Reduction in Incidence of Diabetes,Hypertension and Lipid Disturbances after Intentional Weight Loss Induced by Bariatric Surgery: the SOS Intervention Study

SJÖSTRÖM, c. DAVID, LAUREN LISSNER, HANS WEDEL, and LARS SJÖSTRÖM. Reduction in incidence of diabetes, hypertension and lipid disturbances after intentional weight loss induced by bariatric surgery: the SOS Intervention Study. Obes Res. Objective: To examine the effect of a large, long standing and intentional weight reduction on the incidence of diabetes, hypertension and lipid disturbances in severely obese individuals as compared to weight-stable obese controls. Research Methods and Procedures: The ongoing prospective SOS (Swedish Obese Subjects) intervention consists of a surgically treated group and a matched control group obtaining conventional obesity treatment. This report is based on 845 surgically treated patients and 845 controls (BMI41. 0±4. 6 kg/m² (mean±standard deviation [S])) followed for 2 years. Results: Surgically treated patients lost 28±15 kg and controls 0. 5±8. 9 kg (p<0. 0001). Two-year incidence of hypertension, diabetes, hyperinsulinemia, and lipid disturbances was compared in the two treatment groups. Adjusted odds ratios (95% CI) for the surgically treated group versus controls were 0. 38 (0. 22, 0. 65) for hypertension, 0. 02 (0. 00, 0. 16) for diabetes, 0. 10 (0. 03, 0. 28) for hyperinsulinemia, 0. 10 (0. 04, 0. 25) for hypertriglyceridemia, 0. 28 (0. 16, 0. 49) for low HDL-cholesterol and 1. 24 (0. 84, 1. 8) for hypercholesterolemia. Compared to controls, the 2-year recovery rates from hypertension, diabetes, hypo-HDL, and hypertriglyceridemia were significantly higher in the surgically treated group. Discussion: Intentional weight loss in the obese causes a marked reduction in the 2-year incidence of hypertension, diabetes and some lipid disturbances. The results suggest that severe obesity can and should be treated.     

Serum Leptin Concentration and Insulin Sensitivity in Men with Abdominal Obesity

JOHANNSSON, GUDMUNDUR, CECILIA KARLSSON, LARS LÖNN, PER MÅRIN, PER BJÖRNTORP, LARS SJÖSTRÖM, BJÖRN CARLSSON, LENA M.S. CARLSSON, BENGT-ÅKE BENGTSSON. Serum leptin concentration and insulin sensitivity in men with abdominal obesity. Obes Res. 1998;6:416–421. Objective : We have examined the association between generalized adiposity, abdominal adiposity, insulin sensitivity, and serum levels of leptin in a cross-sectional study of abdominally obese men. Research Methods and Procedures : Thirty men, 48 to 66 years of age with a body mass index (BMI) of between 25 kg/m² and 35 kg/m² and a waist hip ratio of <0.95, were included in the study. Serum leptin concentration was measured using radioimmunoassay. Total body fat percentage was determined from total body potassium, abdominal adiposity was measured by computed tomography, and the glucose disposal rate (GDR) was measured during an euglycemic, hyperinsulinemic glucose clamp. Results : Significant correlations were found between serum leptin concentration and BMI, percentage body fat, abdominal subcutaneous adipose tissue, serum insulin, GDR, and 24-hour urinary-free Cortisol. In a multiple regression analysis, it was shown that abdominal subcutaneous adipose tissue, GDR, and BMI explained 72% of the variability of serum leptin concentration. GDR demonstrated an independent inverse correlation with serum leptin concentration. Discussion : In abdominally obese men with insulin resistance, it was demonstrated that most of the individual variability in serum leptin concentration was explained by the amount of subcutaneous abdominal adipose tissue, insulin sensitivity, and BMI.     

