Drug and Alcohol Dependence 81 (2006) 157–165
Stability and instability in alcohol diagnosis from ages 18 to 21 and ages 21 to 25 years夽 J. Elisabeth Wells a,∗ , L. John Horwood b , David M. Fergusson b a
Department of Public Health and General Practice, Christchurch School of Medicine and Health Sciences, University of Otago, PO Box 4345, Christchurch, New Zealand b Department of Psychological Medicine, Christchurch School of Medicine and Health Sciences, University of Otago, New Zealand Received 31 January 2005; received in revised form 10 June 2005; accepted 21 June 2005
Abstract Background: Only in recent years have longitudinal studies of adolescents diagnosed alcohol use disorders and these have not distinguished between abuse and dependence. This study describes the course of disorder from age 18 to age 25 for abuse and dependence and investigates the extent to which continuities in disorder can be explained by background factors. Methods: A birth cohort of 1265 individuals from Christchurch, New Zealand, followed annually to age 16 years then at 18, 21 and 25 years (1003 at age 25). DSM-IV diagnoses were made from reports of alcohol symptoms at 18, 21 and 25 years. Results: The most stable diagnosis was that of no diagnosis, with 83–91% staying the same from one interview to the next. There were high rates of remission to no disorder; 57–75% for those with initial abuse and 50–54% of those with initial dependence. Nonetheless prior diagnosis was a strong predictor of subsequent diagnosis (ORs of 3.7–27.6). Adjustment for background risk factors reduced these odds ratios but all remained significant and substantial (minimum 2.6). Conclusions: The dual finding of substantial discontinuity and substantial continuity indicates that both public health and treatment interventions are warranted. © 2005 Elsevier Ireland Ltd. All rights reserved. Keywords: Alcohol abuse; Alcohol dependence; Alcohol disorder; Adolescent behaviour; Diagnostic orphans
1. Introduction For at least the last 30 years there has been major public health concern about alcohol consumption and its consequences in late adolescence and early adulthood. Many of the research questions about pathways through the transition to adulthood can be answered only from longitudinal studies. For example, is heavy and problematic drinking in this period the precursor of later alcohol disorder or a temporary rite of passage? How stable or unstable is alcohol diagnosis across this period? To what extent do 夽 Supplemental material for this article can be found by accessing the online version of this paper at http://dx.doi.org by entering doi:10.1016/ j.drugalcdep.2005.06.006. Please see Appendix A for more information. ∗ Corresponding author. Tel.: +64 3 364 3616; fax: +64 3 364 3614. E-mail address:
[email protected] (J.E. Wells).
0376-8716/$ – see front matter © 2005 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.drugalcdep.2005.06.006
young people move in and out of abuse and dependence without treatment, and what implications does this have for the need for public health and health system interventions? A number of the longitudinal studies have used some form of trajectory analysis (Wennberg et al., 2002; Schulenberg et al., 1996; Casswell et al., 2002; Bennett et al., 1999; Bates and Labouvie, 1997), with particular emphasis on distinguishing adolescent limited heavy use or problems from continued or escalating trajectories. Only in the last decade have studies of adolescents included systematic assessment of alcohol use disorders (Clark, 2004). Reducing problem counts to diagnoses does lose information, as with all categorization, but it does permit separation of disorder from no disorder and abuse from dependence and these distinctions are of interest to clinicians and epidemiologists. It also simplifies the analysis of transitions which are a particularly
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appropriate way to study changes when there are only two or three waves of assessment. Follow-up studies of community samples of young adults (Grant et al., 2001) and adults (Hasin et al., 1990; Hasin et al., 1997) have shown substantial changes over time in alcohol diagnoses. Grant et al. (2001) found that after 5 years 53% of those with alcohol abuse at baseline and 48% of those with alcohol dependence no longer had disorder. Nonetheless subsequent dependence was strongly predicted by prior diagnosis; 3% of those without disorder, 8% of those with abuse and 26% of those with dependence initially were dependent at follow-up. These results indicate marked discontinuity but also show that abuse and dependence have a different course. Two longitudinal studies beginning in adolescence (Clark et al., 2003; Rohde et al., 2001) both showed 40–50% of adolescents with alcohol use disorder (AUD) no longer had disorder at age 24. Abuse and dependence were not reported separately presumably because of small numbers with dependence at baseline