peer review (having been through it a few times) is extremely sloppy and reviewers do not do due diligence. Often the reviewers can't even if they wanted to (no raw data released etc) and they have to blindly accept the authors claims. I don't think science dies a little bit each time a dissenting or contradictory result is published. In fact it is a good thing. We need more people to try and reproduce others work. But at the moment we have is a problem of scale. In other words it only looks bad when there are two different conclusions. We need many more reproductions to come to a clear answer.
- TallGuyShort 11y ago
  The problem is that things go from being talked about as a statistical correlation with a probability of error, to being a "link", to being the thing people base their diets and other philosophies on. The anti-vaccine movement resulted in a lot of people touting science as the reason you should trust vaccines, conveniently ignoring the fact that it appears to have started from a phony scientific study. The fact that the phrase "a new study ... has found exactly the opposite" can be published by serious researchers is exactly why we shouldn't be going around proposing that people be legally forced to inject themselves with things because they're considered scientifically illiterate. As Scott Adams said in his piece on the subject, "Science isn’t about being right every time, or even most of the time. It is about being more right over time and fixing what it got wrong." [1] That should be kept in mind by people who are publishing, reporting on, and reading these studies. [1] http://blog.dilbert.com/post/109880240641/sciences-biggest-fail#ixzz3dWKWf6k5 http://blog.dilbert.com/post/109880240641/sciences-biggest-f...

jcroll 11y ago

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.

sramsay 11y ago

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. 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. Given all that, every piece evidence becomes potentially 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. I'm not a biochemist, but I think I would find this work both fascinating and very frustrating.

PaulHoule 11y ago
Note there are at least 14 known serotonin receptors: https://en.wikipedia.org/wiki/5-HT_receptor https://en.wikipedia.org/wiki/5-HT_receptor and this is responsible for the rich pharmacology of serotonin-affecting drugs such as the SSRIs, hallucinogens such as LSD, and MDMA which delivers an entirely different experience, atypical antipsychotics, antimigraine drugs, anti-emetic drugs such as Ondansetron, etc. It doesn't matter "how much" serotonin you have as where it is. Note that serotonogenic drugs have radically different modes of actions such as agonist, antagonist, partial agonist as well as the reuptake inhibitors, and that many serotonin receptors are actually autoreceptors on the other side of the junction which suppress the production of serotonin at the terminals. Personally I think of the SSRI drugs as "antineurotics" and what they seem to do is help me keep compensated under stress. That is, rather than going to pieces, I stay rational under provocation. This might be why Scientology hates SSRIs so much, because it really does seem to make your "reactive mind" much weaker.
- sramsay 11y ago
  Right. I think that's why we get into the "let's try this" mode with doctors, which has been mentioned in this thread. That can be frustrating for patients, but "sertonergic drug" (or effect) is a hugely broad category, and we don't have any way to know in advance which part of what thing needs to be affected in what way -- or even if it's serotonin that's the problem! I hear what you say about "reactive mind." I've never heard it put that way, but man does that capture depression/mania and a whole host of other brain cooties.

tomstokes 11y ago

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. 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." 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. 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. This is another good study to have, but it's important to not be too quick to think that this contradicts our current understandings. [1] http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711 http://archpsyc.jamanetwork.com/article.aspx?articleid=23197... [2] http://www.ncbi.nlm.nih.gov/pubmed/22791197 http://www.ncbi.nlm.nih.gov/pubmed/22791197

don_draper 11y ago

Everyone is different and there is no single elixir to solve all problems, but meditation helped me greatly.

j_baker 11y ago

> 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. 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?

ksenzee 11y ago

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. [1] https://www.psychologytoday.com/blog/mad-in-america/201011/new-rat-study-ssris-markedly-deplete-brain-serotonin https://www.psychologytoday.com/blog/mad-in-america/201011/n...

eivarv 11y ago
Isn't it more that we don't understand why it works (i.e. what kind of connection serotonin has with these mental illnesses) rather than the mechanism of action itself, which is believed to be serotonin staying longer in the synaptic cleft by way of inhibiting reuptake, leading to repeated stimulation of the post-synaptic receptors? I was under the impression that SSRI's were specifically designed to target the serotonin system.

tremols 11y ago

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. 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.

bspates 11y ago

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.

_bdog 11y ago

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: https://news.ycombinator.com/item?id=9476594 https://news.ycombinator.com/item?id=9476594) Easier triggered bodily alertness in unpleasant situations probably creates a feedback-loop which shuts off rational thinking (frontal cortex) further -> anxiety. 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. 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.