Relationships Between Changes in Body Composition and Changes in Cardiovascular Risk Factors: The SOS Intervention Study

SJÖSTRÖM, C DAVID, LAUREN LISSNER, LARS SJÖSTROM. Relationships between changes in body composition and changes in cardiovascular risk factors: The SOS Intervention Study. Relationships between 2-year changes in body composition (estimated from computed tomography-validated anthropometry based on sagittal trunk diameter, weight, and height), adipose tissue (AT) distribution, and cardiovascular risk factors (blood pressure, lipids, glucose, insulin, uric acid) were examined in 842 treated adults with severe obesity with weight changes from ?95. 5 to +30. 6 kg. Although the change (Δ) of visceral AT mass (expressed in % total AT) for a given change in body mass index (ΔBMI) was 6-fold larger in men than in women, Δwaist and Δwaist/hip were similar in both sexes. In men, risk factor changes were similarly related to Awaist, Abodyweight, and ΔBMI, whereas in women, Δbodyweight seemed to be the single independent variable with the highest explanatory power. In multivariate regressions adjusted for ΔBMI and baseline conditions, Δvisceral AT mass was more strongly associated with risk factor changes than were Δwaist and ?waist/hip. When using a three-compartment model (lean body mass, subcutaneous and visceral AT masses) plus neck and thigh girths (indicators of subcutaneous AT distribution), risk factor changes were related both to ?subcutaneous and ?visceral AT masses but not to Δlean body mass. In agreement with cross-sectional findings, Δneck was positively and Δthigh was negatively related to some risk factor changes. Thus, the use of waist as a single risk factor indicator seems less effective for epidemiological studies than the simple anthropometric measures presented here, which are able to separate the effects of visceral AT mass, subcutaneous AT mass, and subcutaneous AT distribution on metabolic parameters under both cross-sectional and longitudinal conditions.     

Inheritance of the Waist‐to‐Hip Ratio in the National Heart,Lung, and Blood Institute Family Heart Study

Objective: Considering that waist‐to‐hip ratio (WHR) is a simple anthropometric measure of obesity and is a better predictor of coronary heart disease than body mass index (BMI), the genetic underpinnings of WHR are of interest. The inheritance pattern of WHR, before and after adjustment for BMI (WHR‐BMI), was investigated in 2713 individuals from 1038 nuclear families in the National Heart, Lung, and Blood Institute Family Heart Study (NHLBI‐FHS). Research Methods and Procedures: Waist and hip measurements were taken twice, and the means of the measurements were used to calculate the WHR. Adjustments for age were carried out separately by sex, using stepwise multiple regression procedures for WHR and WHR‐BMI phenotypes. Segregation analysis was applied using the unified model as implemented in the computer program POINTER. Results: For age‐adjusted WHR, the segregation results suggested an additive major gene that accounts for 35% of the phenotypic variance, and approximately 30% of the sample are homozygous for the “high” genotype. The results for age‐ and BMI‐adjusted WHR were also compatible with a major gene; however, the multifactorial model provided the most parsimonious fit to the data. Discussion: Although the genetic mechanisms for several obesity traits have been studied, tests of Mendelian segregation on this simple anthropometric measure (WHR) have not been reported previously. This study provides evidence for the presence of a major gene for age‐adjusted WHR, suggesting that it is an appropriate trait for further genetic analysis, especially because it has strong predictive value and probably relates biologically to cardiovascular risk.     

Evidence of Pleiotropic Loci for Fasting Insulin,Total Fat Mass,and Abdominal Visceral Fat in a Sedentary Population: The HERITAGE Family Study

Objective: To examine whether there is a major gene effect on fasting insulin and pleiotropic loci for fasting insulin, total fat mass (FM), and abdominal visceral fat (AVF). Research Methods and Procedures: A major gene hypothesis for fasting plasma insulin levels was assessed using segregation analyses of data on 495 members in 98 normolipidemic sedentary families of white descent who participated in the HERITAGE Family Study. Results: Segregation analyses were performed on insulin adjusted for age, on insulin adjusted for age and FM, and on insulin adjusted for age and AVF. Before adjustment for AVF and FM, a major gene effect on fasting insulin levels was indicated. The putative locus accounted for 54% of the variance under a recessive inheritance pattern, affecting 11% of the sample (i.e., allele frequency = 0.33). However, after adjusting for the effects of AVF or FM, neither a major effect alone nor a multifactorial component alone could be rejected, and support for a major gene was equivocal, i.e., neither the hypothesis of Mendelian τ values or that of the equal τs were rejected and the equal τ model fit the data better than the Mendelian τ model. This pattern (i.e., major gene evidence for insulin before but not after adjustment for AVF or FM) suggests that there is a putative locus with pleiotropic effects on both insulin and FM and another pleiotropic locus for both insulin and AVF. Discussion: Although these data do not directly support an additional major gene for insulin independent of AVF and FM, such support cannot be ruled out because there is still a significant major effect on FM‐ or AVF‐adjusted insulin (albeit the Mendelian nature of this effect is ambiguous).     

