Alcohol and You: An Interactive Body

Alcohol makes it harder for the brain areas controlling balance, memory, speech, and judgment to do their jobs, resulting in a higher likelihood of injuries and other negative outcomes. Long-term, heavy drinking causes alterations in the neurons, such as reductions in their size. As a result of these and other changes, brain mass shrinks and the brain’s inner cavity grows bigger. People with alcohol use disorder (AUD) often have problems with memory, sleep, and mood long after the alcohol wears off.

The developing brain is particularly vulnerable to effects of alcohol. Brain development persists into the mid-twenties, and misuse of alcohol during adolescence and early adulthood can alter the trajectory of brain development, resulting in long-lasting changes in brain structure and function.

In the brain, alcohol exerts its effects by interacting with numerous neurotransmitters and their receptors, with different neurotransmitters producing different behavioral effects of alcohol. One neurotransmitter affected by even small amounts of alcohol is called glutamate. Glutamate plays an important role in the ability of the brain to create new memories. Researchers believe that alcohol interferes with glutamate action, and this may be what causes some people to have an alcohol-related blackout.

Blackouts are gaps in a person’s memory for events that occurred while they were intoxicated. These gaps happen when a person drinks enough alcohol to temporarily block the transfer of memories from short-term to long-term storage—known as memory consolidation—in a brain area called the hippocampus. Evidence suggests that, for the developing brain, the hippocampus is more sensitive to alcohol effects, and adolescents and young adults are more susceptible to alcohol-induced memory impairment than adults.

Another neurotransmitter impacted by alcohol is gamma aminobutyric acid, or GABA. Alcohol interactions with GABA receptors contribute to behavioral effects such as motor incoordination and sedation or sleepiness. Someone who is already feeling sleepy probably will feel sleepier after drinking alcohol.

Long-term heavy drinking weakens the heart muscle, causing a disease called alcohol-associated cardiomyopathy. The left ventricle of the weakened heart dilates, stretches out and can’t contract effectively. As a result, it can’t pump enough blood to sufficiently nourish the organs, leading to oxygen deprivation or ischemia. In some cases, this blood flow shortage causes severe damage to organs and tissues. Symptoms of alcohol-associated cardiomyopathy include shortness of breath at rest and/or on exertion, cough, fatigue, swollen legs and feet, and irregular heartbeat. It can even lead to heart failure.

Both binge drinking and long-term drinking can affect how quickly a heart beats. The heart depends on an internal pacemaker system to keep it pumping consistently and at the right speed. Alcohol disturbs this pacemaker system and causes the heart to beat too rapidly, or irregularly. These heart rate abnormalities are called arrhythmias. Both acute and long-term, chronic drinking may change the course of electrical impulses that drive the heart’s beating, which creates arrhythmia.

Both binge drinking and long-term heavy drinking can lead to strokes, even in people without coronary heart disease. In addition, alcohol exacerbates the problems that often lead to strokes, including hypertension, arrhythmias, and cardiomyopathy.

Chronic alcohol misuse, as well as binge drinking, can cause high blood pressure, or hypertension. Heavy alcohol consumption triggers the release of certain stress hormones that in turn constrict blood vessels that elevate blood pressure. In addition, alcohol may affect the function of the muscles within the blood vessels, causing them to constrict and elevate blood pressure.

When alcohol enters the liver, it is broken down by enzymes such as alcohol dehydrogenase. These enzymes break down alcohol into acetaldehyde, which contributes to inflammation, and other compounds that damage liver cells. Chronic heavy drinking causes the liver to become fatty. This condition makes the liver more vulnerable to dangerous inflammation, such as alcoholic hepatitis, and its associated complications. With continued drinking, persistent inflammation causes fibrous tissue to increase in the liver, which prevents the necessary blood supply from reaching the liver cells. Without the oxygen and other nutrients supplied by this blood, the liver cells eventually die and are replaced with scar tissue, creating a condition known as cirrhosis. In mild cases, the liver can actually make repairs and continue to function. However, advanced cirrhosis causes continued deterioration and liver failure.

Abstinence from alcohol can help prevent further injury and keep alcohol-associated liver disease in check. In the more advanced cases (liver failure), however, liver transplant may be the primary treatment option, in which case alcohol abstinence still represents a critical goal, both before and after the surgery.

The stomach is designed to process and transport food.

After ingestion, alcohol travels down the esophagus into the stomach, where some of it is absorbed into your bloodstream. The unabsorbed alcohol continues to move through the gastrointestinal tract. The majority of it will enter the small intestine and get absorbed into the bloodstream through the walls of the small intestine, or it can stay in the stomach and cause irritation.

