OBJECTIVES: Previous studies have suggested that abnormal levels of cortisol and testosterone might increase the risk of serious somatic diseases. To test this hypothesis, we conducted a 5-year follow-up study in middle-aged men. METHODS: A population-based cohort study conducted in 1995 amongst 141 Swedish men born in 1944, in whom a clinical examination supplemented by medical history aimed to disclose the presence of cardiovascular disease (CVD) (myocardial infarction, angina pectoris, stroke), type 2 diabetes and hypertension were performed at baseline and at follow-up in the year 2000. In addition, salivary cortisol levels were measured repeatedly over the day. Serum testosterone concentrations were also determined. Using the baseline data, an algorithm was constructed, which classified the secretion pattern of cortisol and testosterone from each individual as being normal or abnormal. RESULTS: By the end of follow-up, men with an abnormal hormone secretion pattern (n = 73) had elevated mean arterial pressure (P = 0.003), fasting insulin (P = 0.009) and insulin : glucose ratio (P = 0.005) compared with men with a normal secretion pattern (n = 68). Body mass index, waist circumference, and waist : hip ratio were significantly elevated in both groups. However, the 5-year incidence of CVD, type 2 diabetes, and hypertension were significantly higher (P
Diabetes prevalence is associated with low socioeconomic status (SES), but less is known about the relationship between SES and diabetes incidence.
Data from eight cycles of the National Population Health Survey (1994/1995 through 2008/2009) are used. A sample of 5,547 women and 6,786 men aged 18 or older who did not have diabetes in 1994/1995 was followed to determine if household income and educational attainment were associated with increased risk of diagnosis of or death from diabetes by 2008/2009. Three proportional hazards models were applied for income and for education--for men, for women and for both sexes combined. Independent variables were measured at baseline (1994/1995). Diabetes diagnosis was assessed by self-report of diagnosis by a health professional. Diabetes death was based on ICD-10 codes E10-E14.
Among people aged 18 or older in 1994/1995 who were free of diabetes, 7.2% of men and 6.3% of women had developed or died from the disease by 2008/2009. Lower-income women were more likely to develop type 2 diabetes than were those in high-income households. This association was attenuated, but not eliminated, by ethno-cultural background and obesity/overweight. Associations with lower educational attainment in unadjusted models were almost completely mediated by demographic and behavioural variables.
Social gradients in diabetes incidence cannot be explained entirely by demographic and behavioural variables.
Pregnant women commonly undergo screening for gestational diabetes mellitus (GDM) using a 50-g glucose challenge test (GCT), followed by a diagnostic oral glucose tolerance test (OGTT) in those women in whom the GCT is abnormal. Although it has long been recognized that GDM is associated with subsequent Type 2 diabetes, it has recently emerged that any degree of abnormal antepartum glucose homeostasis predicts an increased risk of postpartum glucose intolerance. Thus, in this context, we sought to determine whether women who have a pregnancy complicated by an abnormal GCT, but who do not have GDM, are at increased risk of subsequent diabetes, compared with their peers with an abnormal GCT.
A population-based, retrospective cohort study was conducted. Women referred for an antepartum OGTT indicative of an abnormal GCT (n = 15 381), but without GDM, were matched (for age, region, socioeconomic status, and year of delivery) with up to four other women without such referral (n = 61 237). The two cohorts were followed over a median 6.4 years for the development of diabetes.
The rate of incident diabetes was 5.04 cases per 1000 person-years in the cohort of women who underwent an antepartum OGTT, compared with 1.74 cases per 1000 person-years in women without an OGTT. The hazard ratio for subsequent diabetes in women with an antepartum OGTT was 2.56 (95% confidence interval 2.28, 2.87) (P
The aim of the study was to estimate the effect of the accumulation of major life events (MLE) in childhood and adulthood, in both the private and working domains, on risk of type 2 diabetes mellitus (T2DM). Furthermore, we aimed to test the possible interaction between childhood and adult MLE and to investigate modification of these associations by educational attainment.
The study was based on 4,761 participants from the Copenhagen City Heart Study free of diabetes at baseline and followed for 10 years. MLE were categorized as 0, 1, 2, 3 or more events. Multivariate logistic regression models adjusted for age, sex, education and family history of diabetes were used to estimate the association between MLE and T2DM.
In childhood, experiencing 3 or more MLE was associated with a 69% higher risk of developing T2DM (Odds Ratio (OR) 1.69; 95% Confidence Interval (CI) 1.60, 3.27). The accumulation of MLE in adult private (p-trend = 0.016) and work life (p-trend = 0.049) was associated with risk of T2DM in a dose response manner. There was no evidence that experiencing MLE in both childhood and adult life was more strongly associated with T2DM than experiencing events at only one time point. There was some evidence that being simultaneously exposed to childhood MLE and short education (OR 2.28; 95% C.I. 1.45, 3.59) and work MLE and short education (OR 2.86; 95% C.I. 1.62, 5.03) was associated with higher risk of T2DM, as the joint effects were greater than the sum of their individual effects.
