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Increase in prevalence of obesity and diabetes and decrease in plasma cholesterol in a central Australian Aboriginal community

Robyn McDermott, Kevin G Rowley, Amanda J Lee, Sabina Knight and Kerin O'Dea
Med J Aust 2000; 172 (10): 480-484.
Published online: 15 May 2000
Indigenous Health Research

Increase in prevalence of obesity and diabetes and decrease in plasma cholesterol in a central Australian Aboriginal community

Robyn McDermott, Kevin G Rowley, Amanda J Lee, Sabina Knight and Kerin O'Dea

MJA 2000; 172: 480-484

Abstract - Subject and Methods - Results - Discussion - Acknowledgements - References - Authors' details
- - More articles on Aboriginal health


Abstract Objective: To document change in prevalence of obesity, diabetes and other cardiovascular diease (CVD) risk factors, and trends in dietary macronutrient intake, over an eight-year period in a rural Aboriginal community in central Australia.
Design: Sequential cross-sectional community surveys in 1987, 1991 and 1995.
Subjects: All adults (15 years and over) in the community were invited to participate. In 1987, 1991 and 1995, 335 (87% of eligible adults), 331 (76%) and 304 (68%), respectively, were surveyed.
Main outcome measures: Body mass index and waist : hip ratio; blood glucose level and glucose tolerance; fasting total and high density lipoprotein (HDL) cholesterol and triglyceride levels; and apparent dietary intake (estimated by the store turnover method).
Intervention: A community-based nutrition awareness and healthy lifestyle program, 1988-1990.
Results: At the eight-year follow-up, the odds ratios (95% CIs) for CVD risk factors relative to baseline were obesity, 1.84 (1.28-2.66); diabetes, 1.83 (1.11-3.03); hypercholesterolaemia, 0.29 (0.20-0.42); and dyslipidaemia (high triglyceride plus low HDL cholesterol level), 4.54 (2.84-7.29). In younger women (15-24 years), there was a trebling in obesity prevalence and a four- to fivefold increase in diabetes prevalence. Store turnover data suggested a relative reduction in the consumption of refined carbohydrates and saturated fats.
Conclusion: Interventions targeting nutritional factors alone are unlikely to greatly alter trends towards increasing prevalences of obesity and diabetes. In communities where healthy food choices are limited, the role of regular physical activity in improving metabolic fitness may also need to be emphasised.


The high rates of obesity, diabetes and other cardiovascular disease (CVD) risk factors in Australian Aboriginal communities1-4 lead to high rates of diabetic complications and excess mortality in relatively young people.5-7 With often poor access to appropriate, good quality secondary prevention services,8,9 some communities have sought to emphasise primary prevention of diabetes in community-based health programs aimed at improving individual food choices and the quality of the food supply.10,11

In the community described here, a community-based nutrition awareness and healthy lifestyle program was commenced in 1988, after a 1987 survey showed high rates of obesity, diabetes and other CVD risk factors. The program continued for two years and culminated in a risk factor survey and store turnover study in 1991, followed by a series of family-based workshops to provide feedback on the results. A third survey was carried out in 1995.

We describe the trends in CVD risk factors (anthropometry, lipid levels, and glucose intolerance) and apparent dietary intake over this eight-year period.


Subjects and methods
Cross-sectional surveys were carried out in June 1987, May 1991 and April 1995 at a rural Aboriginal community. The surveys were approved by the Alice Springs Institutional Ethics Committee (which, in 1995, had an Aboriginal subcommittee), and by the Deakin University Ethics Committee, after consultation with the community council and health council. All adult members of the community (those 15 years and over) were invited to participate and volunteers gave written informed consent. Pregnant or non-Indigenous community members were excluded. Results were returned to individual participants and summary reports presented to the community council. The resident population at the time of each survey (excluding visitors from other communities) was determined by household census.

Blood tests: Twelve millilitres of blood was taken after an overnight fast and a second blood sample collected two hours after a 75 g glucose drink. Blood samples were kept cold until centrifugation and the plasma frozen immediately thereafter until analysis. Levels of glucose, total cholesterol, high density lipoprotein (HDL) cholesterol (after precipitation of other lipoproteins with 15% w/v PEG 6000) and triglycerides were measured by standard enzymatic techniques using commercial kits (Boehringer-Mannheim, Mannheim, Germany).