While in the stomach, alcohol acts as an irritant and increases digestive juices (hydrochloric acid) that are secreted from the stomach lining. Alcohol can halt the digestive process, robbing the body of vital vitamins and minerals. Chronic irritation may lead to damage to the lining of the stomach. In summary, alcohol misuse, acutely and/or chronically, can cause stomach irritation, gastritis (inflammation of the stomach lining), ulcers, and bleeding. These clinical conditions may be worsened by drinking alcohol and take medications like aspirin that can also cause the same problems.

Alcohol affects the digestive tract, allowing bacteria to escape and circulate in the bloodstream, potentially causing disease. Even a single episode of binge drinking can cause gut leakage.

Binge drinking or chronic alcohol consumption can interfere with kidney function directly, or indirectly as a consequence of the effects of alcohol on other organs (e.g., alcohol-associated liver disease, alcohol-related hypertension, alcoholic cardiomyopathy).

Normally the rate of blood flow through the kidneys is tightly controlled, so that plasma can be filtered and substances the body needs, such as electrolytes (electrically charged particles, or ions), can be reabsorbed under optimal circumstances. Advanced liver disease impairs this important balancing act, however, by either greatly augmenting or reducing the rates of plasma flow and filtration through a mass of capillaries called the glomeruli.

One of the main functions of the kidneys is to regulate both the volume and the composition of body fluid, including electrolytes, such as sodium, potassium, and chloride ions. However, alcohol can have the diuretic effect of increasing urine volume. This in turn can change the body’s fluid level and disturb the electrolyte balance.

Alcohol can augment urine flow within 20 minutes of consumption. As a result of urinary fluid losses, the concentration of electrolytes in blood serum increases. The mild dehydration that results likely contributes to hangover symptoms such as thirst, fatigue, and a headache. Research has not found a correlation between the extent of electrolyte disruptions and the severity of hangovers, or the impact of added electrolytes on hangover severity. In most people, the body will quickly restore electrolyte balance once the effects of alcohol subside. However, these changes can be profound in people with severe AUD, who may demonstrate clinical evidence of dehydration.

The pancreas sends enzymes to the small intestine to metabolize food. Excessive alcohol use disrupts this process. It causes the pancreas to activate these enzymes prematurely and secrete them internally, rather than sending them to the small intestine.

These enzymes are harmful to the pancreas. If you misuse alcohol over a long time, this continued process can cause inflammation, as well as swelling of tissues and blood vessels

This inflammation is called pancreatitis, and it prevents the pancreas from working properly. Pancreatitis can occur as a sudden attack, called acute pancreatitis. Acute pancreatitis can turn into a condition of constant inflammation of pancreas, which is known as chronic pancreatitis. Chronic pancreatitis is a risk factor for the development of pancreatic cancer and pancreatic diabetes. A heavy drinker may not be able to detect the buildup of pancreatic damage until the problems set off an attack.

An acute pancreatic attack causes symptoms including:

• Abdominal pain, which may radiate up the back
• Nausea and vomiting
• Fever
• Rapid heart rate
• Diarrhea
• Sweating

Chronic pancreatitis can have these symptoms as well, which causes significant reduction in pancreatic function and digestion, and blood sugar problems. In people with alcohol use disorder, acute pancreatitis often presents on top of a chronic pancreatitis (“acute on chronic”) and may in some cases lead to both localized and systemic complications including severe and life-threating medical conditions.

It only recently has been recognized that alcohol misuse also increases the risk of acute lung injury following major trauma, such as a serious motor vehicle accident or other event requiring hospitalization, or the spread of bacteria attributed to infection (i.e., sepsis).

The well-known acute intoxicating effects of alcohol and the concomitant risk of aspiration of secretions or foreign material into the trachea and lungs are components in the development of alcohol-associated lung (i.e., pulmonary) disease. Clinical and experimental evidence has emerged that implicates a chronic imbalance in the cell (i.e., oxidative stress) and consequent cellular dysfunction within the layer of tissue lining the airway (i.e., airway epithelium) as well as pathogen-ingesting white blood cells (i.e., macrophages) in the airway. Moreover, now it is recognized that these disruptions in lung function can occur even in young and otherwise healthy individuals long before they develop clinically apparent signs of alcohol-induced organ damage such as liver disease and/or other end-stage manifestations of longstanding alcohol misuse. Based on these recent studies, the concept of the alcohol-impaired lung is emerging, which is characterized by severe oxidative stress that alone may not cause detectable lung impairment but may predispose those who misuse alcohol to severe lung injury if they are unfortunate enough to suffer serious trauma or other acute illnesses, and makes them more prone to lung infections.