Volume 172 Issue 10

Indigenous Health Research Reducing premature death and renal failure in Australian Aboriginals A community-based cardiovascular and renal protective program Wendy E Hoy, Philip R Baker, Angela M Kelly and Zhiqiang Wang MJA 2000; 172: 473-478 Abstract - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objective: To describe results of a systematic treatment program to modify renal and cardiovascular disease in an Aboriginal community whose rates of renal failure and cardiovascular deaths are among the highest in Australia. Design: Longitudinal survey of people during treatment, and comparison of rates of natural death and renal failure with those in a historical control group. Setting: Tiwi Islands (population, about 1800), November 1995 to December 1998. Participants: All adults with blood pressure ≥ 140/90, with diabetes and urinary albumin/creatinine ratio (ACR) ≥ 3.4 g/mol (microalbuminuria threshold), or with progressive overt albuminuria (ACR ≥ 34 g/mol) were eligible for treatment. The historical control group comprised 229 people who satisfied these criteria in the pretreatment period 1992-1995. Interventions: Perindopril, combined with calcium-channel blockers and diuretics if needed to achieve blood pressure goals; attempts to improve control of blood glucose and lipid levels; health education. Main outcome measures: Blood pressure, ACR, serum creatinine level and glomerular filtration rate (GFR) over two years of treatment; rates of renal failure and natural death compared with control group (analysed on intention-to-treat basis). Results: 258 people enrolled in the program, and 118 had complete data for two years of treatment. In these 118, blood pressures fell significantly, while ACR and GFR stabilised. Rates of the combined endpoints of renal failure and natural death per 100 person-years were 2.9 for the treatment group (95% CI, 1.7-4.6) and 4.8 for the control group (95% CI, 3.3-7.0). After adjustment for baseline ACR category, the relative risk of the treatment group versus the control group for these combined endpoints was 0.47 (95% CI, 0.25-0.86; P = 0.013). Treatment benefit was especially marked in people with overt albuminuria or hypertension and in non-diabetic people. The estimates of benefit were supported by a fall in community rates of death and renal failure. Conclusions: Aboriginal people can participate enthusiastically in chronic disease management, with rapid, dramatic improvement in clinical profiles and mortality. Similar programs should be introduced urgently into other Aboriginal communities nationwide. Aboriginal people in the Northern Territory are experiencing an epidemic of cardiovascular disease (CVD) and end-stage renal disease (ESRD). Age-standardised CVD death rates are three times those of non-Aboriginal people,1 while the incidence of treated ESRD in Aboriginal people is approaching 1000 per million, and doubling every four years.2 ESRD treatment costs, at $100 000 per person annually, are becoming a huge burden,3 but premature death is the greater human catastrophe. These problems are especially serious in the communities of the Tiwi Islands, north of Darwin (population, about 1800) (Box 1). The incidence of ESRD among Tiwi people recently reached 2700 per million, and they have one of the highest CVD mortality rates in Australia.2,4In a community-wide screening program starting in the early 1990s, we found a high prevalence of cardiovascular risk factors, including type 2 diabetes and hypertension, and albuminuria (measured by the albumin/creatinine ratio (ACR) of a random urine specimen).5 Albuminuria correlated inversely with glomerular filtration rate (GFR), and its intensity predicted not only renal failure, but also cardiovascular deaths and all-cause natural deaths.6-9 In the early 1990s, use of antihypertensive drugs was increasing gradually in the Tiwi communities, but systematic management of the huge burden of morbidity identified by the screening program was beyond the capacity of the existing health services. In November 1995, we therefore introduced a systematic treatment program to reduce blood pressure and to modify the expression and progression of renal and cardiovascular disease. We describe the results of this program to the end of 1998. Methods The study was a longitudinal survey of people in the Tiwi Islands communities during treatment, and comparison of endpoints with a historical control group. Treatment was