Institute of Community Medicine, University of Tromsö, Tromsö, Norway
Correspondence: Institute of Community Medicine, University of Tromsö, N-9037 Tromsö, Norway. Tel.: +47 776 44817; Fax: +47 776 44831; E-mail: Odd.Nilssen{at}ism.uit.no
(Received 16 April 2004; first review notified 17 May 2004; in revised form 18 June 2004; accepted 24 August 2004)
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ABSTRACT |
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INTRODUCTION |
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In the Third Tromsø Study (1986), a community based, comprehensive health survey aimed at coronary heart disease and general health, with more than 20 000 participants, we had the opportunity to conduct a randomized controlled trial of brief intervention in 338 (non-dependent) subjects, identified by increased GGT-levels and an alcohol intake of at least 23 times a week, and defined as at-risk alcohol drinkers (Nilssen, 1991). One group received a minor intervention of
10 min (during which they were asked to consider possible reasons for their elevated GGT), and the other a 15 min intervention (during which they were counselled about how to reduce their GGT levels by proposing alcohol-free days, changing to lower alcohol beverages, etc.) with subsequent monthly visits until their GGT values were normalized (major intervention). A third group, the control-group, remained untouched until follow-up 1 year later when they also were subject to brief intervention. Details about identification, intervention and results are described elsewhere (Nilssen, 1991
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At 1-year follow-up we demonstrated a significant reduction in alcohol intake in both intervention groups, and a corresponding reduction in GGT-levels. The control group, however, showed a significant increase both in daily intake and in GGT level.
The current report, somewhat delayed for personal reasons, addresses the question of whether the observed intervention effect only had a short term effect or whether it persisted over time.
In the Fourth Tromsö Study (1995) with more than 27 000 subjects, we were able to re-examine 247 of those who were subject to intervention in 1986, and thereby evaluate the long term effect of our intervention 9 years earlier.
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MATERIALS AND METHODS |
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Of the 338 subjects who, in 1986, were identified as at-risk drinkers and subject to brief alcohol intervention, 247 attended the health screening in 1995. They underwent the same examinations as the larger study population. They were not subject to individual interview on alcohol use. As the control group had received brief intervention at the 1-year follow up in 1987, they were no longer to be used as a control group for the 9-year study. The criteria for inclusion in 1986 were GGT values between 50 and 200 U/l for men, 45200 U/l for women, and an alcohol intake of at least 23 times a week. We therefore established a pseudo-control group of all subjects who, in 1986, had GGT values slightly below inclusion level (i.e. between 45 and 49 U/l for men; 4044 U/l for women) and a reported alcohol intake of at least 23 times a week. In all, 95 subjects met the criteria for pseudo-controls. Of those, 62 subjects were re-examined in 1995, thus constituting our new control group (pseudo-controls).
Statistical analyses were performed using the SAS statistical software package (SAS Institute, 1988). Analyses of variance were used for testing of differences in GGT reduction within and between the groups. The differences were adjusted for mean levels of GGT values in 1986 and 1995. As the basic GGT values (1986 values) are correlated with the change in GGT, we used the means of both measurements (1986 values + 1995 values/2) for the adjustments. These means are uncorrelated with the GGT changes, and also give a more stable standard error (SE).
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RESULTS |
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DISCUSSION |
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Follow-up population
Even though the attendance rate at follow-up was 73.1% (n = 247), 83.7% of those invited (exclusion of participants who had died or who had moved) were re-examined in 1995. This compares favourably with other studies. There had been no contact with the at-risk drinking groups between the 1- and 9-year follow-ups, no special invitation was sent in 1995 and no effort was made to contact them if they did not attend the screening. They were re-assessed in the large health screening for coronary heart disease but were not subject to personal interviews. For the non-attendants, we have reason to believe that many of these subjects were temporarily absent from Tromsö for educational or work-related reasons during the screening period.
Limitations of the study
In 1986 our regional ethical committee insisted that our control group should receive intervention at the 1-year follow-up, thus removing the possibility of having the same control group over time, thereby causing a potential weakness in the study design. A pseudo-control group was therefore established at the 9-year follow-up, consisting of subjects with GGT levels just below the inclusion criteria but with an intake frequency equal to that of the study population. In this study we therefore consider the original control group as a treated group.
For methodical reasons, only one group was asked to quantify their alcohol intake at the intervention. As the participants were randomly assigned into different groups, we assumed that mean alcohol consumption in this group represented a fair estimate of alcohol intake in the two other groups. This assumption is clearly questionable. Hence we feel unable to present data based on volume of alcohol consumed, a fact that impairs the strength in this study.
