Specificity in genetic and environmental risk for prescription opioid misuse and heroin use.

BACKGROUND

Many studies aggregate prescription opioid misuse (POM) and heroin use into a single phenotype, but emerging evidence suggests that their genetic and environmental influences may be partially distinct.

METHODS

In total, 7164 individual twins (84.12% complete pairs; 59.81% female; mean age = 30.58 years) from the Australian Twin Registry reported their lifetime misuse of prescription opioids, stimulants, and sedatives, and lifetime use of heroin, cannabis, cocaine/crack, illicit stimulants, hallucinogens, inhalants, solvents, and dissociatives via telephone interview. Independent pathway models (IPMs) and common pathway models (CPMs) partitioned the variance of drug use phenotypes into general and drug-specific genetic (), common environmental (), and unique environmental factors ().

RESULTS

An IPM with one general and one general factor and a one-factor CPM provided comparable fit to the data. General factors accounted for 55% ( = 14%, = 41%) and 79% ( = 64%, = 15%) of the respective variation in POM and heroin use in the IPM, and 25% ( = 12%, = 8%, 5%) and 80% ( = 38%, = 27%, 15%) of the respective variation in POM and heroin use in the CPM. Across both models, POM emerged with substantial drug-specific genetic influence (26-39% of total phenotypic variance; 69-74% of genetic variance); heroin use did not (0% of total phenotypic variance; 0% of genetic variance in both models). Prescription sedative misuse also demonstrated significant drug-specific genetic variance.

CONCLUSIONS

Genetic variation in POM, but not heroin use, is predominantly drug-specific. Misuse of prescription medications that reduce experiences of subjective distress may be partially influenced by sources of genetic variation separate from illicit drug use.