Diabetes type II, other medical conditions and pancreatic cancer risk: a prospective study in The Netherlands.
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ABSTRACT:
SUBMITTER: Eijgenraam P
PROVIDER: S-EPMC3844907 | biostudies-other | 2013 Nov
REPOSITORIES: biostudies-other
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Project description:ObjectiveTo assess the contribution of modifiable risk factors to social inequalities in the incidence of type 2 diabetes when these factors are measured at study baseline or repeatedly over follow-up and when long term exposure is accounted for.DesignProspective cohort study with risk factors (health behaviours (smoking, alcohol consumption, diet, and physical activity), body mass index, and biological risk markers (systolic blood pressure, triglycerides and high density lipoprotein cholesterol)) measured four times and diabetes status assessed seven times between 1991-93 and 2007-09.SettingCivil service departments in London (Whitehall II study).Participants7237 adults without diabetes (mean age 49.4 years; 2196 women).Main outcome measuresIncidence of type 2 diabetes and contribution of risk factors to its association with socioeconomic status.ResultsOver a mean follow-up of 14.2 years, 818 incident cases of diabetes were identified. Participants in the lowest occupational category had a 1.86-fold (hazard ratio 1.86, 95% confidence interval 1.48 to 2.32) greater risk of developing diabetes relative to those in the highest occupational category. Health behaviours and body mass index explained 33% (-1% to 78%) of this socioeconomic differential when risk factors were assessed at study baseline (attenuation of hazard ratio from 1.86 to 1.51), 36% (22% to 66%) when they were assessed repeatedly over the follow-up (attenuated hazard ratio 1.48), and 45% (28% to 75%) when long term exposure over the follow-up was accounted for (attenuated hazard ratio 1.41). With additional adjustment for biological risk markers, a total of 53% (29% to 88%) of the socioeconomic differential was explained (attenuated hazard ratio 1.35, 1.05 to 1.72).ConclusionsModifiable risk factors such as health behaviours and obesity, when measured repeatedly over time, explain almost half of the social inequalities in incidence of type 2 diabetes. This is more than was seen in previous studies based on single measurement of risk factors.
| S-EPMC3424226 | biostudies-literature
Project description:BackgroundSocioeconomic adversity in early life has been hypothesized to "program" a vulnerable phenotype with exaggerated inflammatory responses, so increasing the risk of developing type 2 diabetes in adulthood. The aim of this study is to test this hypothesis by assessing the extent to which the association between lifecourse socioeconomic status and type 2 diabetes incidence is explained by chronic inflammation.Methods and findingsWe use data from the British Whitehall II study, a prospective occupational cohort of adults established in 1985. The inflammatory markers C-reactive protein and interleukin-6 were measured repeatedly and type 2 diabetes incidence (new cases) was monitored over an 18-year follow-up (from 1991-1993 until 2007-2009). Our analytical sample consisted of 6,387 non-diabetic participants (1,818 women), of whom 731 (207 women) developed type 2 diabetes over the follow-up. Cumulative exposure to low socioeconomic status from childhood to middle age was associated with an increased risk of developing type 2 diabetes in adulthood (hazard ratio [HR]?=?1.96, 95% confidence interval: 1.48-2.58 for low cumulative lifecourse socioeconomic score and HR?=?1.55, 95% confidence interval: 1.26-1.91 for low-low socioeconomic trajectory). 25% of the excess risk associated with cumulative socioeconomic adversity across the lifecourse and 32% of the excess risk associated with low-low socioeconomic trajectory was attributable to chronically elevated inflammation (95% confidence intervals 16%-58%).ConclusionsIn the present study, chronic inflammation explained a substantial part of the association between lifecourse socioeconomic disadvantage and type 2 diabetes. Further studies should be performed to confirm these findings in population-based samples, as the Whitehall II cohort is not representative of the general population, and to examine the extent to which social inequalities attributable to chronic inflammation are reversible.
