The dysfunction of these systems is responsible for acute alcohol intoxication, alcohol dependence, and withdrawal syndrome. It covers the process of the progression from habit to compulsion. You can read more about the neurobiological basis of addiction in a previous post we covered. Levels of MAO‑A expression (an enzyme that breaks down serotonin), and this decrease in MAO‑A levels correlates with an increase in antisocial behaviour, which is a risk factor for alcohol dependence.Īlcohol (ethanol) is liposoluble and can cross the blood-brain barrier where it has been shown to interact directly, and indirectly, with a wide range of neurotransmitters and hormones such as γ-aminobutyric acid (GABA), glutamate, dopamine, opioids, epinephrine, norepinephrine, serotonin, acetylcholine, cannabinoids, corticotropin-releasing factor (CRF), and neuropeptide Y.Īlcohol dependence is characterised by deficits in the physiological dysregulation of motivation and reward systems, such as those in the limbic system, hippocampus, amygdala, caudate nucleus, frontal lobe and nucleus accumbens.
Young males who have experienced a traumatic event can develop low Variation in genes encoding enzymes involved in the metabolism of alcohol dehydrogenase or aldehyde dehydrogenase has been shown to influence the risk of alcohol dependence. However, one of the strongest predictors is the genetic disposition of an individual, with heritability estimated to range between 50% and 64% of cases. The etiopathogenesis of alcoholism involves a complex interplay between biological, psychological and socio-environmental factors.
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