Whitney R. Robinson

The female-male disparity in obesity prevalence among black American young adults: contributions of sociodemographic characteristics of the childhood family

BACKGROUND In the United States, black women are at much greater risk of obesity than are black men. Little is known about the factors underlying this disparity. OBJECTIVE We explored whether childhood sociodemographic factors (parental education, single-mother household, number of siblings, number of minors in household, birth order, and female caregivers age) were associated with the gender disparity in obesity prevalence in young black adults in the United States. DESIGN An analytic data set (n = 7747) was constructed from the nationally representative National Longitudinal Study of Adolescent Health. Childhood sociodemographic factors were assessed in 1994-1995 in nonimmigrant black and white youths aged 11-19 y. Obesity was assessed in 2001-2002. For each childhood sociodemographic factor, we evaluated whether the prevalence difference (female obesity minus male obesity) was modified by the factor. We described the contribution of each variable category to the overall prevalence difference. RESULTS In unadjusted and multivariable-adjusted models, parental education consistently modified gender disparity in blacks (P = 0.01). The gender gap was largest with low parental education (16.7% of men compared with 45.4% of women were obese) and smallest with high parental education (28.5% of men compared with 31.4% of women were obese). In whites, there was little overall gender difference in obesity prevalence. CONCLUSIONS To our knowledge, this was the first study to document that the gender disparity in obesity prevalence in young black adults is concentrated in families with low parental education. In these low-socioeconomic-status families, obesity development is either under the control of distinct mechanisms in each gender, or men and women from these households adopt different obesity-related behaviors.

Getting Over Testosterone: Postulating a Fresh Start for Etiologic Studies of Prostate Cancer

JNCI Vol. 100, Issue 3 | February 6, 2008 Assessing progress in our understanding of prostate cancer etiology is difficult, although it is certainly clear that we have much to learn. Despite a substantial research investment spanning dozens of years, prostate cancer remains as enigmatic as it is burdensome. We know that increasing age, African American race, residence in a Western nation, and family history are associated with increased prostate cancer risk, although we have yet to identify risk factors that are of substantial magnitude and are amenable to preventive intervention. This is not due to a lack of candidates, including a multitude of environmental, lifestyle, or nutritional factors ( 1 ). Among endogenous factors, elevated androgen levels have been persistently associated with prostate cancer despite previous literature reviews pointing to a dearth of supportive epidemiologic evidence ( 2 , 3 ). The intense and sustained interest in confi rming an androgen-driven hypothesis likely arises from the key role that androgens play in normal prostate development and from Huggins’ Nobel Prize – winning observation that suppression of testosterone in men with advanced prostate cancer can lead to dramatic regression of the disease ( 3 , 4 ). An androgen etiology of prostate cancer would have immediate implications for prevention, such as screening for higher androgen levels and, if elevated, subsequent use of more systematic or intensive screening and possibly specifi c strategies or medications to lower androgen levels. Dihydrotestosterone-suppressing 5 -reductase inhibitors remain a tantalizing possibility for effective prostate cancer chemoprevention, even without a link between prostate cancer and androgen level. However, results from the Prostate Cancer Prevention Trial temper potential preventative benefi ts with possible perils for men using fi nasteride. This prevention trial of 18 882 men found an association between fi nasteride and a 25% reduction in prostate cancers, although it also found a simultaneous increase in high-grade prostate cancers ( 5 ). Ironically, the hypothesis that provided the theoretical foundation for the Prostate Cancer Prevention Trial has been convincingly debunked in the accompanying article by the Endogenous Hormones and Prostate Cancer Collaborative Group ( 6 ). The group’s fi ndings suggest an underappreciated difference between excess prostate cancer risk conferred by elevated endogenous androgen levels and prostate cancer risk reduction from drug-induced suppression of androgens among men who may have low or normal androgen levels. In this issue of the Journal, the Endogenous Hormones and Prostate Cancer Collaborative Group ( 6 ) presents an im pressive pooled analysis examining the widely hypothesized link be tween circulating levels of sex hormones and prostate cancer risk. Analyzing 18 prospective studies of 3886 men with prostate cancer and 6438 control subjects, the authors use conditional logistic regression to determine that there are no associations between prostate cancer risk and serum concentrations of testosterone, calculated free testosterone, dihydrotestosterone, dehydroepiandrosterone sulfate, androstenedione, androstanediol glucuronide, estradiol, or calculated free estradiol and that there is a modest inverse association for sex hormone – binding globulin. This collaborative research project is commendable on a number of levels. The study is an impressive example of collaboration and coordination among 18 research groups and dozens of research centers spanning the globe — a heartening display of scientifi c collaboration. By combining the data from their unique efforts, they are able to examine an important issue to a degree that extends beyond the capability of any one study. Lending strength to its fi ndings, this analysis examines only studies including prediagnostic serum samples from case patients with prostate cancer. Because prostate cancer can infl uence hormone levels in men, the exclusion of studies of men already diagnosed with the disease helps to prevent confusion between the cause and effect of higher hormone levels and prostate cancer. Perhaps related to the issue of excess risk from elevated hormone levels vs reducing risk through hormone suppression among those with low-to-normal levels, the factors that promote localized or nonaggressive prostate cancer may be entirely different than those that promote fast-growing, high-grade prostate cancers. Because most of the cancers included in these studies were localized and low grade, pooling data from many studies allowed a sample size that was large enough to perform subanalyses of advanced and high-grade cancers and the power to investigate interactions among hormones and sex hormone – binding globulins. This study is not without limitations. The main analysis presented pooled data from these 18 different studies. To standardize the data, participants in each study were divided into quintiles that were assigned values of 0, 0.25, 0.5, 0.75, and 1. Such categorization and subsequent analysis of the data as if it were continuous may have underestimated the error in their models. The analysis also assumes that the association between the androgens and

