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      Ethnic differences in prediabetes incidence among immigrants to Canada: a population-based cohort study

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          Abstract

          Background

          Prediabetes appears to be increasing worldwide. This study examined the incidence of prediabetes among immigrants to Canada of different ethnic origins and the age at which ethnic differences emerged.

          Methods

          We assembled a cohort of Ontario adults (≥ 20 years) with normoglycemia based on glucose testing performed between 2002 and 2011 through a single commercial laboratory database ( N = 1,772,180). Immigration data were used to assign ethnicity based on country of origin, mother tongue, and surname. Individuals were followed until December 2013 for the development of prediabetes, defined using either the World Health Organization/Diabetes Canada (WHO/DC) or American Diabetes Association (ADA) thresholds. Multivariate competing risk regression models were derived to examine the effect of ethnicity and immigration status on prediabetes incidence.

          Results

          After a median follow-up of 8.0 years, 337,608 individuals developed prediabetes. Using definitions based on WHO/DC, the adjusted cumulative incidence of prediabetes was 40% (HR 1.40, CI 1.38–1.41) higher for immigrants relative to long-term Canadian residents (21.2% vs 16.0%, p < 0.001) and nearly twofold higher among South Asian than Western European immigrants (23.6%; HR 1.95, CI1.87–2.03 vs 13.1%; referent). Cumulative incidence rates based on ADA thresholds were considerably higher (47.1% and 32.3% among South Asians and Western Europeans, respectively). Ethnic differences emerged at young ages. South Asians aged 20–34 years had a similar prediabetes incidence as Europeans who were 15 years older (35–49 years), regardless of which prediabetes definition was used (WHO/DC 14.4% vs 15.7%; ADA 38.0% vs 33.0%).

          Conclusion

          Prediabetes incidence was substantially higher among non-European immigrants to Canada, highlighting the need for early prevention strategies in these populations.

          Electronic supplementary material

          The online version of this article (10.1186/s12916-019-1337-2) contains supplementary material, which is available to authorized users.

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          Deriving Ethnic-Specific BMI Cutoff Points for Assessing Diabetes Risk

          Maria Chiu, Peter C Austin, Douglas G. Manuel … (2011)
          OBJECTIVE The definition of obesity (BMI ≥30 kg/m2), a key risk factor of diabetes, is widely used in white populations; however, its appropriateness in nonwhite populations has been questioned. We compared the incidence rates of diabetes across white, South Asian, Chinese, and black populations and identified equivalent ethnic-specific BMI cutoff values for assessing diabetes risk. RESEARCH DESIGN AND METHODS We conducted a multiethnic cohort study of 59,824 nondiabetic adults aged ≥30 years living in Ontario, Canada. Subjects were identified from Statistics Canada’s population health surveys and followed for up to 12.8 years for diabetes incidence using record linkages to multiple health administrative databases. RESULTS The median duration of follow-up was 6 years. After adjusting for age, sex, sociodemographic characteristics, and BMI, the risk of diabetes was significantly higher among South Asian (hazard ratio 3.40, P < 0.001), black (1.99, P < 0.001), and Chinese (1.87, P = 0.002) subjects than among white subjects. The median age at diagnosis was lowest among South Asian (aged 49 years) subjects, followed by Chinese (aged 55 years), black (aged 57 years), and white (aged 58 years) subjects. For the equivalent incidence rate of diabetes at a BMI of 30 kg/m2 in white subjects, the BMI cutoff value was 24 kg/m2 in South Asian, 25 kg/m2 in Chinese, and 26 kg/m2 in black subjects. CONCLUSIONS South Asian, Chinese, and black subjects developed diabetes at a higher rate, at an earlier age, and at lower ranges of BMI than their white counterparts. Our findings highlight the need for designing ethnically tailored prevention strategies and for lowering current targets for ideal body weight for nonwhite populations.
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            Lifetime risk of developing impaired glucose metabolism and eventual progression from prediabetes to type 2 diabetes: a prospective cohort study.

            Symen Ligthart, Thijs van Herpt, Maarten J. G. Leening … (2016)
            Data are scarce for the lifetime risk of developing impaired glucose metabolism, including prediabetes, as are data for the risk of eventual progression from prediabetes to diabetes and for initiation of insulin treatment in previously untreated patients with diabetes. We aimed to calculate the lifetime risk of the full range of glucose impairments, from normoglycaemia to prediabetes, type 2 diabetes, and eventual insulin use.
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              The natural history of progression from normal glucose tolerance to type 2 diabetes in the Baltimore Longitudinal Study of Aging.

              Kelly D Blake, , Frank-Michael Müller … (2003)
              The natural history of progression from normal glucose tolerance (NGT) to impaired fasting glucose (IFG), impaired glucose tolerance (IGT), and type 2 diabetes is not well defined. We studied this progression using biennial oral glucose tolerance tests performed in the Baltimore Longitudinal Study of Aging and survival analysis to assess progression from NGT to abnormal fasting plasma glucose (FPG; > or =6.1 mmol/l), abnormal 2-h plasma glucose (2hPG; > or =7.8 mmol/l), IFG (FPG 6.1-6.9 mmol/l, 2hPG or =7.0 mmol/l or 2hPG > or =11.1 mmol/l). At baseline, the 815 subjects had a mean age of 57 years, 35% were women, and 60% had NGT. Of the 488 subjects with NGT, over half were followed for at least 10 years. By 10 years, 14% had progressed to abnormal FPG and 48% to abnormal 2hPG. Of the 267 subjects who progressed to IFG-IGT, 216 had additional follow-up. By 10 years, 8% of these progressed to diabetes by FPG whereas 27% progressed by 2hPG. In subsidiary analyses, we defined "abnormal" FPG as > or =5.55 mmol/l and "diabetic" FPG as > or =6.1 mmol/l, making the baseline prevalence of IFG similar to that of IGT. By these criteria, 43% progressed to abnormal FPG and 43% to abnormal 2hPG by 10 years of follow-up; among subjects developing impaired FPG or 2hPG, 22% progressed to diabetes by FPG whereas 17% progressed by 2hPG at 10 years. Nonetheless, 42% of subjects developing abnormal FPG did not develop abnormal 2hPG, and vice versa. We conclude that, although phenotypic differences in rates of progression are partly a function of diagnostic thresholds, fasting and postchallenge hyperglycemia may represent phenotypes with distinct natural histories in the evolution of type 2 diabetes.
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                Author and article information

                Contributors
                Ghazal S. Fazli: ghazal.fazli@utoronto.ca
                Rahim Moineddin: rahim.moineddin@utoronto.ca
                Arlene S. Bierman: arlene.bierman@utoronto.ca
                Gillian L. Booth: boothg@smh.ca
                Journal
                Journal ID (nlm-ta): BMC Med
                Journal ID (iso-abbrev): BMC Med
                Title: BMC Medicine
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1741-7015
                Publication date (Electronic): 23 May 2019
                Publication date PMC-release: 23 May 2019
                Publication date Collection: 2019
                Volume: 17
                Electronic Location Identifier: 100
                Affiliations
                [1 ]GRID grid.415502.7, MAP Centre for Urban Health Solutions, , Li Ka Shing Knowledge Institute, St. Michael’s Hospital, ; 209 Victoria Street, Toronto, Ontario M5C 1N8 Canada
                [2 ]ISNI 0000 0000 8849 1617, GRID grid.418647.8, Institute for Clinical Evaluative Sciences, ; G1 06, 2075 Bayview Avenue, Toronto, Ontario M4N 3M5 Canada
                [3 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Department of Medicine, , University of Toronto, ; 1 Kings College Circle, Toronto, Ontario M5S 1A8 Canada
                [4 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Department of Family and Community Medicine, , University of Toronto, ; 263 McCaul Street, Toronto, Ontario M5T 1W7 Canada
                [5 ]ISNI 0000 0001 2157 2938, GRID grid.17063.33, Institute of Health Policy Management and Evaluation, , University of Toronto, ; 155 College Street Health Science Building, Toronto, Ontario M5T 3M7 Canada
                Article
                Publisher ID: 1337
                DOI: 10.1186/s12916-019-1337-2
                PMC ID: 6533737
                PubMed ID: 31122233
                SO-VID: e918898f-bfdb-4104-bbeb-5f822bd356b2
                Copyright © © The Author(s). 2019
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 27 December 2018
                Date accepted : 30 April 2019
                Funding
                Funded by: Canadian Institute for Health Research
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Medicine
                Keywords: prediabetes,ethnicity,epidemiology,population-based study,immigrant health
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: prediabetes, ethnicity, epidemiology, population-based study, immigrant health

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