when participants were aged 14–18 years. As in the study of Grant et al. (2001), a high rate of remission co-existed with prediction of outcome; those with AUD in adolescence were also much more likely to have AUD in early adulthood. Understanding of these changes and continuities would be enhanced by separation of abuse from dependence, which is possible in late adolescence. Also, since alcohol consumption, problems and diagnoses peak at around age 21 (Jernigan, 2001) it is important to have reports over this period when diagnostic change must be at a maximum. Because of this peak, it is simpler to interpret transitions when cohort members are of the same age, rather than a range of ages. Therefore there is a need for studies of diagnostic stability from around late adolescence to early adulthood, preferably with single age cohorts. Nelson and Wittchen (1998) have provided analyses of diagnostic transitions in this age group. However their analyses were based on cross-sectional data obtained at the baseline of a longitudinal study. They measured transitions by comparing reports of past symptoms (more than a year ago) and those reported for the last 12 months. What continuity is observed over time need not arise from the characteristics of a diagnostic state itself. Alcohol abuse or dependence at two time periods may be related because of common background factors. Stratification by disadvantageous background may show that, within a stratum, diagnosis at one time bears little relation to diagnosis at the next although this pattern does appear in the combined data set. Therefore to interpret observed continuity it is necessary to adjust for all likely background covariates which may be the cause of the observed continuity. If the addition of common background covariates has little impact on the transition probabilities from Time 1 to Time 2 then this implies that how someone reached their Time 1 state is of little importance; what matters is the state the person is in at Time 1. Alternatively, if the transition probabilities are affected then this indicates that they were confounded by some background covariates.
To address these issues of discontinuity and continuity in alcohol diagnoses in late adolescence and early adulthood, the present study uses data from the Christchurch Health and Development Study, a birth cohort of over 1000 young people interviewed annually from birth until age 16 and then at ages 18, 21 and 25 years. The aims of this study are: (a) To describe stability and instability in alcohol diagnoses across the transition from age 18 to age 21, and from age 21 to age 25. (b) To describe the background risk factors from the period from birth to 16 years of age in relation to alcohol diagnosis at age 18. (c) To model the transitions from ages 18 to 21 and from 21 to 25, taking account of common background risk factors.
2. Methods 2.1. Design The data reported here were gathered during the course of the Christchurch Health and Development Study (CHDS). The CHDS is a longitudinal study of an unselected birth cohort of 1265 children born in the Christchurch (New Zealand) urban region during a 4-month period in mid-1977. This cohort has been studied at birth, 4 months, 1 year, annual intervals to age 16 years, and at ages 18, 21 and 25 years. Fergusson et al. (1989) and Fergusson and Horwood (2001) provide overviews of this study which has collected data from a variety of sources including self-reports, parental interview, psychometric tests, teacher reports, medical and other official records. 2.2. Participants The cohort members included in this study were the 1025, 1011 and 1003 interviewed at 18, 21 and 25 years respectively. The number interviewed at age 25 consists of 79% of the original cohort and 89% of the cohort members resident in New Zealand at this age. For the transition from age 18 to age 21 there were 983 with data from both interviews; for the transition from age 21 to age 25 the number was 978. Alcohol diagnosis at age 18 (none, abuse only, dependence) did not predict loss to follow-up at age 21 (p = 0.53) nor did alcohol diagnosis at age 21 predict loss to follow-up at age 25 (p = 0.31). 2.3. Missing data At each interview there were almost no items missing. The problem with missing data arose from missed interviews. Analysis of transitions included only cohort members present for both interviews. For covariates measured before age 18 multiple imputation was carried out using 10 imputations with multiple chain Markov Chain Monte Carlo imputation
