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      The association between parental attitudes and alcohol consumption and adolescent alcohol consumption in Southern Ireland: a cross-sectional study

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          Abstract

          Background

          Alcohol plays a complex role in society. A recent study showed that over half of Irish adults drink hazardously. Adolescents report increased levels of alcohol consumption. Previous research has inferred the influence of the parent on their adolescent. Thus, the aim of the current study was to investigate the association between adolescent alcohol consumption and their parent’s consumption pattern and attitude toward alcohol use in Southern Ireland.

          Methods

          A cross-sectional survey was undertaken in November 2014. This involved distributing a survey to adolescents ( n = 982) in their final two years of second level education and at least one of their parents from a local electorate area in Southern Ireland. This survey included: alcohol use, self- reported height and weight, smoking status, mental health and well-being along with attitudinal questions. Chi-square tests and multivariate logistic regression were utilised.

          Results

          A 37 % response rate was achieved. Over one-third (34.2 %) of adolescents and 47 % of parents surveyed reported hazardous drinking. Over 90 % of parents disagreed with allowing their adolescent to get drunk and rejected the idea that getting drunk is part of having fun as an adolescent. The majority (79.5 %) of parents surveyed believed that their alcohol consumption pattern set a good example for their adolescent. Multivariate logistic regression highlights the association between adolescent hazardous alcohol consumption and hazardous drinking by the father. Furthermore either parent permitting their adolescent to drink alcohol on special occasions was associated with hazardous alcohol consumption in the adolescent.

          Conclusion

          The findings of this research notes a liberal attitude to alcohol and increased levels of consumption by the parent are linked to hazardous adolescent drinking behaviour. Future action plans aimed at combatting adolescent hazardous alcohol consumption should also be aimed at tackling parents’ attitudes towards and consumption of alcohol.

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          Most cited references49

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          Parenting factors associated with reduced adolescent alcohol use: a systematic review of longitudinal studies.

          To identify parenting strategies associated with adolescent alcohol consumption that parents can use to implement new national guidelines regarding alcohol consumption by people under the age of 18. A systematic search of academic literature employing the PRISMA method identified 77 relevant articles. Inclusion criteria for the review were (i) longitudinal cohort studies; (ii) measurement of one or more parenting factors during adolescence or pre-adolescence (between the ages of 8 and 17) as a predictor (iii) outcome measurement of any alcohol use and/or alcohol related problems during adolescence at least one time point after the initial parenting factor was measured, and/or problem drinking in adulthood. Studies were excluded if alcohol use was combined with other substance use or problem behaviour as an outcome variable, or if different parenting factors were combined as a single predictor variable for analysis. Stouffer's method of combining p values was used to determine whether associations between variables were reliable. Twelve parenting variables were investigated in these studies: parental modelling, provision of alcohol, alcohol-specific communication, disapproval of adolescent drinking, general discipline, rules about alcohol, parental monitoring, parent-child relationship quality, family conflict, parental support, parental involvement, and general communication. We found that delayed alcohol initiation was predicted by: parental modelling, limiting availability of alcohol to the child, parental monitoring, parent-child relationship quality, parental involvement and general communication. Reduced levels of later drinking by adolescents were predicted by: parental modelling, limiting availability of alcohol to the child, disapproval of adolescent drinking, general discipline, parental monitoring, parent-child relationship quality, parental support and general communication. A number of parenting strategies were identified that parents can use to reduce their adolescent's alcohol consumption. These could be promoted to parents to help them implement new national guidelines on alcohol use.
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            Global status report on alcoholand health

            (2011)
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              Adult Consequences of Late Adolescent Alcohol Consumption: A Systematic Review of Cohort Studies

