Antisocial personality disorder (ASPD) is a mental condition in which a person exhibits a pattern of repeated disregard for and violation of others’ rights. The Diagnostic and Statistical Manual of Mental Disorders (DSM) provides the framework for diagnosing ASPD. The prevalence rate of ASPD is high in prisons. Genetics, epigenetics, neuroscience, sociology, epidemiology, psychology, and other behavioral science fields have attempted to find a primary etiology. Despite decades of research, the precise etiology of ASPD has not been found, and its pathophysiology remains a complex question. The interaction between genes and the environment appears to be a significant factor in the development of ASPD. Brain imaging in subjects with ASPD has revealed structural brain changes in those with ASPD. Individuals with ASPD are challenging to manage for health care providers because of their complicated clinical presentation, high comorbidity of medical and mental disorders, lack of licensed pharmacotherapies for ASPD, and increased utilization of healthcare resources. ASPD requires tremendous effort from treating clinicians. Clinicians can successfully manage individuals with ASPD if they remain aware of the unique challenges of these patients while thoughtfully applying available research.

A single perspective cannot explain the entirety of serial murder. In psychology, we promote a biopsychosocial model of understanding any behavior or mental process. The author provides a summary of various perspectives, starting with behavioral neuroscience (i.e., biopsychology). She summarizes direct evidence from case studies showing neural issues in serial murderers, implied evidence of brain dysfunction of serial murders, and evidence of no neural issues in serial murderers. She then discusses the biological correlates of violence in general. The case of MSK Joseph DeAngelo highlights crime solved through forensic genetic genealogy.

People often find statistics confusing because anecdotes more effectively tell stories and no one’s direct experience matches the statistical realities. The younger any individual is introduced to any drug the higher the risk of developing dependence. This is especially true for marijuana because it affects neurodevelopment in early adolescence. However, Horwood has shown than the lifetime rate of marijuana dependence does not accurately portray the overall progression of use because the majority of those who ever become dependent discontinue or reduce use sufficiently to no longer meet the DSM criteria for Cannabis Use Disorder (CUD). While 43% of those with onset of marijuana use at 13 years old meet criteria for CUD at some time by age 30, only 15% are dependent during the previous year at 30. The generally accepted rate of CUD for those 12 and older who have ever used marijuana is approximately 9%, compared to a 15% dependence rate for alcohol. The more frequently individuals use marijuana, the more they use on each occasion. The increased rates of marijuana use in Conduct Disorder (CD), Antisocial Personality Disorder (ASPD) and Attention Deficit Hyperactivity Disorder (jsADHD) are discussed.