Providing alcohol to children is associated with alcohol-related harms. There is no evidence to support the view that parental supply protects from adverse drinking outcomes by providing alcohol to their child. Parents should be advised that this practice is associated with risk, both directly and indirectly through increased access to alcohol from other sources.

Between September, 2010, and June, 2011, we recruited 1927 eligible parents and adolescents (mean age 12·9 years [SD 0·52]). Participants were followed up until 2016, during which time binge drinking and experience of alcohol-related harms increased. Adolescents who were supplied alcohol only by parents had higher odds of subsequent binge consumption (odds ratio [OR] 2·58, 95% CI 1·96–3·41; p<0·0001), alcohol-related harm (2·53, 1·99–3·24; p<0·0001), and symptoms of alcohol use disorder (2·51, 1·46–4·29; p=0·0008) than did those reporting no supply. Parental supply of alcohol was not significantly associated with the odds of reporting symptoms of either alcohol abuse or dependence, compared with no supply from any source. Supply from other sources was associated with significant risks of all adverse outcomes, compared with no supply, with an even greater increased risk of adverse outcomes.

We did this prospective cohort study using data from the Australian Parental Supply of Alcohol Longitudinal Study cohort of adolescents. Children in grade 7 (mean age 12 years), and their parents, were recruited between 2010 and 2011 from secondary schools in Sydney, Perth, and Hobart, Australia, and were surveyed annually between 2010 and 2016. We examined the association of exposure to parental supply and other sources of alcohol in 1 year with five outcomes in the subsequent year: binge drinking (more than four standard drinks on a drinking occasion); alcohol-related harms; and symptoms of alcohol abuse (as defined by Diagnostic and Statistical Manual of Mental Disorders, 4th edition [DSM-IV]), alcohol dependence, and alcohol use disorder (as defined by DSM-5). This trial is registered with ClinicalTrials.gov , number NCT02280551

Some parents supply alcohol to their children, reportedly to reduce harm, yet longitudinal research on risks associated with such supply is compromised by short periods of observation and potential confounding. We aimed to investigate associations between parental supply and supply from other (non-parental) sources, with subsequent drinking outcomes over a 6-year period of adolescence, adjusting for child, parent, family, and peer variables.

We aimed to study parental and non-parental supply of alcohol and adjusted associations with five primary outcome variables in adolescents: binge drinking, alcohol-related harms, and the experience of symptoms of alcohol abuse, alcohol dependence, and alcohol use disorder.

Parental provision of alcohol to adolescents is associated with subsequent binge drinking, alcohol-related harm, alcohol use disorder symptoms, and increased access to alcohol from non-parental sources, and these associations persist after controlling for confounding variables. These findings have importance for parents, policy makers, and clinicians, and highlight parents as an important target for prevention.

To the best of our knowledge, this is the first study to examine, over a long period of time, prospective associations between both parental supply of alcohol and supply from other sources, and subsequent adolescent drinking outcomes, and to adjust for known covariates. We found a developing pattern of harm associated with parental supply, such that by the sixth follow-up (mean age 17·8 years), parental supply during previous years was associated with binge drinking, alcohol-related harms, and alcohol use disorder symptoms. The findings also showed that parental supply of alcohol not only risks adverse outcomes itself, it also risks increasing supply from other non-parental sources. Non-parental supply was associated with an even greater increased risk of adverse outcomes.