  • Glucose tolerance was classified according to WHO criteria.12

  • Hypercholesterolaemia was defined as a plasma cholesterol concentration ≥ 5.5 mmol/L; and

  • Dyslipidaemia was defined as the combination of a low HDL cholesterol level ( ≤ 0.9 mmol/L) plus hypertriglyceridaemia (a fasting plasma triglyceride level ≥ 2.0 mmol/L).

Anthropometry: Measurements were made by trained staff using standard techniques.13 Body weight was measured to 0.1 kg, with the subject in light clothing, using digital electronic scales; height was measured to 0.1 cm using a stadiometer; and waist and hip circumferences were measured to 0.1 cm.

  • Obesity was defined as a body mass index (BMI) > 30 kg/m2.

Smoking status: Current smoking status was ascertained in 1991 and 1995 using a yes/no questionnaire.

Dietary intake: Apparent dietary intake was measured using the store turnover method14 for the three months before each of the surveys. This method estimates general trends in food consumption, as the local store is the main source of food for the community. Expressing data as nutrient density (ie, as a proportion of total energy intake) avoids estimating per capita intake and gives a valid measure of dietary quality for the community.10,14

Intervention: A community-based nutrition awareness and healthy lifestyle program was conducted from 1988 to 1990. The program, which included a resident non-Aboriginal project officer and Aboriginal coworker, concentrated mainly on raising awareness of diabetes in the community, promoting healthy food-buying habits and improving the quality of food purchased by the community store. Some details of the intervention are given in Scrimgeour et al.15

Statistical analyses: Although some community members were screened on more than one occasion (Box 1), analyses were performed assuming purely cross-sectional data. Trends in continuous variables were tested by linear regression using SPSS.16 Separate analyses were performed for men and women. Regression models included year of survey, age group and an interaction term of year of survey with age group. Also included was a dummy variable indicating whether that individual was screened once only or on more than one occasion, the interaction terms of this dummy variable with year of survey and age group, and a three-way interaction term. The latter two variables were excluded from the final model if found to be non-significant.

For categorical data, trends in prevalence were tested by a χ2 test for linear association. Confidence intervals for prevalence data were calculated assuming a binomial distribution and adjusted using the finite sampling factor: (N-n)/(N-1), where N is the population size and n is the sample size. Mantel-Haenszel age-weighted odds ratios and exact 95% confidence intervals for risk factors were calculated using EpiInfo software.17 Sensitivity analyses were performed to test for selection bias in the 1991 and 1995 survey samples.


Results

Response rates
Survey participation rates were 87% of the adults normally resident and present at the time of the survey in 1987, 76% in 1991 and 68% in 1995 (Box 1). Participation rates by younger people were progressively lower with each survey.

 
Anthropometry There was no statistically significant change in mean BMI among men (Box 2A; the regression analysis had sufficient statistical power to detect a difference in BMI over time of 0.15 kg/m2). Although mean BMI rose in the two older age groups, this was because men returning for repeat screenings tended to have a higher mean BMI than those screened only once (P = 0.062). Similarly, there was no significant change in waist circumference or waist : hip ratio among men (Box 2). Among women, there was a significant increase in mean BMI, particularly in those aged 15-24 years (Box 2A). The increase in mean BMI (equivalent to about 10 kg in body weight) among women aged 15-24 years was accompanied by an increase in mean waist circumference, but no significant change in waist : hip ratio. Among women 35 years and older, mean BMI remained very high over the eight-year period.

For the community as a whole, the prevalence of obesity increased significantly over the survey period:

1987 -- 22.8% (95% CI, 22.2%-23.5%);

1991 -- 32.0% (95% CI, 30.6%-33.3%);

1995 -- 37.0% (95% CI, 35.1%-38.8%);

χ2 = 15.5, df = 1, P < 0.001.

There was a trebling in prevalence of obesity among women in the age group 15-24 years over the eight-year period (χ2 = 14.4, df = 1, P < 0.001), but no change among men of the same age group (χ2 = 0.2, df = 1, P = 0.636; Box 3). For the older age groups, there was already a high prevalence of obesity among women in 1987, which remained high (Box 3). The prevalence of obesity increased significantly among men aged 25-34 years during the follow-up period (χ2 = 5.2, df = 1, P = 0.022; Box 3). The increase among men aged 35 years and older was not statistically significant (χ2 = 2.0, df = 1, P = 0.155). The statistical power of analyses of prevalence changes in age and sex subgroups was somewhat low because of sparse data and, in some cases, low prevalence.