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with a run in of 200 iterations. Estimates were combined across imputations as calculated by Rubin (1987) (see also http://www.sas.com/statistics/). The covariates imputed were those used in analysis, namely the imputer’s model was also the analyst’s model. This meant that the whole imputation process was carried out separately for the age 18–21 transition and for the age 21–25 transition. Without imputation the sample sizes would have been 868 instead of 983 and 847 instead of 978. Sample sizes for covariates in Table 2 indicate that the amount missing for any individual covariate was always less than 9%. 2.4. Measurements 2.4.1. Alcohol diagnosis At the ages 18, 21 and 25 years interviews sample members were asked about alcohol problems in the years back to the previous interview. The questions came from the CIDI (the Composite International Diagnostic Interview) (World Health Organization Division of Mental Health, 1993). Individuals who met the relevant DSM-IV criteria (American Psychiatric Association, 1994) within a year were classified as having alcohol dependence or alcohol abuse for that year. In the analyses in this paper only the year prior to interview is included except for data from the age 18 interview which asked about symptoms since the previous interview at age 16. To investigate diagnostic transitions in this study, diagnostic algorithms set aside the DSM-IV requirement that alcohol dependence at any previous time prohibits the subsequent diagnosis of alcohol abuse or no diagnosis. DSM-IV requires everyone previously meeting criteria for dependence to be classified by levels of remission (full or partial) and duration of remission. Such detailed breakdowns are appropriate for follow-up of clinical populations but are overly complex for the main analyses investigating diagnostic instability in the general population. 2.4.2. Alcohol consumption For the previous 12 months alcohol consumption was reported for the largest amount of alcohol consumed on a single drinking occasion and for the last drinking occasion. Using questions similar to those used by Casswell et al. (1991), consumption was recorded separately for each type of beverage and container which should have reduced underreporting (Feunekes et al., 1999). It was then converted to millilitres of pure alcohol. For analysis of log consumption 5 ml was added to the 0 ml reported by abstainers. 2.4.3. Treatment At each interview at ages 18, 21 and 25 all participants were asked if they had ever consulted a doctor or sought other advice, counselling or treatment because of their drinking or problems associated with their drinking in the period since the previous interview. The source of treatment, the number of visits and reasons for seeking treatment were also recorded.
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2.4.4. Background factors up to age 16 2.4.4.1. Situation at birth. These were (i) whether the cohort member was born into a single parent or two parent family, (ii) maternal education (no formal qualifications, high school qualification or tertiary qualifications), and (iii) socio-economic status according to the Elley and Irving revised scales of socio-economic status for New Zealand (Elley and Irving, 1976). This six-point scale was collapsed into three levels: professional/managerial; clerical/technical/skilled; semiskilled/unskilled/unemployed. 2.4.4.2. Experiences up to age 16. (i) Parental change (0–16 years). This index of family instability was based on a count of the number of parental changes experienced by the child including parental separation or divorce, reconciliation, remarriage, death, fostering, etc. (ii) Inter-parental violence (0–16 years). At age 18 sample members were asked to report on the extent to which they had witnessed episodes of inter-parental violence by either parent up until they were 16, using items from the Conflict Tactics Scale (Straus, 1979). (iii) Physical punishment. At ages 18 and 21 sample members reported on the extent of parental physical punishment until they were 16. This was coded on a four-point scale; physical punishment was never used (1), seldom used (2), at least one parent regularly used it (3), or at least one parent used physical punishment too often, or too severely or treated the child in a harsh or abusive manner (4). (iv) Sexual abuse. Reports of sexual abuse prior to 16 were obtained in interviews at ages 18 and 21. These were coded as no abuse (0), non-contact abuse only (1), contact abuse but not attempted or completed intercourse (2), and abuse involving attempted or completed oral, anal or vaginal intercourse (3) (Fergusson et al., 1996). 2.4.4.3. Alcohol background. (i) Parental history of alcohol problems. When the adolescent was aged 15 a parental history of alcoholism or alcohol problems was derived from parental reports. (ii) Early use of alcohol. At age 14 participants were asked about the frequency of alcohol consumption in the previous 3 months and the most drunk per occasion, the usual amount drunk and the last amount. 2.4.4.4. Mid-adolescent behaviours. (i) Cannabis use (14–16 years). The number of occasions of use in the previous year was reported at the age 15 and age 16 interviews. The total was truncated to 50 for analyses. (ii) Early sex. This was defined as consensual sexual intercourse prior to age 16.
