>> 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