A Proposed Neurodevelopmental Model of Alcoholism (pp. 35-48)
Authors: Ann M. Manzardo (University of Kansas Medical Center, USA)
Abstract: The Danish Longitudinal Study on Alcoholism has identified several specific developmental markers in childhood that appear to predict Lifetime Alcohol Dependence in adult men. These markers resemble neurodevelopmental and molecular abnormalities that are associated with oxidative insults occurring in the perinatal period. This observation has led to the hypothesis that perinatal oxidative insult may contribute to the etiology of alcoholism. The Neurodevelopmental Model of Alcoholism proposes that the vulnerability to alcoholism in adults is increased by oxidative insults or other perinatal events that interfere with, or disrupt, the normal development of brain reward systems. Oxidative brain injury in neonates can arise from many sources: premature birth; perinatal hypoxia or hemorrhage; severe nutritional deficiency; prenatal viral infection, fetal alcohol exposure or exposure to other drugs and toxins. Such insults can result in relatively mild to severe developmental abnormality. The model suggests that oxidative insult very early in life has at least two major effects that can increase the risk for developing alcoholism. First, brain abnormalities acquired early in life could impair communication between important reward centers in adulthood. This disruption in communication could alter the perception of rewarding events, leading to an increased risk for alcoholism (direct effects). Second, abnormal development of brain systems important for behavioral regulation could impair internal controls over impulse-driven behaviors leading to escalated alcohol abuse (indirect effects). Differing contributions of both direct and indirect effects may offer the best explanation for the true clinical manifestation of the disorder. The proposed Neurodevelopmental Model of Alcoholism shifts the focus of research on the etiology of alcoholism to early developmental events that might ultimately define how an individual responds to alcohol. The model broadens the scope of research in the field to include an array of systems never before considered as possible mediators of alcoholism. This novel perspective on the origins of alcoholism could have far-reaching implications for research and treatment.