              Introduction Alcohol is responsible for approximately 4% of the global burden of disease [1]. This burden is higher in high income countries and among men, accounting for 11% of all male deaths in the World Health Organization (WHO) European region in 2004 [1]. There is global concern about drinking trends among young people, particularly in heavy episodic or “binge” drinking. Prominent among policy responses, in the UK and elsewhere, have been attempts to manage antisocial behaviour related to intoxication in public spaces [2]. Much less attention has been given to risks to adult health and well being. There have been many cohort studies of the longer term harms associated with adolescent drinking. Some studies suggest that individuals “mature out” of late adolescent drinking patterns [3], whilst others identify enduring effects on drinking and broader health and social functioning in adulthood [4]. In the only available meta-analysis of life-course variability, Johnstone and colleagues [3] evaluated stability in drinking frequency and found settled patterns after the age of 30 following earlier marked discontinuity. There has, however, been no systematic review addressing the consequences of late adolescent drinking in adulthood. If adolescent drinking does not cause later difficulties with which it may be associated, early intervention on and management of the acute consequences of alcohol consumption, such as antisocial behaviour and unintentional injuries [5], may be the most appropriate community safety and public health responses. If causal relationships do exist, however, this approach will not address the cumulative harms produced by alcohol, unless such intervention successfully modifies the long-term relationship with alcohol, which seems unlikely. The obstacles to causal inference are well known, and bias and confounding in particular must be addressed in cohort studies. A systematic review of cohort studies provides the strongest observational study design to evaluate evidence for causal inference [6]. We thus applied this approach to study the consequences of late adolescent drinking. Methods Adolescent alcohol involvement and the potential for subsequent harm have been conceptualised and studied in many different ways. We sought therefore to evaluate the possible effects of any behavioural measure of adolescent alcohol consumption on any adult outcome. The durability of any observed effects is an important study theme due to the likely implications for public health. Search Strategy and Selection Criteria The data collection process is illustrated in Figure 1 and the PRISMA checklist is included as Text S1. The literature covering 1964 to 2008 inclusive was initially accessed via electronic databases as proposed by Egger and Davey Smith [7]. This start date identified the oldest cohort study included in the study by Johnstone and colleagues [3]. After piloting the following databases were searched: Medline (via both PubMed and MeSH); Web of Knowledge (including ISI Proceedings); Global Health Archive; Cinhal; PsychInfo; Embase; and HMIC. Configured for a PubMed search, the search terms were (1) Adolescen* OR teen* OR young person OR young people OR young adult; (2) Alcohol* OR binge drinking OR drinking culture OR problem drinking OR drinking problem* OR hazardous drinking OR substance [TI]; (3) Adult* [TI] OR cohort OR longitudinal OR prospective OR lifetime [TI]. Initial screening removed studies that were clearly unrelated to this review. 10.1371/journal.pmed.1000413.g001 Figure 1 PRISMA Flowchart. Citation searching used both backward and forward procedures, with the bibliographies of relevant studies checked and Science Citation Index used for subsequent citations of these papers. Three journals were hand searched: Addiction Abstracts; Addiction; and Journal of Studies on Alcohol and Drugs. The latter two have been published continuously during 1964 to 2008 and were selected following piloting. A data collection protocol was developed and the entire process was undertaken twice, on the second occasion by a research assistant blinded to the outcome of the first. All subsequent study tasks were also duplicated. Only peer-reviewed published data were used and further unpublished information was not sought from authors. Finally, experts, including the authors of included primary studies, were contacted to identify additional studies that had been missed. The following selection criteria were applied independently by two researchers. Studies of drinking behaviour were included if they collected data on at least two points in time, were at least 3 y apart, and from the same cohort. Data collection regarding alcohol consumption was required between the ages of 15 and 19 y old (or between 9th grade at school or first year of university if age not specified). Drinking is normative in this age group and approaches peak levels towards the end of this age range and into the early 20s in most high income countries [8]. Studies were also required to include a report of at least one quantitative measure of effect, such as an odds ratio (OR), between alcohol involvement and any later outcome assessed at age 20 or greater. Cohorts formed from general population sources, including college students and military conscripts, were included. Studies based on selected or special populations such as children of alcoholics, mental health patients, and offenders were excluded. Data Analysis Quality appraisal of included studies was undertaken to evaluate the potential for bias and the adequacy of control for confounding. We gave particular attention to socioeconomic