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(iii) Cigarette smoking (16 years). The frequency of smoking was categorised into non-smoking, less than monthly, monthly, weekly or daily smoking. (iv) Deviant peer affiliations (16 years). This was the selfreported extent of affiliations with delinquent or substance using peers (Fergusson and Lynskey, 1996). 2.4.4.5. Mid-adolescent mental health. DSM-III-R criteria were used on symptoms reported at the age 15 and age 16 interviews. Major depression and anxiety were assessed through questions from the Diagnostic Interview for Children (Costello et al., 1982) and the Diagnostic Interview Schedule (Robins et al., 1981). All participants reported on whether they had experienced suicidal thoughts, planned suicide or made a suicide attempt in the previous 12 months (Fergusson and Lynskey, 1995). 2.4.4.6. Individual characteristics. (i) Conduct problems at age 8 years. A scale score indicating the extent of problems was derived from a combination of parent and teacher reports on a checklist that combined items from the Rutter (1970) and Conners (1969, 1970) questionnaires. A detailed description of this scale and its properties is given by Fergusson et al. (1991). (ii) Novelty seeking (16 years). This was the novelty seeking scale from Cloninger’s personality questionnaire (1987). 2.4.5. Statistical analysis The diagnostic transitions were first described using simple cross-tabulations to relate alcohol diagnosis at one interview to the risk of diagnosis at the next interview. These transitions were also reported using logistic regression to show the odds ratio for disorder or for dependence at the next interview, given abuse or dependence at the previous interview. Note that instead of carrying out polychotomous logistic regression with three outcomes (no diagnosis, abuse only and dependence) two logistic regressions were used, one to predict subsequent alcohol disorder (abuse or dependence) and one to predict dependence. The relationship between background factors and diagnosis at age 18 is presented for dichotomized risk factors and was analysed using the Cochran–Armitage test for trend and chi-square tests for contingency tables. To take account of these background factors, using their original metrics, the logistic regressions predicting subsequent diagnosis were run again with these covariates included. Estimates of the adjusted transition matrices were derived from the coefficients in the fitted models, using the method described by Lee (1981) and Korn and Graubard (1999). Analyses were carried out in SAS 8.02 (http://www.sas.com). When imputation was required for background factors PROC MI was used to produce multiple imputations, these were analysed using PROC LOGISTIC and then PROC MIANALYZE was used to combine the estimates (see Section 2.3).
3. Results 3.1. Observed stability and instability As expected from the usual peak in alcohol consumption and problems around 21 years of age (Casswell et al., 2002; Jernigan, 2001), the prevalence of alcohol abuse alone rose from 14% at age 18 to 18% at 21 and then dropped to 10% at 25. These prevalences were calculated using all cohort members interviewed at each age and considering only symptoms in the year prior to interview except that the age 18 interview symptoms covered the 2-year period since the last interview at age 16. The longer period asked about at age 18 means that prevalences at this age may be biased upwards relative to prevalences at ages 21 and 25. In contrast to the pattern for abuse, the prevalence of dependence was more constant at 6, 4 and 4% as was the percent abstinent for the year before interview (7, 4 and 4%). Nonetheless similar prevalences do not imply that the same cohort members were dependent or abstinent throughout this period. Of the 953 interviewed at all three ages only 18 (1.9%) were abstinent in all three 12-month periods although 69, 42 and 40 were abstinent in each period. Only 5 (0.5%) met criteria for dependence at all three ages although 52, 41 and 34 were dependent at each age, again considering only the 12 months prior to interview (or for the age 18 interview, the period since the age 16 interview). The transitions in alcohol diagnosis from one interview to the subsequent interview are shown in Table 1. The most stable diagnosis was that of no disorder; 83% of those without disorder at age 18 also had no disorder at age 21 and 91% of those without disorder at age 21, the peak age for disorder, also had no disorder at age 25. Moving from no disorder at age 18 into abuse at age 21 was not uncommon (15%) but this transition was seen less often from age 21 to age 25 (7%). For both transition periods only 2% of those initially without disorder were dependent at the subsequent interview. Abuse and dependence were less stable states. The most striking finding was that half of those with dependence at one time no longer met criteria for any alcohol disorder at the next time. For participants with such a change the average reduction in the total number of DSM-IV symptoms of abuse and dependence was 5.1 (S.D. 1.6) by age 21 and 4.9 (S.D. 1.8) by age 25. Few had any residual symptoms of dependence; for both transitions one person still had two symptoms and two still had one symptom out of totals of 27 and 22 people who changed from dependence to no disorder. Treatment could not account for this remission as only 1/27 and 2/22 sought treatment in the relevant interval since the previous interview. Nonetheless almost all continued to drink; only two had become abstinent at 21, and one of those was drinking moderately at 25 but without any symptoms. Even those who changed from dependence to abuse mostly had a marked reduction in the number of symptoms: 3.5 (S.D. 1.8) and 4.1 (S.D. 2.0) for the two transitions. Thus while some of the instability seen in the transition matrices
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Table 1 Alcohol diagnosis transitions from ages 18 to 21 years and from 21 to 25 years Transition
Initial diagnosisa
N
Subsequent diagnosisa Percent with each diagnosis
Disorderb
Dependence
None (%)
Abuse only (%)
Dependence (%)
OR (CI)
OR (CI)
18–21 years
None Abuse only Dependence
793 136 54
83 57 50
15 33 19
2 10 31
1.0 3.7 (2.5, 5.4) 5.0 (2.8, 8.7)
1.0 6.3 (2.9, 14.0) 27.6 (12.5, 61.0)
21–25 years
None Abuse only Dependence
763 174 41
91 75 54
7 18 24
2 7 22
1.0 3.4 (2.2, 5.1) 8.6 (4.4, 16.6)
1.0 4.0 (1.8, 8.7) 15.0 (6.1, 37.3)
a b
The diagnosis is based only on the year prior to interview except at age 18 for which it covers the prior 2 years since the previous interview at age 16. Disorder is alcohol abuse or alcohol dependence.
