QJM Advance Access originally published online on September 17, 2006
QJM 2006 99(10):665-671; doi:10.1093/qjmed/hcl090
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Risk factors associated with body mass index increase in men at 28 years follow-up
From the 1Norwegian Knowledge Centre for the Health Services, Oslo,2The Norwegian Institute of Public Health, Oslo and3Centre for Preventive Medicine, Ullevål University Hospital, Oslo, Norway
Address correspondence to Dr L. Lund Haheim, Norwegian Knowledge Centre for the Health Services, PO Box 7004, St. Olavs Plass, N–0130, Oslo, Norway. email: lise.lund.haheim{at}kunnskapssenteret.no
Received 6 February 2006 and in revised form 28 June 2006
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Summary |
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Background: Several studies have reported a general increase in body mass index (BMI).
Aim: To identify factors influencing BMI changes at 28 years follow-up.
Design: Prospective screening study.
Methods: The cohort of the Oslo I study of 1972/73 had another screening in 2000 (Oslo II). We present data for these men, and men from Oslo I who participated in five similar studies during 1996–2001. In all, 7157 men aged 20–49 years at first screening attended two health screenings, and complete data were available for 7104. BMI change from 1972/73 to 2000 was the dependent variable in multiple regression analyses.
Results: The percentage with obesity (BMI 
30) increased overall from 2.5% to 13.5%. The overall mean (SD) BMI increased from 24.2 (2.6) kg/m2 to 26.2 (3.4) kg/m2. The increase was largest (3.9 (2.5) kg/m2) among men aged 20–24 in 1972/73 and least (1.6 (2.5) kg/m2) in those aged 45–49 years. No age trend was observed for those with BMI 30.0 kg/m2 in 1972/3. On multiple regression analysis, increasing triglycerides, systolic blood pressure, age and non-fasting glucose, decreasing physical activity and not smoking were all significantly related to increasing BMI. Having stopped smoking was also related to increased BMI. Daily smoking in both 1972/73 and 2000, and daily smoking in 2000 but not in 1972/73, were inversely related to increased BMI.
Discussion: There was a substantial increase in BMI, with the largest increase in the younger men, except in those who were already obese at first screening. Overall, obesity increased by 11% in the study period and was associated with multiple life-style factors.
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Introduction |
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Concerns have been raised worldwide1–6 at reports of increases in Body Mass Index (BMI) that affects people's risk for several diseases associated with obesity. Obese people are at increased risk of diabetes,7 hypertension,4,8 heart disease,9–11 stroke12 and total mortality.11,13–16 In Norwegian national cross-sectional data for 40–42-year-olds, the mean male weight increased by 5.6 kg over the period 1966–1995.6 Two Norwegian studies show a high correlation for BMI from both teenagers advancing into adulthood17 and people aged 20–61 years followed for 16 years.18
The Oslo-study of 1972/73 was the first large population-based study on the risk of cardiovascular disease in Norway. The 21-year follow-up of this cohort showed a trend in increasing BMI risk for fatal (but not non-fatal) myocardial infarction (MI) with increasing length of follow-up.19 The second survey (Oslo II) in 2000 made it possible to study the actual increase in BMI and the factors associated. The aim of the present study was to investigate any associated increase (unless otherwise stated) in the values of other risk factors that might influence the observed change in BMI between 1972/73 and 2000, to help us understand the current BMI increase in men. Such knowledge may illuminate whether new preventive measures are needed or if existing ones should be intensified.
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Methods |
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The cohort attended the first screening in 1972/73 in Oslo recording risk factors for cardiovascular disease. The first screening involved all men in Oslo aged 40–49 years (n = 25 915) and a 7% sample of men aged 20–39 years (n = 4110).20 A total of 16 209 men aged 40–49 years and 1763 men aged 20–39 years attended. The standardized procedures involved having a non-fasting blood sample taken to record the level of total serum cholesterol, triglycerides and glucose, and measurement of height and weight. The men answered a questionnaire about the presence of symptoms and diseases of cardiovascular origin, smoking, mental stress, physical activity at leisure and work. Two intervention studies were included; one on diet and smoking intervention and another on drug treatment of hypertension. A low-risk group was examined, with special focus on ECG. With the exception of the men participating in the two intervention studies, this cohort of men had not been to a second screening prior to the Oslo II screening in 2000.
