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.
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.
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.
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.
For me, it's a lot of accepting what I can change and putting things I can't in to perspective. Treating others as I'd like to be treated. And really, trying to find peace without creating conflict.
Think of it as a form of meditation, without the sitting and relaxing part. It is hard to explain because there are many layers to the technique, but keeping different aspects of your life in isolation is another important factor.
Bad day at work? When you walk out of your office, throw it away. Argument with your partner? When you leave your house, don't dwell on it. Stop beating yourself up about things... materialism isn't jut about physical objects, it's also about your environment. If you feel self entitled, you feel like things conspire against you more frequently. Accept that you're no better than anyone else, learn to love the incomprehensible..
There's no magic fix. Accept that. Drugs can mask your symptoms, but they can't fix the underlying problem if your attitude towards life doesn't also change.
This is all pretty vague I know, but without trying to sound like psychobabble - take what you can from my suggestions and reject what you doesn't work. And never let anyone tell you you're cured or still ill... you're cured when you feel cured. You will relapse, but if you fall back to your mecanism to survive all should fall back in to place.
Not OP, but here's my story: I did not enjoy being on any SSRI or NRI so all my work has to be behavior. In general, all the approaches that have worked for me when it comes to changing behavior follows a pattern of:
Perceive -> accept -> insight. This is in the context of a reaction to a stimulus.
1. Perceive the feeling and its reaction. First step is actually recognizing that I feel something and that I have a reaction to it. When something makes me anxious, I have a deeply uncomfortable physical reaction that starts in my diaphragm and radiates outwards. It's a cold, empty, hollow feeling tinged with fear. Before I started being aware of my reactions, I'd feel something and it might only be "bad" or "good." Focusing specifically on the reaction has allowed me to identify physical responses to feelings, which has helped me identify the feeling. This was a long and hard (but fulfilling) process for me which by its nature was very fraught - to practice this, I had to feel negative emotions. But with deliberate practice, and deliberate probing, I started to identify patterns and was able to 'map' reactions to the stimuli that produced them.
2. Accept the reaction. I used to spend a lot of energy avoiding the "bad" and increasing the good. An obvious lack of confidence in my own ability to deal with emotions. It's not possible to avoid "bad" emotions; you're going to feel them. Much better to learn how to accept them so they don't kill your entire day. I like the analogy of living in a city where it rains: It's going to rain whether I want it to or not. I can spend all my time indoors not getting wet and also not experiencing anything. I can try to be a badass and walk around without an umbrella and get soaked; now I don't ever have to check the weather and I don't need to invest in rain gear, but whether I get soaked or not is completely at the mercy of some other force. The ideal way is to accept the rain, put on a raincoat, and go about my day. In this case, the rain coat is the ability to accept a reaction to a stimulus, accept that it might have been negative, then let it pass.
3. Insight. For me, this is all about why I felt a certain way, what underlying values were being stressed for me that caused me to react. It's also about preparing myself to feel those emotions again, and trying to react better the next time. I do a lot of visualizing and projecting here. I try to think of someone, be it a real person or a character, who reacts the way I'd like to react. I imagine the stimulus that upset me, then try to picture myself reacting like they would.
I hope this is helpful. It's a high level, general way to change your behavior. I've done a lot of work with therapists and life coaches to suss this out. If you're on the fence at all about getting help, do it. Easily one of the best decisions I've ever made. At the very least, a book called the Power of Habit by Charles Duhig (kind of pop-sciency, but insightful) might be worth reading.
Also, as other people have suggested: Exercise, but the one most people forget: Sleep. When I start prioritizing 7 - 7.5 hours a night (can't really sleep longer) my mood drastically improves. Getting a good night's sleep is probably the biggest bang for your buck, by a long long margin in the mental health department. If you are getting sleep, exercise is next. When I lift weights 3x a week, I have more energy, I sleep better, my mental reflexes are sharp (I don't feel foggy or hazy).
Yep: being able to tell the difference between feeling, perception and will is essential to my life.
And acceptance: that is crucial as well. This is the fact: "I feel bad. OK, now what was I about to do with my classes today?" (This is a very simplified figure obviously).
Al lot of both really. Also, realising that you are generally amplifying most situations through a self destructive filter and trying as much as possible to be selfless and calm in most situations. This all helps.
