PL-3. Biochemical and Molecular Genetic Factors in Habitual Violence and Antisocial Alcoholism: Control and Preventive Interventions

Serotonin has been found to be in central place in impulsive and habitual violent tendencies and personality disorders. Low brain serotonin turnover (CSF 5HIAA) together with glucose metabolism aspects in the shorter and together with low noradrenaline turnover (CSF MHPG) in the longer follow up have in biological factors been able to predict further violences among   prisoners with antisocial personality disorder (ASP). ASP offenders make even 80 per cent of all habitual violence. There are preliminary molecular genetic findings in sibpair linkage analysis of serotonin 1 B receptor gene in chromosome 6 or area near it being the genetic base in antisocial alcoholism (ASP and type 2 alcoholism connected with it). This suits to this serotonin receptor, alcohol and aggression studies among laboratory animals. Treatments with medicines and dietary means in violent tendencies are in a very preliminary phase. There are, however, findings that at least serotonin uptake inhibitor, fluoxetin, lithium carbonate, beta adrenergic blockers and atypical neuroleptic, clozapine can be effective in violence. The most interesting class of medicines possibly coming to the picture is serotonin 1B agonists also because of the new molecular genetic findings. It is possible that also by changing nonesterified fatty acids in the diet and especially omega-3 fatty acid, docosahexaenoic acid (22:6n3) we can get results in impulsive habitually violent tendencies and even in the ASP. This fatty acid has been found to correlate with CSF 5HIAA among adult violent offenders and early onset alcoholics. Maternal smoking during pregnancy is connected with conduct disorder problems of the child which is often known to continue to ASP in the adulthood. So this also makes an important means of prevention but the exact biological mechanism is unclear. In the future treatment and preventive studies it is important to understand the normal progress in ASP and why the disorder diminishes often in the middle age and what are the brain transmitter and metabolic changes connected with it.