We did a systematic review, searching eight electronic databases on Sept 10, 2016 (Medline, MEDLINE In-Process and Other Non-Indexed Citations, EMBASE, PsycINFO, CINAHL, Scopus, Dissertations and Theses, and Cochrane Library), with the search terms “parental provision”, “social hosting”, “parental source of alcohol”, “youth”, “student”, teenage”, “underage”, “minor”, “risky drinking”, “excessive drinking”, and “binge drinking”. Inclusion criteria were that studies must be peer-reviewed, prospective, longitudinal studies, and analyse parental supply on the basis of reports from adolescent, parent, or both, and were from any publication year. We found seven cohort studies of parental supply of alcohol; the results of these showed that parental supply of alcohol was associated with subsequent risky drinking (pooled estimate odds ratio 2·00, 95% CI 1·72–2·32), but there was substantial risk of confounding bias and publication bias (assessed with the Newcastle–Ottawa scale). In all studies, measurement of exposure was problematic, follow-up times were short, and confounding was poorly controlled. Our cohort study has previously shown that, between age 12–15 years, parental supply of alcohol was associated with increased risk of consuming standard drinks (a standard drink being equal to 10 g of alcohol), but not of binge drinking. Parentally supplied children consumed fewer alcohol beverages on a typical drinking occasion than those who obtained their alcohol from non-parental sources. No study has reported on prospective associations between parental and other sources of supply of alcohol and subsequent adolescent drinking outcomes, harms, and symptoms of abuse, dependence, or alcohol use disorders, taking into account important potential confounders of any observed association.

Our previous Australian adolescent cohort studyfound that between ages 12 and 15 years, parental supply of alcohol was associated with increased risk of consuming standard drinks, but not of binge drinking.Although there was no protective effect associated with early parental supply, parentally supplied children did consume fewer alcohol beverages on a typical drinking occasion than did children who obtained their alcohol from other, non-parental sources. Adolescents who sourced their alcohol from non-parental sources (eg, peers, other relatives, themselves) had greater odds both of drinking standard drinks and of binge drinking. No longitudinal research has examined the development of alcohol use disorder symptoms associated with parental supply. In view of the associations between supply of alcohol and adverse drinking behaviours in our cohort to date, it is important to examine whether these patterns continue (possibly more moderated drinking associated with parental supply compared with more excessive drinking associated with accessing alcohol from non-parental sources), and to examine risk of alcohol-related harm and alcohol use disorders symptoms.

Alcohol use is an important public health issue associated with increased disease burden, and is of special concern in late adolescence and young adulthood, when alcohol use disorders have their peak age of onset.In many countries (such as the UK), parents are an important provider of alcohol to adolescents before they reach the legal age of purchase.Parents reportedly provide alcohol to mitigate harm,but evidence about the associated risks of such parental provision is absent—partly because of the dearth of any prospective studies spanning more than a 2–3-year period, and substantially because of the failure to adequately adjust for confounders in the handful of available cohort studies.

The funders of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report. RPM, PJC, AA, and MW had access to the raw data. RPM had full access to all the data and had final responsibility for the decision to submit for publication.

We used data from the Australian Parental Supply of Alcohol Longitudinal Study (APSALS) cohort of adolescents, which is registered with ClinicalTrials.gov NCT02280551 ).

To test for a dose–response relationship, we did planned secondary analyses examining the association between the number of waves of parental or other supply (between 0 and 5 years of supply) and harms reported in wave 6, using fixed-effect logistic or negative binomial regression, and the same five outcomes as the primary analyses and the four secondary count variables, using multiple imputation to reduce bias due to missing data ( appendix pp 33–35 ). We also did random intercept analyses of the frequency of supply within each wave on the five primary outcomes. We did post-hoc sensitivity analyses of associations with 11 individual symptoms of alcohol abuse, dependence, or use disorders (in light of the rates of endorsement of alcohol use disorder symptoms). Finally, in another post-hoc analysis, we examined the association between parental supply and subsequent other supply using random intercept models. We did all analyses in Stata (version 14.1), using a decision-wise error rate of p<0·05 for planned analyses, reduced to p<0·01 for post-hoc analyses.

We analysed data from six annual waves, with supply (parental only, other only, and both) compared with no supply from each year, examined against the outcomes from the following year. The analysis thus included five paired time periods (period 1 [waves 1–2], period 2 [waves 2–3], period 3 [waves 3–4], period 4 [waves 4–5], and period 5 [waves 5–6]). Variables were included in adjusted analyses if they showed unadjusted significance at an α of 0·05.