Segregation Analysis of Body Mass Index in an Unselected French-Canadian Sample: The Québec Family Study

Interest in a single gene etiology for obesity, as assessed by the body mass index (BMI), has been spurred recently by reports of a putative recessive major gene for extreme values, which accounts for as much as 40% of the variance. The major gene hypothesis was evaluated here in the Québec Family Study, a random sample of 375 French-Canadian volunteer families. This report represents one component in a more complete investigation of obesity in these families. In contrast to the recent studies, a major gene hypothesis for BMI was not verified here. Although there was a major effect, it did not conform to a Mendelian pattern of transmission. A multifactorial component (i.e., polygenic and/or common environmental factors) accounted for 42% of the phenotypic variance. In addition, evidence of heterogeneity between the generations was found. The heterogeneity was traced to the major non-Mendelian component (which accounted for 0.01% of the variance in parents and over 40% in offspring) rather than to the multifactorial one. These results would suggest that a simple recessive gene mixed model may not be sufficient to explain the familial distribution of the BMI. Several factors which may have contributed to these results include temporal trends and surrogate effects such as those related to variation in body composition and energy balance components. (OBESITY RESEARCH 1993; 1:288–294)     

Segregation analysis of non-insulin-dependent diabetes mellitus in Pima Indians: evidence for a major-gene effect.

Non-insulin-dependent diabetes mellitus (NIDDM) has a high prevalence in Pima Indians. The disorder is familial, but the extent to which genetic factors are involved in its etiology is largely unknown. Segregation analysis was used to determine whether familial aggregation of NIDDM in this population could reflect the action of a single major gene. The analysis included 2,697 subjects from 653 nuclear families in which both parents and at least one offspring had been examined in the course of a longitudinal epidemiological study. The REGTL program of the SAGE package was used to fit models in which age at onset of NIDDM is transmitted from parent to offspring under the unified model for segregation analysis. Likelihood-ratio tests were used to test hypotheses related to genetic transmission. The hypothesis of no major effect was strongly rejected (P < .01), as was that of no transmission of the major effect (P < .01). Mendelian transmission was not rejected (P = .91). Similar results were obtained when covariates for obesity and birth cohort were added to the models and when a power transformation of age at onset was estimated. A strong effect of birth cohort with earlier age at onset in the later born cohorts was observed (P < .01). The findings are consistent with the hypothesis that a major gene influences the risk for NIDDM in Pima Indians by affecting age at onset. The expression of this gene may depend on environmental factors that have become more prevalent in recent-birth cohorts.     

Body mass index and depressive symptoms: instrumental‐variables regression with genetic risk score

The causal role of obesity in the development of depression remains uncertain. We applied instrumental‐variables regression (Mendelian randomization) to examine the association of adolescent and adult body mass index (BMI) with adult depressive symptoms. Participants were from the Young Finns prospective cohort study (n = 1731 persons, 2844 person‐observations), with repeated measurements of BMI and depressive symptoms (modified Beck's Depression Inventory). Genetic risk score of 31 single nucleotide polymorphisms previously identified as robust genetic markers of body weight was used as a proxy for variation in BMI. In standard linear regression analysis, higher adult depressive symptoms were predicted by higher adolescent BMI (B = 0.33, CI = 0.06–0.60, P = 0.017) and adult BMI (B = 0.47, CI = 0.32–0.63, P < 0.001). These associations were replicated in instrumental‐variables analysis with genetic risk score as instrument (B = 1.96, CI = 0.03–3.90, P = 0.047 for adolescent BMI; B = 1.08, CI = 0.11–2.04, P = 0.030 for adult BMI). The association for adolescent BMI was significantly stronger in the instrumented analysis compared to standard regression (P = 0.04). These findings provide additional evidence to support a causal role for high BMI in increasing symptoms of depression. However, the present analysis also demonstrates potential limitations of applying Mendelian randomization when using complex phenotypes.     