deprivation and other early life sources of vulnerability, as well as indications of other adolescent behavioural problems, in assessing confounding. We designated studies as having stronger capacity for casual inference in relation to the aims of this review if residual confounding in these areas was assessed as unlikely to be important by two reviewers and they had at least one of the following characteristics: (1) follow-up rates of 80% or greater; or (2) sample sizes of 1,000 participants or more. These characteristics identify two forms of bias at the individual study (attrition bias) and at the review level (small studies having disproportionate influence in reviews), respectively. Also if a study had both these characteristics, it was deemed to have stronger capacity for causal inference if both reviewers agreed there was reasonable control of confounding even though residual confounding was nevertheless still likely. We considered that adjustment for some factors while leaving major individual psychosocial confounders uncontrolled, did not constitute reasonable control of confounding. This subset of studies with stronger capacity for causal inference is individually discussed in the narrative presentation of results in order to summarise the evidence base. Two researchers agreed on all bar two studies (Kappa 0.91) [9],[10], for which disagreements about the strength of control for confounding were resolved by discussion. Meta-analysis of pooled outcomes from these observational studies was deemed inappropriate only after consideration of the nature of findings from included studies, because of the potentially misleading nature of such summary effect estimates in the context of uncontrolled bias and confounding [7]. Results The majority of included studies (n = 35) were multiple reports from ten cohorts (see Table 1), with the Swedish Conscript Study (SCS) of male conscripts providing nine separate reports [11]–[19]. The remainder of included studies (n = 19) originated from separate cohorts (see Table 2). Tables 1 and 2 present selected study characteristics including variables involved in eligible measures of effect. Altogether a total of 54 studies were eligible for inclusion in this review [9]–[62]. This literature has grown rapidly in recent years, with approximately two-thirds of studies (n = 35) published since 2001. Approximately half of all reports (n = 26) were from US studies, ten were from Sweden, eight from Britain, four from New Zealand, three from Australia, two from Finland, and one from the Netherlands. More than half (n = 30) originated from school-based cohorts. Birth cohorts were more likely to be the subject of multiple studies (n = 11/14). Nineteen (35%) studies, based on eight different cohorts, were assessed as having stronger capacity for causal inference (see Tables 1 and 2), and we focus primarily on these studies. The presentation of main results is organised by principal outcomes evaluated, with quantitative data presented only from the subset of 19 studies. 10.1371/journal.pmed.1000413.t001 Table 1 Multiple reports for ten cohort studies. Study Cohort Type Author Name Year Age T1 (y) Age T2 (y) Final Sample Size (n) Follow-up Rate (%) T1 Adolescent Behavioural Variable(s) T2 Adult Outcomes Stronger Capacity for Causal Inference British Cohort Study National birth cohort Viner 2007 16 30 4,911 81 Binge drinking; frequent regular drinking Social class; AD (CAGE); weekly AU above recommended limits; illicit drug use; heavy smoking; psychological morbidity; mental health problems; homelessness; conviction; education; pregnancy, significant accidents No Cable 2008 16 30 13,919 Not clear AU frequency and quantity - in typologies AD (CAGE) No CHDS Local birth cohort Wells 2004 16 21 859 90 AU frequency and quantity, problems (modified Rutgers Alcohol Problem Index) to form a latent class AU, AA, AD; nicotine and illicit drug dependence; mental health outcomes; education and employment; sexual relationships; offending Yes Wells 2006 18 21 983 96 AUD (AA and AD) AUD (AA and AD) Yes Dunedin Multidisciplinary Health and Development Study Local birth cohort Casswell 1997 18 21 770 84 AU frequency and quantity AU frequency and quantity, related problems (latent variable) No McGee 2000 15, 18 21 871 Not clear AU at both ages Mental disorder; cannabis use No MFCS National school cohort Schulenberg 1996 18 23/24 6,862 63 Binge drinking Binge drinking No Merline 2004 18 35 10,225 61 Heavy drinking Heavy drinking No Merline 2008 18 22; 26; 35 21,137a 80 AU frequency and heavy drinking AU frequency and heavy drinking: AA and AD (DSM) (measured only at age 35) Yes National Child Development Study National birth cohort Ghodsian 1987 16 23 9,337 79 AU frequency and quantity AU quantity and frequency No Power 1990 16 23 12,311 76 AU frequency and quantity AU frequency and quantity; employment variables No Jefferis 2005 16 23; 33; 42 9,527, 8,620, 8,600 79, 72, 72 Binge drinking Binge drinking No Maggs 2008 16 23 Not clear Not clear AU weekly quantity AU weekly quantity Yes Staff 2008 16 42 9,107 76 AU weekly quantity (categorised) Educational attainment Yes RAND Adolescent/Young Adult Panel (Project ALERT) School cohort Tucker 2003 18 23 1,534b 71 AU frequency on 0–11 scale Regular smoking No D'Amico 2005 18 23; 29 1,986 30 AU as above AUD (DSM) No Bogart 2005 18 29 1,138c Not clear AU as above AU quantity and frequency; negative consequences; heavy episodic drinking Yes Bogart 2007 18 29 2,376 Not clear AU as above Life satisfaction Yes Collins 2007 18 29 454d Not clear AU as above Marital status (divorce) No Seattle Social Development Project School cohort Guo 2001 16 21 Approx. 