Missing quantification in individual drinking frequency at intervention represent another potential weakness. The way the categories for inclusion were defined in 1986 (23 times a week, daily or about daily) did not allow for an exact determination of frequency. Even though information on frequency was more accurate in 1995, our possibility to estimate individual change over time is limited.
Comparison with other studies
Effect from the intervention was still visible after 9 years. The effect was not only seen in the initial intervention groups but also in the control group, who received brief intervention at the 1-year follow-up. Similar results were found in the Malmö Study (Kristenson et al., 1983), one of the studies with more than 1-year follow-up. They also reported significant reductions in GGT level after 4 years, both in the intervention and in the control groups, but effect on level of alcohol use was not reported. In contrast to the Tromsö study, however, their participants were offered continuing contact throughout the follow-up period. When the GGT value had stabilized at an acceptable level, the frequency of therapeutic contacts was reduced but not stopped. Their control group also received intervention during the follow-up, as they were informed that they had an impaired liver test and were asked to restrict their alcohol intake.
In a randomized control study on brief intervention from Wisconsin (Fleming et al., 2002), the treatment group exhibited significant reductions in 7-day alcohol use at 48-month follow-up. They also reported significant fewer episodes of binge drinking and lower frequency of excessive drinking.
An Australian study found no effect of brief intervention after 10 years (Wutzke et al., 2002). The median consumption in the intervention and the control groups was similar, and mean reduction in consumption from baseline to follow-up was larger in the intervention group than in the control group, but this latter difference was not statistically significant. Although the Tromsö and the Australian studies included only non-dependent alcohol consumers, participants were recruited differently. In the Australian study the participants had a higher consumption level at baseline, different criteria were used for the definition of unsafe drinking and elevated GGT levels, and the criteria for inclusion and exclusion were also somewhat different, all of which might limit the comparability with our study.
Interpretation of results
In 1995 our participants were re-identified in the larger population study, which primarily focused on coronary heart disease, with more than 27 000 participators. An eager-to-please bias does not seems likely as the participants were not informed about our follow-up.
We had expected an increase in GGT levels, mainly for two reasons. First, according to the distribution of GGT in a normal population (Nilssen et al., 1990) an age-related 10% increase in men and a 20% increase in women would have been expected after 9 years. Second, as argued in the theoretical basis for early identification and early intervention, at-risk drinkers tend to increase their alcohol intake (and thereby their GGT level) over time. Nevertheless, a reduction in GGT level for the total risk drinking population was seen after 9 years (Table 3). The reduction (unadjusted) was strongest in the major and minor intervention groups (20.3 and 20%, respectively), although a somewhat smaller reduction for the control group (8%) was also observed. Regression towards the mean may explain parts of this reduction, but as the reduction in GGT was significantly larger for the treated groups than for the pseudo-control group, we suggest this might be interpreted as an effect of the intervention in 1986. The alcohol consumption trend, both in Tromsö and in the society at large, slowly increased during this period (from
4.2 to 5.7 l annual intake per capita). Increased awareness of health hazards as a result of repeated health investigations is possible but not very likely, as the large, background population displayed a significant increased (3.9 %) in GGT level during the same period (data not shown).
In analysis of variance (Table 3), after adjustment for mean levels of GGT in 1986 and 1995, no difference in GGT reduction between the trial groups was seen. This fits well with the findings at the 1-year follow-up. In 1986, we concluded that the minor intervention proved just as effective in reducing alcohol intake as the major intervention. This conclusion also seems valid after 9 years. A 15-min consultation with subsequent monthly control of GGT until normalization (major intervention) resulted in an equal GGT reduction as a single 10-min brief of information about the risk status without any further control (minor intervention).
The trial groups, however, displayed significantly greater GGT reduction than did the pseudo-control group (Table 3, column 3), indicating a beneficial effect of the intervention.
If, for the benefit of an analysis by intention-to-treat, all non-attendants were given the same GGT value in 1995 as in 1986 and included in the variance analysis, the difference between the trial groups and the pseudo-control group would have been further increased. An analysis of this kind must assume that the non-attendants did not change their alcohol intake, an assumption that can not be justified from our data.
For methodical reasons, only one group (the major intervention group) quantified their alcohol intake at the time of the intervention, reporting an average intake of 32.6 g pure alcohol per day. At the 1-year follow-up, the original control group reported an intake of 39.2 g (before receiving intervention). After 9 years the three intervention groups reported intake between 8 and 10 g pure alcohol per day (less than 1 alcohol unit), which is far below international recommendations for a safe level of intake (Bondy et al., 1999). In addition, frequency of any alcohol intake was reported as being reduced after 9 years. While the criteria for enrolment in 1986 was intake of alcohol 23 times per week or daily or about daily intake, average intake in 1995 was less than 1.4 drinking episodes per week, thus indicating a reduction in drinking frequency by more than 50%. Both the reduction in volume and frequency of alcohol intake lends support to the demonstrated GGT reduction, thus completing the picture of the efficacy of brief intervention.