Blood Pressure in Adolescence and Early Adulthood Related to Obesity and Birth Size

Objective: Obesity is an established risk factor for higher systolic (SBP) and diastolic (DBP) blood pressure in adolescence and early adulthood, but birth size may also have a role. We analyzed the effects of adolescent and adult obesity and birth size on BP in the young adult. Research Methods and Procedures: In a prospective longitudinal study, anthropometric measurements were obtained at birth on 67 boys and 67 girls bom in Boston. Their body mass indices (BMI) and BP were recorded 17 years and 30 years later. Results: For women, adolescent and early adult obesity appeared to be the stronger determinants of higher BP, although smaller head and chest circumferences at birth may also be related. We found some evidence of birth (ponderal index [PI] and head circumference) anthropometric influences on age 17 BP levels in boys. By age 30, body mass variables were the dominant predictors of male BP levels. Female BMI at age 17 was positively correlated with birth adiposity (PI), but BMI at 30 was related only to age 17 BMI. Similarly, male BMI at 17 years was higher for those who weighed more at birth, but BMI at 30 years was again related only to age 17 BMI. Discussion: We conclude that adult weight and weight gain are the major determinants of adult BP.     

Maternal obesity is associated with younger age at obesity onset in U.S. adolescent offspring followed into adulthood

Objective: The objective was to test the hypothesis that maternal obesity is associated with younger age of offspring's obesity onset. Research Methods and Procedures: We used prospective, nationally representative, longitudinal data collected across Waves I (1995; 12 to 20 years), II (1996; 13 to 20 years), and III (2001; 18 to 28 years) of the National Longitudinal Study of Adolescent Health (N = 14,654; 49% female). Interval regression analysis was used to assess the association between maternal obesity and age at offspring's obesity onset (International Obesity Task Force BMI ≥30 equivalent age‐ and sex‐specific cut‐off points for adolescents and BMI ≥30 for young adults) using self‐reported heights and weights, adjusting for race/ethnicity, sex, parental education, and family income, accounting for complex sampling design. Results: The net effect of having an obese mother varied by race/ethnicity and was associated with a significantly earlier age at obesity onset (p = 0.0001) for whites [β= ?8.1 year, 95% confidence interval (CI), ?9.3; ?6.9)], blacks (β = ?10.8 years, 95% CI, ?12.4; ?9.2), Hispanics (β = ?7.0 years, 95% CI, ?9.2; ?4.8), and Asians (β = ?8.6 years, 95% CI, ?13.3; ?3.9). Earlier obesity onset (<18 years) was associated with increased severity at young adulthood (mean BMI, 36.0 ± 0.3 kg/m²) vs. onset after age 18 (mean BMI, 34.4 ± 0.2 kg/m²; p = 0.0001). There were no sex differences in the association of maternal obesity to age at obesity onset. Conclusions: Having an obese mother was associated with earlier age at obesity onset across all race/ethnic groups, particularly non‐Hispanic blacks. Early obesity onset has important health consequences because of its association with more severe adult obesity.     

Complex segregation analysis of obsessive-compulsive disorder in families with pediatric probands

OBJECTIVE: The purpose of this study was to assess the mode of inheritance for obsessive-compulsive disorder (OCD) in families ascertained through pediatric probands. METHODS: We ascertained 52 families (35 case and 17 control families) through probands between the ages of 10 and 17 years. Direct interviews were completed with 215 individuals. Family informant data were collected on another 450 individuals without direct interviews, forming two data sets with one contained within the other. Complex segregation analyses were performed using regressive models as programmed in REGTL in the S.A.G.E. package.All models used in the analyses included sex-specific age and type parameters. RESULTS: All models that excluded a residual effect of an affected parent were rejected. With that parameter included, the environmental and sporadic models were rejected in comparisons with the most general model in both data sets (all p < 0.005). With the direct interview data, the general codominant Mendelian model was not rejected when compared with the most general model (p = 0.140). We could not distinguish between any of the simple Mendelian models using either data set. However, the dominant Mendelian model provided a somewhat better fit than the other Mendelian models to the direct interview data. CONCLUSIONS: The results provide evidence for a major susceptibility locus in families with OCD when age at onset is incorporated into the model. Mendelian factors at most partially explained the familial aggregation of the phenotype, and residual familial effects were necessary to fit the data adequately. The results support the importance of linkage efforts by suggesting that a major locus is segregating within a proportion of families with OCD ascertained through pediatric probands.     