offered to eligible people as part of improved standard care. All participants gave informed consent to have their course followed up for the projects The epidemiology and prevention of Aboriginal renal disease, Parts 1 and 2. These projects were approved by the Joint Institutional Ethics Committee of the Menzies School of Health Research and Territory Health Services, Darwin, and its Aboriginal subcommittee, and by the Tiwi Land Council (Part 1) and the Tiwi Health Board (Part 2). Treatment program The program relied considerably on screening and treatment algorithms. Interventions included education about diet, exercise, health behaviours and medical treatment. Medical treatment centred around use of a long-acting angiotensin-converting enzyme inhibitor (ACEi) (perindopril; Coversyl [Servier]), aggressive blood pressure control,10,11 and, where appropriate, oral hypoglycaemic and lipid-lowering drugs. The choice of an ACEi was based on the well recognised antihypertensive and cardiovascular-protective effects of this class of drug12 and several reports, subsequently substantiated, of an additional renal protective effect.13-23 If antihypertensive drugs had been prescribed before entry into the study, they were discontinued or tapered when perindopril was started. Objectives were to achieve a minimum daily dose of 4 mg perindopril and to lower blood pressure, initially to < 130/85, but more recently to < 120/75.10 A stepped approach to achieve these blood pressures included increasing perindopril to 8 mg, with addition of long-acting calcium-channel blockers and/or diuretics if needed. Participants were seen at least monthly while medications were introduced or changed, then at least every three months for the first year, and at least every six months thereafter. Each examination included a minimum of a brief history, medication review, and measurement of weight, blood pressure, urinary ACR and serum creatinine level and, in diabetics, evaluation of blood glucose control. After a start-up period, the day-to-day program was largely conducted by local health workers and community project officers, who were supported by telephone contacts and regular visits by nurse coordinators from Darwin. Doctors, who reviewed eligibility assessments, supported or made treatment decisions and modified the protocols, were less intensively involved. The program has run in parallel with other clinic activities in Nguiu, Bathurst Island, but has been integrated into regular clinic activities at the Melville Island communities of Milikapiti and Pirlangimpi. Participants Treatment group: People eligible for ACEi therapy were those with: hypertension (blood pressure ≥ 140/90 mmHg); diabetes and ACR ≥ 3.4 g/mol (microalbuminuria threshold), regardless of blood pressure; or progressive overt albuminuria (ACR ≥ 34 g/mol on first testing and increasing over time), regardless of blood pressure or diabetes status. All qualifying features needed to be confirmed on at least two occasions. People with past adverse reactions and breastfeeding women were ineligible for ACEi therapy. Fertile women were advised about teratogenic risks and the options of contraception or discontinuation of ACEi medication early in unplanned pregnancy. People with serum creatinine levels over 250 µmol/L were considered ineligible for long-acting ACEi therapy in the first six months of the program, but were later enrolled when treatment proved safe and effective in people with mild and moderate renal insufficiency. To some extent, enrolment was prioritised by disease severity. Thus, most people with overt albuminuria, uncontrolled blood pressure and renal insufficiency were enrolled in the first year of the program. Control group: In the absence of a parallel control group, rates of renal failure and natural death in participants were compared with those of a historical control group from the pre-program period. This control group comprised adults whose results on a single screening examination between July 1992 and September 1995 met the eligibility criteria later used for the treatment program. Selection was blinded to their future course, which was followed to 30 October 1995. Data analyses Analyses were performed using STATA statistical software.24 Clinical profiles in the treatment group were described at baseline, six, 12, and 24 months of treatment, regardless of compliance, and were compared by analysis of variance, using geometric means for ACR and