After 28 years, 12 764 of the men who had been invited to the first screening, and now were living in Oslo or the surrounding county of Akershus, were invited to the second screening, Oslo II, in coordination with the Oslo Health Study.21 In all, 5323 of these men attended both health screenings. Some men from the Oslo study cohort were not invited, because they were instead invited to attend The Oslo Health Study and the associated MORO (Exercise at Romsås; in Norwegian, Mosjon på Romsås) study, according to their year of birth. We also did not invite the men who previously attended two intervention studies and now were currently taking part in three new intervention studies. Thus, in addition to Oslo II, data from 1834 participants from the five studies of 3960 eligible men of the Oslo study cohort were included, with informed consent from the men involved and permission of the Norwegian Data Inspectorate. The study population being analysed thus comprised 7157 men.
At the second screening, the men underwent a health screening where a non-fasting blood sample was taken for total serum cholesterol, HDL-cholesterol, triglycerides and glucose. Height and weight were measured. Two questionnaires were used according to age of the participants. They answered a questionnaire on medical history, sickness in family, memory (only the older men), mental health, muscular or skeletal pain, relation to family and friends, physical activity, education, diet, drinking, smoking, physical functioning and feeling of safety (only the older men), use of health services, pattern of habitation and medication.
Statistical analyses
Analyses were based on the change in risk factors from 1972/73 to 2000. Body Mass Index was calculated as weight in kg divided by the square of the height in m (kg/m2). BMI was first stratified into five levels according to the World Health Organization definition.13 However, to gain enough power in the statistical analyses, the BMI strata were reduced to three levels: <25.0 kg/m2, 25.0–29.9 kg/m2 and 30.0 kg/m2.
Risk factors were presented as means and standard deviation (SD) or percentages. Multiple linear regression analysis was used to study the association of other factors with BMI (continuous term). Analyses were made separately for the different age-groups and the total cohort.
The definition of attendance was a SBP value for both screenings. Not all men had all risk factors measured, hence numbers are lower for some of the analyses. Significance was set at p < 0.05.
At the first screening in 1972/73, the values of total serum cholesterol, triglycerides and glucose were measured in mg/dl. Recalculations as mmol/l were made according to specifications of The Oslo Study Laboratory Protocol 2: total serum cholesterol in mmol/l=(0.92 x value in mg/dl x 0.02586) + 0.03; triglycerides in mmol/l = (0.90 x value in mg/dl x 0.01129)–0.11; glucose in mmol/l = (0.0518 x value in mg/dl)–0.58. Analyses used SPSS 12.0.1.22
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Results |
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An increase in mean BMI was clear. At the first screening, obesity (defined as BMI
30 kg/m2) ranged from 0.6% to 2.7% among the six age groups (Table 1). In 2000, these values ranged from 12.3% to 21.5%. The differences ranged from 9.9% among the eldest (aged 45–49 years in 1972/73) to 20.9% among men aged 30–34 years. The overall increase in the proportion of obese people in this cohort was 11%. This coincides with the reported change in physical activity at leisure: 3611 men reduced their level of activities vs. 954 who increased their level of activities (results not shown).
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BMI increased in all six five-year age groups (Table 2), but the younger ones increased the most, with an increase of 3.9 kg/m2 in men aged 20–24 years in 1972, compared to a change of 1.6 kg/m2 in men aged 45–49 years. At the screening in 1972/73, the mean (SD) value of BMI increased gradually over the age groups from 22.3 (2.8) kg/m2 (20–24 years old) to 24.4 (2.6) kg/m2 (45–49 years old). In 2000, the BMI change was not systematically different between the age groups, at 26.2 (3.6) and 26.0 (3.3), respectively. Analyses of the three BMI strata showed marked changes for BMI <30.0 compared to BMI
30.0 kg/m2. For BMI <25.0, the increase in BMI was larger in the younger age groups: men aged 20–24 years had a 4.0 unit increase, whereas men aged 45–49 years had a 1.8 unit increase. The same trend was observed for BMI of 25.0–29.9 kg/m2, with an increase of 4.0 units vs. 1.4 units respectively. In men with BMI 30.0 kg/m2 in 1972/73, an appreciable mean change in BMI was not observed between first and second screening, but the numbers in some of the age groups were small. The change ranged from 1.1 units (3.4) in the youngest men to 0.6 (3.8) in the oldest.