Race, childhood insulin, childhood caloric intake, and class 3 obesity at age 24: 14-year prospective study of schoolgirls

The prevalence of Class 3 obesity (BMI ≥40 kg/m²) has more than doubled in the past 25 years. In a 14‐year prospective study from age 10 to 24 of a biracial schoolgirl cohort (293 black, 256 white), we assessed childhood correlates of Class 3 BMI at age 24. Of 42 girls with Class 3 BMI at age 24, 36 (86%) were black. By logistic regression, significant explanatory variables of Class 3 BMI at age 24 included top decile waist circumference at age 11 (odds ratio (OR) 5.7, 95% confidence interval (CI) 2.3–13.9, P = 0.0002), age 10 BMI ≥ the Center for Disease Control (CDC) 2000 top 15% (OR 7.0, 95% CI 2.5–19.3, P = 0.0002), and a three‐way interaction between race, childhood insulin, and average caloric intake from age 10 to age 19 (for each unit increase, OR 1.7 95% CI 1.3–2.2, P = 0.0003). Age 10 BMI, age 11 waist circumference, and interaction of race, childhood insulin, and childhood caloric intake predict Class 3 obesity in young adulthood, facilitating childhood identification of girls at high risk for developing Class 3 obesity.     

Lack of Evidence for a Major Gene in the Mendelian Transmission of BMI in Chinese

Objectives: To determine the heritability of BMI and to examine the mode of inheritance of BMI variation in Chinese. Research Methods and Procedures: Familial correlation and complex segregation analyses for BMI were undertaken in a Chinese sample composed of 392 nuclear families, with 1190 total individuals. Results: A moderate heritability was found for BMI (h² = 0.419 ‐ 0.492). The obtained results do not support a major gene for BMI in our samples. BMI may be inherited in a complex and non‐Mendelian manner in Chinese. Discussion: The findings of this study suggest that identification of specific genes for BMI in Chinese, at least within the same data set, is a serious challenge because of the lack of evidence of a major gene for BMI in our Chinese sample.     

Obesity and Depression in US Women: Results From the 2005–2006 National Health and Nutritional Examination Survey

Research is needed to better elucidate the relationship between obesity and depression, which has been most consistently demonstrated for women, but not for men. We examined exclusively a population‐based sample of US women who participated in the 2005 or 2006 National Health and Nutritional Examination Survey. Current depression was defined as having a score of ≥10 (a conventional threshold for moderate symptoms of depression) or meeting the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM‐IV) diagnostic criteria for major depression on the nine‐item Patient Health Questionnaire. Weight and height were measured and BMI was calculated. Waist circumference, a clinical measure of abdominal obesity, was also measured. BMI was positively associated with the probability of moderate/severe depressive symptoms (r = 0.49, P = 0.03) and major depression (r = 0.72, P < 0.0001). The probability curves increased progressively, beginning at BMI of 30. Degree of obesity was an independent risk factor for depression even within the obese population, and women in obesity class 3 (BMI ≥40) were at particular risk (odds ratio (OR) = 4.91, 95% confidence interval (CI): 1.17–20.57), compared to those in obesity class 1 (BMI 30 to <35). Abdominal obesity was positively associated with depressive symptoms, but not major depression, independent of general obesity (BMI). In addition to severe obesity, compromised physical health status, young or middle‐aged adulthood, low income, and relatively high education were also independently associated with greater odds of depressive symptoms among obese women. These characteristics may identify specific at‐risk subgroups of obese women in which hypothesized causal pathways and effective preventive and therapeutic interventions can be profitably investigated.     