759 Approx. 94 AU any in past month AUD and AD (DSM) No Oesterle 2008 15–18 21; 24; 27 773 96 Heavy episodic drinking Positive functioning; AUD (DSM) No SCS National conscription for military service Andreasson 1988 18–20 33–35 49,464 99 AU weekly quantity (categorised) Mortality Yes Andreasson 1990 18–20 33–35 8,226e 95–99 AU as above Hospitalisation for accidents, or gastro-intestinal, respiratory, musculo-skeletal, or infectious disorders Yes Andreasson 1991a 18–20 38–40 49,464 99 AU as above Mortality Yes Andreasson 1991b 18–20 33–35 49,464 99 AU as above Psychiatric hospital admission Yes Andreasson 1993 18–20 33–35 49,464 99 AU as above Hospital admission for alcoholism Yes Stattin 1995 18–20 33–35 7,577e 99 Composite problems measure (incl. AU, hangover, intoxication, relief drinking, arrested drunk) Criminal convictions, mortality Yes Karlsson 1997 18–20 25–27 8,122e 99 AU quantity, intoxication and hangover regularity, relief drinking Drink driving; public drunkenness Yes Romelsjo 1999 18–20 43–45 49,618 99 AU daily quantity (categorised) Mortality, myocardial infarction, stroke Yes Stenbacka 2003 18–20 45–47 7,577e 93 Composite problems measure (incl. AU, hangover, intoxication, relief drinking, arrested drunk) Hospitalisation or mortality for alcohol or drugs (separately) Yes UCLA Longitudinal Study of Growth and Development School cohort Locke 2001 18 26; 35 426 Not clear Latent alcohol involvement factor (AU quantity and frequency, drinking at school/work, intoxication) Latent alcohol involvement factor (as in adolescence except AUD replacing intoxication measure); latent dysphoria factor No Locke 2003 18 26; 35 305f Not clear Latent alcohol involvement factor (as above) Latent alcohol involvement and dysphoria factors as above at age 26, age 35 marital satisfaction, perceived opportunity, divorce, relationship and job satisfaction, job stability No Locke 2004 18 26; 35 305f Not clear Latent alcohol involvement factor (as above) Latent alcohol involvement and dysphoria factors as above No Victorian Adolescent Health Cohort School cohort Bonomo 2004 15–17 20/21 1,601 82 AU frequency and binge drinking AD No Patton 2007 15–17 24 1,520 78 AU quantity (categorised) AU, weekly/daily cannabis use concurrent high risk alcohol/cannabis use, education, employment, relationships, parenthood, tobacco smoking, other drug use and problems measures No AA, alcohol abuse; AD, alcohol dependence; AU, alcohol use; AUD, alcohol use disorder; Beh, behaviour. a Selected those who completed first postschool follow-up. b Nonweekly smokers only. c Women not married at age 18 only. d Married by age 23 only. e Stockholm County only. f Women only. 10.1371/journal.pmed.1000413.t002 Table 2 Individual cohort reports. Study Cohort Type Author Name Year T1 Age (y) T2 Age (y) Final Sample Size (n) Follow-up Rate (%) T1 Adolescent Behavioural Variable(s) T2 Adult Outcomes Stronger Capacity for Causal Inference AHRS Community cohort Jackson 2002 13–20 (mean 16.7) 18–25 1,814 88 AU frequency and heavy drinking Au frequency and heavy drinking; regular and heavy tobacco smoking initiation and cessation Yes Alcohol Misuse Prevention Study School cohort Bingham 2005 17–18 23–24 1,987a Not clear AU quantity and frequency, drunkenness, binge drinking, drinking consequences AU quantity and frequency, drunkenness, bingeing, AU disorders, drinking consequences No Amsterdam Growth and Health Longitudinal Study School cohort Koppes 2000 16 21 150 52 Total and beverage specific AU quantity Total and beverage specific AU quantity No Boston 13 year Longitudinal Project School cohort Stein 1993 15– 18 26 785 79 AU frequency AU quantity and frequency. Cannabis and other drug use. Work-related variables No Cambridge Study of Delinquent Development School cohort Shepherd 2004 16– 18 32 378b 94 Heavy weekly drinking Illness and injuries No FinnTwin 16– 25 Study National birth cohort Viken 2007 18 25 3,028c 92 Alcohol problems (Rutgers Alcohol Problem Index) Alcohol problems (Rutgers Alcohol Problem Index) No Health in Transition Study School cohort Toumbourou 2004 17– 19 21 1,596 48 AU quantity (within recommended limits) AU quantity (within recommended limits), alcohol related harms No Michigan Study of Adolescent Life Transitions School cohort Peck 2008 18 21; 28 578 67 AU AU frequency and heavy drinking (intoxication) No Minnesota Longitudinal Study of Parents and Children Local birth cohort Englund 2008 16 23; 26; 28 178d Not clear AU quantity AU (quantity at 23, 26); AUD (DSM) at 28 No National Education Longitudinal Study National school cohort Chatterji 2006 15– 16; 17– 18 26 7,604e Not clear AU any past month; heavy drinking Graduated high school on time, diploma achievement, college entry, college graduation No NYLS School cohort Kandel 1986 15– 16 24– 25 1,004 83 Lifetime drinking ten times or more Frequency of tobacco, alcohol, illicit drug use, prescription drug use, employment and family role measures, education, delinquency, physical and mental health Yes North Karelia Youth Project School cohort Paavola 2004 15 21; 28 657; 640 73; 71 AU frequency AU, smoking, physical activity (all frequencies) No Oregon Adolescent Depression Project School cohort Rohde 2001 15– 19 24 940f 85 AUD diagnosed, symptoms only or nonproblematic AUD, substance use disorder, depression, anxiety (all DSM), daily smoking, borderline and antisocial personality disorder symptoms No Project Family School cohort Mason 2008 16; 18 21– 22 313 Not clear AU frequency and quantity; heavy drinking Major depressive disorder (DSM) No Young Adult Follow-up Study School cohort Donovan 1983 15– 16 21– 22 403g 93 AU beverage