We analysed the four secondary count outcomes (reported number of different harms, total number of harms, number of abuse symptoms, and number of dependence symptoms) using a priori planned negative binomial regression, with results presented as incidence rate ratios (IRRs).

We included data from 6 years (waves 1–6) in this study. We planned primary analyses a priori, and did analyses using random intercept mixed-effects (controlling for within-respondent clustering or correlation over time), to examine the unadjusted and adjusted associations between the exposures and five main outcomes. We also analysed these five outcomes using logistic regression, with results presented as odds ratios (ORs) and CIs. We analysed severity of alcohol use disorder (mild, moderate, severe) and binge drinking (none, 5–10, ≥11 drinks) using multinomial logistic regression with results presented as relative risk ratios.

Covariates, which we chose on the basis of the literature on adolescent drinking, and measured at each annual wave, are described elsewhere.These include parental report of their own alcohol consumption (quantity and frequency), presence of familial alcohol problems, potential home access to alcohol without parental knowledge, parental religiosity, family conflict or positive relations, the presence of older siblings in the home, socioeconomic status of area of residence, parental employment and income, and country of birth. Children reported on the supply of alcohol from parental and from other sources; parental responsiveness, demandingness, or consistency; parental use of alcohol-specific rules; parental monitoring of the child's activities; whether they were living in a one-parent or two-parent household; child sex and age; availability of money to purchase alcohol; child tobacco use; child externalising behaviour; child anxiety and depression symptoms; and their peer's substance use and disapproval of alcohol and tobacco use ( appendix pp 13–19 ).

For the primary analysis, exposures were coded as a four-level variable: no supply of alcohol, parental supply only, other supply only, or both parental and other supply. In other analyses, parental supply and other supply were coded as separate variables. For a secondary planned dose–response analysis, the exposure variables were coded into two measures of the number of years in which supply occurred (0, 1, 2, 3, 4, or 5).

A further source of alcohol exposure—other supply—included alcohol supply from non-parental adults, friends, siblings, or self-supply, compared with adolescents reporting no supply from these sources. Parental supply and other supply were not mutually exclusive, and since supply could be derived from both sources, each source was controlled for separately in all analyses.

Adolescents were asked about who supplied them alcohol (sips or standard drinks) in the past 12 months, including mother, father, other adults, friends, siblings, and self-supply. From this, a dichotomous exposure variable—parental supply—was coded, indicating participants who had received alcohol from parents and those who had not. Adolescent report of parental supply was used because adolescent measures have been shown to be more predictive of adolescent behaviours than have parent measures,and adolescent self-report correlated well with parental report of supply (intraclass correlation 0·69–0·79; appendix p 29 ).

Finally, we assessed symptoms of an alcohol use disorder from wave 5 using the alcohol dependence items from DISC-IV,including an International Classification of Diseases item assessing craving, which corresponded with DSM-5 criteria ( appendix p 27 ). A categorical variable was coded on the basis of number of alcohol use disorder symptoms experienced in the past year (no alcohol use disorder [none or one symptom], mild [2–3 symptoms], moderate [4–5 symptoms], or severe [≥6 symptoms]).

We assessed symptoms of alcohol dependence from wave 5 using the alcohol dependence items from DISC-IV.A binary variable (no or yes) was coded, indicating whether three or more of the dependence symptom items had been experienced in the past 12 months, corresponding to DSM-IV criteria ( appendix p 26 ). We constructed an additional count outcome by summing the number of dependence symptoms experienced (possible range 0–7).

We assessed symptoms of alcohol abuse from wave 2 using the alcohol abuse items from the Diagnostic Interview Schedule for Children-IV (DISC-IV).A binary variable (no or yes) was coded, indicating whether any of the abuse symptom items had been experienced or not in the past 12 months, corresponding to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria ( appendix p 25 ). We constructed an additional count outcome by summing the number of abuse symptoms experienced (possible range 0–4).