Long-term effects of obesity on employment and work limitations among U.S. Adults, 1986 to 1999

Objective: To determine the relationships between BMI and workforce participation and the presence of work limitations in a U.S. working‐age population. Research Methods and Procedures: We used data from the Panel Study of Income Dynamics, a nationwide prospective cohort, to estimate the effect of obesity in 1986 on employment and work limitations in 1999. Individuals were classified into the following weight categories: underweight (BMI < 18.5), normal weight (18.5 ≤ BMI < 25), overweight (25 ≤ BMI < 30), and obese (BMI ≥ 30). Using multivariable probit models, we estimated the relationships between obesity and both employment and work disability. All analyses were stratified by sex. Results: After adjusting for baseline sociodemographic characteristics, smoking status, exercise, and self‐reported health, obesity was associated with reduced employment at follow‐up [men: marginal effect (ME) ?4.8 percentage points (pp); p < 0.05; women: ME ?5.8 pp; p < 0.10]. Among employed women, being either overweight or obese was associated with an increase in self‐reported work limitations when compared with normal‐weight individuals (overweight: ME +3.9 pp; p < 0.01; obese: ME +12.6 pp; p < 0.01). Among men, the relationship between obesity and work limitations was not statistically significant. Discussion: Obesity appears to result in future productivity losses through reduced workforce participation and increased work limitations. These findings have important implications in the U.S., which is currently experiencing a rise in the prevalence of obesity.     

Intelligence Test Score and Educational Level in Relation to BMI Changes and Obesity

Objective: To investigate whether intelligence and education are related to subsequent BMI changes and development and persistence of obesity in men from young adulthood through middle‐age. Research Methods and Procedures: Subjects were selected among men (median age, 19 years; examined between 1956 and 1977) appearing at Danish draft boards: a group with juvenile‐onset obesity, including all men with a BMI of ≥31.0 kg/m²; and a nonobese group randomly selected as a 1% sample of the study population. The obese group and 50% of the nonobese group were invited to participate in follow‐up studies between 1982 and 1984 and between 1992 and 1994. Among 907 men with juvenile‐onset obesity and 883 nonobese men, age, examination region, intelligence test score, education, and BMI from baseline to first follow‐up were analyzed by multiple linear and logistic regressions analyses. Results: Education and intelligence, analyzed separately, were inversely related to BMI changes in both groups and to the development of obesity in the nonobese group. When adjusted for education, the association between intelligence score and BMI changes and development of obesity vanished, whereas the inverse relationship for education persisted only for BMI changes. Intelligence score was not associated with the persistence of obesity in the obese group, whereas inverse relationships were found for education. Discussion: Intelligence test score was inversely related to risk of BMI changes and the risk of development of obesity, perhaps with education acting as a mediator or indicator of cognitive ability. Education, but not intelligence, was inversely associated with risk of remaining obese.     

Prevalence of Pre‐obesity and Obesity in Urban Adult Mexicans in Comparison with Other Large Surveys

Objective: 1. To estimate the prevalence of pre‐obesity and obesity in a 1992 to 1993 national survey of the Mexican urban adult population. 2. To compare our findings with other national surveys and with data for Mexican Americans. Research Methods and Procedures: The national representative sample of the Mexican urban adult population included 8462 women and 5929 men aged 20 to 69 years from 417 towns of >2500 people. Body mass index (BMI), calculated from measured weight and height, was classified using the World Health Organization categories of underweight (BMI < 18.5 kg/m²), normal weight (BMI 18.5 to 24.9 kg/m²), pre‐obesity (PreOB = BMI 25 to 29.9 kg/m²) and obesity (OB = BMI 30+ kg/m²). Estimates for Mexican Americans were calculated from U.S. survey data. Results: Overall, 38% of the Mexican urban adult population were classified as pre‐obese and 21% as obese. Men had a higher prevalence of pre‐obesity than women did at all ages, but women had higher values of obesity. Both pre‐obesity and obesity increased with age up to the age range brackets of 40 to 49 or 50 to 59 years for both men and women. Both pre‐obesity and obesity prevalence estimates were remarkably similar to data for Mexican Americans from 1982 through 1984. Comparison with other large surveys showed that countries differed more in the prevalence of obesity than of pre‐obesity, leading to differences in the PreOB/OB ratio, and that countries also differed in the gender ratio (female/male) for both pre‐obesity and obesity. Discussion: Pre‐obesity and obesity were high in our population and increased with age. Our approach of characterizing large surveys by PreOB/OB and gender ratios appeared promising.     