Glucose tolerance
For the community as a whole, there was a trend to an increasing prevalence of diabetes:

1987 -- 11.6% (95% CI, 11.1%-12.0%);

1991 -- 18.6% (95% CI, 17.4%-19.7%);

1995 -- 20.7% (95% CI, 17.7%-22.2%);

χ2= 9.9, df = 1, P = 0.002; with significant increases in prevalence among men aged 25-34 years (χ2 = 4.8, df = 1, P = 0.029) and women aged 35 years and older (χ2 = 3.9, df = 1, P = 0.048; Box 3).

However, the prevalence of impaired glucose tolerance (IGT) did not change significantly:

1987 -- 8.4% (95% CI, 8.0%-8.8%);

1991 -- 9.4% (95% CI, 8.6%-10.3%);

1995 -- 7.5% (95% CI, 5.6%-8.5%).

χ2= 0.13, df = 1, P = 0.721.

Plasma lipids
There was a highly significant decrease in mean levels of plasma cholesterol between 1987 and 1991 (Box 2B). This decrease occurred across all ages and in both sexes. This fall in total cholesterol level was partly due to decreases in HDL cholesterol levels, which also occurred in all age- and sex-specific categories, with the largest decrease among women aged 15-24 years (Box 2B). Conversely, among both men and women, there was an increase of similar magnitude in mean fasting plasma triglyceride level in all age groups (Box 2B). After excluding subjects with diabetes from the analysis, these trends to lower total and HDL cholesterol and higher triglyceride levels were still apparent (data not shown).

Changes in CVD risk factor profile
Box 4 shows the changing prevalence of cardiovascular risk factors as odds ratios compared with baseline. By 1995, community members were more likely to be obese, diabetic and dyslipidaemic (high plasma triglyceride and low plasma HDL cholesterol levels), whereas the risk of hypercholesterolaemia declined.

Apparent dietary macronutrient intake
Box 5 summarises changes in apparent community intake of sugar, total fat and saturated fat. As a proportion of total energy intake, there was a decline in total and saturated fat and sugar intake. Complex carbohydrate intake was 22%, 21% and 30% of total energy in 1987, 1991 and 1995, respectively. Store turnover data also suggested that, compared with 1987, there were decreases in the approximate per capita daily intake of sugar, fruit and vegetables and increases in flour and bread consumption (data not shown).

Representativeness of the survey samples
The sensitivity analyses performed assumed that the non-responders in 1991 and 1995 were all non-diabetic and non-obese. With this assumption, the linear trend to an increase in prevalence remained for obesity (χ2 = 5.0, df = 1, P = 0.025) but not for diabetes (χ2 = 1.0, df = 1, P = 0.320). A more realistic, but still conservative, assumption is that the non-responders in the 1991 and 1995 surveys had the same prevalence of obesity and diabetes as in the first survey sample. With this assumption, there were significant increases in estimated prevalences of obesity (23%, 30% and 32% in 1987, 1991 and 1995, respectively; χ2 = 9.4; df = 1; P = 0.002) and diabetes (12%, 17% and 18%; χ2 = 6.1; df = 1; P = 0.014).

Among men, regression analysis indicated that those who were screened on more than one occasion had a greater increase in waist : hip ratio with time (P = 0.014) and lower HDL cholesterol levels (P = 0.004) compared with men screened only once. Among women, those who were screened on more than one occasion had higher BMI (P = 0.020) compared with women screened only once. There were no other significant differences apparent between these groups, nor were there any other significant interactions with time. Furthermore, a comparison of baseline data for subjects screened in 1987 and again at either or both of the subsequent surveys with those who were not rescreened revealed no significant differences in mean age, BMI, cholesterol and triglyceride levels or glucose tolerance among either men or women. Together, these observations make it unlikely that the observed trends in obesity, diabetes and plasma lipids are artifacts due to sampling bias.


