Burke, J. P.

OBJECTIVE—The aim of this study was to examine associations between diabetes and clinical markers of benign prostatic hyperplasia (BPH) in community-dwelling white and black men aged 40–79 years. RESEARCH DESIGN AND METHODS—Data from the Olmsted County Study of Urinary Symptoms and Health Status and the Flint Men's Health Study were combined for a total study sample of 2,484 men. Severity of lower urinary tract symptoms (LUTS), peak urinary flow rates, prostate volume, and serum prostate-specific antigen (PSA) levels were examined by self-reported physician-diagnosed diabetes. RESULTS—Overall, 170 men (6.8%) reported a history of diabetes. Increased irritative LUTS and specifically nocturia were positively associated with diabetes. These patterns were consistent across race and persisted after adjustment for age, BMI, and various indicators of socioeconomic status. Furthermore, the relationship between irritative LUTS and diabetes was greater in black men. No significant associations were observed between diabetes and prostate volume, PSA level, and peak urinary flow rate. CONCLUSIONS—Our multiethnic community-based study demonstrates positive associations between diabetes and irritative LUTS and nocturia. Moreover, the association between irritative LUTS and diabetes is increased in black men. There was no strong evidence for an association between diabetes and BPH across measures more specific to BPH (i.e., prostate volume, PSA, and peak urinary flow rate). Taken together, our findings suggest that the presence of diabetes may be less related to prostate growth and more related to the dynamic components of lower urinary tract function. Further evaluations of the association between diabetes and BPH and related racial variations are warranted.

Women with type 1 diabetes have a delayed menarche and a greater prevalence of menstrual disorders than women without diabetes. However, little is known about the menopause transition among type 1 diabetic women. The Familial Autoimmune and Diabetes (FAD) Study recruited both adult individuals who were identified from the Children’s Hospital of Pittsburgh Type 1 Diabetes Registry for the years 1950–1964 and their family members. Unrelated nondiabetic control probands and their relatives were also evaluated. Women with type 1 diabetes (n = 143) compared with nondiabetic sisters (n = 186) or unrelated control subjects (n = 160) were more likely to have an older age at menarche (13.5, 12.5, and 12.6 years, respectively, P < 0.001), more menstrual irregularities before 30 years of age (45.7, 33.3, and 33.1%, respectively, P = 0.04), and a younger age at menopause (41.6, 49.9, and 48.0 years, respectively, P = 0.05). This resulted in a 6-year reduction in the number of reproductive years (30.0, 37.0, and 35.2 years, respectively, P = 0.05) for women with type 1 diabetes. Risk factors univariately associated with earlier menopause included type 1 diabetes (hazard ratio [HR] 1.99, P = 0.04), menstrual irregularities before 30 years of age (HR 1.87, P = 0.04), nulliparity (HR 2.14, P = 0.01), and unilateral oophorectomy (HR 6.51, P < 0.0001). Multivariate analysis confirmed that type 1 diabetes (HR 1.98, P = 0.056), menstrual irregularities by 30 years of age (HR 2.36, P = 0.01), and unilateral oophorectomy (HR 9.76, P < 0.0001) were independent determinants of earlier menopause in our cohort. We hypothesize that an earlier menopause, which resulted in a 17% decrease in reproductive years, is a major unstudied complication of type 1 diabetes.

OBJECTIVE—Birth weight is a risk factor for both diabetes and mortality. Diabetes is a risk factor for mortality. Whether the excess mortality observed for diabetes varies with birth weight is unclear. RESEARCH DESIGN AND METHODS—Among all 2,508 Rochester, Minnesota, residents who first met research criteria for adult-onset diabetes in 1960–1995, 171 were born locally in-hospital after 1922 (i.e., birth weights available) as singleton, term infants. Each case subject and two age- and sex-matched nondiabetic control subjects (born locally, residing locally when the case subject met the criteria for diabetes) were followed through 31 December 2000 for vital status. RESULTS—Of the diabetic case subjects, 16% (27 of 171) died vs. 7% (25 of 342) of control subjects (P = 0.004). The difference was less for normal-birth-weight (NBW) (2,948–<3,856 g) individuals (12% [12 of 102] vs. 8% [20 of 246], P = 0.31) than for abnormal-birth-weight individuals (low birth weight [LBW] 20% [8 of 39] vs. 2% [1 of 46], P = 0.01; high birth weight [HBW] 23% [7 of 30] vs. 8% [4 of 50], P = 0.16), as confirmed with age- and sex-adjusted Cox proportional hazards (diabetes-associated hazard ratio 1.4 [95% CI 0.69–2.90] for NBW vs. 4.8 [1.7–13.3] for abnormal birth weight, test for interaction P = 0.056). The observed diabetes deaths were greater than expected, based on mortality for the general population (27 vs. 13.3, P < 0.001), with 70% of excess deaths occurring among LBW (8 vs. 2.2, P < 0.001) and HBW (7 vs. 3.1, P = 0.03) individuals. CONCLUSIONS—The excess mortality observed for diabetes appears disproportionately concentrated among abnormal-birth-weight individuals, thus identifying a subset of at-risk diabetic individuals and reinforcing the importance of NBW deliveries.

OBJECTIVE—To examine the influence of obesity and prevention of weight gain on the incidence of type 2 diabetes. RESEARCH DESIGN AND METHODS—We examined participants in the San Antonio Heart Study, a prospective population-based study of Mexican Americans and non-Hispanic whites residing in San Antonio, Texas. BMI was stratified into four categories: normal (<25 kg/m2), overweight (≥25 kg/m2 and <30 kg/m2), obese (≥30 kg/m2 and <35 kg/m2), and very obese (≥35 kg/m2). The number and proportion of incident cases prevented by targeting each BMI category were estimated. In addition, we calculated the decrease in risk of developing type 2 diabetes associated with weight gain prevention across both the BMI and age spectra. RESULTS—Preventing normal individuals from becoming overweight would result in the greatest reduction in incidence of type 2 diabetes. This would result in a 62 and 74% reduction in the incidence of type 2 diabetes in Mexican Americans and non-Hispanic whites, respectively. Preventing the entire population from gaining, on average, 1 BMI unit would result in a reduction in incidence of type 2 diabetes of 12.4 and 13.0% in Mexican Americans and non-Hispanic whites, respectively. CONCLUSIONS—The majority of cases of type 2 diabetes were in individuals who were overweight or mildly obese with a family history of type 2 diabetes. Public health resources should be directed toward the prevention of weight gain among normal and overweight individuals in order to prevent the maximum number of cases of type 2 diabetes.

OBJECTIVE—To compare the incidence of type 2 diabetes between low-income Mexican-Americans residing in San Antonio, Texas, and low-income residents in Mexico City, Mexico. RESEARCH DESIGN AND METHODS—Using data from the San Antonio Heart Study and the Mexico City Diabetes Study, we compared the incidence of type 2 diabetes in 35- to 64-year-old low-income Mexican-American residents of San Antonio with similarly aged low-income residents of Mexico City. Because of the different follow-up times in the two studies, Poisson regression was used to compare the rates of diabetes. Potential risk factors for diabetes were also analyzed to determine whether they explained or contributed to a difference in incidence. RESULTS—The age- and sex-adjusted incidence of type 2 diabetes was significantly higher in San Antonio (RR 2.01) compared with Mexico City. This difference was seen primarily in the oldest age group (55–64 years of age) and remained statistically significant after adjusting for a number of diabetes risk factors, including demographic, anthropometric, and metabolic variables. Follow-up rates were similar in both cities. CONCLUSIONS—We conclude that there was a higher incidence of type 2 diabetes in San Antonio than in Mexico City, and that difference occurred primarily in individuals in the oldest age group. The potential mediating factors we examined did not account for this difference. Other factors, such as exercise and diet, which were not available for analysis in this study, in addition to a cohort effect, may have contributed to the difference in incidence of type 2 diabetes in the two cities. In addition, there was no evidence of a higher case fatality among diabetic individuals from Mexico City compared with San Antonio.