serum creatinine level to normalise their distribution. All endpoint data in the treatment group were analysed on an intention-to-treat basis. Rates of natural death and renal failure were calculated by baseline ACR category for the intention-to-treat and control groups, and the risk ratios for the intention-to-treat group calculated in stratified analysis by ACR category by the Mantel-Haenszel method for cohort studies. Kaplan-Meier survival curves for both groups were derived, and survivals compared by the non-parametric Wilcoxon technique. Results Enrolment By 31 December 1998, 258 people had enrolled in the program (29% of all adults in the island communities) and 227 were still participating. Of these, 39 had completed over three years of treatment, 137 over two years, 168 over one year, and 192 over six months. Of 31 dropouts, nine had died, seven had begun dialysis (two of whom later died), seven had stopped taking the medication because of side effects (cough in four; angioedema, itching and dizziness in one each), four became normotensive without treatment, two chose to quit, one moved, and one entered palliative care with osteomyelitis of the skull. Characteristics of people who enrolled are shown in Box 2: 42% had diabetes, almost two-thirds had hypertension, with a quarter already prescribed enalapril, and almost two-thirds had overt albuminuria. Medications and participation Doses of perindopril prescribed for the 227 people participating at the end of 1998 were 2 mg (5 people; 2%), 4 mg (72; 32%), and 8 mg (150; 66%). Calcium-channel blockers were being taken by 37 people (16%), diuretics by 15 (7%), and both by 13 (6%). Participation was enthusiastic, and compliance increased over time; 65% were taking ≥ 70% of their prescribed dose (assessed by pill counts and interview), 27% were taking medicine occasionally, and 7% were taking little or no medication at the end of 1998. Two-year clinical profiles Of the 137 people who had been treated for at least two years, 118 had largely complete follow-up data and were included in the two-year profile. These 118 were well matched with participants not included in this profile for age, BMI, and blood pressure, but were more likely to have diabetes, overt albuminuria, and to have been taking prior ACEi therapy (Box 2). These differences reflected prioritisation of sicker people for early entry into the program. Two-year clinical profiles for the 118 people are shown in Box 3. Treatment was associated with a swift and sustained fall in blood pressure, as well as stabilisation of ACR and GFR. Results are presented according to participants' clinical categories at baseline in Box 4. The fall in blood pressure was marked in people with hypertension at baseline and less marked but still apparent in those who had been normotensive, as well as in those previously prescribed an ACEi. Good blood pressure responses were seen in people both with and without diabetes, those with micro- and overt albuminuria and those with "normal" and raised levels of serum creatinine. Stabilisation of ACR and GFR was seen in all clinical categories. Indeed, serum creatinine level tended to fall and GFR to rise in all categories. Baseline weight did not change (mean, 74 kg; SD, 16 kg), while mean serum potassium level rose non-significantly from 4.04 mmol/L (SD, 0.46 mmol/L) to 4.14 mmol/L (SD, 0.49 mmol/L). No one developed significant hyperkalaemia. There was no evidence that ACEi therapy accelerated progression to renal insufficiency. Comparisons with control group Two hundred and twenty-nine people qualified as controls from the pre-program period, comprising 123 people who subsequently went onto the treatment program and 106 people who did not. Reasons for not going onto the program included death, dialysis, failure to qualify on subsequent examinations, presence of exclusion criteria (eg, pregnancy, breastfeeding), declining treatment, or moving. Baseline characteristics of the control and intention-to-treat groups are compared in Box 2. The control group was younger at enrolment, had lower BMI, and included fewer people with diabetes or overt albuminuria. The control group was followed up for a total of 564 years (individual mean, 2.5 years; range, 1 month to 3.3 years) and the intention-to-treat group for 560 years (individual mean, 2.2 years; range, 2 weeks to 3.1 years). Endpoints of the two groups are compared in Box 5. The treatment group as a whole had lower rates of