DNA damage
Alcohol-induced DNA damage, when not properly repaired, may have a key role in the neurotoxicity induced by alcohol. Metabolic conversion of ethanol to acetaldehyde can occur in the brain and the neurotoxic effects of ethanol appear to be associated with acetaldehyde induced DNA damages including DNA adducts and crosslinks. In addition to acetaldehyde, alcohol metabolism produces potentially genotoxic reactive oxygen species, which have been demonstrated to cause oxidative DNA damage. Diagnosis
Definition
Misuse, problem use, abuse, and heavy use of alcohol refer to improper use of alcohol, which may cause physical, social, or moral harm to the drinker. The Dietary Guidelines for Americans defines "moderate use" as no more than two alcoholic beverages a day for men and no more than one alcoholic beverage a day for women. The National Institute on Alcohol Abuse and Alcoholism (NIAAA) defines binge drinking as the amount of alcohol leading to a blood alcohol content (BAC) of 0.08, which, for most adults, would be reached by consuming five drinks for men or four for women over a two-hour period. According to the NIAAA, men may be at risk for alcohol-related problems if their alcohol consumption exceeds 14 standard drinks per week or 4 drinks per day, and women may be at risk if they have more than 7 standard drinks per week or 3 drinks per day. It defines a standard drink as one 12-ounce bottle of beer, one 5-ounce glass of wine, or 1.5 ounces of distilled spirits.
There was also a 1973 study showing chronic alcoholics drinking moderately again, but a 1982 follow-up showed that 95% of subjects were not able to maintain drinking in moderation over the long term. Another study was a long-term (60 year) follow-up of two groups of alcoholic men which concluded that "return to controlled drinking rarely persisted for much more than a decade without relapse or evolution into abstinence." Internet based measures appear to be useful at least in the short term. Medications
In the United States there are four approved medications for alcoholism: acamprosate, two methods of using naltrexone and disulfiram. Acamprosate may stabilise the brain chemistry that is altered due to alcohol dependence via antagonising the actions of glutamate, a neurotransmitter which is hyperactive in the post-withdrawal phase. By reducing excessive NMDA activity which occurs at the onset of alcohol withdrawal, acamprosate can reduce or prevent alcohol withdrawal related neurotoxicity. Acamprosate reduces the risk of relapse amongst alcohol-dependent persons. Naltrexone is a competitive antagonist for opioid receptors, effectively blocking the effects of endorphins and opioids. Naltrexone is used to decrease cravings for alcohol and encourage abstinence. Alcohol causes the body to release endorphins, which in turn release dopamine and activate the reward pathways; hence in the body Naltrexone reduces the pleasurable effects from consuming alcohol. Evidence supports a reduced risk of relapse among alcohol-dependent persons and a decrease in excessive drinking. Nalmefene also appears effective and works in a similar manner. Disulfiram prevents the elimination of acetaldehyde, a chemical the body produces when breaking down ethanol.