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Objective: To determine the prevalence of diabetic retinopathy among adults 40 years and older in the United States., Methods: Pooled analysis of data from 8 population-based eye surveys was used to estimate the prevalence, among persons with diabetes mellitus (DM), of retinopathy and of vision-threatening retinopathy-defined as proliferative or severe nonproliferative retinopathy and/or macular edema. Within strata of age, race/ethnicity, and gender, US prevalence rates were estimated by multiplying these values by the prevalence of DM reported in the 1999 National Health Interview Survey and the 2000 US Census population., Results: Among an estimated 10.2 million US adults 40 years and older known to have DM, the estimated crude prevalence rates for retinopathy and vision-threatening retinopathy were 40.3% and 8.2%, respectively. The estimated US general population prevalence rates for retinopathy and vision-threatening retinopathy were 3.4% (4.1 million persons) and 0.75% (899 000 persons). Future projections suggest that diabetic retinopathy will increase as a public health problem, both with aging of the US population and increasing age-specific prevalence of DM over time., Conclusion: Approximately 4.1 million US adults 40 years and older have diabetic retinopathy; 1 of every 12 persons with DM in this age group has advanced, vision-threatening retinopathy.

The uncoupling proteins (UCPs) are a family of mitochondrial transport proteins that promote proton leakage across the inner mitochondrial membrane, uncoupling oxidative phosphorylation from adenosine triphosphate (ATP) production and releasing energy as heat. Variation in these genes may disrupt biochemical pathways influencing thermogenesis, energy metabolism, and fuel substrate partitioning and oxidation, which may in turn predispose to obesity. We genotyped polymorphisms in UCP2 and UCP3 in a sample of nondiabetic participants (n = 722) of the San Luis Valley Diabetes Study (SLVDS) and found female-specific associations between UCP3 polymorphisms and measures of dietary intake and body composition. The UCP3-5 variant was statistically significantly associated with total caloric intake (P =.012), fat intake (P =.011), fat mass (P =.004), and lean mass (P =.013), with the C allele corresponding to higher dietary intake and lower fat mass and lean mass. The UCP3p-55 and the UCP3-3 polymorphisms, which were in high linkage disequilibrium (D' = 0.9776), showed similar patterns of association with total caloric intake (P =.031 and P =.042, respectively) and lean mass (P =.035 and P =.059, respectively), with the rare alleles corresponding to higher total intake and lean mass. No statistically significant associations were detected between the outcome variables and polymorphisms in UCP2. Two-way analysis of covariance (ANCOVA), used to evaluate the multi-locus effects and interactions between UCP3-5 and UCP3p-55, showed association with the main effect terms, but no evidence for statistically significant interaction between UCP3-5 and UCP3p-55 in regard to dietary intake. The UCP3-5 polymorphism was the only statistically significant genetic predictor of fat mass. The lean mass model showed no statistically significant association with either UCP3 variant. These results support a role for UCP3 in fuel substrate management and energy metabolism, which may influence body weight regulation.

Obesity and type 2 diabetes are closely related, multifactorial metabolic conditions characterized by alterations in energy metabolism and glucose homeostasis, respectively. Peroxisome proliferator-activated receptor gamma (PPARgamma) is a ligand-dependent transcription factor that regulates genes involved in lipid and glucose homeostasis, including the adipocyte-specific fatty acid-binding protein (FABP4). In turn, FABP4 binds fatty acids and transports them to the nucleus where the FABP4/fatty acid complex activates PPARgamma in a positive feedback loop. In this study, we tested the hypothesis that the polymorphisms, FABP4-376 and PPARgamma Pro12Ala, interactively influence insulin sensitivity and body composition in nondiabetic, Hispanic and non-Hispanic white males (n = 314) participating in the San Luis Valley Diabetes Study (SLVDS). Although the individual sites were not statistically significantly associated with any of the outcomes, we found statistically significant interaction terms in 2-way analysis of covariance (ANCOVA) models for homeostasis model assessment of insulin resistance (HOMA-IR) (P =.014) and lean mass (P =.019). While the PPARgamma Pro12Ala site was the only statistically significant predictor of fat mass in the 2-way model (P =.012), the FABP4 and PPARgamma main effect terms individually became stronger when considered in one model compared with the analysis of each polymorphism separately. These findings provide evidence that FABP4 and PPARgamma work together to influence a biologic pathway affecting insulin sensitivity and body composition, illustrating the importance of investigating the joint effect of genes in determining susceptibility for complex disease.