specific and overall quantities, being drunk, negative consequences; years as a problem drinker Problem drinker (intoxication frequency and negative consequences) No Youth Development Study School cohort McMorris 2000 17– 18 22 780 78 AU frequency AU frequency; work hours No Unnamed Local birth cohort Wennberg 2000 18 25; 36 212 Not clear AU quantity Frequency of intoxication at 25, AU quantity at 36 No School cohort Shope 2001 15– 16 23– 24 4,403h 100 Alcohol use/misuse (four categories) Serious motoring offences; serious car crashes Yes School cohort Repetto 2004 14– 15 20– 21 458i 67 AU quantity Depressive symptoms No AA, alcohol abuse; AD, alcohol dependence; AHRS, Adolescent Health Risk Study; AU, alcohol use; AUD, alcohol use disorder. a Includes only not married/cohabiting young adults and sampled only those with a driving licence. Also partial overlap between this sample and Shope. b Men only. c Same-sex twins only. d Low income first born sample. e Various earlier data requirements met. f AUD at 18 excluded in analyses examining the course of AUD. g Previously participated in all four survey waves. h Excluded those not living with either parent and those already driving at study entry, and those who did not obtain a driving license during the study period. i Black only. Mortality The risk of premature death associated with late adolescent drinking has been evaluated only in the SCS, after 15, 20, and 25 y [12],[15],[17]. When the male study population was approximately aged 34, late adolescent heavier drinkers (>250 g per week) were twice as likely (OR = 2.1, 95% confidence interval [1.4–3.2]) to have died compared to moderate drinkers ( 250 g per week) young men at age 19 were 2.3 (1.8–2.9) times more likely to have been hospitalised for alcoholism than low risk drinkers ( 250 g per week) compared to moderate drinkers and 8.0 (2.2–28.9) compared to abstainers after 20 y of follow-up [15]. Moderate drinkers ( 0.5 after adjustment) at age 21 assessed in CHDS [60]. There were no associations between age 15–16 drinking lifetime prevalence and having seen a mental health professional, nor on depressed mood at age 24–25 in the NYLS [33]. As noted above, suicide was the leading cause of death over the 20 y of the SCS mortality studies, with heavier drinkers at greater risk than moderate drinkers (OR = 1.7 [1.0–2.8]) and abstainers [15]. Other risk factors were more strongly associated with suicide, including number of friends (having none compared to having more than 3, OR = 3.1 [1.5–6.2]). Although there was also a greater risk of psychiatric hospitalisation after 15 y in the SCS (OR 1.8 [1.5–2.1]), the nonaddiction mental health consequences are difficult to appreciate as approximately two-thirds of all admissions involved alcoholism or drug addiction [14]. Tobacco Smoking An observed association between age 16 drinking patterns and DSM-IV nicotine dependence at age 21 disappeared after adjustment for covariates in CHDS [60]. In the US Adolescent Health Risk Study (AHRS) [31] small effects of occasional and heavy drinking on smoking initiation and cessation were identified over a 5-y interval into the early 20s. ORs for both regular smoking and half pack a day smoking suggested small effects, with lower confidence intervals near 1. These were statistically significant for all initiation analyses (among nonsmokers) but not in all cessation analyses (among baseline smokers). No effects of having drunk alcohol 10 times or more by age 15–16 on lifetime smoking prevalence by 24–25 y were observed in the NYLS [33]. Other Drug Use and Related Problems In CHDS age 16 drinking latent class was not associated with age 21 cannabis and other illicit drug dependence after control for confounding [60]. No effects of age 15–16 drinking lifetime prevalence on other drug use at 24–25 were observed in the NYLS [33]. Despite this cohort being particularly closely associated with the “gateway” perspective (any prior use of one drug increasing risk of subsequent use of another), only cumulative use measured over the entire intervening period was associated with other drug use, thus “adolescent use retains no direct unique effect once use between adolescence and young adulthood is taken into account” [33]. In the SCS after 26–27 y of follow-up, a summary measure of problematic drinking among those who had not used cannabis at conscription was not associated with hospitalization or mortality with a drug use diagnosis (OR = 1.83 [0.97–3.45]) [18]. Among problem drinkers who had used cannabis, however, elevated risks of such drug problems were found (ever used ≤10 times OR = 5.60 [2.92–10.75], >10 times 3.34 [1.60–6.98]). Educational Attainment No effects of adolescent drinking on any educational outcomes (school qualification, university enrolment, or degree) at age 21 remained after adjustment for confounding in CHDS [60]. In the NYLS there was no effect of having drunk alcohol ten times or more by age 15–16 on number of years in education by 24–25 y [33]. In the British NCDS, however, an effect of heavier past week drinking (>4 units male, >3 units female) at age 16 on subsequent educational attainment by age 42 was found among men only, using propensity scores to deal with confounding [54]. This effect was greater in working class men, where heavy drinkers were approximately 25% less likely to complete a degree than nonheavy drinkers. The difference was 10% among middle class men [54]. Other Possible Consequences The CHDS found no effect of age 16 drinking latent class on months unemployed, sexually transmitted infections, or pregnancy by age 21 [60]. Effects on numbers of sexual partners were