Discussion The community store intervention and education campaign in this central Australian Aboriginal community was associated with a decrease in apparent dietary intake of total and saturated fats and refined carbohydrates and a corresponding increase in complex carbohydrate intake. Associated with the change in dietary fat intake, there were reductions in plasma cholesterol levels in all age groups and both sexes. However, there were increases in the prevalence of obesity (60% increase) and diabetes (80% increase) over the survey period. While the study design does not allow us to ascribe cause-and-effect relationships between the intervention process and the trends in outcomes, the data imply that an attempt to modify diet alone is insufficient to reverse trends to increasing prevalence of obesity and diabetes.

Although the biochemical assays at baseline were performed on a different instrument to that used in the two follow-up surveys, the apparent changes in lipid profiles between the first and subsequent surveys are unlikely to be due to methodological differences as the same enzymatic methods were used for all three surveys and the kits purchased from the same source; quality control samples were routinely run and did not vary significantly over the study period; and the changes observed are entirely consistent with the changes in dietary fat intake.

Our results are similar to those reported after five years of a non-communicable disease intervention program in Mauritius:18 a major improvement in circulating cholesterol levels, but rapidly increasing prevalence of obesity and diabetes. The increase in prevalence of diabetes that we found approaches the highest recorded.19 The trebling in the prevalence of obesity among women aged 15-24 years was associated with a four- to fivefold increase in prevalence of diabetes. In contrast, there was no change in mean BMI for men in this age range. Thus, weight gain and onset of diabetes in women was apparently accelerated. Anecdotal evidence suggests this sex difference in secular trends in body weight may be due to high participation by young men in vigorous sporting activities such as football, whereas regular exercise by young women is limited in this community. Exercise has been shown to have protective effects against the incidence of diabetes,20 even independently of dietary change. Hence, community-directed interventions aimed at increasing physical activity may improve health outcomes.

The prevalence of diabetes in older age groups was extremely high in both men and women. Prior to 1991, diabetes was absent in men under 25 years and relatively uncommon among young women. By 1995, cases of type 2 diabetes were beginning to appear even at this young age. The decreasing age of onset of diabetes in this community has major public health implications with respect to diabetic complications, hyperglycaemia in pregnancy, and the subsequent intergenerational amplification of diabetes risk.21

We have previously reported that body fat distribution, as indicated by waist : hip ratio, among women in this community was unusual for an Aboriginal population, with the central deposition of body fat being less apparent than in other Aboriginal groups.2 Consistent with this, there were no major changes in mean waist : hip ratio for women in the subsequent surveys, even in the young women who had a large increase in waist circumference.

Despite these adverse trends in obesity and diabetes, the community has achieved significant improvements in dietary quality, as indicated by the changes in the food supply at the store, and in plasma cholesterol levels. However, a healthy diet consistent with National Health and Medical Research Council (NHMRC) guidelines22 has not been achieved. This problem goes beyond the realm of individual choice and reflects endemic poverty, high prices coupled with low incomes, often poor quality of fruit and vegetables in community stores, household economies which discourage the consumption of fresh foods, lack of domestic refrigeration, and unavailability of many nutritious foods.23 Reversal of obesity is difficult even in the absence of such major environmental and social barriers.24 Hence, early intervention to prevent or delay the onset of excessive weight gain is likely to be more effective in reducing diabetes and cardiovascular risk in such communities.25

In conclusion, our results suggest that a focus on nutrition and dietary habits alone may be insufficient to prevent excessive weight gain and diabetes among adults in Aboriginal communities. Further systematic studies of intervention processes, impacts and associated outcomes are required to address this issue.



Acknowledgements
This work was supported by grants from the NHMRC (No. 954605) and the Commonwealth Department of Health and Family Services. Special thanks to Fiona McLachlan, Sunil Piers, Nick Williams, Kathy Abbott and the health workers and nursing staff of Territory Health Services in Central Australia. We gratefully acknowledge the expert technical assistance of Connie Karschimkus and Olga Strommer and statistical advice of Elmer Villanueva.


References
  1. O'Dea K, Guest CS. Diabetes in Aborigines and other Australian populations. Aust J Public Health 1992; 16: 340-349.
  2. O'Dea K, Patel M, Kubisch R, et al. Obesity, diabetes and hyperlipidemia in a central Australian Aboriginal community with a long history of acculturation. Diabetes Care 1993; 16: 1004-1010.
  3. Gault A, O'Dea K, Rowley KG, et al. Abnormal glucose tolerance and other coronary heart disease risk factors in an isolated Aboriginal community in central Australia. Diabetes Care 1996; 19: 1269-1273.
  4. O'Dea K. Westernization and non-insulin-dependent diabetes in Australian Aborigines. Ethnicity Dis 1991; 1: 171-187.
  5. Phillips CB, Patel MS, Weeramanthri TS. High mortality from renal disease and infection in Aboriginal central Australians with diabetes. Aust J Public Health 1995; 19: 482-486.
  6. Veroni M, Gracey M, Rouse I. Patterns of mortality in Western Australian Aboriginals, 1983-1989. Int J Epidemiol 1994; 23: 73-81.
  7. Thomson NJ. Recent trends in Aboriginal mortality. Med J Aust 1991; 154: 235-239.
  8. Phillips CB, Patel MS, Carbaron Y. Utilisation of health services by Aboriginal Australians with diabetes. Diab Res Clin Practice 1993; 20: 231-239.
  9. Deeble J, Mathers C, Smith L, et al. Expenditure on health services for Aboriginal and Torres Strait Islander People. Canberra: Australian Institute of Health and Welfare, 1998. (Catalogue No. HWE 6.)
  10. Lee AJ, Bonson APV, Yarmirr D, et al. Sustainability of a successful health and nutrition program in a remote Aboriginal community. Med J Aust 1995; 162: 633-635.
  11. Spinks M, White G. Looma, Western Australia: Diabetes Program. In: Bear-Wingfield R, editor. Sharing good tucker stories. A guide for Aboriginal and Torres Strait Islander communities. Canberra: Commonwealth Department of Health and Family Services, 1996: 63-69.
  12. World Health Organization: Diabetes Mellitus: Report of a WHO Study Group. World Health Organ Tech Rep Ser 1985; No. 727.
  13. Callaway CW, Chumlea WC, Bouchard C, et al. Circumferences. In: Lohman TG, Roche AF, Masturell R, editors. Anthropometric standardisation reference manual. Champaign, Ill: Human Kinetics Books, 1988: 39-54.
  14. Lee AJ, O'Dea K, Mathews JD. Apparent dietary intake in remote Aboriginal communities. Aust J Public Health 1994; 18: 190-197.
  15. Scrimgeour D, Rowse T, Knight S. Food purchasing behaviour in an Aboriginal community. 2. Evaluation of an intervention aimed at children. Aust J Public Health 1994; 18: 67-70.
  16. SPSS [computer program], version 9.0. Chicago Ill: SPSS Inc, 1998.
  17. EpiInfo [computer program], version 6. Atlanta, Ga: Centers for Disease Control and Prevention, 1993.
  18. Dowse GK, Gareeboo H, Alberti KGMM, et al, for the Mauritius Non-communicable Disease Study Group. Changes in population cholesterol concentrations and other cardiovascular risk factor levels after five years of the non-communicable disease intervention programme in Mauritius. BMJ 1995; 311: 1255-1259.
  19. Dowse GK, Spark RA, Mavo B, et al. Extraordinary prevalence of non-insulin-dependent diabetes mellitus and bimodal plasma glucose distribution in the Wanigela people of Papua New Guinea. Med J Aust 1994; 16: 767-774.
  20. Pan X-R, Li G-W, Hu Y-H, et al. Effects of diet and exercise in preventing NIDDM in people with impaired glucose tolerance. The Da Qing IGT and diabetes study. Diabetes Care 1997; 20: 537-544.
  21. Pettit DJ, Nelson RG, Saad MF, et al. Diabetes and obesity in the offspring of Pima Indian women with diabetes during pregnancy. Diabetes Care 1993; 16: 310-314.
  22. National Health and Medical Research Council. Dietary guidelines for Australians. Canberra: NHMRC/AGPS, 1992.
  23. Leonard D, Beilin R, Moran M. Whichway kaikai blo umi? Food and nutrition in the Torres Strait. Aust J Public Health 1995; 19: 589-595.
  24. World Health Organization. Obesity: preventing and managing the global epidemic. Geneva: WHO, 1998: 107-158.
  25. Macaulay AC, Paradis G, Potvin L, et al. The Kahnawake Schools Diabetes Prevention Project: intervention, evaluation and baseline results of a diabetes primary prevention program with a native community in Canada. Prev Med 1997; 26: 779-790.

(Received 11 Oct 1999, accepted 20 Mar 2000)


Authors' details
Health Surveillance, Queensland Health, Tropical Public Health Unit, Cairns, QLD.
Robyn McDermott, MPH, FAFPHM, Director.

Monash University, Centre for Population Health and Nutrition, Monash Medical Centre, Melbourne, VIC.
Kevin G Rowley, BAppSci, PhD, Research Fellow; currently, Research Fellow, Department of Medicine, St Vincent's Hospital, Melbourne.
Kerin O'Dea, BSc, PhD, Head.

Menzies School of Health Research, Darwin, NT.
Amanda J Lee, GradDipDiet, PhD, Public Health Nutrition Consultant.

Territory Health Services, Alice Springs, NT.
Sabina Knight, RN, MTH, Staff Development Officer (Remote).

Reprints will not be available from the authors.
Correspondence: Dr K G Rowley, Department of Medicine, Clinical Sciences Building, St Vincent's Hospital, Fitzroy, VIC 3065.
rowleykATmail.medstv.unimelb.edu.au


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1: Age- and sex-specific response rates for the three cross-sectional surveys in a rural Aboriginal community
 Men

Women

 15-24 y25-34 y35 y +15-24 y25-34 y35 y +

1987
Population, N
Sample, n
Response rate
% Of sample rescreened
90
71
79%
56%
54
42
78%
41%
58
48
83%
58%
87
81
93%
69%
47
45
96%
49%
68
61
90%
56%
1991
Population, N
Sample, n
Response rate
% Of sample rescreened
87
51
59%
37%
61
35
57%
60%
63
54
86%
46%
95
72
76%
46%
57
50
88%
54%
72
69
96%
67%
1995
Population, N
Sample, n
Response rate
% Of sample rescreened
81
48
59%
40%
72
38
53%
61%
63
43
68%
74%
94
49
52%
33%
58
56
97%
73%
81
71
88%
62%
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2: Trends in anthropometric variables and plasma lipid levels, stratified by age and sex
 
 15-24 years25-34 years35 years and overP*P†

A: Anthropometric variables
Body mass index (BMI), kg/m2
Men
1987
1991
1995
24.5 (23.4-25.6)
24.1 (22.9-25.4)
24.8 (23.3-26.3)
26.3 (24.7-28.0)
27.0 (25.0-29.0)
28.7 (27.2-30.2)
26.0 (24.7-27.3)
27.8 (26.2-29.5)
28.2 (26.6-29.9)

 
 
0.514
 

 
 
0.992
 
Women
1987
1991
1995
24.5 (23.2-25.7)
24.6 (23.1-26.1)
29.1 (27.3-31.0)
27.8 (26.0-29.7)
28.8 (26.9-30.7)
29.7 (27.7-31.8)
30.2 (28.3-32.1)
31.8 (30.0-33.6)
30.4 (28.7-32.1)

 
 
<0.001
 

 
 
0.004
 
Waist circumference, cm
Men
1987
1991
1995
86.2 (83.0-89.4)
85.3 (82.0-88.7)
84.8 (81.2-88.4)
91.0 (87.3-94.6)
93.9 (89.4-98.4)
95.1 (91.1-99.2)
97.9 (93.4-102.5)
99.0 (95.2-102.8)
98.2 (93.1-103.3)

 
 
0.834
 

 
 
0.340
 
Women
1987
1991
1995
81.5 (78.7-84.4)
82.3 (79.3-85.4)
90.0 (86.7-93.4)
92.0 (87.8-96.2)
95.4 (90.5-100.2)
92.2 (88.2-96.3)
98.3 (94.1-102.4)
99.9 (96.3-103.5)
94.0 (90.9-97.2)

 
 
<0.001
 

 
 
<0.001
 
Waist:hip ratio
Men
1987
1991
1995
0.87 (0.85-0.88)
0.87 (0.86-0.89)
0.88 (0.87-0.90)
0.92 (0.90-0.94)
0.94 (0.92-0.96)
0.94 (0.93-0.96)
0.97 (0.96-0.98)
0.99 (0.97-1.01)
1.00 (0.98-1.02)

 
 
0.293
 

 
 