Studies have linked low birth weight to elevated risk for adult hypertension and insulin resistance. However, the relation between birth weight and later risk for pregnancy-induced hypertension (PIH), a disorder associated with insulin resistance and predictive of chronic hypertension, has not been well studied. This case-control study used linked hospital discharge and vital record data from New York State. Subjects were healthy women born in New York State who completed a first pregnancy there between 1994 and 1998. Records from each woman's own birth (1970-1985) were linked to those from her first pregnancy. Cases were 2,180 women diagnosed with PIH. Controls were the 22,955 remaining women with no record of PIH. Birth weight showed a U-shaped relation to risk for PIH, with the highest risks associated with very low and very high birth weights. Relative to women born at 3.5-4.0 kg, odds ratios adjusted for gestational age were 2.1 (95% confidence interval (CI): 1.1, 3.9) and 1.6 (95% CI: 1.1, 2.4), respectively, for women with birth weights less than 1.5 kg and greater than 4.5 kg. Adjustment for other perinatal factors reduced the association with high birth weight to 1.1 (95% CI: 0.7, 1.7) but strengthened that with lower birth weights, leaving a strong, inverse relation between birth weight and PIH risk (p for trend < 0.0001). These findings support a possible role for early life factors, particularly fetal growth, in the etiology of PIH.

There are environmental determinants and genetic susceptibility to coronary heart disease (CHD); however, identifying factors that modify genetic risk has been difficult. Evidence suggests that a common polymorphism in the hepatic lipase gene (LIPC-480C>T) may be related to susceptibility to CHD and that physical activity is a behavioral factor associated with CHD. This population-based prospective study in the San Luis Valley of Colorado investigated the role of the LIPC-480C>T polymorphism in predicting clinical CHD and the modifying effect of physical activity. Hispanics and non-Hispanic Whites (n = 966) were followed for 14 years (1984-1998); 91 CHD events occurred. The LIPC-480 TT genotype predicted an increase in CHD in both ethnic groups, and physical activity altered this relation. In the full cohort, the rate of CHD was significantly elevated among subjects with the high-risk genotype and normal levels of physical activity (hazard ratio = 2.58, 95% confidence interval: 1.39, 4.77) but was not elevated among those with the high-risk genotype who participated in vigorous physical activity (hazard ratio = 0.52, 95% confidence interval: 0.12, 2.19) (reference group: LIPC-480 CC/CT, normal physical activity). Thus, in this prospective cohort study, the LIPC-480 TT genotype increased susceptibility to CHD only in those subjects with normal levels of physical activity, not in those with the high-risk genotype who were vigorously active.

Type 2 diabetes affects over 150 million adults worldwide and this figure is expected to double over the next 25 yr. This increase will be accompanied by a marked increase in the number of patients with ESRD due to diabetes. We hypothesized that a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes We randomly assigned 3234 nondiabetic persons with elevated fasting and postload plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle-modification program with the goals of at least a 7% weight loss and at least 150 min of physical activity per week. The mean age of the participants was 51 yr, and the mean body mass index was 34.0 kg/m(2); 68% were women, and 45% were members of non-Caucasian racial/ethnic groups. The average follow-up was 2.8 yr. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence of diabetes by 58% (95% CI: 48 to 66%) and metformin by 31% (95% CI: 17 to 43%), compared with placebo; the lifestyle intervention was significantly more effective than metformin. In conclusion, lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk and the lifestyle intervention was more effective than metformin. Because the lifestyle changes worked equally in all racial/ethnic groups in the Diabetes Prevention Program, they should be applicable to high-risk populations worldwide and may be able to reduce the projected progressive rise in the incidence of diabetes and the expected increase in ESRD.

