Ethanol addiction
Ethanol addiction, commonly referred to as alcoholism, is a condition characterized by an individual's compulsive consumption of alcoholic beverages, leading to physical and psychological dependence. Ethanol is a psychoactive substance found in various alcoholic drinks, and its effects on the body can result in both immediate and long-term health risks. The metabolism of ethanol occurs in the liver, where it is broken down into acetaldehyde, a toxic byproduct that can contribute to adverse effects such as hangovers and liver damage.
The neurologic impact of ethanol is significant, as it interacts with brain receptors and neurotransmitters, influencing behavior, coordination, and judgment. Factors such as genetic variations and cultural practices can affect individual susceptibility to addiction and the way ethanol is metabolized in different populations. With a rich history of use in many cultures, ethanol consumption is often intertwined with social rituals and activities, though the rise of trends like mixing alcohol with energy drinks raises additional concerns about its health implications. Understanding ethanol addiction requires a nuanced approach that considers biological, psychological, and social factors, ensuring respectful and informed discussions around the topic.
Subject Terms
Ethanol addiction
Also known as: Alcohol; ethyl alcohol; EtOH; grain alcohol; neutral spirit
Definition: Ethanol, a small molecule with the chemical formula CH3CH2OH, occurs as a natural result of the microbial fermentation of sugars. Humans control fermentation and distillation to produce ethanol for use in alcoholic beverages and for industrial purposes.
Status: Usually legal but highly regulated and taxed in the United States and many other countries
Classification: Controlled by various federal, state, and local laws
Source: Produced for human consumption in alcoholic beverages; produced industrially to use as a solvent, a fuel additive, and for other applications; amateur winemakers and brewers may make small quantities legally in the United States; occurs naturally in foods such as fresh bread and some fruit juices
Transmission route: Ingestion, almost entirely of ethanol-containing liquids
History of Use
Consumption of ethanol predates written human history. Even animals may behave as if inebriated when consuming overripe fruit containing ethanol naturally. Characteristic fermented grain and fruit beverages are part of many cultures. A current trend is mixing alcoholic beverages with so-called energy drinks containing caffeine and other pharmacologically active substances.
Effects and Potential Risks
Ethanol metabolizes in a deceptively simple manner in animals, including humans. Ethanol oxidizes in two steps to acetate, which enters normal metabolism without pharmacologic effect. Acetate accounts for the high caloric content of ethanol (7.1 calories per gram). Reduced cofactors generated by oxidizing ethanol explain its fat-sparing ability and how it causes hypoglycemia (high blood sugar) and lactic acidosis when taken in excess.
Oxidative conversions are carried out by two enzymes widely distributed in nature: alcohol dehydrogenase and aldehyde dehydrogenase. The intermediate acetaldehyde is toxic and accounts for some of ethanol’s toxic effects, such as hangover symptoms and cirrhosis (irreversible liver damage), and accounts for ethanol sensitivity in some people. Ethanol itself accounts for neurologic effects like inebriation (with loss of inhibition and coordination) and addiction (alcoholism).
After ingestion and absorption from the gut, ethanol in the bloodstream reaches liver, lungs, and other tissues and organs. Ethanol affects the brain directly, in a variety of complex and little-understood interactions. Excess imbibition leads to delayed oxidation in liver, inebriation and other brain effects, and release of acetaldehyde into the blood, which causes headache, nausea, and other delayed symptoms typical of hangovers.
Ethanol’s neurologic effects on the brain result from the direct interaction of the ethanol molecule with protein receptors in the membranes of neurons. Several proteins and the genes that encode them have been implicated, including those responsible for neurotransmitters involved in addiction to other substances. Different gene frequencies probably account for ethnogeographic variation of ethanol metabolism and alcoholism among various human groups.
Bibliography
Berg, Jeremy M., John L. Tymoczko, and Lubert Stryer. Biochemistry. 8th ed. New York: Freeman, 2010.
Haseba, T., and Y. Ohno. “A New View of Alcohol Metabolism and Alcoholism: Role of the High-Km Class III Alcohol Dehydrogenase (ADH3).” International Journal of Environmental Research and Public Health 10 (2010): 1076–92. Print.
Manzo-Avalos, Salvador, and Alfredo Saavedra-Molina. “Cellular and Mitochondrial Effects of Alcohol Consumption.” International Journal of Environmental Research and Public Health 12 (2010): 4281–4304. Print.