Findings from this study suggest that the accumulation of MLE in childhood, private adult life and work life, respectively, are risk factors for developing T2DM.
Enlarged subcutaneous abdominal adipocytes have been shown to predict incidence of type 2 diabetes (T2D) in the Pima population of Arizona (USA). We investigated the role of subcutaneous abdominal adipocyte size (AAS), as well as femoral adipocyte size (FAS), as predictors of T2D in a population-based Swedish cohort. In 1974-1975, a sample of 1302 middle-aged women underwent a health examination, including anthropometry and evaluation of parental medical history. In addition, body composition (total body potassium and total body water), AAS and FAS (adipose tissue needle biopsy) were assessed in a subsample of 245 women. Incidence of T2D was followed until 2001, with 36 cases eligible for inclusion in this analysis. Women developing T2D had larger AAS at baseline vs. women remaining healthy (age/heredity-adjusted hazard ratio for increase of AAS by 1 sd [AAS-HR] 1.91; P
OBJECTIVE: The aim of this study was to investigate associations of adiponectin, leptin, C-reactive protein (CRP), interleukin (IL)-6, and serum amyloid A (SAA), individually or in combinations, with risk of incident type 2 diabetes in a Aboriginal Canadian [corrected] population. RESEARCH DESIGN AND METHODS: Of the 606 Sandy Lake Health and Diabetes Project cohort subjects who were free of diabetes at baseline, 540 (89.1%) participated in 10-year follow-up assessments. Concentrations of fasting adiponectin, leptin, CRP, IL-6, SAA, and covariates were measured at baseline. Fasting glucose and a 75-g oral glucose tolerance test were obtained at baseline and follow-up to determine incident type 2 diabetes, defined as clinically diagnosed type 2 diabetes or as fasting plasma glucose > or =7.0 mmol/l or 2-h postload plasma glucose > or =11.1 mmol/l at follow-up. RESULTS: Low adiponectin, high leptin, and low adiponectin-to-leptin ratio at baseline were associated with increased risk of incident type 2 diabetes after adjustment for age, sex, triglycerides, HDL cholesterol, hypertension, and impaired glucose tolerance (odds ratio 0.63 [95% CI 0.48-0.83], 1.50 [1.02-2.21], and 0.54 [0.37-0.77], respectively). When the models were additionally adjusted for waist circumference or BMI, however, only low adiponectin remained significantly associated with increased incident diabetes (0.68 [0.51-0.90]). Combinations of leptin, CRP, IL-6, and/or SAA with adiponectin, assessed using either the ratio or joint effects, did not improve diabetes prediction. CONCLUSIONS: Low baseline adiponectin is associated with increased risk of incident type 2 diabetes independent of leptin, CRP, IL-6, SAA, and metabolic syndrome variables including obesity.
Latent autoimmune diabetes (LADA) is a common form of diabetes, yet the risk factors are poorly characterised. The aim of this study was to investigate the influence of age, overweight and physical activity on the risk of LADA.
We analysed age, overweight and physical inactivity and the incidence of LADA in 38,800 men and women, observed between 1984 and 1986 and 1995 and 1997 as part of the Nord-Tr?ndelag Health Survey. We also compared such factors with incident cases of type 2 (n = 738) and 'classic' type 1 diabetes (n = 18). Patients classified as LADA (n = 81) had antibodies against GAD and were insulin independent at diagnosis.
The proportion of those who were older, overweight and inactive before diagnosis was almost identical in LADA and type 2 diabetes patients. BMI >or=30 kg/m(2) was strongly associated with LADA incidence (relative risk [RR] = 15.0, 95% CI 7.51-29.97). The association was similar for type 2 diabetes (RR = 15.37, 95% CI 12.07-19.57) but not for type 1 diabetes. Similarly, age (>or=60 years) was an important risk factor for LADA (RR = 5.62, 95% CI 2.36-13.4) as well as for type 2 diabetes (RR = 6.78, 95% CI 5.07-9.06) in contrast to type 1 diabetes. Physical inactivity was associated with an increased risk of both LADA and type 2 diabetes.
This study suggests that increased age, overweight and physical inactivity are as strong risk factors for LADA as for type 2 diabetes. These findings suggest a role for insulin resistance in the pathogenesis of LADA.
According to records kept by The Swedish Child Diabetes Register the incidence of childhood diabetes type I before 15 years of age has increased. The increase is most noticeable in children before the age of 5. The genetic basis of this disease is complex and the different risk genes have a low penetrance, thus indicating non-genetic factors to have a great impact. One risk factor for type I diabetes is rapid growth, measured either as weight or as height gain. As a high standard of living favours rapid growth in children this may contribute to the onset of the disease.