Research scientists, laboratory technicians, and animal handlers who work with animals frequently report respiratory and skin symptoms from exposure to laboratory animals (LA). However, on the basis of prick skin tests or RASTs, only half are sensitized to LA. We hypothesized that aerosolized endotoxin from mouse work is responsible for symptoms in nonsensitized workers. We performed a cross-sectional study of 269/310 (87%) workers at a research institution. Subjects completed a questionnaire and underwent prick skin tests (n = 254) or RASTs (n = 16) for environmental and LA allergens. We measured airborne mouse allergen and endotoxin in the animal facility and in research laboratories. Of 212 workers not sensitized to mice, 34 (16%) reported symptoms compared with 26 (46%) of mouse-sensitized workers (p < 0.001). Symptomatic workers were more likely to be atopic, regardless of mouse sensitization status. Symptomatic non-mouse-sensitized workers spent more time performing animal experiments in the animal facility (p = 0.0001) and in their own laboratories (p < 0.0001) and had higher daily endotoxin exposure (p = 0.008) compared with asymptomatic coworkers. In a multivariate model, daily endotoxin exposure most strongly predicted symptoms to mice in non-mouse-sensitized workers (odds ratio = 30.8, p = 0.003). We conclude that airborne endotoxin is associated with respiratory symptoms to mice in non-mouse-sensitized scientists and technicians.

Despite a worse cardiovascular disease (CVD) risk profile, Hispanics have lower CVD mortality than non-Hispanic Whites in studies based on death certificates. This study examined 310 deaths that occurred between 1984 and 1998 among 1,862 Hispanic and non-Hispanic White participants in the San Luis Valley Diabetes Study, using medical records to classify cause of death. Among persons without diabetes, the age-adjusted all-cause mortality rate was 6.1/1,000 person-years in non-Hispanic Whites and 7.4/1,000 person-years in Hispanics. Among persons with diabetes, it was 24.3/1,000 person-years in non-Hispanic Whites and 21.9/1,000 person-years in Hispanics. Among nondiabetics, the age-adjusted CVD mortality rate was 2.5/1,000 person-years in non-Hispanic Whites and 1.6/1,000 person-years in Hispanics. Among diabetics, it was 12.9/1,000 person-years in non-Hispanic Whites and 8.8/1,000 person-years in Hispanics. Among nondiabetics, the adjusted hazard ratio for CVD death in Hispanics compared with non-Hispanic Whites was 0.65 (95% confidence interval (CI): 0.34, 1.23). The hazard ratio for coronary heart disease death was 0.95 (95% CI: 0.35, 2.59). Among diabetics, the hazard ratio for CVD death, after adjustment for conventional and diabetes risk factors, was 0.44 (95% CI: 0.26, 0.74), and for coronary heart disease death it was 0.43 (95% CI: 0.21, 0.91). A statistically significant decreased risk of CVD death was observed only in male Hispanics with diabetes. Competing mortality or factors that interact with diabetes may explain these differences.

The San Luis Valley Health and Aging Study is a population-based epidemiologic study of chronic illness and disability among Hispanic and non-Hispanic white persons over the age of 60 in two counties in rural southern Colorado, USA. Between 1993 and 1995, we examined the prevalence of impaired executive cognitive functioning in a sample of 1,313 individuals living both in the community and in nursing homes. Overall, 1 person in 3 was found to have at least mild impairment, while 1 in 6 had moderate to severe deficits. Increasing levels of executive functioning impairment were associated with lower education, advancing age, and Hispanic ethnicity. After controlling for education and acculturation, the differences by ethnic group were no longer significant., (Copyright 2002 S. Karger AG, Basel)