in Table 1 is due to participants just crossing the symptom threshold for criteria much of the change is considerably more substantial. Reports of changes in drinking behaviour paralleled changes in reports of symptoms and consequently changes in diagnosis. Those changing from dependence to no diagnosis reduced the amount consumed on their heaviest drinking occasion in the previous year by 48% (ages 18–21) and 53% (ages 21–25). The amount consumed on the last drinking occasion decreased by 39% (18–21 years) and 40% (ages 21–25). Further analyses of current consumption for the whole cohort showed that drinking behaviours corresponded to current diagnoses and were little affected by past diagnosis (see supplementary material for this paper). Supplementary analyses were carried out to look at transitions with four diagnostic categories formed by splitting the no diagnosis category into those with no symptoms of dependence and those with one or two symptoms, sometimes referred to as ‘diagnostic orphans’ (Eng et al., 2003; Hasin and Paykin, 1999; Pollock and Martin, 1999; Sarr et al., 2000). There were 42 of these at age 18 and 40 at age 21. Diagnostic orphans at age 18 had outcomes at 21 no different from those without dependence symptoms (χ2 (3) = 0.65, p = 0.88) but did better than those with abuse (χ2 (3) = 13.91, p = 0.004) and those with dependence (χ2 (3) = 15.68, p = 0.001). In contrast those who were diagnostic orphans at age 21 had outcomes at age 25 more like those for participants with abuse at 21 (χ2 (3) = 1.48, p = 0.69), their outcomes were significantly worse than for those without symptoms (χ2 (3) = 11.27, p = 0.01) and they were better than for those with dependence (χ2 (3) = 8.78, p = 0.03). For both transitions the diagnostic orphans had very low probabilities of meeting criteria for dependence at the next interview – 2.4 and 2.5% – so they were not young people on the verge of developing dependence. All further analyses retained the standard DSM-IV single category of no diagnosis. The transition matrices in Table 1 demonstrate the extent to which there is instability in alcohol diagnosis over these ages. The odds ratios derived from these matrices indicate how well alcohol diagnosis at one time predicted alcohol
diagnosis at the next time and serve as a measure of continuity. For each transition two separate logistic regressions were carried out. In the first regression abuse and dependence were combined to give a single outcome variable of alcohol disorder whereas in the second regression the outcome was dependence. For both transitions the pattern was for higher odds ratios from dependence than from abuse at the initial interview, and for higher odds ratios when predicting dependence than when predicting disorder. In the transition from 18 to 21 years, relative to no disorder at 18, dependence at 18 has OR = 5.0 for disorder at 21 whereas for abuse only at 18 OR = 3.7. These ORs are higher again when predicting dependence (27.6 and 6.3 respectively). A similar pattern is seen for the transition from 21 to 25 years. These odds ratios are substantial. Table 1 shows both instability and continuity in alcohol diagnosis. This double message occurs because even large odds ratios arise from matrices with dispersion across the outcomes. It is possible that some of the continuity observed has arisen from common background factors rather than from causal connections between diagnostic states across time. The next section documents the background risk factors related to alcohol diagnosis at the start of the transitions considered here, namely at age 18. Then these background risk factors are taken into account in the following section. 3.2. Background risk factors related to alcohol diagnosis at 18 years There are complex pathways leading from birth circumstances through childhood to patterns of drinking and their consequences in late adolescence. Some analyses of such pathways leading to alcohol abuse at age 16 have already been carried out on this cohort (Fergusson et al., 1995) and subsequent psychosocial outcomes of drinking at age 16 have also been reported (Wells et al., 2004). Table 2 merely describes the prevalence of various risk factors in those with no alcohol disorder, alcohol abuse or alcohol dependence at age 18 and does not attempt to look at the extent to which some risk factors mediate the impact of earlier factors or independently
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Table 2 Alcohol diagnosis at 18 years—percent with each risk factor N
Alcohol diagnosis at age 18a None
Linear trend (P)b
Abuse only
Dependence
Situation at birth Single parent family Family semiskilled/unskilled/unemployed Mother lacked formal educational qualifications