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The possible influence of other risk factors on the increase in BMI was studied by multiple linear regression. We studied the risk profiles overall and for each of the three BMI levels (Table 3). The analyses were controlled for use of cholesterol lowering and antihypertensive drugs. Overall, analyses showed increasing age, systolic blood pressure (SBP), triglycerides, total cholesterol, glucose, increased physical activity relative to no change (inversely) and being a smoker in 2000 (inversely) and quitting smoking in 2000 to be independently associated with BMI increase. Inactivity at leisure relative to no change was not significantly associated. The men with BMI <25.0 had the same risk factor profile except for physical activity at leisure (p > 0.05) and smoking at last screening but not at first screening (p > 0.05). The risk profile for men with BMI 25.0–29.9 kg/m2 differed from the overall results, in that total cholesterol and glucose were not significantly associated. For the obese men, a further increase in BMI was only independently associated with SBP and being smoker at both screenings (inversely).
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The relationship between BMI increase and age was analysed by stratifying age into three ten-year age groups. These analyses were adjusted for age within the age strata. All three strata shared the significant predictors of increasing levels of SBP, triglycerides, glucose and quitting smoking (inversely). For the older age group, the additional risk factors increasing total cholesterol, increased physical activity (inversely) and being a smoker in 2000 (inversely) were significantly associated. Age was not significant in the middle age group of 30–39 years.
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Discussion |
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TopSummaryIntroductionMethodsResultsDiscussionAcknowledgementsReferences |
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The percentage of obese men (BMI
30.0 kg/m2) increased by a factor of 5.4 in our cohort, with a marked increase in mean BMI, over the 28-year period. This change was larger in younger men. Overall, all the risk factors studied, except for reduced level of physical activity at leisure, were independently associated with BMI increase. The reference group was no change in activity and it might be that the difference on BMI between no change and decreased activity at leisure is small among these men. In the largest age group (40–49 years at screening) the independent predictors of BMI increase were age, total cholesterol, increased level of physical activity at leisure (inversely) and smoking in 2000 (inversely). Four risk factors—SBP, triglycerides, glucose and quitting smoking—were common through the three ten-year age groups. Little change was seen among the men with BMI 30.0 kg/m2 at first screening, but numbers in this category were low. The increase in BMI seen in this cohort accords with the previously reported increase in weight (5.6 kg change from 1966 to 1995) in cross-sectional data among Norwegian men aged 40–42 years.6 Our study shows a significant age-related change of men over an age span of 30 years. The men were aged 20–49 years at the first screening in 1972/73, and the change has been larger in the younger men, suggesting a future burden of disease for a longer period of their lives. It was therefore of great interest to investigate what risk factors were associated with BMI increase.
Our results indicate a multi-factorial profile. In the NHANES study (n=9790) obesity was associated with increased CVD mortality, with a significant hazard ratio of 1.24.15 Low levels of physical activity were also associated, but not caloric intake. In the MONICA study of 38 populations in 21 countries over 10 years follow-up, several known cardiovascular risk factor levels were decreasing, but BMI was on the increase, especially among men, and smoking was increasing among women.1 SBP showed a decreasing trend as well as total cholesterol although changes were smaller. In Rosengren et al., after 19.7 years of follow-up of 6874 Swedish men, risk of coronary death and non-fatal myocardial infarction increased with increasing weight gain.11 Smokers are known to be leaner than non smokers, but the risk of CHD death is greater from smoking than from increased BMI.14 In the Diverse Populations Collaborations study of 21 prospective cohorts, 15.9 kg/m2 BMI units were required to offset the detrimental effects of smoking among men.14 Lyratzopoulos et al.24 studied the relationship between increased BMI and deprivation status among persons aged 35–55 years. They found that BMI increased over time independently of deprivation status, except among obese people. In the 21-year follow-up of this study, however, the risk effect of BMI took 10–15 years to become significant for fatal myocardial infarction.19 The multi-factorial risk factor profile associated with BMI increase shows the complexity of weight gain. However, this multi-factorial aspect gives scope for several preventive strategies for individuals to achieve a stable BMI that does not increase the risk of serious disease.
