There will be no statistics in this article. There will be no suggestive statements or propaganda intending to downplay the level of alcohol consumption by college students. Students drink alcohol, and alcohol is the major staple of social events in college. The purpose of this column is to provide a practical primer on the use and physiological effects of this drug.
Ethanol, generally referred to as alcohol, is the oldest drug known to man, and as a consequence it has been well characterized. It is important, however, not to mistake this familiarity for safety. One should take the following measures when drinking, especially when intending to drink heavily:
-- Have friends that are with you the entire night
-- Eat a substantial meal
-- Drink water between each alcoholic drink
-- Take a multivitamin containing complex B vitamins, vitamin C, vitamin E, but not vitamin A, caffeine, salicylic acid (Aspirin) or acetaminophen (Tylenol).
The majority of ethanol-related maladies and fatalities occur from physical harm due to poor decisions or motor control (i.e. motor vehicle accidents, drowning, risky sexual behaviors, etc.), not from the toxic effects of ethanol exposure. Thus, the most dangerous effects of ethanol are upon cognitive functioning and decision-making, making external control and security through other individuals vitally important.
The immediate observable consequences of ethanol intake are mostly attributed to its effects on neuron firing. High concentrations of ethanol block calcium channels necessary for synaptic release of neurotransmitters in normal cognitive function. Additionally, ethanol induces the increased release of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter. These two actions are the basis for regarding ethanol as a depressant and the relaxed state associated with ethanol consumption.
A state of euphoria associated with an initial rise in blood alcohol levels likely results from increased dopamine and endogenous opioid release in the mesolimbic and prefrontal cortex, respectively (Alcohol, 1996). It should be noted that these two interconnected circuits have important consequences on reward and drive behavioral responses, especially related to sex and food, providing possible explanatory power to certain ethanol-related phenomena including reduced adherence to socially-imposed inhibitions.
The fact that ethanol can induce both euphoria and depression is demonstrative of a biphasic effect: At lower levels, ethanol can potentiate neurotransmitter release and brain activity as measured through electroencephalograms (EEG), yet higher levels of ethanol yield central nervous system (CNS) depression, loss of consciousness, suppression of autonomic processes such as respiration, coma and death.
Having a substantial meal prior to ingestion of ethanol alters the manner in which ethanol reaches the bloodstream. The effects of ethanol that we associate with drinking occur as a result of higher concentrations of the alcohol in the blood. Under fasting conditions, the majority of the ethanol is absorbed by the small intestine, a faster route of entry to the bloodstream than the stomach. When one consumes a full meal, the pyloric valve between the stomach and the small intestine closes, thus slowing access of ethanol to the bloodstream providing more time for the liver to break down ethanol into acetaldehyde and acetic acid.
Further, drinking water will counteract the diuretic effects of ethanol that result in dehydration, but will not restore vitamins lost in this process. Thus, it is necessary to supplement these vitamins. Certain vitamins, including B vitamins (especially thiamine), vitamin C and vitamin E have been shown to counteract some of the detrimental neurological and liver effects of ethanol consumption.
One should not, however, take aspirin, Tylenol (acetomeniphen), or vitamin A while consuming alcohol as these agents may potentiate the damaging effects of ethanol to the gastrointestinal tract and the liver.
As a final cautionary note, repeated consumption of excessive amounts of ethanol (i.e. binge drinking) has been shown to result, both statistically and mechanistically, in increased incidences of liver damage, memory loss and even certain types of cancer. Although alcohol is often treated as a fairly innocuous substance with positive cardiovascular and neurological effects in low doses, the damage done by excessive consumption will outweigh those positive effects.
Michael can be reached at michaelmcduffie@cavalierdaily.com
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