0.160
 
Women
1987
1991
1995
0.82 (0.80-0.83)
0.85 (0.82-0.87)
0.85 (0.83-0.88)
0.85 (0.83-0.87)
0.89 (0.85-0.92)
0.85 (0.84-0.87)
0.85 (0.84-0.87)
0.89 (0.87-0.91)
0.86 (0.84-0.88)

 
 
0.134
 

 
 
0.095
 

Data are means (95% confidence interval). *P-value for change over time. †P-value for interaction of change over time with age group.
Back to text
B: Plasma lipids
Total cholesterol, mmol/L
Men
1987
1991
1995
5.3 (5.0-5.6)
4.5 (4.3-4.8)
4.5 (4.3-4.8)
6.0 (5.7-6.3)
4.8 (4.6-5.1)
5.3 (5.0-5.6)
6.2 (5.7-6.6)
5.5 (5.1-5.9)
5.5 (5.2-5.8)

 
 
0.034
 

 
 
0.571
 
Women
1987
1991
1995
5.2 (4.9-5.4)
4.3 (4.1-4.5)
4.5 (4.3-4.8)
5.7 (5.3-6.1)
4.8 (4.5-5.0)
4.8 (4.5-5.1)
5.5 (5.3-5.8)
5.0 (4.7-5.3)
5.0 (4.8-5.3)

 
 
0.001
 

 
 
0.317
 
HDL cholesterol, mmol/L
Men
1987
1991
1995
1.17 (1.10-1.24)
0.88 (0.82-0.94)
0.83 (0.76-0.90)
1.23 (1.10-1.36)
0.84 (0.77-0.91)
0.79 (0.73-0.85)
1.05 (0.96-1.14)
0.78 (0.72-0.84)
0.76 (0.70-0.81)

 
 
<0.001
 

 
 
0.180
 
Women
1987
1991
1995
1.45 (1.33-1.57)
0.98 (0.91-1.05)
0.88 (0.81-0.95)
1.25 (1.12-1.38)
0.81 (0.75-0.87)
0.86 (0.81-0.92)
1.18 (1.10-1.27)
0.84 (0.79-0.89)
0.82 (0.78-0.86)

 
 
<0.001
 

 
 
0.011
 
Triglycerides, mmol/L
Men
1987
1991
1995
1.1 (1.0-1.3)
1.6 (1.4-1.9)
1.7 (1.5-1.9)
1.6 (1.3-2.0)
2.3 (1.9-2.7)
2.1 (1.8-2.5)
2.1 (1.8-2.5)
3.0 (2.5-3.6)
2.9 (2.4-3.6)

 
 
0.004
 

 
 
0.419
 
Women
1987
1991
1995
1.0 (0.9-1.1)
1.2 (1.1-1.4)
1.6 (1.4-1.8)
1.3 (1.2-1.6)
1.8 (1.6-2.1)
1.8 (1.5-2.0)
1.6 (1.4-1.8)
2.2 (2.0-2.5)
2.2 (2.0-2.4)

 
 
<0.001
 

 
 
0.248
 


Data are means (95% confidence interval), except triglycerides, which are geometric means (95% CI). *P-value for change over time. †P-value for interaction of change over time with age group.
Back to text
 
Box 3
Back to text

 
4: Risk ratios for cardiovascular risk factors in the follow-up surveys (1991 and 1995) compared with baseline (odds ratios and 95% CIs)*
 198719911995

Obesity
Impaired glucose tolerance (IGT)
Diabetes
Hypercholesterolaemia
Dyslipidaemia
Smoking
1.00
1.00
1.00
1.00
1.00
-
1.50 (1.03-2.17)
1.04 (0.58-1.87)
1.63 (0.98-2.69)
0.24 (0.17-0.35)
4.73 (3.06-7.61)
1.00
1.84 (1.28-2.66)
0.76 (0.41-1.41)
1.83 (1.11-3.03)
0.29 (0.20-0.42)
4.54 (2.84-7.29)
0.73 (0.52-1.03)

*Compared with 1987 (or 1991 for smoking), Mantel-Haenszel-weighted (for age) odds ratios and exact 95% confidence intervals.
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Box 5
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Received 24 September 2018, accepted 24 September 2018

  • Robyn McDermott
  • Kevin G Rowley
  • Amanda J Lee
  • Sabina Knight
  • Kerin O'Dea


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