Adolescents were also asked about the frequency of experiencing a range of alcohol-related harms, using a scale that included 17 alcohol-related harms.A binary variable (no or yes) was coded, indicating whether any of the harms had been experienced. Two additional count outcomes were derived: number of different harms experienced (possible range 0–17), and total number of harms experienced, which was constructed by summing the six frequency response categories for each item (possible range 0–85; appendix pp 9–10 ).

We defined binge drinking as consumption of more than four standard drinks (a standard drink being equal to 10 g of alcohol)on any single occasion in the past year, which was coded into a binary variable (no or yes). This definition is in line with Australian guidelines for adults, which recommend that healthy adults drink no more than four standard drinks on a single occasion to reduce the risk of alcohol-related injury.

There were five variables, based on adolescent report of: binge drinking; experience of alcohol-related harms; and experience of symptoms of alcohol abuse, alcohol dependence, and alcohol use disorder.

Adolescents and parents completed paper or online questionnaires independently of each other to minimise reporting biases; adolescent self-report on alcohol behaviours has been shown to be reliable and valid ( appendix pp 9–24, 85–99 ).

The validity of self-reports of alcohol consumption: state of the science and challenges for research.

Ethics approval was given by UNSW Sydney, and Universities of Tasmania, Newcastle, Queensland, and Curtin University. We obtained signed parental consent for each adolescent participant.

Between September, 2010, and June, 2011, a cohort of 1927 adolescents, and their parents, were recruited from grade 7 classes in 24 private independent (49%), six Catholic (12%), and 19 government (39%) secondary schools in Sydney, Perth, and Hobart. A detailed description of the recruitment methods, cohort characteristics, and representativeness is provided in the appendix (pp 4–8) . The parents of grade 7 adolescents had to provide signed informed consent to be eligible.The cohort was similar to the Australian population on important demographic measures, parental alcohol use, and child alcohol use.At wave 1 (grade 7 of secondary school), adolescents were a mean age of 12·9 years (SD 0·52), and similar to the Australian population in terms of sex distribution, household composition, racial background, and parental education. Groups of lower socioeconomic status are somewhat under-represented in the cohort; the predominance of students from non-government schools is likely to have biased the cohort towards higher levels of advantage compared with the general population.

Results

Figure Study profile Show full caption *Parents were not assessed in wave six. †Participants did not have to respond at all waves to be included in the analysis and those not responding at a particular wave were still contacted at subsequent waves unless they actively withdrew from the study or were lost to follow-up because they had no valid contact details; see table 2 The study profile is shown in the figure . The mean age of adolescent participants was 12·9 years (SD 0·52) in wave 1, 13·9 years (0·54) in wave 2, 14·8 years (0·56) in wave 3, 15·8 years (0·55) in wave 4, 16·9 years (0·50) in wave 5, and 17·8 years (0·51) in wave 6. At wave 6, 1494 (92%) of 1629 participants were attending high school. All forms of parental supply of alcohol (ie, adolescents who had parental supply only or both parental and other supply) increased across the six waves of observation, with such supply reported by 291 (15%) of 1910 adolescents in wave 1, 472 (26%) of 1836 in wave 2, 486 (27%) of 1776 in wave 3, 583 (34%) of 1705 in wave 4, 729 (44%) of 1671 in wave 5, and 916 (57%) of 1618 respondents in wave 6 (2 of 1673 cases had missing data at wave 5, and 11 of 1629 cases had missing data on this measure at wave 6; appendix p 36 ). Parental, familial, child, and peer characteristics associated with parental supply are shown in the appendix (p 38) , with information related to the context of supply (special occasion, dinners, parties, etc), and the frequency and typical quantity supplied by parents (p 37).

