That should have been a red flag. When humans regularly drink alcohol, only 15 percent or so become dependent on the stuff. Why them and not the other 85 percent? After training rats to self-administer alcohol, he offered them some sugary water, too. This better mimics real life, in which drugs exist simultaneously with other pleasurable substances. Given a choice between booze and nectar, most rats chose the latter. But not all of them: Of the 32 rats that Augier first tested, four ignored the sugar and kept on shooting themselves up with alcohol.
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Consistently, 15 percent of them choose alcohol over sugar—the same number as the proportion of human drinkers who progress to alcoholism. Those alcohol-preferring rats showed other hallmarks of human addiction, too. They spend more effort to get a sip of alcohol than their sugar-preferring peers, and they kept on drinking even when their booze supply was spiked with an intensely bitter chemical or paired with an electric shock. Many lab studies treat animals as if they were identical, and any variation in their behavior is just unhelpful noise.
That is exactly what the team did next. They compared the alcohol-preferring and sugar-preferring rats and looked for differences in the genes that were active in their brains. They focused on six regions that are thought to be involved in addiction, and found no differences in five. The amygdala is an almond-shaped region that sits deep within the brain, and is heavily involved in processing emotions. When Augier looked at the amygdala of alcoholic rats, he found signs of unusually low activity in several genes, all of which are linked to a chemical called GABA.
G ABA is a molecular red light: Certain neurons make and release it to stop their neighbors from firing. But in the amygdala of alcohol-preferring rats, the gene that makes GAT3 is much less active, and makes just half the usual levels of the pump.
G ABA accumulates around the neighboring neurons, making them abnormally inactive. They are naturally more anxious, which might explain their vulnerability to alcohol. He predicts it will take another five years of work to fully close this loop. They took rats that prefer sugar and deliberately reduced the levels of GAT3 in their amygdala.
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This characteristic is inconsistent with the medical model, which implies that alcoholism is either present or absent—as is the case, for example, with pregnancy or a brain tumour. For such reasons, the sociological definition regards alcoholism as merely one symptom of social deviance and believes its diagnosis often lies in the eyes and value system of the beholder.
For example, periodic intoxication can cause sickness necessitating days of absence from work. In a modern industrial community , this makes alcoholism similar to a disease. In a rural Andean society, however, the periodic drunkenness that occurs at appointed communal fiestas and results in sickness and suspension of work for several days is normal behaviour. It should be noted that this drunkenness at fiestas is a choice and does not produce regret.
If the sociological model were entirely correct, alcoholism should often be expected to disappear with maturation as is the case with many other symptoms of social deviance. This does not occur, however. Finally, epidemiologists need a definition of alcoholism that enables them to identify alcoholics within a population that may not be available for individual examination.
To define alcoholism they may rely on quantity and frequency measurements of reported community drinking and alcohol-related hospitalizations, on a formula based on the frequency of deaths from cirrhosis within the population, or on arrests for alcohol-related misbehaviour.
Alcoholism & Alcoholics
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