| S-EPMC3699448 | biostudies-literature
Project description:ObjectivesTo assess the performance of a panel of common single nucleotide polymorphisms (genotypes) associated with type 2 diabetes in distinguishing incident cases of future type 2 diabetes (discrimination), and to examine the effect of adding genetic information to previously validated non-genetic (phenotype based) models developed to estimate the absolute risk of type 2 diabetes.DesignWorkplace based prospective cohort study with three 5 yearly medical screenings.Participants5535 initially healthy people (mean age 49 years; 33% women), of whom 302 developed new onset type 2 diabetes over 10 years.Outcome measuresNon-genetic variables included in two established risk models-the Cambridge type 2 diabetes risk score (age, sex, drug treatment, family history of type 2 diabetes, body mass index, smoking status) and the Framingham offspring study type 2 diabetes risk score (age, sex, parental history of type 2 diabetes, body mass index, high density lipoprotein cholesterol, triglycerides, fasting glucose)-and 20 single nucleotide polymorphisms associated with susceptibility to type 2 diabetes. Cases of incident type 2 diabetes were defined on the basis of a standard oral glucose tolerance test, self report of a doctor's diagnosis, or the use of anti-diabetic drugs.ResultsA genetic score based on the number of risk alleles carried (range 0-40; area under receiver operating characteristics curve 0.54, 95% confidence interval 0.50 to 0.58) and a genetic risk function in which carriage of risk alleles was weighted according to the summary odds ratios of their effect from meta-analyses of genetic studies (area under receiver operating characteristics curve 0.55, 0.51 to 0.59) did not effectively discriminate cases of diabetes. The Cambridge risk score (area under curve 0.72, 0.69 to 0.76) and the Framingham offspring risk score (area under curve 0.78, 0.75 to 0.82) led to better discrimination of cases than did genotype based tests. Adding genetic information to phenotype based risk models did not improve discrimination and provided only a small improvement in model calibration and a modest net reclassification improvement of about 5% when added to the Cambridge risk score but not when added to the Framingham offspring risk score.ConclusionThe phenotype based risk models provided greater discrimination for type 2 diabetes than did models based on 20 common independently inherited diabetes risk alleles. The addition of genotypes to phenotype based risk models produced only minimal improvement in accuracy of risk estimation assessed by recalibration and, at best, a minor net reclassification improvement. The major translational application of the currently known common, small effect genetic variants influencing susceptibility to type 2 diabetes is likely to come from the insight they provide on causes of disease and potential therapeutic targets.
| S-EPMC2806945 | biostudies-literature
Project description:ObjectiveTo examine whether established diabetes risk factors and diabetes risk algorithms are associated with future frailty.DesignProspective cohort study. Risk algorithms at baseline (1997-1999) were the Framingham Offspring, Cambridge, and Finnish diabetes risk scores.SettingCivil service departments in London, United Kingdom.ParticipantsThere were 2707 participants (72% men) aged 45 to 69 years at baseline assessment and free of diabetes.MeasurementsRisk factors (age, sex, family history of diabetes, body mass index, waist circumference, systolic and diastolic blood pressure, antihypertensive and corticosteroid treatments, history of high blood glucose, smoking status, physical activity, consumption of fruits and vegetables, fasting glucose, HDL-cholesterol, and triglycerides) were used to construct the risk algorithms. Frailty, assessed during a resurvey in 2007-2009, was denoted by the presence of 3 or more of the following indicators: self-reported exhaustion, low physical activity, slow walking speed, low grip strength, and weight loss; "prefrailty" was defined as having 2 or fewer of these indicators.ResultsAfter a mean follow-up of 10.5 years, 2.8% of the sample was classified as frail and 37.5% as prefrail. Increased age, being female, stopping smoking, low physical activity, and not having a daily consumption of fruits and vegetables were each associated with frailty or prefrailty. The Cambridge and Finnish diabetes risk scores were associated with frailty/prefrailty with odds ratios per 1 SD increase (disadvantage) in score of 1.18 (95% confidence interval: 1.09-1.27) and 1.27 (1.17-1.37), respectively.ConclusionSelected diabetes risk factors and risk scores are associated with subsequent frailty. Risk scores may have utility for frailty prediction in clinical practice.
