Yet another study showing that mainstream medicine’s claims about the origins of a mental health condition are just about the opposite of the true underlying cause(s). Namely, compulsive sexual behavior disorder (CSBD), which medicine has claimed for decades to be driven by excessive dopamine levels/signalling. The study below demonstrated that patients with CSBD have reduced expression of the so-called serotonin transporter (SERT) – a protein responsible for the uptake and deactivation of 5-HT – thus leading to elevated extracellular levels of 5-HT. It just so happens that SERT inhibition is the main target of the selective serotonin reuptake inhibitor (SSRI) drugs – the “standard of care” therapy for a plethora of mental health conditions, especially clinical depression, anxiety, PTSD, etc. In contrast, the study found no difference in dopamine signalling between healthy people and CSBD patients. Since SSRI drugs are so widely used globally, it would not be too far-fetched for a reasonable person to conclude that the epidemic of CSBD (as well as most other mental health disorders) is iatrogenic in nature and largely driven by the indiscriminate prescription and use of said SSRI drugs, as well as chronic stress (which also inhibits SERT while also increasing 5-HT synthesis, especially in the gut).
https://www.sciencedirect.com/science/article/abs/pii/S0166432825004590
“…Analysis revealed significantly higher methylation of the 5HTT/SLC6A4 (serotonin transporter gene), suggesting reduced central expression of the serotonin transporter in the CSBD individuals. Group differences in 5HT3A receptor gene methylation were non-significant; however, the threshold of significance reached was suggestive of a potential effect. Larger sample size and increased statistical power would be needed to provide stronger statistical evidence. These findings were further supported by correlations between the methylation status of these two serotonergic genes and sexual outlet indicators in the control group. Importantly, no such association was observed in CSBD patients, which may suggest a lack of epigenetic regulatory feedback, potentially leading to suboptimal signalling of sexual drive and satiety. Notably, no epigenetic differences were observed for dopaminergic targets (DRD2 receptor gene and DAT/SLC6A3 transporter gene).”