Objective: To explore the relationship between serum selenium and cervical cancer., Methods: We conducted a case-control study of cervical cancer in five areas around Birmingham, AL; Chicago, IL; Denver, CO; Miami, FL; and Philadelphia, PA. Community controls were selected by random-digit dialing and were matched to invasive cervical cancer cases by age, race/ethnicity, and telephone exchange. Serum selenium was determined by neutron activation analysis. Logistic regression analysis controlling for known risk factors of cervical cancer, including human papillomavirus (HPV) type-16 measured serologically, was performed on 227 invasive cases, 127 in-situ cases, and 526 controls., Results: Values of serum selenium ranged from 67.5 to 185.0 ng/ml. Adjusted odds ratios for invasive cervical cancer by quintile were: 1.0 (highest selenium), 1.1, 1.0, 0.8, and 1.0 (lowest selenium), p for trend = 0.82. Similar patterns were observed for Stage I invasive, and Stages II-IV invasive cases, suggesting severity of disease did not influence the null results. Although no associations were seen among current or never smokers, a protective effect of selenium was suggested among former smokers. Effect modification was not evident for other variables examined., Conclusions: This study does not support a relationship between serum selenium and invasive cervical cancer at typical serum selenium levels in the US.

Objectives: To evaluate whether the risk of bladder cancer is greater in individuals with spinal cord injury (SCI) than in the general population and whether indwelling catheter (IDC) use is a significant independent risk factor for bladder cancer., Design: Historical cohort study in which subjects with SCI were stratified according to bladder management method and followed for the development of bladder cancer., Setting: A large rehabilitation hospital in the Spinal Cord Injury Model Systems., Participants: A total of 3670 patients with SCI who were evaluated for bladder cancer on at least 1 occasion by cystoscopy over a period of 1 to 47 years., Interventions: Not applicable., Main Outcome Measures: Bladder cancer occurring after SCI determined by diagnosis at our facility, by subject report, or by report of next of kin., Results: Twenty-one cases of bladder cancer were found in the 3670 study participants. The risk of bladder cancer for subjects with SCI using IDC is 77 per 100,000 person-years, corresponding to an age- and gender-adjusted standardized morbidity ratio (SMR) of 25.4 (95% confidence interval [CI], 14.0--41.9) when compared with the general population. After controlling for age at injury, gender, level and completeness of SCI, history of bladder calculi, and smoking, those using solely IDC had a significantly greater risk of bladder cancer (relative risk [RR] = 4.9; 95% CI, 1.3--13.8) than those using nonindwelling methods. Mortality caused by bladder cancer in individuals with SCI was significantly greater than that of the US population (SMR = 70.6; 95% CI, 36.9--123.3)., Conclusions: Bladder cancer risk and mortality are heightened in SCI compared with the general population. IDC is a significant independent risk factor for the increased risk of and mortality caused by bladder cancer in the SCI population., (Copyright 2002 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation)

The San Luis Valley Health and Aging Study, was designed to examine Hispanic versus non-Hispanic White differences in prevalence and incidence of aging-related outcomes in a rural population (1,358 community dwellers and 75 nursing home residents). Data presented here were gathered between 1993 and 1997. Previously reported analyses identified greater prevalence of functional dependence in daily living activities among Hispanic elderly, especially females, than among non-Hispanic White elderly. This analysis explored the degree to which incident changes explain these patterns. Comparisons of incidence, recovery, and mortality rates after 22 months revealed no significant ethnic differences, although trends were as hypothesized: greater Hispanic incidence, lower Hispanic recovery rates, and less Hispanic mortality. Overall age-adjusted incidence (activities of daily living = 9.5; instrumental activities of daily living = 15.1 per 100 person-years) exceeded reports from most other studies, while rates of recovery (activities of daily living = 14.5; instrumental activities of daily living = 9.9) and mortality (4.8 among community dwellers; 6.7 including nursing home residents) were similar to those of other reports. Patterns of new dependence, recovery, and mortality did not increase the previously observed disparity. Greater prevalent disability in the Hispanic cohort, especially in women, may reflect a reservoir accumulated during younger years and related to culture and socioeconomic status as well as to older age.

Background: Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors--elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle--are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes., Methods: We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle-modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups., Results: The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin., Conclusions: Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin.