Hypersexual disorder or sex addiction is defined as an overactive sex drive and is listed as an impulse-control disorder by the World Health Organization (WHO).

The disorder is characterised by a compulsion to perform sexual acts, obsessive thoughts about sex, a lack of control or sexual habits that may harm the individual or others.

It has been said that approximately 3–6% of the population are affected, and now research has found that the hormone oxytocin may be to blame. 

Altered regions of DNA

The study, published in Epigenetics, found that hypersexual disorder could potentially be treated by engineering a way to suppress oxytocin activity. DNA patterns in the blood of 60 patients with hypersexual disorder were measured and compared to 33 samples from healthy volunteers.

8 852 regions of DNA methylations were investigated to identify any variations between the samples. DNA methylation can affect gene expression and the function of genes, which can reduce their activity. Findings were also compared to samples from 107 subjects, of which 24 were alcohol dependent, in order to explore an association with addictive behaviour. 

It was revealed that there were two region of DNA that were altered in hypersexual patients. The DNA identified targets genes that are not normally expressed at particularly high levels in the brain and are involved in the regulation of oxytocin. Oxytocin plays a central role in the regulation of pair-bonding behaviour.

Treatment for hypersexuality

The comparison with alcohol-dependent subjects revealed the same DNA region to be significantly under-methylated, suggesting that it may be primarily associated with addictive components of hypersexual disorder, which include sex addiction, dysregulated sexual desire, compulsivity and impulsivity. 

Adrian Bostrom, from the department of Neuroscience at Uppsala University, Sweden, who conducted the study with researchers from the Andrology/Sexual Medicine Group (ANOVA) at Karolinska Institutet said, “We set out to investigate the epigenetic regulatory mechanisms behind hypersexual disorder so we could determine whether it has any hallmarks that make it distinct from other health issues.” According to Bostrom, this study is the first of its kind seeking treatment for hypersexuality.

The authors noted that the mean difference in DNA methylation was around 2.6% between patients with hypersexual disorder and healthy volunteers, so the impact on physiological changes could be questioned. However, evidence suggests that even subtle methylation changes could have wide-ranging consequences for more complex conditions such as depression or schizophrenia. 

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Deeanne Daniels