Inferiority of hyperprolactinergics (SSRIs, D2 antagonists)

Currently, various common mental disorders, and especially depression, OCD, and schizophrenia, are treated with drugs whose most prominent effect is to cause hyperprolactinemia. Such drugs include the SSRIs, and the D2 receptor antagonists, such as risperidone and paliperidone. Hyperprolactinemia causes long-term sexual anhedonia, probably via an epigenetic mechanism that shuts down a dopamine-related gene in neurons, in response to the very high prolactin.

The pharmaceutical companies that manufacture the hyperprolactinergics deceptively call them 'anti-depressants' and 'anti-psychotics', yet they are not very effective for those purposes, especially when compared to some other drugs. The pharmaceutical companies have even propagated neuropsychological falsehoods for the purpose of marketting such drugs, by saying that depression and OCD are caused by low serotonin, and that schizophrenia is caused by high dopamine. The truth is that depression is caused by the neurotransmitter glutamate binding to NMDA receptors that have NR2B subunits; OCD is caused by excessive glutamate activity in the caudate nucleus; and the efficacy of 'antipsychotic' drugs is due to their blockage of sigma-1 receptors, rather than their effects on dopamine. The sigma-1 receptor is the same receptor that is activated by the recreational drug PCP.

Therefore depression can be eliminated with absorbable forms of magnesium (glycinate and taurinate forms have proven very effective), as magnesium blocks NR2B-containing NMDA receptors; OCD can be eliminated with the glutamate release inhibitor riluzole; and schizophrenia can be eliminated with the selective sigma-1 receptor antagonist rimcazole.

I was on amisulpride, its one of the worst on prolactin.

I am now on Aripiprazole, it does not increase prolactin. It is, better than the others, so far.