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.
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.
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.
>> 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.
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.
> "The problem is not these supposed 'reversals', but rather how this information is being reported."
The reporting is terrible, but I think there is a problem with the research itself. There's little apparent awareness by many researchers of the limitations of single studies, perhaps because they have been heavily indoctrinated re: the significance of p-values, etc., or perhaps because their careers depend on it.
It's the researchers themselves writing "We show that ____", as if their single study with 20 participants all of whom are starving college freshmen CONCLUSIVELY proves such-and-such completely bizarre point which all previous observations have flatly contradicted. Then the media gobble it up, with all the authority of "science" to back them up, and when further research refutes the flawed study, nobody pays attention.
It's not just pop media though. There's a general attitude among many people I know who have advanced degrees in science that our current understanding is close to perfect, and that every correlation between two variables validates the entire theory that motivated the experiment. There's also a general attitude to just believe headlines and not look for authoritative or in-depth sources. The fact that pop media reports the way it does is a side effect of these underlying problems IMO. We ought to value accuracy in statements and healthy skepticism more than we do, I think.
> 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.
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?
To express it as a spectrum. Dogma has an almost infinite amount of resistance, science tries to reach to zero, but sometimes has too much (IIRC people became emotional about Einstein's theory)
Dogma frequently undergoes change, perhaps to a greater degree than science (which is generally the refinement of earlier theories and methods). See, for example, the Protestant Reformation.
Reversals based on further evidence are part of science, inherently. Science shouldn't have a magical reputation, because it's not magic. Like all other means of explaining there material world, it's guesswork. There only difference is that science is guesswork with systematic effort to find holes in the guesses and improve them and reject there ones that don't work, while every other approach to explaining material phenomena had some form of guesswork and some method of closing which guesses to accept that is not based on what demonstrably works or fails.
I think a lot of the harm comes from people treating science as some sort of monolithic entity. Science says X! Science says Y! When really it's more like some scientists over here have found some evidence for X, some over here did some work that points to Y.
It's neat that mainstream enthusiasm for science has grown so much in the last few years, but it seems like a lot of times this kind of treatment oversimplifies things.
Don't forget the Science community itself is always shouting "Trust us, we're impartial scientists, don't ignore us!". Some scientists over here have found some evidence for X, and the media that cover their story, REALLY want you to believe their story. You can't treat the Science community as impartial here.
It's a pretty simple fact that the more people who strongly trust a signal, the more value there is in mimicry of it. Because birds understand that Monarchs are poisonous, there's great value to the Viceroy in being a good mimic of it.
So the more strongly people trust science, the more value there will be to con men in passing themselves off as scientists. We can mitigate that to some extent with scientific reputation and whatnot, but I don't think we have trust fully figured out in general, as there's always the bootstrapping problem.
Is any of this even solvable to the general mainstream public? They need to think in absolutes, as in, this medicine does x to fix, prevent, or repair y. That is how the general public measure things.
In reality, an anti depressant for example, probably works out to something like: it works about 50% of the time, with a bit of a lean over 50%, but if we calculate in spontaneous remission, placebo effect, and some other variable, now it looks like it is either a net zero effect, or in many cases, like AA meetings, statistically detrimental. But the general public will need a binary answer.
And I consider myself part of this general public, I just know there is more than meets the eye on anything, and in general I feel correlation and causation more often then not don't agree.
I see a lot of positive reactions to how happy we should be that science changes. I mean, look how long it took us to get out of the dark ages, right?
But no, the liberality of changes like this one is what separates fluff science from actual science. There is a vast chasm of difference between stuff like this one and, say, aether theories.
People who came up with aether theories were the brightest of their ages. That is really the best they could come up with -- and the reason why it took us so long to disprove aether-based theories was that they had some bloody solid science behind them -- at least back in those ages. People were unable to come up with anything better because, for a very long time, they lacked both theoretical and experimental tools with which to conclusively prove (or disprove) their hypotheses.
We needed significant developments in mathematics, fluid mechanics and optics in order to test these theories, and we needed special relativity to come up with something better.
Whereas claims like the one this article refutes need only a correct application of double-blind testing and not falling into well-known (at least to statisticians) traps in order to be tested.
The fact that we have 180 degree spins in understanding such matters every six months is not a testament to how modern science cares only about truth. It's a testament of how important it is to publish papers.
