Why Do People With Alcohol Use Disorder Drink?

Environmental Factors

Like most behavioral health disorders, AUD is a combination of genetic and environmental factors. Research indicates the influence of a person’s genetic makeup and surroundings are equally responsible for the development of substance use and often influence one another. While biology impacts some aspects of personality, most people cannot control the world into which they are born. 

Society, community, and social networks are three primary mechanisms contributing to substance use. These mechanisms either nurture and create opportunity – therefore preventing substance use – or they can contribute to the development of addiction by providing adverse, constraining experiences.

Societal mechanisms responsible for AUD include poverty, racial disclusion, and a lack of job opportunities. Within the community, advertising, the presence of easily accessible alcohol retailers, and elevated crime rates contribute to higher rates of alcohol misuse. Individuals exposed to excessive alcohol use in the home also tend to engage in problematic drinking more often than those raised in a home where alcohol use was monitored and limited. Likewise, a history of childhood abuse or exposure to traumatic stressors in adolescence can trigger negative drinking behaviors in young adults.

Chemical Imbalance

Besides the role environment plays in alcohol dependence, biological elements are equally provoking. Brain chemicals (neurotransmitters) are responsible for mood, energy levels, sleep, stress, pain, and other bodily functions. Several neurotransmitters are implicated in alcohol use and mental health conditions linked to excessive drinking. Because alcohol is a nervous system depressant (or “downer”), It blocks some excitatory brain chemicals while triggering some inhibitory neurotransmitters. 

GABA

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter. Alcohol intensifies GABA’s effects, leading to short-term memory loss and poor muscle control. The anxiety-reducing and sedating properties associated with alcohol’s effects on GABA receptors contribute significantly to its addictive potential. Approximately 75% of individuals with AUD have a pre-existing anxiety disorder, indicating alcohol is frequently used to self-medicate.

Glutamate

Glutamate is an excitatory neurotransmitter or “upper.” It is strongly implicated in developing alcohol dependence due to the changes drinking triggers in the brain. Alcohol blocks glutamate’s stimulating effects, resulting in memory impairment and sedation. Long-term drinking may increase the number of glutamate receptors in the brain to offset the inhibitory effects of alcohol. When someone reduces their alcohol intake, the newly formed receptors remain, leaving the brain in a more anxious, excitatory state that reinforces the need for a substance.

Dopamine

More than other neurotransmitters, dopamine is heavily linked to the brain’s reward system. Drinking causes a dopamine surge that increases the experience of pleasure. The more alcohol a person consumes, the greater the feel-good sensations. As a result, the pleasant effects of alcohol use encourage acute intoxication and contribute to the unpleasant withdrawal symptoms preceding relapse.

Serotonin

Serotonin is the brain chemical associated with feelings of satisfaction and well-being. Drinking depletes serotonin, potentially increasing anxiety and depression. Individuals with AUD continue drinking to mitigate these adverse effects. Most importantly, under the influence of alcohol, serotonin triggers an increase in GABA and dopamine activity to reinforce drinking habits.