identified to be robust to adjustment for background variables. Hospitalisation during 15 y of follow-up for any accidents, or gastro-intestinal, respiratory, musculo-skeletal, or infectious disorders in Stockholm County in the SCS was not significantly higher (OR 1.2 [0.9–1.6]) for heavier drinkers as compared to moderate drinkers as defined above [13]. The NYLS found no direct effects on a wide range of possible consequences of having ever drank alcohol ten times or more by age 15–16. Given the limitations of this measure it is perhaps not surprising that alcohol consequences, compared to other substances, were characterised as “benign” [33]. Finally, there were no effects of drinking frequency at age 18 on life satisfaction at age 29 in a western US school cohort [10], again in contrast to other substances. Additional Evidence from Other Studies Evidence from studies not assessed as having stronger capacity for inference broadly agreed with the findings presented above. There was consistent evidence of effects on subsequent alcohol consumption and related problems. There were similarly mixed findings on possible mental health, tobacco smoking, and educational consequences. There are two principal exceptions: Although no effects on pregnancy among young women were found in CHDS, contrary findings emerged from two other cohorts [46],[59], one of which was restricted to pregnancy outcome by age 18 [59]. Also in three of the four studies that investigated possible effects on adult drug use or related problems, associations with at least one outcome measure in this area were identified [40],[46],[59]. In both cases, the vulnerability of these findings to bias and/or confounding should be remembered. Discussion This systematic review has investigated whether late adolescent alcohol consumption is a time-limited activity without significant longer term consequences or whether it impacts upon adult health and well being. It is clear that the evidence base on long-term consequences is not as extensive nor as compelling as it could be. There are sparse data of sufficient quality to warrant making causal inferences on the broader health and social consequences of late adolescent drinking on the basis of the data evaluated here. There is evidence from a single population-based cohort that late adolescent drinking can cause early death among men, principally through car crashes and suicides [12],[15]. There is a large evidence base attesting to the ongoing impacts of late adolescent drinking on adult drinking behaviours, though most studies cannot strongly support causal inferences because of their designs. There is robust evidence from one national cohort that apparent effects on later alcohol consumption persist beyond the age of 30, which is longer than had previously been understood [43]. Possible effects on subsequent alcohol problems including dependence are somewhat more complex than effects upon subsequent alcohol consumption per se. Evidence from multiple well-designed cohort studies indicates that other factors indicative of heightened psychosocial risk more broadly are also implicated. It is nonetheless striking that effects on alcohol problems assessed in the mid 30s appear to have been produced by elevated consumption in late adolescence in both SCS and MFCS, and to earlier ages in other studies. Findings from a rigorous birth cohort study on nonalcohol outcomes, however, demonstrate that many apparent effects of late adolescent drinking may be due to uncontrolled confounding [60]. Certainty about the long-term consequences of late adolescent drinking is thus not easily achieved. Caution is also required because of the limitations of the present study. Our approach to the investigation of confounding in individual studies was necessarily constrained by weaknesses of the literature as a whole and by the comprehensive nature of our appraisal of possible consequences. For example, there are few studies that address family influences, both siblings and parents. Similarly, there was only a single study included that investigated genetic inheritance [58]. Confounding also needs to be considered in relation to more specific outcomes. For example, a CHDS study not included here by virtue of not having a drinking behavioural measure, found that the contribution of drink driving to traffic accidents is much reduced when other risky driver behaviours are taken into account [63]. Unless otherwise indicated in the Results section, traditional methods of investigation of confounding have been used in the studies covered and these can be criticised for their adequacy in dealing with residual confounding. Being designated as having stronger capacity for casual inference here should not be mistaken to indicate support for causal inference in relation to observed associations, nor that we view the treatment of psychosocial factors to have eliminated residual confounding. Conversely, not being so designated does not imply that a study is weak, rather, simply that it does not contribute as much as others to the aims of this review. Bias was considered in relation to sample size and study attrition in our appraisal of study quality. Whilst this latter variable is long established as important to the evaluation of cohort studies, thinking about the former has been more recently advanced, and thus deserves elaboration and consideration of the impact on review findings. Small study effects have been recently observed within meta-analyses of trials [64]. These effects are related to publication bias (see below) though are more fundamentally due to the greater likelihood of bias in effect estimates