dialysis, natural death and the combined endpoint (dialysis or death) than the control group, although the differences were not significant. However, rates of endpoints were strongly correlated with baseline ACR category. Indeed, renal failure necessitating dialysis was confined to people with ACR ≥ 100 g/mol at baseline, and in these people the treatment group had an estimated 57% lower dialysis rate than the control group. In contrast, rates of natural death and of the combined endpoint were lower in the treatment group than in the control group for all categories of baseline overt albuminuria. After adjustment for ACR category, the treatment group had an estimated 45% lower rate of natural death and an estimated 53% lower rate of the combined endpoint. Box 6 shows estimates of the survival advantage in people with various baseline clinical profiles after adjustment for ACR category. Treatment benefit was strong in people with overt albuminuria, non-diabetic people and people with hypertension. It was less marked in diabetic or normotensive people. Survival estimates for people with overt albuminuria at baseline are shown in Box 7. Although the intention-to-treat group showed attrition during the first year (representing ESRD and deaths of seriously ill people prioritised for early entry), a survival advantage over the control group was clear by two years of the treatment program. Discussion This study found that the introduction of a systematic treatment program to the Tiwi Island communities was associated with marked improvements in blood pressure and stabilisation of renal function in people receiving treatment. These changes contrasted sharply with the increase in blood pressure and ACR and fall in GFR noted previously in people matched for ACR category in the pretreatment status quo.10 The treatment program was also associated with a swift and dramatic decrease in rates of renal failure and natural death in the treated group compared with a historical control group, suggesting that the program prevented or at least delayed these outcomes. Further evidence for the existence of this estimated survival benefit was the decrease in community-wide rates of ESRD and natural death -- previously increasing -- after introduction of the program (Box 8). In contrast, ESRD continued to increase among non-Tiwi Aboriginal people in the Top End (Box 9), arguing against a chance background effect. Preliminary estimates of cost effectiveness of the program, based solely on avoidance or delay of dialysis, are already startling.3,25 These results show that Aboriginal people are interested in health issues and receptive to health messages, and will take medications over the long term to protect against future health risk, with excellent response. They also show that a systematic approach, with testing and treatment algorithms and clear goals, is superior to the previous approach of gradually improving medical management. While we cannot apportion relative benefit to individual elements of the treatment program, the observed fall in blood pressures alone would be expected to markedly reduce cardiovascular deaths and progression of renal disease,10,11 compatible with the effects we found. Our intention-to-treat analyses probably underestimate the therapeutic efficacy of treatment, as a third of the intention-to-treat group took the prescribed medications only occasionally or not at all. Use of the historical control group was also a potential source of bias. On the one hand, it may have also led to underestimates of treatment benefit because of the group's potentially better survival prospects, based on its younger mean age, milder disease and the probable inclusion of people with borderline blood pressure or ACR readings, as eligibility for the group was not confirmed by a second examination. On the other hand, the 123 controls who subsequently entered the treatment program might have had superior survival characteristics to the controls who did not enter the program, potentially inflating the apparent benefit of the program. Another source of bias was the prioritisation of the sickest people for early enrolment in the treatment program, many of whom were failing previous management regimens. This predisposes to poor short term outcomes of the program and underestimates of its benefits. Analyses of program results at four and five years, when more people have passed through one to two years of treatment, will dilute the impact of these early events. Longer-term analyses will also be needed to evaluate any survival effect of treatment in people without overt albuminuria, and the extent to which treatment has delayed rather than prevented ESRD and death in people with overt albuminuria. The program could still be improved. Blood pressure control should be better; at two-year follow-up, 31% of people had blood pressures ≥ 140/90, and 50% had blood pressures ≥ 120/75.10 Hypertension, and therefore eligibility for treatment even in the absence of albuminuria, should probably be redefined as blood pressures ≥ 130/80 in this high-risk population.10 Control of blood glucose and lipid levels needs to improve. Finally, we might reassess the notions of the maximally renal-protective dose of ACEi and/or add other renal-protective drugs, such as angiotensin II receptor blocking agents,26,27 for poor responders. Much of the success of this particular program derives from a strong sense of community ownership and control, a non-judgemental, non-authoritarian style, and respect for competing personal and community perspectives and priorities. Individuals appreciate personalisation of their health goals, and many are slowly adopting lifestyle changes. This program is now being integrated into normal clinic activities at Nguiu. Its protocols have also been incorporated into standard care guidelines for Aboriginal adults in the Top End of the NT.28 Extension of its principles to other Aboriginal communities with high burdens of disease nationwide is a matter of urgency.29 Allocation of adequate resources is a challenge, but the clinical benefit and cost-effectiveness mandate the short- and intermediate-term investment. Acknowledgements This study was supported by Servier Australia, the Australian Kidney Foundation, Rio Tinto, the National Health and Medical Research Council, the Stanley Tipiloura Fund, and Territory Health Services. We gratefully acknowledge the support, enthusiasm and participation of the Tiwi community and the staff of the Tiwi Island clinics at Nguiu, Milikapiti and Pirlangimpi. We especially thank the Tiwi Health Board for review of this manuscript, and Treatment Program Coordinators Susan Jacups and Kiernan McKendry, Aboriginal Health Workers Jerome Kerinauia and Nellie Punguatji, and Community Project Officers Eric Tipiloura and Elizabeth Tipiloura for their dedicated work. Finally, we thank Resident Medical Officer, Dr Chris Harrison, for his support and participation. Dr Alan Cass updated the Top End ESRD rates. References Cunningham J, Condon J. Premature mortality in Aboriginal adults in the Northern Territory. Med J Aust 1996; 165: 309-312. Spencer JS, Silva D, Hoy WE. An epidemic of renal failure among Australian Aborigines. Med J Aust 1998; 168: 537-541. You J, Hoy W, Beaver C, Zhao Y. Costs of hemodialysis and hospitalisations for patients with end stage renal disease in the Top End of the Northern Territory. Presented at the 35th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology; 1999 Mar 3-5; Brisbane (Qld). Jain SK, editor. Trends in mortality by causes of death in Australia, the States and Territories during 1971-1992, and in statistical subdivisions during 1991-1992. Canberra: National Center for Epidemiology and Population Health and Australian Bureau of Statistics, 1994. (ABS catalogue no. 3313.0)Hoy WE, Pugsley DJ, Normal RJ, Hayhurst BG. A brief heath profile of adults in a Northern Territory Aboriginal community: with an emphasis on preventable morbidities. Aust N Z J Public Health 1997; 21: 121-126. Hoy WE, Mathews JD, Pugsley DJ, et al. The multidimensional nature of renal disease: rates and associations of albuminuria in a high risk Aboriginal community. Kidney Int 1998; 54: 1296-1304. Cockcroft D, Gault MK. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16: 31-41. Hoy WE, Wang Z, Baker P, et al. The natural history of renal disease in an Australian Aboriginal community. Presented at the 35th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology; 1999 Mar 3-5; Brisbane (Qld). McDonald S, Wang Z, Hoy WE. Physical and biochemical predictors of death in an Australian Aboriginal cohort. Clin Exp Pharmacol Physiol 1999; 26: 618-621. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC VI). Arch Intern Med 1997; 157: 2413-2446. Collins R, Peto R, MacMahon S. Blood pressure, stroke and coronary artery disease. Part 2. Short term reductions in blood pressure: overview of randomised drug trials in their epidemiological context. Lancet 1990; 335: 827-838. Lonn EM, Yusuf S, Jha P. Emerging role of angiotensin converting enzyme inhibitors in cardiac and vascular protection. Circulation 1994; 90: 2056-2068. Mogensen CE. Angiotensin converting enzyme inhibitors and diabetic nephropathy. BMJ 1992; 304: 327-328. Ravid M, Savin H, Lang R, et al. Proteinuria, renal impairment, metabolic control, and blood pressure in type 2 diabetes mellitus. A 14-year follow up report on 195 patients. Arch Intern Med 1992; 152: 1225-1229. Ravid M, Savin H, Jutrin I, et al. Long term stabilizing effect of angiotensin converting enzyme inhibition on plasma creatinine and on proteinuria in normotensive type 2 diabetic patients. Ann Intern Med 1993; 118: 577-581. Gansevoort RT, de Zeeuw D, de Jong PE. Long term benefits of the antiproteinuric effect of angiotensin converting enzyme inhibition in nondiabetic renal disease. Am J Kidney Dis 1993; 22: 202-206. Lewis EJ, Hunsicker LG, Bain RP, et al. The effect of angiotensin converting enzyme inhibition on diabetic nephropathy. N Engl J Med 1993; 329: 1456-1462. Bedogna V, Valvo E, Casagrande P, et al. Effect of ACE inhibition in normotensive patients with chronic glomerular disease and normal renal function. Kidney Int 1994; 38: 101-107. Cattran DC, Greenwood C, Ritchie S. Long term benefits of angiotensin converting enzyme inhibitor therapy in patients with severe immunoglobulin A nephopathy: a comparison to patients receiving treatment with other antihypertensive agents and patients receiving no therapy. Am J Kidney Dis 1994; 23: 247-254. Mogensen CE, Keane WF, Bennett PH, et al. Prevention of diabetic renal disease with special reference to microalbuminuria. Lancet 1995; 346: 1080-1084. Maschio G, Alberti D, Janin G, et al. Effect of angiotensin converting enzyme inhibitor benazapril on the progression of chronic renal insufficiency. N Engl J Med 1996; 334: 939-945. The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia). Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, nondiabetic nephropathy. Lancet 1997; 349: 1857-1863. Ruggenenti P, Perna A, Gheradi G, et al. Renoprotective properties of ACE inhibition in nondiabetic nonnephrotic proteinuria. Lancet 1999; 354: 359-364. Statcorp. Stata statistical software, release 6.0. College Station (TX): Stata Corporation, 1999. Baker P, Hoy WE, Wang Z, et al. Towards evaluation of the cost-effectiveness of a treatment program for renal disease in Australian Aborigines. Presented at the 35th Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology; 1999 Mar 3-5; Brisbane (Qld). Mackenzie HS, Ziai F, Omer SA, et al. Angiotensin receptor blockers in chronic renal disease: the promise of a bright future. J Amer Soc Nephrol 1999; 10 Suppl 12: S283-S286. Mimran A, Ribstein J. Angiotensin receptor blockers: pharmacology and clinical significance. J Amer Soc Nephrol 1999; 10 Suppl 12: S273-S277. Hoy WE. Screening and treatment for renal disease: the community model. Nephrology 1998; 4 Suppl iii-iv: S90-S95. Minutes of the Inaugural Meeting of the National Aboriginal and Torres Strait Islander Renal Disease Scientific Working Group and its Guidelines Subcommittee. Office of Aboriginal and Torres Strait Islander Health. 1999; Nov 16 Alice Springs (NT). (Received 14 Jul 1999, accepted 6 Apr 2000) Authors' details Menzies School of Health Research, Darwin, NT. Wendy E Hoy, FRACP, Senior Renal Consultant; Philip R Baker, BSc, NHMRC PhD Student, Menzies School of Health Research, and Department of Social and Preventive Medicine, University of Queensland, Brisbane, QLD; Angela M Kelly, RN, BAppSc, Senior Program Coordinator; Zhiqiang Wang, PhD, Epidemiologist and Statistician, and Senior Research Officer. Reprints will not be available from the authors. Correspondence: Dr W E Hoy, Menzies School of Health Research, PO Box 41096, Casuarina, NT, 0811. wendyATmenzies.su.edu.au Make a comment Back to text 2: Baseline characteristics of participants in the treatment program and the historical control group All participantsIncluded in 2-year profiles Historical control group (n=258)Yes (n=118)No* (n=140)(n=229)P?% Men43%47%40%51%0.13Mean age in years (SD)43.4 (11.1)43.5 (10.4)43.4 (11.7)40.8 (12.8)0.02Mean body mass index27.0 (5.7)27.1 (5.7)27.0 (5.8)25.2 (5.4)< 0.001(kg/m2) (SD) Blood pressure (mm Hg) Mean systolic (SD)135 (20)135 (20)135 (21)134 (20)0.58Mean diastolic (SD)82 (14)81 (13)82 (15)85 (15)0.01% With hypertension?65%66%63%65%0.91% With diabetes42%46%37%26%0.001% With ACR ≥34g/mol65%74%58%58%0.02% With raised serum creatinine level§12%13%11%12%0.62Previous ACEi25%33%16%NR ACR=urinary albumin/creatinine ratio. ACEi=angiotensin-converting enzyme inhibitor. NR=no result. *90 had been enrolled less than 2 years, 19 had been enrolled ≥ 2 years but did not have complete data for all visits, and 31 had dropped out. ?For test of significance of difference between all participants (intention-to-treat group) and control group. ?Blood pressure ≥140/90 or taking antihypertensive treatment. §Serum creatinine level > 106µmol/L (women), > 120µmol/L (men). Back to text 3: Clinical profiles over two years of treatment in 118 Tiwi people VariableBaseline6 months12 months24 monthsP*Blood pressure (mm Hg) Mean systolic (SD)135 (20)126 (21)124 (20)122 (22)< 0.001Mean diastolic (SD)81 (13)75 (14)77 (14)74 (14)< 0.001Mean? ACR (g/mol) (95% CI)55 (43-70)50 (39-64)53 (41-69)55 (43-69)0.36Mean? serum creatinine level (µmol/L) (95% CI)89 (85-93)88 (84-92)88 (84-92)84 (79-89)0.44Mean GFR (mL/min/1.73m2) (SD)89 (26)91 (28)89 (26)93 (29)0.54ACR=urinary albumin/creatinine ratio. GFR=glomerular filtration rate. *Test for significance of difference in values among the four intervals by analysis of variance. ?Geometric mean. Back to text 4: Clinical profiles over two years of treatment in 118 Tiwi people, by clinical category at baseline Blood pressure PreviousDiabetes < 140/90 (n=69)≥ 140/90 (n=49)ACEi (n=39)No (n=64)Yes (n=54)BP (mm Hg) Mean systolicBaseline123 (11)152 (17)136 (19)135 (21)136 (19)(SD)24 months117 (20)130 (22)128 (23)122 (15)122 (23)Mean diastolicBaseline75 (9)90 (12)83 (11)81 (15)81 (10)(SD)24 months72 (14)77 (13)78 (14)76 (15)72 (11)Mean ACRBaseline66 (50-87)43 (27-61)62 (40-97)48 (34-68)62 (45-91)(g/mol) (95% CI)24 months75 (57-98)35 (23-54)66 (45-98)50 (36-70)60 (41-87)Mean serumBaseline88 (82-94)90 (85-95)94 (85-103)90 (85-95)87 (81-93)creatinine level (µmol/L) (95% CI)24 months84 (77-92)84 (77-91)93 (82-105)83 (77-89)86 (78-94)Mean GFR (SD)Baseline91 (29)86 (21)91 (31)90 (26)88 (26)(mL/min/1.73m2)24 months95 (32)91 (25)92 (32)96 (28)90 (24) Albuminuria Serum creatinine level Micro-* (n=28)Overt? (n=86)Normal (n=98§)Raised? (n=15§)BP (mm Hg)Mean systolicBaseline 134 (24)135 (18)135 (20)139 (19)(SD)24 months 123 (23)120 (21)123 (22)118 (20)Mean diastolicBaseline 82 (15)81 (12)82 (13)78 (13)(SD)24 months 73 (15)74 (14)75 (14)71 (13)Mean ¶ ACRBaseline 16 (13-19)104 (90-121)49 (38-65)125 (83-187)(g/mol) (95% CI)24 months 19 (15-25)90 (72-112)50 (38-66)88 (45-174)Mean¶ serumBaseline 85 (79-92)90 (85-95)83 (82-88)137 (123-153)creatinine level (µmol/L) (95% CI)24 months 75 (70-81)88 (82-95)78 (75-81)119 (98-144)Mean GFR (SD)Baseline 88 (23)89 (28)95 (23)55 (18)(mL/min/1.73m2)24 months 102 (24)91 (28)99 (24)57 (30) ACEi=angiotensin-converting enzyme inhibitor. BP=blood pressure. ACR=urinary albumin/creatinine ratio. GFR=glomerular filtration rate. *ACR, 3.4-33g/mol. ?ACR >34g/mol. ?Serum creatinine level >106µmol/L (women), >120µmol/L (men). §Data not available for all participants. ¶Geometric mean. Back to text 5: Rates of endpoints in historical control and intention-to-treat groups Historical control group (n=229) BaselineEndpointACR (g/mol)CasesPerson-yearsRate per 100 person-years (95% CI)DialysisAll ≥ 1009 9564 1201.6 (0.8-3.1) 7.5 (3.9-14.4)Natural deathAll < 34 34-99 ≥ 10018 2 9 7555 226 205 1243.2 (1.0-5.1) 0.9 (0.2-3.5) 4.4 (2.2-8.4) 5.6 (2.7-11.2)Combined (dialysis or natural death)All < 34 34-99 100-199 ≥ 20026? 2 9 6 9543 227 205 74 374.8 (3.3-7.0) 0.9 (0.2-3.5) 4.4 (2.3-8.4) 8.1 (3.6-18.0) 24.2 (12.6-46.5) Intention-to-treat group (n=258) Endpoint CasesPerson-yearsRate per 100 person-years (95% CI)Dialysis 7 7548 1971.3 (0.6-2.6) 3.6 (1.7-7.0)Natural death 11 3 3 5560 178 194 1882.0 (1.1-3.4) 1.7 (0.5-5.2) 1.5 (0.4-4.8) 2.7 (1.1-6.4)Combined (dialysis or natural death) 16 3 3 3 7549 178 193 104 732.9 (1.7-4.6) 1.7 (0.5-5.2) 1.6 (0.5-4.8) 2.9 (0.9-8.9) 9.6 (4.6-20.2) Relative risk (RR) (95% CI) Endpoint Crude*Adjusted?P (for adjusted RR)Dialysis 0.77 (0.24-2.33)0.43 (0.17-1.12)0.08Natural death 0.59 (0.25-1.31)0.55 (0.26-1.16)0.11Combined (dialysis or natural death) 0.59 (0.30-1.14)0.47 (0.25-0.86)0.01 ACR=urinary albumin/creatinine ratio. *Overall estimate for treatment group versus control group. ?Relative risk adjusted for baseline ACRcategory. ?People who underwent dialysis and later died were counted only once for the combined endpoint. Back to text 6: Estimated survival advantage for intention-to-treat versus control group, adjusted for ACR category Clinical category at baselineRelative risk (95% CI)?PAll0.47 (0.25-0.86)0.01Overt albuminuria0.36 (0.18-0.72)0.004DiabetesNo0.28 (0.09-0.93)0.02Yes0.65 (0.28-1.51)0.31HypertensionNo0.59 (0.25-1.44)0.24Yes0.38 (0.15-0.98)0.04* ACR=urinary albumin/creatinine ratio. Categories: < 3.4 3.4-33, 34-99, 100-199, ≥ 200 g/mol. ? For combined endpoints of natural death and renal failure, intention-to-treat versus control group. Back to text Back to text Back to text Back to text