| S-EPMC3820037 | biostudies-literature
Project description:BACKGROUND:Exposure to persistent organic pollutants (POPs) may predispose to the development of type 2 diabetes (T2D), but prospective human evidence is scarce. OBJECTIVES:We investigated the association between plasma-POP concentrations in the late 1990s and incident T2D over 11 years of follow-up in the Nurses' Health Study II. DISCUSSION:Three organochlorine pesticides and 20 polychlorinated biphenyls (PCBs) were measured in banked plasma from 793 case-control pairs of T2D. In a multiviarate-adjusted model, T2D ORs (95%CIs) comparing extreme POP tertiles (high vs. low) were 1.67 (1.24, 2.23; Ptrend < 0.001) for hexachlorobenzene (HCB), 3.62 (2.57, 5.11; Ptrend < 0.001) for β-hexachlorocyclohexane (β-HCH), 1.55 (1.13, 2.13; Ptrend = 0.05) for p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE), and 1.95 (1.42, 2.69; Ptrend < 0.001) for total dioxin-like PCBs (DL-PCBs) which included 5 mono-ortho congeners, PCB-105, 118, 156, 157, and 167. Adjustment for previous weight change and body mass index (BMI) at blood draw attenuated these associations, but that for DL-PCBs remained (OR[95% CI] = 1.78[1.14, 2.76]; Ptrend = 0.006). Age, breastfeeding history, previous weight change and BMI at blood draw were significant predictors of plasma POP concentrations. In addition, we found significant interactions of POPs and weight change before blood draw on T2D risk. ORs (95%CIs) of T2D comparing extreme (high vs. low) POP groups were 2.00 (1.02, 3.92; Ptrend = 0.01) for HCB, 2.69 (1.34, 5.40; Ptrend < 0.001) for β-HCH, and 2.41 (1.22, 4.77; Ptrend < 0.001) for DL-PCBs in the lowest weight gain group, whereas these values were 1.29 (0.73, 2.28; Ptrend = 0.46; Pinteraction = 0.04) for HCB, 1.41 (0.77, 2.60; Ptrend = 0.24; Pinteraction = 0.003) for β-HCH, and 0.90 (0.50, 1.63; Ptrend = 0.61; Pinteraction = 0.01) for DL-PCBs in the highest weight-gain group. CONCLUSIONS:Our findings suggest that elevated POP exposure may have diabetogenic potential. These data also highlight the impact of lifestyle factors, especially history of weight gain, on circulating POP concentrations and their associations with subsequent T2D risk.
| S-EPMC5899920 | biostudies-literature
Project description:ObjectiveTo evaluate the association between snoring frequency and type 2 diabetes mellitus (T2DM) according to age and gender in Chinese population.DesignA cohort study was performed in Suzhou site of the China Kadoorie Biobank. Residents who didn't suffer from T2DM at baseline survey (2004-2008) and in half a year after baseline were enrolled in this study and followed cause-specific morbidity until 31 December 2013. All participants were requested to complete a detailed questionnaire and undergo anthropometric measurements. Cox regression models were used to estimate HRs and 95% CIs for the snoring and T2DM association.SettingWuzhong district, Suzhou, China.ParticipantsA total of 49 453 participants (men: 41.8%; mean age: 51.14±10.28 years) were enrolled in this study.Outcome measuresT2DM cases were defined as International Classification of Diseases 10th Revision code of E11 and were identified through disease registries and health insurance databases.ResultsDuring a media of 7.18 years follow-up, 1120 T2DM cases were identified. Higher T2DM incidence was observed in participants with frequent and occasional snoring compared with those without (4.80 and 2.87 vs 2.39 per 1000 person-years). The multivariable-adjusted model found snoring was independently associated with T2DM (HR 1.28, 95% CI 1.20 to 1.38), both in men (HR 1.25, 95% CI 1.10 to 1.41) and women (HR 1.28, 95% CI 1.17 to 1.39). Moreover, a significant multiplicative interaction effect between snoring and age was detected on T2DM risk (p=0.015).ConclusionsSnoring was independently associated with an increased risk of T2DM in Chinese population, both in men and women. Meanwhile, there was an interaction effect between snoring and age on T2DM risk.
| S-EPMC8126309 | biostudies-literature
Project description:ObjectiveTo evaluate the association between type 2 diabetes and newly reported Parkinson's disease.Research design and methodsOur study included 21,841 participants in the Physicians' Health Study, a cohort of U.S. male physicians. Diabetes and Parkinson's disease were self-reported via questionnaire. We used time-varying Cox regression to calculate adjusted relative risk (RR) for Parkinson's disease.ResultsOver 23 years, 556 individuals with Parkinson's disease were identified. Subjects with diabetes had an increased Parkinson's disease risk (multivariable-adjusted RR 1.34 [95% CI 1.01-1.77]). The association remained significant after exclusion of those with known vascular disease. The diagnosis of diabetes was clustered around the diagnosis of Parkinson's disease and was more apparent among men with short diabetes duration and those without complications from diabetes.ConclusionsResults of this large prospective study in men do not suggest that diabetes is a preceding risk factor for Parkinson's disease. Whether the positive association may be explained by ascertainment bias or a common underlying biological mechanism remains to be established.
