INTRODUCTION
Ethanol consumption in moderate amounts is generally not injurious (and may even protect against some disorders). But in excessive amounts alcohol causes serious physical and psychologic damage.
Epidemiology/prevalence of alcohol abuse-
Despite all the attention given to illicit drugs such as cocaine and opiates, alcohol abuse is a far more widespread hazard and claims many more lives. According to a 2017 survey conducted by the National Institute on Alcohol Abuse and Alcoholism, 60% of the people reported using alcohol in the previous month. Even more worrisome is the fact that 14 million of adults (over 18 years of age) suffer from alcohol abuse disorder (AUD) in the United States (5.7% of this age group).
[What is AUD??
AUD( alcohol abuse disorder) is a chronic relapsing brain disease characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences.]
It is estimated that alcohol consumption is responsible for more than 80,000 deaths annually. More than 50% of these deaths result from accidents caused by drunken driving and alcohol-related homicides and suicides,and about 15,000 annual deaths are a consequence of cirrhosis of the liver. Worldwide, alcohol accounts for approximately 3.3 million deaths per year (5.9% of all
deaths).
ALCOHOL METABOLISM…
After consumption, ethanol is absorbed unaltered in the stomach and small intestine. Then ethanol distributes throughout the body in direct proportion to the blood level. Less than 10% ehanol is excreted unchanged in the urine, sweat, and breath.
How does the traffic police do alcohol test??
Traffic police do alcohol test in drunker by the BREATH TEST.
The amount exhaled is proportional to the blood level and forms the basis for the breath test used by law enforcement agencies. A concentration of 80 mg/dL in the blood coconstitutes the legal definition of drunk driving in most states.
For an average individual, alcohol concentration is reached after consumption of three standard drinks, about three (12 ounce) bottles of beer, 15 oz of wine, or 4 to 5 oz of 80-proof distilled spirits.Drowsiness occurs at 200 mg/dL, stupor at 300 mg/dL, and coma, with possible respiratory arrest, at higher levels.
The rate of metabolism affects the blood alcohol level. Chronic alcoholics develop tolerance to alcohol. They metabolize alcohol at a higher rate than normal.
Most of the alcohol in the blood is metabolized to acetaldehyde in the liver by three enzyme systems: alcohol dehydrogenase, cytochrome P-450 isoenzymes, and lastly catalase . Of these, the main enzyme involved in alcohol metabolism is alcohol dehydrogenase, located in the cytosol of hepatocytes.
At high blood alcohol levels, however, the microsomal ethanol oxidizing system also plays an important role. This system involves cytochrome P-450 enzymes, particularly the CYP2E1 isoform, located in the smooth endoplasmic reticulum.
Alcohol may delay other CYP2E1 substrates metabolism………
However, when alcohol is present in the blood at high concentrations, it competes with other CYP2E1 substrates and may delay the catabolism of other drugs, thereby potentiating their effects.
Catalase is of minor importance, being responsible for only about 5% of alcohol metabolism. Acetaldehyde produced by these systems is in turn converted by acetaldehyde dehydrogenase to acetate, which is used in the mitochondrial respiratory chain or in lipid synthesis.
Several toxic effects result from ethanol metabolism. Listed here are only the most important of these….
• Acetaldehyde,
Acetaldehyde direct product of alcohol oxidation, has many toxic effects and is responsible for some of the acute effects of alcohol. Many individual are completely unable to oxidize acetaldehyde and cannot tolerate alcohol, experiencing nausea, flushing, tachycardia,and hyperventilation after its ingestion.
•furthermore, Alcohol oxidation by alcohol dehydrogenase causes the reduction of nicotinamide adenine dinucleotide (NAD) to NADH, with a consequent decrease in NAD and increase in NADH. NAD is required for fatty acid oxidation in the liver and for the conversion of lactate into pyruvate. Its deficiency is a main cause of the accumulationof fat in the liver of alcoholics. The increase in the NADH/NAD ratio in alcoholics also causes lactic acidosis.
• ROS ( reactive oxygen species)generation.
Metabolism of ethanol in the liver by CYP2E1 produces ROS, which cause lipid peroxidation of hepatocyte membranes.
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Alcohol also provokes the release of endotoxin (lipopolysaccharide) from gramnegativebacteria in the intestinal flora, which stimulates the production of tumor necrosis factor. (TNF) and other cytokines from macrophages and Kupffer cells, leading to hepatic injury.
Adverse effects of ethanol
The adverse effects of ethanol can be classified as acute or chronic.
Acute alcoholism.
Acute alcoholism exerts its effects mainly on the CNS, but it may induce hepatic and gastric changes that are reversible if alcohol consumption is discontinued. Even with moderate intake of alcohol, multiple fat droplets accumulate in the cytoplasm of hepatocytes (fatty change or hepatic steatosis). The gastric changes are acute gastritis and ulceration. In the CNS, alcohol is depressants. progressively higher blood levels, cortical neurons and then lower medullary centers are depressed, including those that regulate respiration.Respiratory arrest may follow.
Chronic alcoholism.
Chronic alcoholism affects not only the liver and stomach, but virtually all other organs and tissues as well.Chronic alcoholics suffer significant morbidity and have a shortened lifespan, related principally to damage to the liver, gastrointestinal tract, CNS, cardiovascular system, and pancreas.
• firstly the liver is the main site of chronic injury.
Chronic alcoholism causes fatty changes in liver, alcoholic hepatitis and cirrhosis. Cirrhosis is associated with portal hypertension and an increased risk for the development of hepatocellular carcinoma.
• In the gastrointestinal tract,
chronic alcoholism can cause massive bleeding from gastritis, gastric ulcer, or esophageal varices (associated with cirrhosis), which may be fatal.
• Neurologic effects.
Thiamine (vitamin B1) deficiency is common in chronic alcoholics; the principal lesions resulting from this deficiency are peripheral neuropathies and Wernicke-Korsakoff syndrome ; cerebral atrophy, cerebellar degeneration,and optic neuropathy may also occur.
• Cardiovascular effects.
Alcohol has diverse effects on the cardiovascular system. Injury to the myocardium may produce dilated congestive cardiomyopathy (alcoholic cardiomyopathy. Chronic alcoholism is also associated with an increased incidence of hypertension, and heavy alcohol consumption, with attendant liver injury, results in decreased levels of highdensity lipoprotein (HDL), increasing the likelihood of coronary heart disease.
• Pancreatitis.
Excessive alcohol intake increases the risk of both acute and
chronic pancreatitis .
• Fetus.
The use of ethanol during pregnancy can cause fetal alcohol syndrome. which is marked by microcephaly, growth retardation, and facial abnormalities in the newborn and reduction in mental functions as the child grows older. It is difficult to establish the minimal amount of alcohol consumption that can cause fetal alcohol syndrome.But consumption during the first trimester of pregnancy is particularly harmful.
• Carcinogenesis.
Chronic alcohol consumption is associated with an increased incidence of cancer of the oral cavity, esophagus, and liver. In women, low to moderate intake (12 oz beer or 5 oz of wine) incurs a slightly higher risk of breast cancer. Undoubtedly, Alcohol and cigarette smoke synergize in the causation of various cancers.
• Malnutrition.
Ethanol is a substantial source of energy (empty calories). Chronic alcoholism leads to malnutrition and nutritional deficiencies, particularly of the B vitamins.