Coffee and energy drink use patterns in college freshmen: associations with adverse health behaviors and risk factors.

BACKGROUND: Public health concern over college students mixing caffeine-containing energy drinks (EDs) and alcohol has contributed to an array of ED-focused research studies. One review found consistent associations between ED use and heavy/problem drinking as well as other drug use and risky behaviors (Nutr Rev 72:87-97, 2014). The extent to which similar patterns exist for other sources of caffeine is not known. The present study examined associations between coffee and ED consumption and alcohol, tobacco and other drug use; alcohol use problems; and parental substance abuse and mental health problems in a sample of college freshmen. METHODS: Subjects were N = 1986 freshmen at an urban university who completed an on-line survey about demographics; caffeine; alcohol, tobacco and other drug use; and family history. The sample was 61% female and 53% White. Chi-square analyses and multivariable binary or ordinal logistic regression were used to compare substance use, problem alcohol behavior, and familial risk measures across 3 caffeine use groups: ED (with or without Coffee) (ED + Co; N = 350); Coffee but no ED (Co; N = 761); and neither coffee nor ED (NoCE; N = 875) use. RESULTS: After adjusting for gender and race, the 3 caffeine use groups differed on 8 of 9 symptoms for alcohol dependence. In all cases, the ED + Co group was most likely to endorse the symptom, followed by the Co group and finally the NoCE group (all p < .002). A similar pattern was found for: use 6+ times of 5 other classes of drugs (all p < .05); extent of personal and peer smoking (all p < .001); and paternal problems with alcohol, drugs and anxiety/depression as well as maternal alcohol problems and depression/anxiety (p < .04). CONCLUSIONS: The response pattern was ubiquitous, with ED + Co most likely, Co intermediate, and NoCE least likely to endorse a broad range of substance use, problem alcohol behaviors, and familial risk factors. The finding that the Co group differed from both the ED + Co and NoCE groups on 8 measures and from the NoCE group on one additional measure underscores the importance of looking at coffee in addition to EDs when considering associations between caffeine and other risky behaviors.

Long-Chain ω-3 Levels Are Associated With Increased Alcohol Sensitivity in a Population-Based Sample of Adolescents.

BACKGROUND: The levels of the ω-3 long-chain polyunsaturated fatty acids (ω-3 LC-PUFAs), including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have been associated with alcohol sensitivity in vertebrate and invertebrate model systems, but prior studies have not examined this association in human samples despite evidence of associations between ω-3 LC-PUFA levels and alcohol-related phenotypes. Both alcohol sensitivity and ω-3 LC-PUFA levels are impacted by genetic factors, and these influences may contribute to observed associations between phenotypes. Given the potential for using EPA and DHA supplementation in adjuvant care for alcohol misuse and other outcomes, it is important to clarify how ω-3 LC-PUFA levels relate to alcohol sensitivity. METHODS: Analyses were conducted using data from the Avon Longitudinal Study of Parents and Children. Plasma ω-3 LC-PUFA levels were measured at ages 15.5 and 17.5. Participants reported on their initial alcohol sensitivity using the early drinking Self-Rating of the Effects of Alcohol (SRE-5) scale, for which more drinks needed for effects indicates lower levels of response per drink, at ages 15.5, 16.5, and 17.5. Polygenic liability for alcohol consumption, alcohol problems, EPA levels, and DHA levels was derived using summary statistics from large, publicly available datasets. Linear regressions were used to examine the cross-sectional and longitudinal associations between ω-3 LC-PUFA levels and SRE scores. RESULTS: Age 15.5 ω-3 LC-PUFA levels were negatively associated with contemporaneous SRE scores and with age 17.5 SRE scores. One modest association (p = 0.02) between polygenic liability and SRE scores was observed, between alcohol problems-based polygenic risk scores (PRS) and age 16.5 SRE scores. Tests of moderation by genetic liability were not warranted. CONCLUSIONS: Plasma ω-3 LC-PUFA levels may be related to initial sensitivity to alcohol during adolescence. These data indicate that diet-related factors have the potential to impact humans' earliest responses to alcohol exposure.

An extended Swedish national adoption study of alcohol use disorder.

IMPORTANCE: Alcohol use disorder (AUD) runs strongly in families. It is unclear to what extent the cross-generational transmission of AUD results from genetic vs environmental factors. OBJECTIVE: To determine to what extent genetic and environmental factors contribute to the risk for AUD. DESIGN, SETTING, AND PARTICIPANTS: Follow-up in 8 public data registers of adoptees, their biological and adoptive relatives, and offspring and parents from stepfamilies and not-lived-with families in Sweden. In this cohort study, subtypes of AUD were assessed by latent class analysis. A total of 18,115 adoptees (born 1950-1993) and 171,989 and 107,696 offspring of not-lived-with parents and stepparents, respectively (born 1960-1993). MAIN OUTCOMES AND MEASURES: Alcohol use disorder recorded in medical, legal, or pharmacy registry records. RESULTS: Alcohol use disorder in adoptees was significantly predicted by AUD in biological parents (odds ratio, 1.46; 95% CI, 1.29-1.66) and siblings (odds ratio, 1.94; 95% CI, 1.55-2.44) as well as adoptive parents (odds ratio, 1.40; 95% CI, 1.09-1.80). Genetic and environmental risk indices created from biological and adoptive relatives acted additively on adoptee AUD liability. Results from biological and adoptive relatives were replicated and extended from examinations of, respectively, not-lived-with parents and stepparents. Multivariate models in these families showed that AUD in offspring was significantly predicted by AUD, drug abuse, psychiatric illness, and crime in not-lived-with parents and by AUD, drug abuse, crime, and premature death in stepparents. Latent class analyses of adoptees and offspring of not-lived-with parents with AUDs revealed 3 AUD classes characterized by (1) female preponderance and high rates of psychiatric illness, (2) mild nonrecurrent symptoms, and (3) early-onset recurrence, drug abuse, and crime. These classes had distinct genetic signatures in the patterns of risk for various disorders in their not-lived-with parents and striking differences in the rates of recorded mood disorders. CONCLUSIONS AND RELEVANCE: Parent-offspring transmission of AUD results from both genetic and environmental factors. Genetic risk for AUD reflects both a specific liability to AUD and to other externalizing disorders. Environmental risk reflects features of both parental psychopathology and other aspects of the rearing environment. Alcohol use disorder is a heterogeneous syndrome and meaningful subtypes emerged from latent class analysis, which were validated by patterns of disorders in biological parents and specific psychiatric comorbidities. The general population contains informative family constellations that can complement more traditional adoption designs in clarifying the sources of parent-offspring resemblance.