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Treatment of alcohol withdrawal is, however, only the beginning of rehabilitation and, for many, a necessary precursor to a longer-term treatment process. According to WHO, alcohol is implicated as a risk factor in over 60 health disorders including high blood pressure, stroke, coronary heart disease, liver cirrhosis and various cancers. The AAF for alcoholic liver disease and alcohol poisoning is 1 (or 100% alcohol attributable) (WHO, 2000). For other diseases such as cancer and https://ecosoberhouse.com/article/10-useful-sobriety-sayings-that-can-help/ heart disease the AAF is less than 1 (that is, partly attributable to alcohol) or 0 (that is, not attributable to alcohol). Also, as noted earlier, the risk with increasing levels of alcohol consumption is different for different health disorders. Risk of a given level of alcohol consumption is also related to gender, body weight, nutritional status, concurrent use of a range of medications, mental health status, contextual factors and social deprivation, amongst other factors.
But the ICD has yet to catch up and since American billing systems and other records often rely on ICD, this conflation continues to cause problems both in the United States and rest of the world. There is no justification physiological dependence on alcohol for keeping this misleading term in light of what we now know about the nature of addiction. For one, depending on a substance to avoid physical withdrawal symptoms is neither necessary nor sufficient to define addiction.
Glutamate systems have long been implicated in the acute reinforcing actions of alcohol, and alcohol effects perceived by an organism can be mimicked with NMDA receptor antagonists (Colombo and Grant 1992). In contrast to its effects on GABA, alcohol inhibits glutamate activity in the brain. For example, acute alcohol exposure reduces extracellular glutamate levels in a brain region called the striatum, which contains the nucleus accumbens, among other structures (Carboni et al. 1993). Acute alcohol administration also suppresses glutamate-mediated signal transmission in the central nucleus of the amygdala, an effect that is enhanced following chronic alcohol exposure (Roberto et al. 2004b).
Comorbid psychiatric disorders are considered to be ‘the rule, not the exception’ for young people with alcohol-use disorders (Perepletchikova et al., 2008). Data from the US National Comorbidity study demonstrated that the majority of lifetime disorders in their sample were comorbid disorders (Kessler et al., 1996). This common occurrence of alcohol-use disorders and other substance-use disorders along with other psychiatric disorders notes the importance of a comprehensive assessment and management of all disorders. Disruptive behaviour disorders are the most common comorbid psychiatric disorders among young people with substance-use disorders. Those with conduct disorder and substance-use disorders are more difficult to treat, have a higher treatment dropout rate and have a worse prognosis.
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