In conclusion, the view that the effects from brief intervention in at-risk alcohol drinkers only represent short-term effects was not confirmed in this study. On the contrary, at-risk drinkers seem to respond beneficially to brief intervention.
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REFERENCES |
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Bien, T. H., Miller, W. R. and Tonigan, J. S. (1993) Brief intervention for alcohol problems: a review. Addiction 88, 315336.[ISI][Medline]
Bjartveit, K., Foss, O. P., Gjervig, T. and Lund-Larsen, P. G. (1979) The cardiovascular disease study in Norwegian counties. Acta Medica Scandinavica 643(Suppl.), 170.
Bondy, S. J., Rehm, J., Ashley, M. J., Walsh, G., Single, E. and Room, R. (1999) Low-risk drinking guidelines: the scientific evidence. Canadian Journal of Public Health 90, 264270.[ISI][Medline]
Fleming, M. F., Mundt, M. P., French, M. T., Manwell, L. B., Stauffacher, A. E. and Barry, K. L. (2002) Brief physician advice for problem drinkers: long term efficacy and benefitcost analysis. Alcohol: Clinical and Experimental Research 26, 3643.[ISI][Medline]
Kristenson, H., Öhlin, H., Hultèn-Nosslin, M. B., Trell, E. and Hood, B. (1983) Identification and intervention of heavy drinking in middle-aged men: results and follow-up of 2460 months of long-term study with randomised controls. Alcohol: Clinical and Experimental Research 20, 203209.
Nilssen, O. (1991) The Tromsö Study: identification of and a controlled intervention on a population of early stage risk drinkers. Prev Med 20, 518528.[CrossRef][ISI][Medline]
Nilssen, O., Förde, O. H. and Brenn, T. (1990) The Tromsö Study; distribution and population determinants of gamma-glutamyltransferase. American Journal of Epidemiology 132, 318326.[Abstract]
Saunders, J. B. and Conigrave, K. M. (1990) Early identification of alcohol problems. Canadian Medical Association Journal 143, 10601069.[Abstract]
Saunders, J. and Aasland, O. (1987) WHO collaborative project on identification and treatment of persons with harmful alcohol consumption. Report on phase 1. Development of a screening instrument. World Health Organization, Division of Mental Health, Geneva.
Saunders, J. B. and Foulds, K. (1992) Brief and early intervention: experience from studies on harmful drinking. Australian and New Zealand Journal of Medicine 22, 224232.[ISI][Medline]
SAS Institute (1988) SAS/STAT User's Guide, release 6.03. SAS Institute, Cary, NC.
Shaw, L. M., Strömme, J. H., London, J. L. and Theodorsen, L. (1983) International Federation of Clinical Chemestry, Scientific Committee, Analytical Section: IFCC methods for the measurement of catalytic concentration of enzymes. Part 4. IFCC method for gamma-glutamyltransferase [(gamma-glutamyl)-peptide: amino acid gamma-glutamyltransferase, EC 2.3.2.2]. Journal of Clinical Chemistry and Clinical Biochemistry 21, 633646.[ISI][Medline]
Stensland-Bugge, E., Bönaa, K. H. and Joachimsen, O. (1997) Reproducibility of ultrasono-graphically determined intima media thickness is dependent on arterial wall thickness. The Tromsö Study. Stroke 28, 19721980.
Strømme, J. H. and Löhne, K. (1990) Europeiske bruksmetoder for bestemmelse av ASAT, ALAT, GT og CK: Referanseverdier og relasjoner til nordiske metoder. Teknisk kjemisk avdeling, Ullevål sykehus, Oslo. [European methods for the determination of ASAT, ALAT, GT and CK: Reference values and relations to the Nordic methods. Department of Technical chemistry, Ullevål Teaching Hospital, Oslo.]
The Committee on Enzymes of Scandinavian Society for Clinical Physiology (1976) Recommended method for the determination of gamma-glutamyltransferase in blood. Scandinavian Journal of Clinical and Laboratory Investigation 36, 119125.[ISI][Medline]
Wutzke, S. E., Conigrave, K. M., Daunders, J. B. and Hall, W. D. (2002) The long-term effectiveness of brief interventions for unsafe alcohol consumption: a 10-years follow-up. Addiction 97, 665675.[CrossRef][ISI][Medline]
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