People are asserting that these reversals are a normal part of science and therefore good. I think they are a normal part of science but reveal a huge flaw in the method: scientists frequently over extrapolate and end up drawing erroneous conclusions based on limited data. The widespread presence of basic methodological flaws in many scientific papers such as misunderstanding the meaning of p values means a lot of so-called science is built on faulty reasoning. This is worse than merely presenting a model that imperfectly represents the data, it is simply wrong: reaching conclusions that the data do not justify and never could.
You see this most often with efforts to reduce complex systems down to the effect of single variables; such efforts are almost guaranteed to miss the point. The serotonin story is a good example. The notion that the complexity of human psychology that led to depression could be reduced to the activity level of a single neurotransmitter should strike us as an absurd exercise on its face. It's not even wrong, it's a basic misreading of the problem space.
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.
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.
In the link he brings up the "fatty food makes you fat" thing. My memory is that fatty foods were shown to be bad for your heart back in the 1980's and I always wondered where the "makes you fat" part came from. It's almost like once something is labeled (fatty food = bad) people forget the why and substitute their own reasons.
Similar stuff is going on now with saturated vs unsaturated fat. The problem is trans-fat which tends to form in the commercial process for saturating fat, and in the deep fryer. I don't recall any other research, but now there seems to be another "reversal" on saturated fat. Or is it unsaturated? IDK, but the public opinion is getting altered again.
These aren't fully contradictory results. The paper is referring in serotonin in one brain structure, the amygdala. The article was wrong to cast such a broad stroke.
>But every time the accepted explanation does a 180 science dies a little bit
So let's just keep the earth flat then, shall we ;)
This is the beauty of science. If a report on memory that claims X and then another scientist is unable to replicate their results X, what can we say about the validity of X?
It would be the beauty of science if people referred to the weight of the evidence in more accurate language, and if policy makers didn't every now and then find excuses in weakly established conclusions.
I wouldn't treat this as a complete reversal just yet. These kinds of "paradigm changing" studies get shown to be flawed all the time. It's just that the press rarely reports when that happens.
I suspect the reason for the reversal is the accessibility of new tools, namely the PET scan. Whereas in the past, the results were probably based on polling people about their anxiety levels while on SSRIs.
>> 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.
the actual paper contains no such language of course, let me quote the introduction:
> Anxiety disorders are debilitating psychiatric conditions that impose a considerable burden on patients1 and society,2 and social anxiety disorder (SAD) is one of the most common of these conditions.3 The neural underpinnings of excessive social anxiety are not fully characterized, although serotonin (5-hydroxytryptamine) has been suggested to be involved etiologically.4,5
> However, only a few studies have used molecular neuroimaging to examine serotonin dysfunction in SAD directly. A single-photon emission tomography study6 found increased serotonin transporter availability in the thalamus, but not in the raphe nuclei, in patients with SAD relative to healthy control individuals. Also, a positron emission tomography (PET) study7 showed that SAD is associated with reduced serotonin 1A receptor binding. Somatodendritic serotonin 1A autoreceptors in the raphe nuclei, which inhibit serotonin synthesis and release,8 and postsynaptic serotonin 1A heteroreceptors, which convey inhibitory signals in the amygdala, anterior cingulate cortex (ACC), and insula cortex, were downregulated.7 In addition, functional neuroimaging studies of SAD9 have demonstrated heightened, fear-induced neural reactivity in the amygdala, which is densely innervated by serotonin,10 with alterations in the hippocampus, ACC, insula cortex, and striatum.9,11 Moreover, the first line of pharmacologic treatment for SAD consists of selective serotonin reuptake inhibitors (SSRIs),12- 14 which reduce excessive amygdala reactivity, restore initially suppressed ventromedial prefrontal cortex response to emotional challenge,15- 18 and attenuate resting brain perfusion in the ACC and insula.19 Thus, findings from molecular and functional neuroimaging and treatment studies indicate that serotonergic neurotransmission in the amygdala, raphe nuclei, striatum, thalamus, hippocampus, insula cortex, and ACC may be compromised in SAD.