Analyses stratified by age gave consistent results across the age groups, with SBP, triglycerides, glucose and quitting smoking as common predictors of BMI change. The older men also had the additional predictors of cholesterol, physical inactivity and being smokers, which may indicate additional changes that occur with increasing age. This age difference may necessitate slightly different approaches for BMI-reducing strategies. It may indicate that the long-term effects of obesity are more complex, given that the older men had been obese for a longer time than the younger ones.
There is a general increase in BMI in many cohorts,1–6 and there is a growing concern about the consequences of an obesity 'epidemic'. The consequences for increased cardiovascular disease incidence and mortality and diabetes appear to be real.7–15 This study sheds some light on which factors are associated and may be the subject of preventive strategies. There is an overall association between increasing glucose level and BMI, relating the results to risk of diabetes. The factors glucose, triglycerides, SBP and BMI are major factors constituting the metabolic syndrome,23 and these factors were also related. It is unfortunate that there appears to be a rise in BMI due to quitting smoking, as smoking is a well-known risk factor for cardiovascular diseases.
The limitations of this study relate to the fact that the study involves a selection of the men who were alive in 2000. We also lack information on men emigrating and moving out of the greater Oslo area. We are potentially missing people with a high risk, which might strengthen the associations. Subgroup analyses of the two ten-year age groups have a power limitation in comparison to the overall analysis, as do the comparisons between BMI 30.0 kg/m2 vs. lower BMI.
The response rate was not uniform through the six studies (Table 5). The studies were different in design and aim, and all studies except Oslo II and DOIT (Diet and Omega-3 Intervention Trial on atherosclerosis) included additional subjects not in the Oslo study cohort. In the Oslo II study, response rate was highest among those who had attended the Oslo cohort. They had the benefit of comparing their health status in 2000 to that in 1972/73 (study response rate was 65% after one reminder of former participants and 52% overall, with no reminder to those not attending in 1972/73). More than 60% was considered satisfactory in the Oslo II study. From earlier analyses,25,26 we know that the non-attenders had a higher mortality and morbidity rate. As a consequence the results are biased towards healthier people, and the risks underestimated.
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Conclusions
The proportion of obese men increased from 2.5% to 13.5% over a 28-year period. The increases in BMI were greater in younger than in older men. The overall association between the BMI increase and other risk factors was multi-factorial, confirming known independent and modifiable risk factors as serum lipids, glucose, smoking and (inversely) physical activity at leisure.
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Acknowledgements |
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Data were collected in coordination with, and prior to, the Oslo Health Study 2000–2001, in collaboration with the National Health Screening Service of Norway, now part of the Norwegian Institute of Public Health, the City of Oslo and Ullevål University Hospital in Oslo. The second screening in 2000, Oslo II, was supported by the Norwegian Council for Cardiovascular Diseases of the Norwegian National Association for Public Health. Results were presented in part at the 10th conference of the Norwegian Society for Epidemiology, Trondheim, Norway, November 2001.
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References |
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1. Evans A, Tolonen H, Hense HW, Ferrario M, Sans S, Kuulasmaa K. WHO MONICA Project. Trends in coronary risk factors in the WHO MONICA project. Int J Epidemiol 2001;(Suppl. 1), S35–40.
2. Arnett DK, McGovern PG, Jacobs DR Jr, Shahar E, Duval S, Blackburn H, Luepker RV. Fifteen-year trends in cardiovascular risk factors (1980–1982 through 1995–1997): the Minnesota Heart Survey. Am J Epidemiol 2002; 156:929–35.
3. Lahti-Koski M, Pietinen P, Mannisto S, Vartiainen E. Trends in waist-to-hip ratio and its determinants in adults in Finland from 1987 to 1997. Am J Clin Nutr 2000; 72:1436–44.
4. Nissinen A, Kastarinen M, Tuomilehto J. Community control of hypertension-experiences from Finland. J Hum Hypertens 2004; 18:553–6.[CrossRef][Web of Science][Medline]
5. Liu L, Choudhury SR, Okayama A, Hayakawa T, Kita Y, Ueshima H. Changes in body mass index and its relationships to other cardiovascular risk factors among Japanese population: results from the 1980 and 1990 national cardiovascular surveys in Japan. J Epidemiol 1999; 9:163–74.[Medline]
6. Tverdal A. Height, weight and body mass index of men and women aged 40–42 years. Tidsskr Nor L
geforen 1996; 116:2152–6.[Medline]
7. Midthjell K, Krüger O, Holmen J, Tverdal A, Claudi T, Bjorndal A, Magnus P. Rapid changes in the prevalence of obesity and known diabetes in an adult Norwegian population. The Nord-Trondelag Health surveys: 1984–1986 and 1995–1997. Diabetes Care 1999; 22:1813–20.