in small studies compared to large studies [65]. We are not aware that the influence of small study effects has previously been considered within systematic reviews of cohort studies despite their potential for bias. At the outset, we judged that it was important to consider this possibility, and to use a simple means of so doing, given the challenges involved in summarising a large number of observational studies with substantial problems of bias and confounding. We took the decision to give additional weight to larger studies after piloting and before the main study data collection and analysis. The particular threshold we chose may be somewhat arbitrary, though it is not clear that moving this threshold upwards or downwards by a few hundred study participants would substantially influence our findings. Two other important forms of bias were not directly involved in the determination of study quality. Almost all adolescent behavioural data were self-reported. These data are most likely to involve underestimation of true levels of drinking and its consequences for reasons of social desirability, though the possibility of exaggeration should also not be ignored [66],[67]. Self-report bias leads to underestimation of the true extent of the relationships between adolescent exposure and adult consequences, as would also be true if reporting error was random rather than systematic. This problem is compounded by the fact that the vast majority of the adult outcome data are also self-reported, making probable further underestimation of the true effects [68], notwithstanding the effects of repeated measures within cohorts. The SCS studies are a noteworthy exception to the reliance on self-reported outcomes. It would have been possible to have selected data reliability as a criterion for bias evaluation; this would not have meaningfully changed the results beyond giving greater prominence to SCS data. Publication bias exerts influence in the opposite direction [69],[70]. If the studies reviewed here represent a biased sample of all the relevant studies that have been undertaken, then overestimation of actual effects occurs, which seems highly likely given the paucity of negative findings for alcohol outcomes. This threat to valid inference perhaps has its origins in the context of preliminary explorations of cohort study datasets. In these situations, if drinking is not found to be associated with outcomes of interest then the analyses may not be pursued. We may also have missed studies that meet inclusion criteria by virtue of their publication characteristics. This risk is inherent in the nature of this exercise and is heightened given the breadth of the outcomes investigated here. It seems likely, therefore, that the possibility of not having successfully identified all relevant studies is greater for nonalcohol compared to alcohol outcomes. At the outset we expected publication bias to be a greater threat to the validity of inferences made than small study effects. By its nature, however, we were not in a position to attribute this risk to individual included studies. Both publication and reporting bias pose profound threats to valid inference in this review whose magnitude is difficult to appreciate quantitatively. Studies from a range of different national and cultural contexts have been included here and identified as providing a stronger basis for causal attribution, though these are entirely restricted to Anglophone and Northern European countries. There are no included studies from low- and middle-income countries, nor from any country with a Mediterranean drinking culture. Previous meta-analytic study in this area has identified national context to be particularly important to findings on alcohol consumption from cohort studies [3]. These studies also cover limited historical periods. Period effects were investigated across the different cohorts in the MFCS where only limited differences were identified [43]. Because there have been no previous systematic reviews of this literature, the research question addressed here is unusually broad. This approach led us to specify an end date for formal inclusion in the review, and inevitably further studies have since been published. For example, Huurre and colleagues [71] robustly identified continuities between heavy drinking at age 16 and hazardous drinking at age 32 in a Finnish study. A later MFCS report demonstrates the application of multilevel analyses to examine more advanced research questions on mediators and moderators of effects [72]. Other more recent studies that may have been included [73],[74] do not substantially change the picture obtained, though there will be other studies of which we are unaware and we expect this literature to continue to grow rapidly. Notwithstanding the limitations of the evidence base and of this review, and attenuations over time in the strength of the direct effects, late adolescent alcohol consumption appears a probable cause of increased drinking well into adulthood, through to ages at which adult social roles have been achieved. Heavier drinking seems most likely, however, to be only one component in a complex causal process, whose contribution has probably been overestimated in previous studies because of uncontrolled confounding, setting aside the uncertainties induced by self-reported data. The importance of these data is highlighted in the context of work showing strong stability of drinking patterns through the fourth and fifth decades of life [3],[31],[75]. A wide range of health and other harms, such as liver cirrhosis, are caused by alcohol at middle and older ages [76],[77]. Late