Individual and environmental predictors of health risk behaviours among Dutch adolescents: the HBSC study.

OBJECTIVE: To examine unique and common predictors of tobacco smoking, binge drinking, cannabis smoking, early sexual intercourse and multiple health risk behaviours. STUDY DESIGN: Cross-sectional survey study. METHODS: The Dutch Health Behaviour in School-aged Children (HBSC) study was used to provide data on 1742 adolescents aged 15 and 16 years of age. This study focused on a variety of individual and environmental predictors of health risk behaviours, tapping into four domains (mental health, family, peers and school), retrieved by adolescent self-reports and corrected for sociodemographic variables. Logistic and linear regression analyses were performed. RESULTS: Unique predictors (i.e., gender, low and very low education level, general health, hyperactivity problems, conduct problems, incomplete family, religion, knowledge of mother, parental rules on alcohol drinking, time spent with friends, number of friends, perceived tobacco use of classmates, truancy) were identified. In addition, common predictors (i.e., permissive rules on alcohol drinking and much time spent with friends) were also identified, explaining an increase in engagement in all investigated health risk behaviours in adolescence, including multiple risk behaviours. CONCLUSIONS: A prevention strategy targeting restrictive parenting and time spent with friends may be effective to reduce/discourage engagement in health risk behaviours.

Predicting transitions in low and high levels of risk behavior from early to middle adolescence: the TRAILS study.

The present study examined the joint development of substance use and externalizing problems in early and middle adolescence. First, it was tested whether the relevant groups found in previous studies i.e., those with an early onset, a late onset, and no onset or low levels of risk behavior could be identified, while using a developmental model of a single, underlying construct of risk behavior. Second, departing from Moffitt's taxonomy of antisocial behavior, it was tested if early, but not late, onset risk behavior is predicted by a problematic risk profile in childhood. Data were used from TRAILS, a population based cohort study, starting at age 11 with two follow-ups at mean ages of 13.6 and 16.3 years. Latent transition analyses demonstrated that, both in early and middle adolescence, a single underlying construct of risk behavior, consisting of two classes (labeled as low and high risk behavior), adequately represented the data. Respondents could be clearly classified into four possible transition patterns from early to middle adolescence, with a transition from high to low being almost non-existent (2.5 %), low to low (39.4 %) and low to high (41.8 %) being the most prevalent, and high to high (16.2 %) substantial. As hypothesized, only the high-high group was characterized by a clear adverse predictor profile in late childhood, while the low-high group was not. This study demonstrates that the development of substance use is correlated with externalizing problems and underscores the theory that etiologies of early and later onset risk behavior are different.

DRD2 and DRD4 in relation to regular alcohol and cannabis use among adolescents: does parenting modify the impact of genetic vulnerability? The TRAILS study.

AIMS: The aims of the present study were to determine the direct effect of DRD2 and DRD4, as well as their interaction with parenting (i.e. rejection, overprotection and emotional warmth), on the development of regular alcohol and cannabis use in 1192 Dutch adolescents from the general population. METHODS: Information was obtained by self-report questionnaires. Perceived rejection, overprotection and emotional warmth were assessed at age 10-12. Regular alcohol and cannabis use were determined at age 15-18 and defined as the consumption of alcohol on 10 or more occasions in the past four weeks, and the use of cannabis on 4 or more occasions in the past four weeks. Models were adjusted for age, sex, parental alcohol or cannabis use, and externalizing behavior. RESULTS: Carrying the A1 allele of the DRD2 TaqIA polymorphism, or the 7 repeat DRD4, was not directly related to regular alcohol or cannabis use. In addition, adolescent carriers of these genetic risk markers were not more susceptible to the influence of less optimal parenting. Main effects for parenting indicated that overprotection increased the risk of regular alcohol use, whereas the risk of cannabis use was enhanced by parental rejection and buffered by emotional warmth. CONCLUSIONS: Our findings do not support an association between DRD2/DRD4 and regular alcohol and cannabis use in adolescents. Given the substance-specific influences of rejection, overprotection and emotional warmth, these parenting factors might be promising candidates for prevention work.

Parental communication appears not to be an effective strategy to reduce smoking in a sample of Dutch adolescents.

This longitudinal study examined the reciprocal effects of the frequency of parent-adolescent communication on tobacco-related issues (smoking-specific communication), and adolescents' smoking. Participants were 428 Dutch older and younger siblings between 13 and 16 years old. Smoking-specific communication did not affect youth smoking in general; however, among younger, but not older, siblings, smoking-specific communication was associated with a higher likelihood of smoking over time. In addition, when adolescents already smoked parents started to talk more frequently about smoking-related issues with their older and younger adolescents later on. Neither the quality of smoking-specific communication, the quality of parent-adolescent relationship, nor parental smoking moderated these reciprocal effects. In conclusion, prevention campaigns encouraging parents to undertake smoking-specific communication might not be desirable.

Parental smoking and respiratory tract infections in children.

The adverse health consequences of exposing children to tobacco smoke have been well documented. Re-calculation of the data available from cohort and cross-sectional studies worldwide shows that between 500-2500 excess hospitalisations and between 1000 to 5000 excess diagnoses per 100 000 young children as result from respiratory infections can be directly attributed to parental smoking. Results of published meta-analyses support these figures, which are probably under-estimated because of the effects of non-differential misclassification bias. These excess infections are a source of preventable morbidity and have a high cost to the community. They also have important long-term consequences because children who have respiratory infections in early life are at an increased risk of developing asthma in later childhood. More effective strategies that prevent smoking in young people before they become parents have the potential to lead to reductions in these high rates of unnecessary morbidity in the next generation of children.