8. Stamler J. Epidemiologic findings on body mass and blood pressure in adults. Ann Epidemiol 1991; 1:347–62.[Medline]
9. Kenchaiah S, Evans JC, Levy D, Wilson PWF, Benjamin EJ, Larson MG, Kannel WB, Vasan RS. Obesity and the risk of heart failure. N Engl J Med 2002; 347:305–13.
10. Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation 1983; 67:968–77.
11. Rosengren A, Wedel H, Wilhelmsen L. Body weight and weight gain during adult life in men in relation to coronary heart disease and mortality. A prospective population study. Eur Heart J 1999; 20:269–77.
12. Kurth T, Gaziano JM, Berger K, Kase CS, Rexrode KM, Cook NR, Buring JE, Manson JE. Body Mass Index and the Risk of Stroke in Men. Arch Intern Med 2002; 162:2557–62.
13. Meyer HE, Søgaard AJ, Tverdal A, Selmer R. Body mass index and mortality: the influence of physical activity and smoking. Med Sci Sports Exerc 2002; 34:1065–70.
14. Diverse Populations Collaboration. Smoking, body weight, and CHD mortality in diverse populations. Prev Med 2004; 38:834–40.[CrossRef][Web of Science][Medline]
15. Fang J, Wylie-Rosett J, Cohen HW, Kaplan RC, Alderman MH. Exercise, body mass index, caloric intake, and cardiovascular mortality. Am J Prev Med 2003; 25:283–9.[CrossRef][Web of Science][Medline]
16. Engeland A, Bjorge T, Selmer RM, Tverdal A. Height and body mass index in relation to total mortality. Epidemiology 2003; 14:293–9.[CrossRef][Web of Science][Medline]
17. Kvaavik E, Tell GS, Klepp K-I. Predictors and tracking of body mass index from adolescence into adulthood: follow-up of 18 to 20 years in the Oslo Youth Study. Arch Pediatr Adolesc Med. 2003; 157:1212–18.
18. Wilsgaard T, Jacobsen BK, Schirmer H, Thune I, Lochen ML, Njolstad I, Arnesen E. Tracking of cardiovascular risk factors: the Tromso study, 1979–1995. Am J Epidemiol 2001; 154:418–26.
19. Lund Håheim L, Tonstad D, Hjermann I, Leren P, Holme I. Predictiveness of body mass index and other risk factors for fatal coronary heart disease: a 21-year prospective cohort study. Scand J Public Health 2006; in press. Preview at [http://www.journalsonline.tandf.co.uk/openurl.asp?genre=article&id=doi:10.1080/14034940510032293].
20. Leren P, Askevold EN, Foss OP, Frøili A, Grymyr D, Helgeland A, Hjermann I, Holme I, Lund-Larsen PG, Norum KR. The Oslo Study. Cardiovascular disease in middle-aged and young Oslo men. Acta Med Scand 1975; 588:Suppl., 1–38.
21. Søgaard AJ, Selmer R, Bjertness E, Thelle D. The Oslo Health study: The impact of self-selection in a large population-based study. Int J Equity Health 2004; 3:3.[CrossRef][Medline]
23. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, And Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA 2001; 285:2486–97.
24. Lyratzopoulos G, McElduff P, Heller RF, Hanily M, Lewis PS. Mid-term Body Mass Index increase among obese and non-obese individuals in middle life and deprivation status: A cohort study. BMC Public Health 2005; 5:32.[CrossRef][Medline]
25. Lund Håheim L, Holme I, Hjermann I, Leren P. The predictability of risk factors with respect to incidence and mortality of myocardial infarction and total mortality. A 12-year follow-up of the Oslo Study, Norway. J Int Med 1993; 234:17–24.[Web of Science][Medline]
26. Lund Håheim L, Holme I, Hjermann I, Leren P. Risk factors of stroke and mortality. A 12-year follow-up of the Oslo Study. Stroke 1993; 24:1484–9.
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