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Alcohol < Back

By Erik Buchholz

History   

Alcohol has a long history. Beer can be traced back to 3700 B.C. in Egypt, and wine can be traced back to 1700 B.C. in Babylonia. Some historians claim alcohol as a contributing factor to the fall of Rome: members of the Roman upper classes enhanced the flavors of their alcohol with compounds containing lead, which may have contributed to symptoms of confusion and dementia in their leaders. In Europe, alcohol use was divided along social class lines: the poor drank gin, and the rich drank beer. In America, the Continental Army provided rations of rum to its soldiers. By the 1830s, the temperance movement blamed alcohol for all societal ills, such as broken families, poverty, and aggression. Consequently, the United States passed the Eighteenth Amendment in 1917, forbidding the sale of alcohol. However, illegal alcohol production skyrocketed, organized crime controlled the production, and toxic forms of alcohol were sold. As a result, the amendment was repealed in 1933.



Alcohol is the natural product of yeast fermenting objects that contain sugar, such as grapes, rice, barley, honey and other fruits. The type of alcohol produced by the fermentation depends on the fermented material. Fermentation produces alcohol and carbon dioxide as by-products. By the time the alcohol concentration reaches 15%, the yeast dies. To create “harder” liquors (e.g., rum, whiskey, brandy, etc.), the alcohol must be distilled, a process in which heat is applied to the alcohol, which boils off in steam and condenses in cooling tubes. Beverages above 15% are often rated by their “proof,” which is twice the percentage of alcohol. The term comes from the time when soldiers were given rations of rum. To prove the purity of the alcohol rations, a small portion was dumped on gunpowder and ignited. If it burned, the beverage was 100% “proof”, or at least 50% alcohol.

How It’s Used

Alcohol is traditionally consumed orally, often in a social setting. In America it is generally considered acceptable to consume a modest amount of alcohol, especially as part of a meal. Excessive alcohol intake can be hard to quantify, but it is generally understood by servers that someone who is exhibiting poor motor control, slurred speech, and lack of situational awareness should not be served more alcohol. Since alcohol impairs reaction times, decision making, and movement, it is very dangerous to drive a car after drinking alcohol. It is a crime in the United States to drive with a blood alcohol content higher than 0.08%, roughly the equivalent of 2 drinks. Due to individual differences in alcohol metabolism, it can be difficult to estimate blood alcohol content from the number of drinks someone has had, and some people, suffering from impaired decision-making as a result of alcohol intoxication, overestimate their ability to drive safely. Nearly one-third of all traffic-related deaths involve alcohol. In 2013, 3.3 million deaths world-wide were attributed to alcohol use, whether due to traffic accidents, overdose, or adverse health effects such as liver failure.

How It Works

Alcohol primarily affects four neurotransmitters: glutamate, GABA, dopamine, and endogenous opioids. Glutamate is a neurotransmitter that binds to NMDA receptors and increases the firing rate of neurons. When alcohol binds to an NMDA site, it turns down the excitatory signal of glutamate, inhibiting NMDA. Memory loss often results. GABA is the primary inhibitory neurotransmitter in the brain, binding to GABA receptors and decreasing the firing rate of neurons. Alcohol binding alters the GABA receptor, making it more sensitive and thus increasing the inhibitory effects of GABA. Anxiety reduction and motor impairment often result. Third, alcohol triggers dopamine release, which leads to feelings of pleasure and craving for alcohol. Finally endogenous opioids, such as endorphins, increase in response to alcohol, which reduce pain and increase pleasure.

Because of these changes in the neurotransmitter system, the body must compensate. The body produces more NMDA receptors, fewer GABA receptors, fewer dopamine receptors, and fewer endogenous opioids. Consequently, individuals must drink more alcohol to create the same neurotransmitter effects. Alternatively, if they stop drinking alcohol, withdrawal symptoms can result. Alcohol withdrawal can be fatal, as the brain adapts to the constant presence of an inhibitory chemical. When alcohol is removed, the brain can become hyperexcitable, leading to seizures and death.

Treatment

The first step in treatment is detoxification, in which individuals are weaned off alcohol to minimize withdrawal symptoms. Substitutes for alcohol can mimic the effects of alcohol, such as benzodiazepines (e.g., valium), which activate the GABA receptors to prevent seizures. Next, individuals may enter psychosocial rehabilitation, which may include individual therapy, group therapy, Alcoholics Anonymous, Rational Recovery, or the Community Reinforcement Approach. Individuals may also take medication to aid recovery. Successful quitting rates increase when individuals use both medication and therapy.

Medication tends to focus on increasing negative reactions to alcohol or decreasing positive reactions to alcohol. For instance, Antabuse inhibits the enzyme that breaks down alcohol. Consequently, less alcohol is metabolized so more alcohol remains present in the body, causing face flushing and intense hangovers. Alcohol can then be associated with an aversive response. Alternatively, naltrexone blocks opioid receptors, yielding less pleasure from drinking. Consequently, individuals may be less likely to continue drinking alcohol. It is important to note that 40-70% of people in alcohol abuse programs relapse within one year. It is therefore important to avoid looking at relapse as failure and instead treat it as a step on the road toward recovery.


References

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