Addiction Psychiatry Pass Rates

The correct answer is: E. Opioid receptor mu 1 A118G.

Presently, the US Food and Drug Administration has approved the use of disulfiram, naltrexone, and acamprosate for the treatment of AUD. One of the most constant results of naltrexone has been the decline in heavy drinking relapse, heavy drinking days, overall drinking, and alcohol craving.
It has been noted that therapeutic responses to naltrexone in AUD are regulated by variations at the mu-opioid receptor gene locus (OPRM1). There are certain alcohol-dependent individuals who respond better to naltrexone treatment and they would be carriers of the OPRM1 118G allele. People low on dopamine beta-hydroxylase exhibit lack of disulfiram effects on their cocaine use while those with the Human dopamine D2 receptor E8 A/A genotype were noted to need higher doses of tiapride for alcohol use disorder, as well as increased depression and anxiety upon admission and 2 weeks after admission. Carriers of the ANKK1 rs1800497 T allele showed fewer cocaine-positive urines during the disulfiram pharmacotherapy while dopamine active transporter 1 10/10 repeat homozygotes do not reduce drinking in response to naltrexone.
Source Patriquin MA, Bauer IE, Soares JC, Graham DP, Nielsen DA. Addiction pharmacogenetics. Psychiatric Genetics. 2015;25(5):181-193. doi:10.1097/ypg.0000000000000095. Bilbao A, Robinson JE, Heilig M, et al. A Pharmacogenetic Determinant of Mu–Opioid Receptor Antagonist Effects on Alcohol Reward and Consumption: Evidence from Humanized Mice. Biological Psychiatry. 2015;77(10):850-858. doi:10.1016/j.biopsych.2014.08.021. Medications Development Program. November 2017. https://www.niaaa.nih.gov/research/major–initiatives/medications–development–program. Sub-Topic Genetics