
Individuals with social phobia have too much serotonin - forloop
http://www.sciencedaily.com/releases/2015/06/150617115327.htm
======
henderson101
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.

~~~
Eduard
> I still get bouts, but I have a mechanism in place to handle the symptoms
> and they mostly dissipate.

Can you tell me about the mechanism that helps you?

~~~
richmt
Not OP, but the biggest thing my therapist recommended me was practicing
mindfulness through meditation. The idea is that it makes it easier to fall
back in that same mental state when suffering everyday anxiety.

Another thing she recommended which I just started doing was exercising
regularly. I just started lifting a few weeks ago with a friend at the gym,
and already its had a huge boost on my confidence levels.

Sorry if you've heard these before, but they do help a ton, trust me.

~~~
heroku
I started exercising and it gave me a huge confidence boost that further lead
to being attracted by girls. After a year though I got used to lifting weights
and I wasn't progressing as I wanted to be so that didn't help. But I am sure
if you get shredded you will be cured.

~~~
justacat
Dude…getting shredded has always been the cure.

~~~
testingonprod
It's the natural cure

~~~
yeison
There are truly a lot of reasons why exercise contributes to good mental
health. One of them is that it helps produce the correct balance of hormones
in your system, which in turn also impact the correct balance of
neurotransmitters. It's very easy, especially for us coders, to forget that
we're sitting all day. Sitting all day is far from natural and has a
tremendous amount of health impact. Exercise is extremely beneficial.

------
dschiptsov
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
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=23197...](http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711)

------
phkahler
>> 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.

~~~
anthony_romeo
It's a good thing that science can change. This is what distinguishes science
from dogma.

The problem is not these supposed 'reversals', but rather how this information
is being reported. Pop-science media reports modest studies as absolute truths
to catch eyeballs. When one study merely suggests research in one direction,
it's emblazoned as fact on the tabloids.

In the example you identified: "Fatty food is bad - no it's good" the issue is
not the studies flip-flopping. Rather, it's a problem of regular people taking
what are likely modest reports way too far and massively integrating them into
their daily lives, without ever reading the study and understanding the
context or scope of it. A study indicating that, say, there may be health
problems associated with consuming excess saturated fat seems to compel people
to follow no-fat diets. So I'd argue that the bigger problem is people reading
oversimplified reports of scientific information

I mean, I'm not terribly familiar with this field, but the study itself
indicates that whether high or low serotonin levels were contributory was "a
matter of debate" and that "only a few studies have used molecular
neuroimaging to examine serotonin dysfunction in SAD directly."[1] So this
doesn't appear to be a reversal at all, but rather a study which helps clarify
the role of serotonin in SAD.

[1]
[http://archpsyc.jamanetwork.com/article.aspx?articleid=23197...](http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711#yoi150011r5)

~~~
primroot
> So I'd argue that the bigger problem is people reading oversimplified
> reports of scientific information.

And what about the AHA[1] and other policy makers and shapers? What leads them
to make recommendations based on weakly established conclusions?

I think the pressure to deliver, and the lack of generalist knowledge are
somehow involved here. In the case of food and drugs, I would also blame
elitism.

[1]
[http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter...](http://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/The-
American-Heart-Associations-Diet-and-Lifestyle-
Recommendations_UCM_305855_Article.jsp)

~~~
eivarv
I know nothing of the AHA's methods or qualifications, but in my view bad
policies purportedly based upon science usually come from lack of these, in
addition to lack of scientific literacy. Alternatively, from a predefined
goal, i.e. a political agenda.

I'm curious: in what way would you blame elitism in those cases?

------
sramsay
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
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
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.

------
snarfy
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
With most biological systems, it's a pretty safe bet that things are more
complicated than that.

~~~
zyb09
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
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.

------
sunnyelements
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

------
tvm
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
honest question: is that phobia a real problem for you? or did somebody tell
you it is?

~~~
tvm
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
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?

~~~
sramsay
An actual panic attack is completely and totally devastating. The entire
fight/flight system goes haywire, and people think they're about to die. It's
even possible to start hallucinating. Lots of sufferers wind up in the ER
absolutely convinced they're having a heart attack.

What's worse, this can lead to a whole range of phobias (I'm in the middle of
this theater. What if I have an attack? Then you start having one. Now you're
afraid of theaters and theater-like spaces).

It can take many, many years for people to learn how to "talk themselves down"
out of this (or, more accurately, to endure the onset of one without letting
it get full blown). It's not life threatening, but it's a very serious illness
indeed.

~~~
tvm
Yes, the main deal is that the fight/flight system gets triggered too often,
even in inappropriate situations. The result is devastating.

~~~
stephendedalus
I feel for you so much. I've gone through this for the last 14 years. On and
off. Mostly off since I've been on medication, but it's debilitating. When you
don't go places or do things because you're afraid of simply being there for a
panic attack. Always sitting on aisles (when you finally get to the point
where you can go to a movie) so you have an easy escape.

And yeah, often you don't look at people, wear headphones or do other things
like that. That's when you're doing "well" and not having panic attacks. When
you've learned how to manage it.

------
hndude
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
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
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.

------
_bdog
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.

------
glasz
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
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
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.

------
j_baker
> 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?

------
martijn_himself
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
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
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.

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

~~~
eivarv
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
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
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.

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

------
mpg33
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.

------
jcroll
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.

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

~~~
devdoomari
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'

------
deepnet
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
Definitely not, it's not the same mental state, one is pleasant the other one
not.

~~~
deepnet
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
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.

~~~
deepnet
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.

~~~
Dylan16807
I understand you when you say there isn't a direct link between serotonin and
anxiety.

I don't understand how that bears any relation to whether anxiety and
positive-excitement are the same thing.

Also, when I'm excited in a happy way, I don't feel the compounding negative
effects of stress hormones. You think that's all perception?

------
tomstokes
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=23197...](http://archpsyc.jamanetwork.com/article.aspx?articleid=2319711)

[2]
[http://www.ncbi.nlm.nih.gov/pubmed/22791197](http://www.ncbi.nlm.nih.gov/pubmed/22791197)

------
anti-shill
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...

------
spacko
Taking half a litre blood from somebody suffering hypertension obviously
solves that problem ...

... so great - now we have the solution to social phobia!

</irony>