| S-EPMC2551644 | biostudies-literature
Project description:Aims/hypothesisTreatment guidelines recommend the UK Prospective Diabetes Study (UKPDS) risk engine for predicting cardiovascular risk in patients with type 2 diabetes, although validation studies showed moderate performance. The methods used in these validation studies were diverse, however, and sometimes insufficient. Hence, we assessed the discrimination and calibration of the UKPDS risk engine to predict 4, 5, 6 and 8 year cardiovascular risk in patients with type 2 diabetes.MethodsThe cohort included 1,622 patients with type 2 diabetes. During a mean follow-up of 8 years, patients were followed for incidence of CHD and cardiovascular disease (CVD). Discrimination and calibration were assessed for 4, 5, 6 and 8 year risk. Discrimination was examined using the c-statistic and calibration by visually inspecting calibration plots and calculating the Hosmer-Lemeshow ?(2) statistic.ResultsThe UKPDS risk engine showed moderate to poor discrimination for both CHD and CVD (c-statistic of 0.66 for both 5 year CHD and CVD risks), and an overestimation of the risk (224% and 112%). The calibration of the UKPDS risk engine was slightly better for patients with type 2 diabetes who had been diagnosed with diabetes more than 10 years ago compared with patients diagnosed more recently, particularly for 4 and 5 year predicted CVD and CHD risks. Discrimination for these periods was still moderate to poor.Conclusions/interpretationWe observed that the UKPDS risk engine overestimates CHD and CVD risk. The discriminative ability of this model is moderate, irrespective of various subgroup analyses. To enhance the prediction of CVD in patients with type 2 diabetes, this model should be updated.
| S-EPMC3017299 | biostudies-literature
Project description:Aims/hypothesisIn this study, we aimed to examine the association between age at natural menopause and risk of type 2 diabetes, and to assess whether this association is independent of potential mediators.MethodsWe included 3639 postmenopausal women from the prospective, population-based Rotterdam Study. Age at natural menopause was self-reported retrospectively and was treated as a continuous variable and in categories (premature, <40 years; early, 40-44 years; normal, 45-55 years; and late menopause, >55 years [reference]). Type 2 diabetes events were diagnosed on the basis of medical records and glucose measurements from Rotterdam Study visits. HRs and 95% CIs were calculated using Cox proportional hazards models, adjusted for confounding factors; in another model, they were additionally adjusted for potential mediators, including obesity, C-reactive protein, glucose and insulin, as well as for levels of total oestradiol and androgens.ResultsDuring a median follow-up of 9.2 years, we identified 348 individuals with incident type 2 diabetes. After adjustment for confounders, HRs for type 2 diabetes were 3.7 (95% CI 1.8, 7.5), 2.4 (95% CI 1.3, 4.3) and 1.60 (95% CI 1.0, 2.8) for women with premature, early and normal menopause, respectively, relative to those with late menopause (p trend <0.001). The HR for type 2 diabetes per 1 year older at menopause was 0.96 (95% CI 0.94, 0.98). Further adjustment for BMI, glycaemic traits, metabolic risk factors, C-reactive protein, endogenous sex hormone levels or shared genetic factors did not affect this association.Conclusions/interpretationEarly onset of natural menopause is an independent marker for type 2 diabetes in postmenopausal women.
| S-EPMC6448832 | biostudies-literature
Project description:BackgroundType 2 diabetes (T2D) has been associated with increased breast cancer risk, but commonly prescribed antidiabetic medications such as metformin may reduce risk. Few studies have investigated T2D and medications together in relation to breast cancer.Patients and methodsData came from 44 541 Sister Study participants aged 35 to 74 years at enrollment (2003-2009) who satisfied eligibility criteria, followed through 15 September 2017. Information on time-varying, self-reported, physician-diagnosed, prevalent and incident T2D, use of antidiabetic medications, and covariates was obtained from baseline and follow-up questionnaires. Incident breast cancers were confirmed with medical records. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated.ResultsDuring follow-up (median, 8.6 years), 2678 breast cancers were diagnosed at least 1 year after enrollment. There were 3227 women (7.2%) with prevalent and 2389 (5.3%) with incident T2D, among whom 61% (n = 3386) were ever treated with metformin. There was no overall association between T2D and breast cancer risk (HR 0.99; 95% CI, 0.87-1.13). However, T2D was associated with increased risk of triple-negative breast cancer (HR 1.40; 95% CI, 0.90-2.16). Compared with not having T2D, T2D with metformin use was not associated with overall breast cancer risk (HR 0.98; 95% CI, 0.83-1.15), but it was associated with decreased risk of estrogen receptor (ER)-positive breast cancer (HR 0.86; 95% CI 0.70-1.05) and increased risk of ER-negative (HR 1.25; 95% CI, 0.84-1.88) and triple-negative breast cancer (HR 1.74; 95% CI, 1.06-2.83). The inverse association with ER-positive cancer was stronger for longer duration (≥10 year) metformin use (HR 0.62; 95% CI, 0.38-1.01; P for trend = 0.09). Results were supported by sensitivity analyses.ConclusionOur findings suggest that associations between T2D and breast cancer may differ by hormone receptor status and that associations between T2D and ER-positive breast cancer may be reduced by long-term metformin use.
| S-EPMC7995619 | biostudies-literature