Table 1 Participants reporting binge drinking, alcohol-related harms, abuse, dependence, or alcohol use disorder symptoms, by source of supply of alcohol, and of the total sample Wave 1 Wave 2 Wave 3 Wave 4 Wave 5 Wave 6 Binge drinking (>4 drinks on one occasion) Parental supply only 3/177 (2%) 6/241 (2%) 10/213 (5%) 14/179 (8%) 42/186 (23%) 33/132 (25%) Other supply only 10/63 (16%) 36/126 (29%) 76/193 (39%) 110/243 (45%) 190/361 (53%) 224/361 (62%) Both sources of supply 12/114 (10%) 56/231 (24%) 82/273 (30%) 194/404 (48%) 357/543 (66%) 632/784 (81%) Total 25/1910 (1%) 98/1836 (5%) 168/1776 (9%) 318/1705 (19%) 589/1671 (36%) 889/1618 (55%) Any alcohol-related harms Parental supply only 16/177 (9%) 25/241 (10%) 14/213 (7%) 22/179 (12%) 47/186 (25%) 46/132 (35%) Other supply only 24/63 (38%) 70/126 (56%) 101/193 (52%) 137/243 (56%) 253/361 (70%) 261/361 (72%) Both sources of supply 37/114 (32%) 104/231 (45%) 115/273 (42%) 237/404 (59%) 404/543 (74%) 671/784 (86%) Total 77/1910 (4%) 199/1836 (11%) 230/1776 (13%) 396/1705 (23%) 704/1671 (42%) 978/1618 (60%) Alcohol abuse symptoms (≥1) * * Results for abuse symptoms do not consider diagnostic criterion B from Diagnostic and Statistical Manual of Mental Disorders, 4th edition—that dependence not be diagnosable— but when diagnostic criterion B is considered, percentages with abuse symptoms in wave 6 are 0·8% for participants who did not receive parental supply (n=3), 4·9% for those who did (n=45), and 3·2% for the total sample (n=52). † † Abuse questions were not asked in wave 1. Parental supply only NA 0 0 0 0 0 Other supply only NA 10/126 (8%) 13/193 (7%) 19/243 (8%) 18/361 (5%) 18/361 (5%) Both sources of supply NA 13/231 (6%) 22/273 (8%) 28/404 (7%) 54/543 (10%) 102/784 (13%) Total NA 23/1836 (1%) 35/1776 (2%) 47/1705 (3%) 72/1671 (4%) 120/1618 (7%) Alcohol dependence symptoms (≥3) ‡ ‡ Dependence and alcohol use disorder questions were not asked in waves 1–4. Parental supply only NA NA NA NA 0 0 Other supply only NA NA NA NA 30/361 (8%) 44/361 (12%) Both sources of supply NA NA NA NA 70/543 (13%) 145/784 (18%) Total NA NA NA NA 100/1671 (6%) 189/1618 (12%) Alcohol use disorder symptoms (≥2) ‡ ‡ Dependence and alcohol use disorder questions were not asked in waves 1–4. Parental supply only NA NA NA NA 5/186 (3%) 2/132 (1%) Other supply only NA NA NA NA 55/361 (15%) 67/361 (19%) Both sources of supply NA NA NA NA 132/543 (24%) 284/784 (36%) Total NA NA NA NA 192/1671 (11%) 353/1618 (22%) Data are n/N (%). Figures might differ from figure 1 because of missing data. If a participant was missing data on the parental supply or other supply variable, they were coded as missing because we were unable to confirm whether they also received alcohol from the missing source. NA=not asked. Binge drinking and experience of alcohol-related harms increased markedly over time ( table 1 ). Whereas only 77 (4%) of 1910 adolescents reported experiencing alcohol-related harm at wave 1, by wave 6 this had increased to 978 (60%) of 1618 ( table 1 ). Endorsement of symptoms of abuse (at least one DISC-IV symptom; appendix p 30 ) and dependence (at least three DISC-IV symptoms; appendix p 31 ) were less common, with 120 (7%) of 1618 reporting alcohol abuse symptoms and 189 (12%) reporting alcohol dependence at wave 6; alcohol use disorder symptoms (at least two DISC-IV symptoms; appendix p 32 ) were reported by 353 (22%) adolescents at wave 6.