Wendy E Hoy · Philip R Baker · Angela M Kelly · Zhiqiang Wang

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.10,11In 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 O'Dea K, Guest CS. Diabetes in Aborigines and other Australian populations. Aust J Public Health 1992; 16: 340-349. 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. 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. O'Dea K. Westernization and non-insulin-dependent diabetes in Australian Aborigines. Ethnicity Dis 1991; 1: 171-187. 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. Veroni M, Gracey M, Rouse I. Patterns of mortality in Western Australian Aboriginals, 1983-1989. Int J Epidemiol 1994; 23: 73-81. Thomson NJ. Recent trends in Aboriginal mortality. Med J Aust 1991; 154: 235-239. Phillips CB, Patel MS, Carbaron Y. Utilisation of health services by Aboriginal Australians with diabetes. Diab Res Clin Practice 1993; 20: 231-239. 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.) 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. 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. World Health Organization: Diabetes Mellitus: Report of a WHO Study Group. World Health Organ Tech Rep Ser 1985; No. 727. 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. Lee AJ, O'Dea K, Mathews JD. Apparent dietary intake in remote Aboriginal communities. Aust J Public Health 1994; 18: 190-197. 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. SPSS [computer program], version 9.0. Chicago Ill: SPSS Inc, 1998. EpiInfo [computer program], version 6. Atlanta, Ga: Centers for Disease Control and Prevention, 1993. 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. 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. 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. 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. National Health and Medical Research Council. Dietary guidelines for Australians. Canberra: NHMRC/AGPS, 1992. 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. World Health Organization. Obesity: preventing and managing the global epidemic. Geneva: WHO, 1998: 107-158. 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 Make a comment 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 +1987Population, N Sample, n Response rate % Of sample rescreened90 71 79% 56% 54 42 78% 41%58 48 83% 58% 87 81 93% 69%47 45 96% 49% 68 61 90% 56%1991Population, 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%1995Population, N Sample, n Response rate % Of sample rescreened81 48 59% 40% 72 38 53% 61%63 43 68% 74% 94 49 52% 33%58 56 97% 73% 81 71 88% 62%Back to text 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/m2Men 1987 1991 199524.5 (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 199524.5 (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, cmMen 1987 1991 199586.2 (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 199581.5 (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 ratioMen 1987 1991 19950.87 (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 textB: Plasma lipids Total cholesterol, mmol/LMen 1987 1991 19955.3 (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 19955.2 (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/LMen 1987 1991 19951.17 (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 19951.45 (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/LMen 1987 1991 19951.1 (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 19951.0 (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 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)* 198719911995Obesity Impaired glucose tolerance (IGT) Diabetes Hypercholesterolaemia Dyslipidaemia Smoking1.00 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) 1.001.84 (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. Back to text Back to text

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