Overall and central obesity and risk of type 2 diabetes in U.S. black women

Objective: Obesity has risen to epidemic proportions in the United States, leading to an emerging epidemic of type 2 diabetes. African‐American women are disproportionately affected by both conditions. While an association of overall obesity with increasing risk of diabetes has been documented in black women, the effect of fat distribution, specifically abdominal obesity, has not been studied. We examined the association of BMI, abdominal obesity, and weight gain with risk of type 2 diabetes. Research Methods and Procedures: During eight years of follow‐up of 49,766 women from the Black Women's Health Study, 2472 incident cases of diabetes occurred. Cox proportional hazard models were used to estimate incidence rate ratios (IRRs), with control for age, physical activity, family history of diabetes, cigarette smoking, years of education, and time period of data collection. Results: Sixty‐one percent of participants had a BMI ≥25 kg/m² (WHO definition of overweight). Compared with a BMI of <23 kg/m², the IRR for a BMI of >45 kg/m² was 23 (95% confidence interval, 17.0 to 31.0). The IRR for the highest quintile of waist‐to‐hip ratio relative to the lowest was 2.3 (95% confidence interval, 2.0 to 2.7) after control for BMI. Furthermore, at every level of BMI, an increased risk was observed for high waist‐to‐hip ratio relative to low. Discussion: Central obesity, as well as overall obesity, is a strong risk factor for diabetes in African‐American women. Efforts to reduce the prevalence of obesity in African‐American women are of paramount importance.     

Obesity,End‐stage Renal Disease,and Survival in an Elderly Cohort With Cardiovascular Disease

Obesity is highly prevalent in African Americans and is associated with increased risk of End‐Stage Renal Disease (ESRD) and death. It is not known if the effect of obesity is similar among blacks and whites. The aim of this study is to examine racial differences in the association of obesity with ESRD and survival in elderly patients (age >65). Data were obtained for 74,167 Medicare patients with acute myocardial infarction (AMI) between February 1994 and July 1995. BMI was calculated as weight (kg) divided by height (m²). We evaluated the association of BMI class with ESRD incidence and death using multivariable Cox proportional hazards models, testing for race‐BMI interactions. Compared to whites, African Americans had higher BMI (26.9 vs. 26.0, P < 0.0001) and estimated glomerular filtration rate (72.4 ml/min/1.73 m² vs. 66.6 ml/min/1.73 m², P < 0.0001). Crude ESRD rates increased with increasing obesity among whites but not among blacks. However, after adjusting for age, sex, and other comorbidities, obesity was not associated with increased ESRD rate among blacks or whites and the interaction between race and BMI was not significant. Furthermore, for both races, patients classified as overweight, class 1 obese, or class 2 obese had similar, significantly better survival abilities compared to normal weight patients and the race BMI interaction was not significant. In conclusion, obesity does not increase risk of ESRD among black or white elderly subjects with cardiovascular disease (CVD). However, both obese blacks and whites, in this population, experience a survival benefit. Further studies need to explore this obesity paradox.     

Racial Differences in the Tracking of Childhood BMI to Adulthood

Objective: The possibility that there are racial differences in the patterns of BMI (kilograms per meter squared) change throughout life has not been examined. For example, the high prevalence of obesity among black women could result from a higher prevalence of obesity among black girls or because normal‐weight black girls experience larger BMI increases in adolescence or adulthood than do their white counterparts. Therefore, we examined the tracking of childhood BMI into adulthood in a biracial (36% black) sample. Research Methods and Procedures: Five‐ to 14‐year‐old children (2392) were followed for (mean) 17 years. Childhood overweight was defined as BMI ≥ 95th percentile, and adult obesity was defined as BMI ≥ 30 kg/m². Results: The tracking of childhood BMI differed between whites and blacks. Among overweight children, 65% of white girls vs. 84% of black girls became obese adults, and predictive values among boys were 71% (whites) vs. 82% (blacks). These racial differences reflected contrasting patterns in the rate of BMI change. Although the initial BMI of black children was not higher than that of white children, BMI increases with age were larger among black girls and overweight black boys than among their white counterparts. In contrast, relatively thin (BMI < 50th percentile) white boys were more likely to become overweight adults than were their black counterparts. Discussion: These findings emphasize the black/white differences in BMI changes with age. Because of the adult health consequences of childhood‐onset obesity, early prevention should be given additional emphasis.