Alcohol Dependency | How Does Your Body Signal a Reliance on Alcohol?

Alcohol tolerance is a primary physical sign of developing dependency. It occurs when the body and brain adapt to the persistent presence of alcohol, leading to a diminished response over time. This process unfolds in two main ways. First is 'metabolic tolerance,' where the liver becomes more efficient at breaking down alcohol by increasing the production of specific enzymes, primarily alcohol dehydrogenase. This means alcohol is cleared from the bloodstream faster. Second, and more significantly, is 'functional tolerance,' which happens in the central nervous system. The brain's nerve cells (neurons) adjust their own sensitivity to alcohol. Chronic alcohol exposure suppresses the activity of glutamate, an excitatory neurotransmitter, while enhancing the activity of GABA, an inhibitory neurotransmitter. To counteract this constant suppression, the brain compensates by increasing its baseline level of excitability. As a result of these adaptations, an individual must consume progressively larger amounts of alcohol to achieve the same mood-altering effects, such as relaxation or euphoria, that were once achieved with smaller quantities. This escalating consumption is a key behavioral indicator that tolerance has developed and is a foundational component of alcohol dependency, creating a cycle of increased drinking to overcome the body's adaptations.

Alcohol withdrawal describes the range of symptoms that occur when a person who is physically dependent on alcohol suddenly stops or significantly reduces their intake. These symptoms are the direct result of the brain's previous adaptations to the presence of alcohol. As explained with tolerance, the brain of a chronic drinker operates in a hyper-excited or "up-regulated" state to counteract alcohol's sedative effects. When alcohol is abruptly removed, the sedative agent is gone, but the brain's compensatory hyperactivity remains. This imbalance leads to a state of overstimulation, causing the classic symptoms of withdrawal. These typically begin within 6 to 24 hours after the last drink and can include hand tremors (commonly known as "the shakes"), anxiety, insomnia, sweating, headache, and nausea or vomiting. These initial signs indicate that the central nervous system is rebounding from the depressive effects of alcohol and struggling to re-establish a normal state of equilibrium without the substance it has grown dependent on.

Beyond the initial symptoms, severe alcohol withdrawal can progress to life-threatening conditions. One such condition is alcoholic hallucinosis, where individuals experience auditory, visual, or tactile hallucinations. More dangerous are generalized tonic-clonic seizures, which can occur within 24 to 48 hours of cessation. The most severe form of withdrawal is Delirium Tremens (DTs). This is a medical emergency characterized by profound confusion, disorientation, agitation, fever, dangerously high blood pressure, and rapid heartbeat. DTs typically appear 2 to 3 days after stopping drinking and result from the extreme over-activity of the nervous system. It requires immediate hospitalization as it carries a significant risk of mortality if left untreated.

Long-term alcohol dependency often manifests in noticeable changes to a person's physical appearance. The skin is frequently affected; persistent flushing and redness of the face can occur due to the dilation of blood vessels. Over time, this can lead to the development of spider angiomas, which are small, web-like collections of broken capillaries, especially on the face, neck, and chest. Facial bloating and puffiness are also common, resulting from dehydration, inflammation, and poor nutrition. In cases of significant liver damage, jaundice—a yellowing of the skin and the whites of the eyes—can occur. This is a sign that the liver is failing and can no longer effectively process bilirubin, a yellow pigment.

The long-term consequences of alcohol dependency on the liver and brain are severe and can be irreversible. The liver is particularly vulnerable, as it is the primary site of alcohol metabolism. The damage progresses through stages, beginning with alcoholic fatty liver disease, where fat accumulates in liver cells. This can advance to alcoholic hepatitis, which is inflammation of the liver. The final stage is cirrhosis, a condition where healthy liver tissue is replaced by scar tissue, severely impairing the organ's ability to function. Cirrhosis is irreversible and can lead to liver failure. In the brain, chronic alcohol use leads to significant structural and functional changes. It causes brain shrinkage, particularly in the prefrontal cortex and cerebellum, which are responsible for executive functions (like decision-making and planning) and motor coordination, respectively. This results in cognitive deficits, memory loss, and problems with balance. A specific and devastating brain disorder associated with chronic alcoholism is Wernicke-Korsakoff syndrome, which is caused by a severe deficiency in thiamine (vitamin B1). It presents first as Wernicke's encephalopathy, with confusion and eye movement abnormalities, and can progress to Korsakoff's psychosis, a chronic memory disorder characterized by an inability to form new memories.