1025 1025 1025
6 25 49
6 21 48
9 40 55
Experiences up to age 16 Change of parents Highest quartile inter-parental violence Parental physical abuse Any contact sexual abuse
1025 1025 1025 1025
35 20 15 9
43 28 22 18
48 40 40 24
0.009 <0.0001 <0.0001 <0.0001
952 941
11 3
16 5
21 9
0.009 0.006
946 1025 935 934
16 20 10 18
36 40 27 46
47 60 40 62
<0.0001 <0.0001 <0.0001 <0.0001
946 946 946
8 23 12
17 30 25
20 41 25
0.0001 0.001 <0.0001
1025 969 934
48 23 22
57 31 44
53 43 51
0.08 0.0002 <0.0001
Alcohol background Parental alcohol problems Early use—at least fortnightly at 14 years on averagec Mid-adolescent behaviours Cannabis use 14–16 years Sex before age 16 years Daily cigarette smoking (16 years) Highest quartile deviant peers (16 years) Mid-adolescent mental health Major depression (14–16 years) Anxiety disorder (14–16 years) Suicidal ideation prior to 16 years Individual characteristics Gender (% male) Highest quartile conduct problems (8 years) Highest quartile novelty seeking (16 years)
0.60 0.16 (0.02) 0.56
a
Based on symptoms reported for the period since previous interview at age 16 years. Cochran–Armitage test for trend for dichotomous outcomes. The p value in brackets is that from χ2 and is reported only if it was lower than that from the test for trend. c At least seven times in the previous 3 months. b
contribute to the outcome. For ease of presentation all risk factors have been dichotomized. There was little relation between alcohol disorder at age 18 and socio-economic status at birth but there were strong associations with experiences up to age 16 of parental change, inter-parental violence, parental physical abuse and sexual abuse from any source (p ≤ 0.009). A parental history of alcohol problems was more common in 18-year olds with alcohol abuse and still more common in those with alcohol dependence (p = 0.009). A similar pattern was seen for early frequent drinking (p = 0.006) and for other measures of early drinking not reported in Table 2. For example, at age 14 the percent who drank 60 ml or more on their heaviest drinking occasion was 5, 8 and 22% for those who at age 18 had no disorder, abuse only or dependence respectively (p < 0.0001). Mid-adolescent deviant behaviours, early conduct problems, and novelty seeking were also strongly associated with alcohol disorder at age 18 (p ≤ 0.0002), as were mid-adolescent depression, anxiety and suicidal ideation (p ≤ 0.001). The relation between gender and disorder was weak at age 18; males were slightly over-represented among those with abuse and dependence (p = 0.08).
3.3. Stability and instability adjusted for background risk factors To adjust for background risk factors all those risk factors in Table 2 were entered into models in their original metrics. After adjustment the odds ratios for initial alcohol diagnosis presented in Table 3 were lower than those in Table 1 but still remained substantial and significant (3.7 reduced to 2.6, 5.0 to 3.5, 3.4 to 2.8 and 8.6 to 6.1 for predicting disorder; 6.3 reduced to 3.0, 27.6 to 15.5, 4.0 to 2.7 and 15.0 to 10.0 for predicting dependence). Again the pattern was for dependence to predict subsequent diagnosis more strongly than abuse alone, and for subsequent dependence to be predicted more strongly than subsequent disorder. Only some of the continuity in alcohol diagnosis across ages can be accounted for by background risk factors. The two adjusted transition matrices are another way of indicating the relationship between alcohol diagnosis at one time and at a later time, taking account of background risk factors. The adjusted probabilities (Lee, 1981) are the predictive margins (Korn and Graubard, 1999) obtained from the fitted logistic regression models by first assigning everyone in the sample to an initial alcohol diagnosis of no disorder, then to abuse only,
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Table 3 Alcohol diagnosis transitions from ages 18 to 21 years and from 21 to 25 years adjusted for background risk factors Transition
Initial diagnosis a
N
Subsequent diagnosisa Adjustedb % with each diagnosis
Disorderc
None (%)
Abuse only (%)
Dependence (%)
Adjustedb
Dependence OR (CI)
Adjustedb OR (CI)
18–21 years
None Abuse only Dependence
793 136 54
82 65 60
16 30 21
2 5 19
1.0 2.6 (1.7, 4.1) 3.5 (1.8, 6.7)
1.0 3.0 (1.2, 7.2) 15.5 (6.0, 40.1)
21–25 years
None Abuse only Dependence
763 174 41
90 78 64
8 17 20
2 5 16
1.0 2.8 (1.8, 4.4) 6.1 (2.9, 12.8)
1.0 2.7 (1.2, 6.4) 10.0 (3.4, 29.5)
a b c
The diagnosis is based only on the year prior to interview except at age 18 for which it covers the prior 2 years since the previous interview at age 16. Adjusted for all covariates in Table 2 in their original metric. Disorder is alcohol abuse or alcohol dependence.
