Chemical processes of alcohol consumption and social behavior pattern of alcoholics.

Alcohol consumption remains a major global public health and social challenge, driven by complex interactions between biochemical processes and sociocultural dynamics. This study critically examines the chemical pathways of ethanol metabolism and their relationship with the social behavior patterns observed among individuals with alcohol use disorder (AUD). Drawing on an interdisciplinary narrative review of peer-reviewed literature in biochemistry, neuroscience, psychology, sociology, and public health, the paper synthesizes evidence on how alcohol dehydrogenase, aldehyde dehydrogenase, and cytochrome P450 (CYP2E1) pathways mediate intoxication, tolerance, dependence, and long-term physiological harm through acetaldehyde toxicity and oxidative stress. These biochemical mechanisms are analytically linked to neurochemical adaptations involving GABAergic, glutamatergic, dopaminergic, and stress-related systems that underpin craving, withdrawal, impaired self-control, and compulsive drinking. Beyond biological mechanisms, the study situates alcohol-related behaviors within broader social contexts, highlighting the roles of social learning, peer influence, stress coping, family dynamics, and cultural norms. Particular attention is given to low- and middle-income settings, with reference to Nigeria, where informal alcohol markets, gendered drinking norms, stigma, and weak treatment infrastructures intensify social and health consequences. The review identifies persistent fragmentation between biological and sociological research and underscores gaps in longitudinal, context-specific, and African-centered evidence. The study concludes that alcohol dependence is best understood as both a biochemical disorder and a socially embedded phenomenon, and it advocates for integrated, culturally responsive prevention, treatment, and policy approaches.