Reliability and validity of an internalizing symptom scale based on the adolescent and adult Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA).

BACKGROUND: The Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) is an interview that assesses psychiatric symptoms and diagnoses, including substance use disorders and anxiety and mood (i.e., internalizing) disorders. Although the SSAGA is widely used, there exists no overall internalizing characteristics scale based on items drawn from SSAGA's mood and anxiety disorder sections. OBJECTIVES: To design and assess a SSAGA-based measurement instrument capturing the overall internalizing dimension that underlies more specific internalizing conditions. METHODS: We developed, assessed, and characterized a new scale for measuring internalizing problematic characteristics derived from the SSAGA interview. All samples were drawn from the Collaborative Studies on the Genetics of Alcoholism, a prospective multi-site genetic study of families at high risk for alcohol use disorders. All participants taking part in the study between September 2005 and September 2017 were eligible (n = 904, 52.2% female). RESULTS: The scale had adequate internal consistency (ordinal α = 0.85, 95% CI = [0.81, 0.89]). Construct validity was supported by its association with other measures of internalizing characteristics (Internalizing Scale from Achenbach Self Reports; Neuroticism Scale from the Neuroticism-Extraversion-Openness Five-Factor Personality Inventory). Several indices of alcohol, marijuana, and nicotine misuse were also positively associated with Internalizing Scale scores. CONCLUSIONS: The Internalizing Scale has very good psychometric properties and can be used in studies that incorporate the SSAGA interview to study the association between internalizing characteristics and problematic alcohol and other substance use. These associations can potentially be utilized to identify individuals at risk for substance problems and to design treatments targeting such individuals.

Predictors of sexual debut at age 16 or younger.

The present study examined the extent to which variables within the self system (i.e., symptoms of alcohol dependence and conduct disorder, gender, race, and metropolitan status) and the familial system (i.e., having an alcohol dependent biological parent or second-degree relative, religious background, educational background of parents, and being born to a teenage mother) were associated with sexual debut at 16 years old or earlier. Participants were 1,054 biological relatives, aged 18-25 years, of alcohol dependent probands who participated in the Collaborative Study on the Genetics of Alcoholism project. Comparison participants (N = 234) without alcohol dependent biological parents were also evaluated. Clinical and sociodemographic variables were assessed by structured, personal interviews. Parental history of alcohol dependence was evaluated by direct interview of parents in most cases and family history in uninterviewed parents. In a multivariate survival analysis, increased risk of becoming sexually active at 16 years of age or earlier was significantly associated with 6 of the 10 predictor variables, including race, one or more alcohol dependence symptoms, and/or one or more conduct disorder symptoms. Having an alcohol dependent biological parent or second-degree relative (e.g., aunt, uncle, or grandparent), educational background of mother, and being born to a teenage mother were also significantly associated with increased risk. These results provide evidence that specific variables in the self and familial systems of influence are important in predicting sexual debut at 16 years old or earlier.

A comparison of diagnoses obtained from in-person and telephone interviews, using the semi-structured assessment for the genetics of alcoholism (SSAGA).

OBJECTIVE: The aim of this study was to compare the prevalence of psychiatric diagnoses when the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA-II) interview was administered in person with the prevalence when the SSAGA-II was conducted by telephone. METHOD: As part of the Collaborative Studies on the Genetics of Alcoholism, SSAGAs were administered either by telephone (n = 1,294) or in person (n = 1,484) to adult relatives of probands (42.3% male). The two modes of interview were compared with respect to reported lifetime prevalence of (1) Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) alcohol dependence; (2) other DSM-IV substance-dependence diagnoses (nicotine, marijuana, cocaine, opioid, stimulant, sedative); and (3) DSM-IV nonsubstance diagnoses (i.e., antisocial personality disorder, major depressive disorder, mania, panic, social phobia, obsessive-compulsive disorder, and generalized anxiety disorder). These analyses took into account the potential confounds of gender, age, race, education, income, marital status, and potential within-family correlation. RESULTS: Diagnostic prevalence rates for alcohol dependence and major depressive disorder were lower for telephone interviews than for in-person interviews (7% and 2%, respectively); there were no other significant differences. CONCLUSIONS: When circumstances dictate (e.g., subject out of area, subject preference), telephone administration of the SSAGA should be considered.

Functional variant in a bitter-taste receptor (hTAS2R16) influences risk of alcohol dependence.

A coding single-nucleotide polymorphism (cSNP), K172N, in hTAS2R16, a gene encoding a taste receptor for bitter beta -glucopyranosides, shows significant association with alcohol dependence (P = .00018). This gene is located on chromosome 7q in a region reported elsewhere to exhibit linkage with alcohol dependence. The SNP is located in the putative ligand-binding domain and is associated with an increased sensitivity to many bitter beta -glucopyranosides in the presence of the N172 allele. Individuals with the ancestral allele K172 are at increased risk of alcohol dependence, regardless of ethnicity. However, this risk allele is uncommon in European Americans (minor-allele frequency [MAF] 0.6%), whereas 45% of African Americans carry the allele (MAF 26%), which makes it a much more significant risk factor in the African American population.