> Given the inhibitory role of serotonin 1A autoreceptors on serotonin synthesis,8 previous findings of decreased autoreceptor binding in SAD7 may indicate increased serotonin formation and enhanced serotonergic activity. On the other hand, because blocking the serotonin reuptake with SSRIs attenuates social anxiety symptoms12,13 and because posttreatment dietary depletion of the serotonin precursor tryptophan reverses the anxiolytic effects of SSRIs,20 the notion that increased serotonin availability is pivotal for anxiety reduction also has support. Indeed, whether anxiety conditions such as SAD are best characterized by serotonin overactivity or underactivity remains a matter of debate.5
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.
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.
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.
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.
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.
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.
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
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.
Been there, 4 years of constant panic attacks. Last 2 years have been great, and the solution was simple. Exercise. I still feel the symptoms now and again. I've merely refactored my programming.
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?
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.
I think it's people usually don't get that these are often just random and not always tied to an event, but vice-versa. Certain situations and interactions can lead up to or trigger attacks, but when it's a real disorder with the fight or flight mechanism, there's often no rational meaning to the sense of panic.
In my case my attacks turned out to be related to a disorder of the autonomic nervous system, which (among lots of other things) results in my response system overreacting to stimuli. It took me a long time to get diagnosed and I've learned to cope by rationalizing my panicky feelings as nothing more than flawed biology. I know that there's nothing really wrong, and I can calm myself down, telling myself it's just my screwed up vagus nerve, before an attack becomes full-blown. Thanks to that I was eventually able to taper off taking Xanax regularly.
But while going through that process I had days where I couldn't even work, and even had a boss drive me to an urgent care place once in a full-blown attack. The work at the time was definitely stressful, but I think the panic attacks exacerbated the work more than the other way around.
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.
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.
the last sentence is particularely intetesting to me. from the other things you've told i would have thought (and i don't know shit, really, so please bear with me) that the management stuff wasn't really what you loved which you wouldn't realize but subconciously you've got burned out.
but again, i basically have no idea. however, i honestly whish you all the best.
I know you probably wrote your post in good faith, and you appear sympathetic to the posts you've replied to in this subthread.
I can see how you would jump to the assumption that there is something "wrong" in the person's life, as this is a universal reference point;
Something bad happens in your life, and you feel bad about it.
But the fact is that most mental illnesses generally aren't a results of anything like what you've described.
There's no meaning behind them, and they're not rational - which is one of the reasons why they are described as illnesses.
This, in addition to severity, is some of the difference between an anxiety disorder and an anxious mood.
So the assumption made is basically dependent on your healthy perspective, and does not take into account the experience of people affected by mental illness.
If you really don't know much about mental illnesses (as you say in your post) I urge you to try to read up, as ignorance and stigma (which is to some extent a result of the former) are huge problems, even though mental illness is very common and affects around 20% of people, depending in the source (NIMH says 18.6 percent of all U.S. adults had a mental illness the previous year in 2012 [0]).
thanks for sharing this. Since i'm in a somewhat comparable situation, would you mind getting in touch? you can find my website, alas email, on my profile page and I think talking about some stuff that worked and didn't work might help me. Thank you.
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.
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.
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.
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.
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)
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.
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?
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.
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.
So, you clearly do not have social phobia. Yes, it is a legitimate disorder, and it can be quite disabling when it's severe.
It's not about not being able to speak in public. Imagine suffering from panic attacks and not being able to leave your house for days, because you're afraid someone will say hi to you. That's social anxiety.
Your attitude "STOP IT. tell them to fit in" is the reason many people with social anxiety, and many other psychiatric disorders end up committing suicide.
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.
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.
> 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?
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.
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).
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.
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.
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.
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.
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.
Almost 10 years ago I read a study that attributed (not too much or too little serotonin), but sending the wrong serotonin allele types for various social situations. This correlated to genetic predispositions to both social anxiety and certain forms of autism. It seems odd these later studies seem to be focusing on a far more general use case of whether more or less serotonin in general is a cause.
ssri's have done more harm than good for me. I simply feel numbed out...have little emotion and a poor memory. It basically kills the emotion -> memory feedback loop that you need to learn and grow. In my experience I felt more stuck on the drug than off them.
They don't even know what serotonin does. Every antidepressants action mechanism is just a shot in the dark, trial and error and it's questionable whether any of them work at all. Yes Tom Cruise is right on this one.
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.
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.
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.
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.
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.