adolescent drinking, by virtue of its probable effect on long-term adult alcohol consumption is likely to contribute to the burden of alcohol-related disease. Continuities from adolescence to adulthood in drinking patterns have been observed across a range of measures including frequency of consumption and heavy drinking. In this study it seems that alcohol consumption confers additional risk of alcohol problems both on those who are already more vulnerable in various ways to poorer health and psychosocial outcomes, and strikingly also among those who are not otherwise vulnerable. Possible effects on adult alcohol problems and dependence including hospitalisation identified here result from heavier drinking in adolescence without necessarily involving problems at younger ages. If these effects are confirmed, there are two important implications: (1) Reducing late adolescent alcohol consumption in the general population may be expected to make a long-term contribution to reducing the incidence of adult alcohol problems; (2) In more vulnerable populations, late adolescent drinking may be one cause among many of later difficulties, and its effects may be more severe and long-lasting [78]. Having relatively secure psychosocial resources may somewhat buffer these risks, and their consequent potential for adverse effects, but it does not remove them. These statements should be read with some caution given studies of mediators and moderators of these effects are lacking, limiting our understanding of their nature. Nevertheless, this systematic review affords more secure inference of the likely existence of these effects than has been possible previously. It is possible that relationships with alcohol forged during late adolescence may have cumulative lifetime drinking related consequences that are also simply not well captured by the existing literature. The lack of convincing evidence of effects on nonalcohol outcomes is the product of an absence of evidence rather than strong evidence indicating no effects. A priori, one might expect that effects on nonalcohol outcomes would be weaker simply because they are less direct. To this extent, any such effects would be less durable and may be more likely to occur in high risk subgroups. There is also the possibility of reverse causation in relation to many of these consequences as the initiation of drinking in adolescence may have been preceded by many of the nonalcohol outcomes considered here. Only careful studies of adolescence may address this possibility. There is also a clear need for high quality long-term prospective cohort studies in order to better understand the public health burden that is consequent on late adolescent drinking, both in relation to adult drinking and more broadly. A number of the cohorts included here were originally formed for prevention trials, and obtained some short-term evidence of benefit (for example the RAND and Seattle cohorts in Table 1). There is currently, however, an absence of experimental evidence of successful intervention modifying drinking during the late adolescent years leading to improved adult outcomes [79]. Long-term investment in rectifying this state of affairs should be a public health priority. In addition to making both alcohol and heavy drinking less available, less acceptable, and more expensive [80],[81], these findings indicate a need for policy makers to encourage young people to be more cognisant of the long-term risks to adult health and well-being, and to act on this awareness in their decision making about whether and how much to drink [82]. This encouragement requires much more than the provision of accurate information about risks if it is to have any real prospect of influencing actual behaviour. Alcohol harm reduction has largely been concerned with reducing various risks inherent in drinking situations and their immediate aftermaths [81]. This study demonstrates the need to develop a longer term perspective on harm reduction. Supporting Information Text S1 PRISMA Checklist. (0.07 MB DOC) Click here for additional data file.
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                Author and article information

                Contributors
                eimearmurphy33@gmail.com
                ianosullivan98@gmail.com
                daodonovan@aol.com
                annhope@eircom.net
                +353-21-4205592 , m.davoren@ucc.ie
                Journal
                BMC Public Health
                BMC Public Health
                BMC Public Health
                BioMed Central (London )
                1471-2458
                18 August 2016
                18 August 2016
                2016
                : 16
                : 821
                Affiliations
                [1 ]Department of Epidemiology and Public Health, University College Cork, 4th Floor Western Gateway Building, Western Road, Cork, Ireland
                [2 ]Department of Public Health and Primary Care, School of Medicine, Trinity College Dublin, Dublin 2, Ireland
                Article
                3504
                10.1186/s12889-016-3504-0
                4991068
                27538455
                f034fb1f-49b2-4c57-933c-b8cf669eba98
                © The Author(s). 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 6 April 2016
                : 12 August 2016
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2016

                Public health
                alcohol,adolescent,parent,consumption
                Public health
                alcohol, adolescent, parent, consumption

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