At wave 6, the rates of binge drinking, alcohol-related harm, and symptoms of abuse, dependence, and alcohol use disorder were higher among adolescents who reported both parental and other supply than parental or other supply individually ( table 1 ). Adolescents could get alcohol from parents, other non-parental sources, or both, so these are coded as parental supply only, other supply only, or both sources of supply. Specifically, 632 (81%) of 784 adolescents who received alcohol both from their parents and from others reported that they had binged, 671 (86%) experienced alcohol-related harm, 102 (13%) reported alcohol abuse symptoms, 145 (18%) had at least three dependence symptoms, and 284 (36%) reported at least two alcohol use disorder symptoms ( table 1 ). The most frequently reported alcohol use disorder symptoms in adolescents supplied with alcohol by their parents (n=916) were reported tolerance (n=310 [34%]), drinking larger amounts or for longer than intended (n=283 [31%]), and spending time getting, consuming, or recovering from alcohol (n=159 [17%]; appendix p 28 ). The outcome measures were significantly inter-correlated; for example, binge drinking was moderately correlated with harms (0·66) and weakly correlated with abuse symptoms (0·23), and alcohol use disorder symptoms were strongly correlated with dependence symptoms (0·97; appendix p 39 ).

Table 2 Associations of source of supply at current wave and time with binge-drinking, harms, and symptoms of abuse, dependence, and alcohol use disorder at the subquent wave Binge drinking Any alcohol-related harms ≥1 abuse symptom ≥3 dependence symptoms * * Dependence and alcohol use disorder symptoms were first assessed in wave 5, so only two time periods (waves 4 and 5) were included for analysis. ≥2 alcohol use disorder symptoms * * Dependence and alcohol use disorder symptoms were first assessed in wave 5, so only two time periods (waves 4 and 5) were included for analysis. Current wave supply No supply 1 (ref) 1 (ref) 1 (ref) 1 (ref) 1 (ref) Parental supply only 2·58 (1·96–3·41); p<0·0001 2·53 (1·99–3·24); p<0·0001 0·50 (0·17–1·47); p=0·205 1·67 (0·71–3·93); p=0·241 2·51 (1·46–4·29); p=0·0008 Other supply only 5·58 (4·27–7·29); p<0·0001 3·46 (2·68–4·47); p<0·0001 5·30 (3·14–8·94); p<0·0001 3·01 (1·58–5·72); p=0·0008 3·81 (2·45–5·91); p<0·0001 Both parental and other supply 4·81 (3·75–6·17); p<0·0001 4·25 (3·38–5·36); p<0·0001 5·21 (3·15–8·59); p<0·0001 5·04 (2·70–9·42); p<0·0001 5·79 (3·78–8·86); p<0·0001 Time period 1 (wave 1 to wave 2) 1 (ref) 1 (ref) 1 (ref) NA NA 2 (wave 2 to wave 3) 1·10 (0·78–1·56); p=0·586 0·59 (0·45–0·78); p=0·0002 0·64 (0·34–1·21); p=0·170 NA NA 3 (wave 3 to wave 4) 2·91 (2·06–4·10); p<0·0001 1·41 (1·08–1·84); p=0·011 0·59 (0·31–1·13); p=0·111 NA NA 4 (wave 4 to wave 5) 8·16 (5·63–11·81); p<0·0001 3·71 (2·78–4·95); p<0·0001 0·66 (0·35–1·24); p=0·197 1 (ref) 1 (ref) 5 (wave 5 to wave 6) 16·93 (11·09–25·86); p<0·0001 8·35 (5·92–11·78); p<0·0001 0·85 (0·44–1·65); p=0·627 1·61 (1·08–2·39); p=0·018 1·58 (1·19–2·11); p=0·0015 Cases included (n) 1821 1819 1819 1563 1563 Paired time periods included (n) 7908 7813 7745 2774 2774 Data are adjusted odds ratio (95% CI); p value. Results are from random intercept mixed-effects logistic regression models, which we adjusted for other covariates ( appendix pp 40–45 ). Data are included as paired waves, with covariates from one wave and outcome from subsequent wave. NA=not asked. Adolescents who reported parental supply only had significantly higher odds of binge drinking (OR 2·58, 95% CI 1·96–3·41; p<0·0001) in the subsequent wave, compared with those reporting no supply, a result consistent with higher levels of bingeing ( appendix pp 46–48 ). Adolescents who reported other supply only had even greater odds of binge drinking (5·58, 4·27–7·29; p<0·0001) compared with those reporting no supply. Those who reported both parental and other supply also had increased odds of binge drinking (4·81, 3·75–6·17; p<0·0001), which was higher than for parental supply only, but was lower than would be expected if the effects of receiving parental supply only and other supply only were combined ( table 2 ).

