A genetic mutation that has been found to cause people to act outrageously when they’re drunk also appears to lower the risk of certain metabolic disorders such as diabetes and obesity. Peculiarly, the mutation has so far only been found in Finnish people, and is thought to affect around 100,000 people in the Nordic country.

The mutation in question inhibits the production of serotonin 2B receptors. Since serotonin is a key regulator of mood and behavior, the absence of this receptor unsurprisingly leads to an inability to control one’s actions, and has been blamed for some of the violent, reckless, and downright stupid conduct of some people when drunk.

In a new study appearing in the Journal of Psychiatric Research, scientists from the University of Helsinki reveal how carriers of this mutation also have higher insulin sensitivity (IS) and lower insulin resistance (IR) than non-carriers. Insulin is a hormone that facilitates the transportation of glucose from the bloodstream into body cells. As such, when cells become insensitive or resistant to insulin, this process grinds to a halt, leading to a rise in blood sugar levels and potentially type 2 diabetes.

The researchers recruited 98 Finnish men, all of whom had been diagnosed with antisocial personality disorder (ASPD). Of these, nine were found to carry the mutation – called HTR2B Q20* - while 89 did not. The study authors then measured the serum glucose and insulin levels of all participants in order to calculate IS and IR indices, discovering that the mutant group was much better off on both measures.

^{Type 2 diabetes arises when body cells become resistant to insulin, resulting in high blood glucose levels. dekdoilongkrung/Shutterstock}

Carriers of the mutation also had lower body mass indices than non-carriers, suggesting that they may be at less risk of obesity.

Intriguingly, the study authors also discovered that carriers of HTR2B Q20* were particularly protected against pathological IS and IR scores if they had low testosterone levels as well. This is surprising, as low testosterone in males is normally associated with a higher risk of diabetes. Indeed, non-carriers with low testosterone were found to have lower IS and higher IR than those with high testosterone.

Though the reason for this effect is still unknown, study author Roope Tikkanen mentioned in a statement that “we could speculate that the compound effect the mutation and testosterone have on energy metabolism may have been beneficial in the cool, nutrition-poor environment after the Ice Age, particularly for men with a high physiological level of testosterone – they would have survived with a lower calorie intake.” In other words, the mutation would have allowed men with high testosterone levels to maintain high blood sugar levels with relatively small amounts of food.