While the meta-study only reviewed studies about blocking the 5-HT3 receptor, other studies listed below directly implicate the 5-HT1, 5-HT2 and 5-HT7 receptors as well, which strengthens the hypothesis that serotonin (5-HT) as a whole is the driver of OCD. In addition, consider the fact that the drug Meta-Chlorophenylpiperazine (mCPP) is perhaps the most widely-used and well-researched agent for causing\/exacerbating OCD. That drug is also the perfect synthetic surrogate of serotonin – i.e. it is an agonist on most 5-HT receptors, it increases serotonin release, and also acts as an SSRI. Hard to get more serotonergic than this.<\/p>\n
https:\/\/en.wikipedia.org\/wiki\/Meta-Chlorophenylpiperazine<\/a><\/p>\n The old ergot derivative metergoline<\/a> – a non-selective serotonin antagonist – has been shown to block the pro-OCD effects of mCPP.<\/p>\n https:\/\/pubmed.ncbi.nlm.nih.gov\/2018816\/<\/a><\/p>\n To me at least, the evidence above alone means cased closed on the causes and cures of OCD, but since it is only one study I decided to also add the ones below. If that serotonin-as-a-cause-of-OCD hypothesis is correct, then the current treatment of OCD with the serotonergic SSRI drugs is nothing short of criminally negligent and may explain to a great degree why OCD rates continue rising (especially in children and young adults) – i.e. the rising usage of SSRI drugs by those age groups are likely directly contributing to the rising rates of OCD.<\/p>\n https:\/\/academic.oup.com\/ijnp\/article\/8\/3\/391\/910011<\/a><\/p>\n https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3310222\/<\/a><\/p>\n https:\/\/psycnet.apa.org\/record\/2010-07003-006<\/a><\/p>\n