Similarly, adolescents reporting parental supply only or other supply only had significantly higher odds of experiencing alcohol-related harms than did those reporting no supply (parental supply OR 2·53, 95% CI 1·96–3·34, p<0·0001; other supply 3·46, 2·68–4·47; p<0·0001). Those reporting both parental and other supply also had increased odds of alcohol-related harms (4·25, 3·38–5·36; p<0·0001), however, as with binge drinking, although the odds ratio was higher than parental supply only, it was lower than would be expected if the effects of parental supply only and other supply only were combined ( table 2 ).

Those reporting parental supply only had significantly increased odds of DSM-5 alcohol use disorder compared with no supply (OR 2·51, 95% CI 1·46–4·29; p=0·0008), as did those reporting other supply only (3·81, 2·45–5·91; p<0·0001), and those reporting both parental and other supply (5·79, 3·78–8·86; p<0·0001). Parental supply only was not significantly associated with the odds of reporting symptoms of either DSM-IV outcome (abuse or dependence), compared with no supply from any source. However, other supply only was associated with much higher odds of both abuse symptoms (5·30, 3·14–8·94; p<0·0001) and dependence symptoms (3·01, 1·58–5·72; p=0·0008) compared with no supply from any source. Adolescents who reported both parental and other supply also had higher odds of alcohol abuse symptoms (5·21, 3·15–8·59; p<0·0001) and alcohol dependence symptoms (5·04, 2·70–9·42; p<0·0001; table 2 ).

There were significant random effects for all models used to examine the associations between supply and outcomes: binge drinking (intercept SD 1·33, p<0·0001), reporting any harms (1·21, p<0·0001), reporting abuse symptoms (1·07, p<0·0001), reporting dependence symptoms (1·58, p<0·0001), and reporting alcohol use disorder symptoms (0·96, p=0·0009).

Similar to the results for our primary analysis, when we examined the number of harms and symptoms experienced by adolescents, parental supply of alcohol was associated with higher rates of harms (IRR 1·42, 95% CI 1·27–1·58), total number of harms (1·49, 1·30–1·70), and number of dependence symptoms (1·56, 1·31–1·87)—but not the number of abuse symptoms (0·90, 0·66–1·24)—than was no parental supply ( appendix pp 63–64 ). Abuse symptoms were infrequently endorsed.

Analysis of the number of waves of parental supply showed evidence of a dose–response relationship between number of waves of parental supply and binge drinking and report of harms, but not the DSM outcomes ( appendix pp 65–82 ). There was also evidence of a dose–response relationship with supply of alcohol from other sources, particularly for alcohol abuse, with the ORs increasing as the number of waves of other supply increased ( appendix pp 65–55 ). Analysis of frequency of supply within each year showed significant associations between frequency of parental supply and all outcomes except abuse symptoms, which is consistent with the results from our primary analysis ( appendix pp 65–82 ).

Adjusted analysis of the relationship between parental supply and other supply, to explore whether withholding parental supply leads to higher rates of later other supply, showed that parental supply was associated with double the odds of other supply in the subsequent wave (OR 2·05 95% CI 1·69–2·48), compared with no parental supply. This was true both of supply of sips (2·03, 1·66–2·49) and standard drinks (2·67, 1·81–3·95; appendix pp 83–84 ).