and then to dependence, thus ensuring that the distribution of all other covariates is identical across the initial alcohol diagnosis categories. This procedure was carried out for the logistic regression predicting disorder and also for the logistic regression predicting dependence. The adjusted percent with subsequent abuse only was obtained by subtracting the adjusted percent for subsequent dependence from that for subsequent disorder. If those with alcohol dependence at age 18 had the same distribution of background factors as found in the whole sample, 60% would have had no alcohol disorder at age 21, whereas the observed transition percent was 50%. The disadvantageous background factors found in those with dependence at age 18 contributed to another 10% of them not going into remission. Although gender is included as a background factor it is actually one which has a major impact within the period from 18 to 25. At age 18 the difference in rates of alcohol disorder for young men and young women was 5% (22% versus 17%, OR = 0.7, 95%CI = 0.7, 0.97, p = 0.03) whereas at 21 the difference was 17% (31% versus 14%, OR = 0.4, 95%CI = 0.3, 0.5, p < 0.0001). By age 25 the difference had reduced to 8% (18% versus 10%, OR = 0.5, 95%CI = 0.3, 0.7, p = 0.0002). There was a clear peak in the rate of disorder for young men at 21 whereas for women the peak, which was much lower, was at age 18. Nonetheless, when predicting subsequent disorder, there were no significant interactions between gender and prior abuse alone or prior dependence; p > 0.70 for the age 18–21 transition, and p > 0.28 for age 21–25 transition. Gender comparisons of rates of dependence were imprecise because of low numbers and were not significant until age 25. The rates for males and females were 6% versus 5% at age 18 (OR = 0.8, 95%CI = 0.4, 1.3), 5% versus 4% at 21 (OR = 0.7, 95%CI = 0.5, 1.4) and 5% versus 2% at age 25 (OR = 0.4, 95%CI = 0.2, 0.9). No interactions with prior disorder were significant; p > 0.95 for the age 18–21 transition and p > 0.13 for the 21–25 transition. For young men and for young women, prior diagnosis was an important predictor of subsequent diagnosis with a negligible change in odds ratios for prior diagnosis when gender was added to each model.
Overall only 2% (n = 17) of cohort members sought treatment for alcohol problems in the period between the age 18 and age 21 interviews and only 3% (n = 26) sought help between 21 and 25. In relation to alcohol diagnosis in the year before interview 1% of those with no diagnosis sought help in the next period, 2–5% of those with abuse only, and 9–15% of those with dependence. The number of visits was often only enough for brief intervention and assessment. For these two periods the numbers with just one or two visits were 8/17 and 9/26 respectively.
