Current Treatments Treatments for alcoholism aim to end ethanol consumption and provide social support to prevent relapse. In some cases, sedating medications (benzodiazepines) may be necessary to prevent and/or reduce withdrawal symptoms. These benzodiazepines are only prescribed for a short period time to aid with withdrawal symptoms, for they too can become addictive. Some other commonly used drugs on the market include: ;Disulfiram :Disulfiram (trade name Antabuse) creates a sudden acute response to ethanol consumption by inhibiting an enzyme that metabolizes ethanol. In the liver, ethanol is metabolized by alcohol dehydrogenease to produce acetaladehye which is then metabolized by acetaldehyde dehydrogenease to produce acetic acid. Disulfiram interferes with the acetaldehyde dehydrogenease preventing acetaldehyde metabolism. This buildup of acetaldehyde is responsible for immediate “hangover” effects such as vomiting, nausea, and headaches. Naltrexone :Naltrexone (trade name Revia) is an opioid antagonist that is thought to work by interfering with the dopaminergic mesolimbic (or reward) pathway associated with risk-reward evaluation in the brain. This pathway starts at the ventral tegmental area and makes its way to the nucleus accumbens. Addictions of many drugs, including ethanol is commonly linked to this pathway. Naltrexone is thought to block or attenuate opioid stimulation. Acamprosate :Acamprosate (trade name Campral) is believed to stabilize chemical balances in the brain that ethanol withdrawal would normally induce. In chronic ethanol users, ethanol binds to GABA receptors causing the down-regulation of GABA receptors; which are now less sensitive to the inhibitory GABA neurotransmitter. Acamprosate is thought to act as a GABA agonist that relieves anxiety associated with ethanol withdrawal, thereby promoting the discontinue use of ethanol. These drug treatments are often coupled with social support through counseling, rehabilitation centers, and support groups. These social systems aid in dealing with the underlying social and psychological issues related to ethanol addiction. Future Epigenetic-Based Treatments HDAC Inhibitors Chronic alcohol use up-regulates HDACs through oxidative stress in the brain; this leads to decreased histone acetylation and decreased NPY expression, especially in the amygdala. The lower levels of NPY are associated with increased ethanol consumption and increased anxiety in periods of ethanol withdrawal. Trichostatin A (TSA) is an HDAC inhibitor which has been shown to reverse these histone acetylation and NPY deficits by preventing and reversing HDAC up-regulation. TSA acted as an anxiolytic as it was able to reduce anxiety associated with ethanol withdrawal. Suberanilohydroxamic Acid or SAHA is an HDAC inhibitor that reduces the motivation of rats to consume and/or seek ethanol, SAHA reduced binge drinking in rats by ending ethanol consumption periods sooner than in non-SAHA rats. SAHA was selective for reducing ethanol seeking but not sucrose seeking. DNMT Inhibitors In alcoholics, certain regions of the amygdala are associated with higher levels of DNA methyltransferases. 5-azacitidine (5-AzaC) in mice reduced excessive ethanol consumption. 5-AzaC decreases DNA methylation by inhibiting the activity of DNA methyltransferases. These results suggest ethanol consumption increases DNMT activity and that this histone modification can be reversed by DNMT inhibitors.
Molecular and epigenetic mechanisms of alcoholism
Disease theory of alcoholism
Alcohol and health
Long-term effects of alcohol
Pharmacology of antidepressants
Antidepressants and suicide risk
Digital media use and mental health
Epigenetics of cocaine addiction