4. Discussion The cultural context for the young people in this study was one of widespread consumption of alcohol. In New Zealand (McPherson et al., 2004) about 85% of adults have drunk alcohol in the past year, which is similar to or a little below that seen in other Western countries (World Health Organization, 1999). In 1995 when the cohort members were 18 years of age the legal age for purchase of alcohol was 20 years yet only 7% were abstinent throughout the previous year. In late 1999 when the purchase age was lowered to 18 years the cohort were already aged 22 years. Despite liberalization of access at that time through sales of beer in supermarkets and Sunday trading, consumption per occasion decreased from age 21 to age 25 although there was a small increase in the frequency of drinking (see supplementary material). There was a marked rise in alcohol abuse from 14% at age 18 to 18% at 21 and then a decline to 10% at 25 whereas the prevalence of dependence was more constant at 6, 4 and 4%. Nonetheless transition matrices from age 18 to age 21 and from age 21 to age 25 showed considerable instability in both abuse and dependence diagnoses from one interview to the next. For each transition 50–54% of those with dependence at one interview had no alcohol diagnosis at the next interview; this is extremely close to the 48% remission observed by Grant et al. (2001) over a 5-year period for a cohort several years older. They found that 63% of alcohol abusers later had
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no diagnosis; in our study the percent was 57% from 18 to 21, but 75% from 21 to 25. In both studies only 2–3% initially without dependence became dependent but it was more common to move into abuse (7–15%). Nelson and Wittchen’s (1998) study also suggested that alcohol abuse was more transient than alcohol dependence, although as in our study transience was higher after the peak in alcohol consumption around age 21 than when consumption was increasing during adolescence. Abuse without dependence may be seen as the result of lifestyle decisions, with instability and continuity affected by the access to alcohol, behaviours and attitudes found in an individual’s social milieu and the broader social environment. Dependence however sounds inherently stable without intervention, yet the study of transitions shows that it is not. It may be that dependence is not as permanent a state as DSMIV indicates, especially in young people with only a short history of dependence. Such short duration of dependence may also have been important in the high rates of remission found in drug addicted Vietnam veterans (Robins et al., 1974). Furthermore, the description of dependence in DSMIV, and earlier versions, owes much to clinical research and as Cohen and Cohen (1984) pointed out 20 years ago, stability observed in such populations owes much to selection. However it would be premature to claim that remission over 3 or even over 7 years leaves a young adult no more susceptible to later dependence than someone who has not met criteria for an alcohol diagnosis. There has been debate over the applicability of DSM-IV dependence criteria for young people (Chung et al., 2002). Some of these concerns arise from the way in which the criteria are operationalized, with particular concern that reports of tolerance in adolescents do not reflect what is meant for the DSM-IV criteria, although the adolescents are correctly reporting that they have to drink more than previously to obtain the same effect (Clark, 2004). Problems may also arise with reports of drinking more or for longer than intended that relate to social context rather than compulsion. Chung et al. (2002) have shown wide variation across surveys of young people for these two criteria. False positives on these criteria may account for some of the ‘diagnostic orphans’ found in a number of studies (Eng et al., 2003; Hasin and Paykin, 1999; Pollock and Martin, 1999; Sarr et al., 2000). Measurement error is another potential source of apparent change in diagnosis. Failure to report symptoms is possible, either deliberately or because of forgetting, as is misunderstanding of questions. Nevertheless the magnitude of the instability seen in the present study and other studies (Clark et al., 2003; Grant et al., 2001; Hasin et al., 1990, 1997; Rohde et al., 2001) suggests genuine change for many people. As well as change, this study also found substantial continuity, even after adjustment for a wide range of background risk factors. Since the early influential paper by Temple and Fillmore on variable outcomes for young people (Temple and Fillmore, 1985) there has been dispute about whether to emphasize discontinuity or continuity (Windle, 1988; Rohde
et al., 2001; Clark, 2004). The extent of change not due to treatment indicates the potential for public health interventions and may also indicate the importance of naturally occurring interventions in the lives of individuals. The continuity seen implies that alcohol use disorder, particularly dependence, should not be ignored. As well as the current problems experienced by young people with alcohol disorder, they are likely to experience subsequent or continuing disorder. Therefore treatment, or at least early intervention, is appropriate. Young people with alcohol abuse or dependence are not doomed to later disorder but they are at risk of it. 4.1. Strengths and limitations This study has the advantage which comes from following participants since birth in that risk factors have been measured longitudinally. Loss to follow-up has been relatively low and adjustment for such loss has been shown to have little impact on alcohol analyses in this study or in other analyses (Wells et al., 2004). The cohort is an unselected community sample. Nonetheless this cohort comes from one city in one country, with participants born in the same year, all of which raises issues about generalizability. In spite of this the results seem remarkably congruent with those from several studies from the United States of America. It seems reasonable to expect similar findings for other Western countries since these also show a peak of alcohol consumption and problems at around 21 years of age.
Acknowledgements This research was funded by grants from the Health Research Council of New Zealand, the National Child Health Research Foundation, the Canterbury Medical Research Foundation and the New Zealand Lottery Grants Board.
Appendix A. Supplementary data Supplementary data associated with this article can be found by accessing the online version of this paper at http://dx.doi.org by entering doi:10.1016/j.drugalcdep. 2005.06.006.
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