Birth cohort effects on abdominal obesity in the United States: the Silent Generation, Baby Boomers and Generation X

BACKGROUND:Abdominal obesity predicts a wide range of adverse health outcomes. Over the past several decades, prevalence of abdominal obesity has increased markedly in industrialized countries like the United States No previous analyses, however, have evaluated whether there are birth cohort effects for abdominal obesity. Estimating cohort effects is necessary to forecast future health trends and understand the past population-level trends.METHODS:This analysis evaluated whether there were birth cohort effects for abdominal obesity for the Silent Generation (born 1925–1945), children of the Great Depression; Baby Boomers (born 1946–1964); or Generation X (born 1965–1980). Cohort effects for prevalence of abdominal obesity were estimated using the median polish method with data collected from the National Health and Nutrition Examination Survey (NHANES) between 1988 and 2008. Respondents were aged 20–74 years.RESULTS:After taking into account age effects and ubiquitous secular changes, the Silent Generation and Generation X had higher cohort-specific prevalence of abdominal obesity than the Baby Boomers. Effects were more pronounced in women than men.CONCLUSIONS:This work presents a novel finding: evidence that the birth cohorts of the post-World War II Baby Boom appeared to have uniquely low cohort effects on abdominal obesity. The growing prosperity of the post-World War II US may have exposed the baby-boom generation to lower levels of psychosocial and socioeconomic stress than the previous or subsequent generations. By identifying factors associated with the Baby Boomers’ low cohort-specific sensitivity to the obesogenic environment, the obesity prevention community can identify early-life factors that can protect future generations from excess weight gain.

Birth cohort effects among US-born adults born in the 1980s: foreshadowing future trends in US obesity prevalence

Background:Obesity prevalence stabilized in the US in the first decade of the 2000s. However, obesity prevalence may resume increasing if younger generations are more sensitive to the obesogenic environment than older generations.Methods:We estimated cohort effects for obesity prevalence among young adults born in the 1980s. Using data collected from the National Health and Nutrition Examination Survey between 1971 and 2008, we calculated obesity for respondents aged between 2 and 74 years. We used the median polish approach to estimate smoothed age and period trends; residual non-linear deviations from age and period trends were regressed on cohort indicator variables to estimate birth cohort effects.Results:After taking into account age effects and ubiquitous secular changes, cohorts born in the 1980s had increased propensity to obesity versus those born in the late 1960s. The cohort effects were 1.18 (95% CI: 1.01, 1.07) and 1.21 (95% CI: 1.02, 1.09) for the 1979–1983 and 1984–1988 birth cohorts, respectively. The effects were especially pronounced in Black males and females but appeared absent in White males.Conclusions:Our results indicate a generational divergence of obesity prevalence. Even if age-specific obesity prevalence stabilizes in those born before the 1980s, age-specific prevalence may continue to rise in the 1980s cohorts, culminating in record-high obesity prevalence as this generation enters its ages of peak obesity prevalence.

Body Mass Index Is Associated with Gene Methylation in Estrogen Receptor–Positive Breast Tumors

Background: Although obesity is associated with breast cancer incidence and prognosis, the underlying mechanisms are poorly understood. Identification of obesity-associated epigenetic changes in breast tissue may advance mechanistic understanding of breast cancer initiation and progression. The goal of this study, therefore, was to investigate associations between obesity and gene methylation in breast tumors. Methods: Using the Illumina GoldenGate Cancer I Panel, we estimated the association between body mass index (BMI) and gene methylation in 345 breast tumor samples from phase I of the Carolina Breast Cancer Study, a population-based case–control study. Multivariable linear regression was used to identify sites that were differentially methylated by BMI. Stratification by tumor estrogen receptor (ER) status was also conducted. Results: In the majority of the 935 probes analyzed (87%), the average beta value increased with obesity (BMI ≥ 30). Obesity was significantly associated with differential methylation (FDR q < 0.05) in just two gene loci in breast tumor tissue overall and in 21 loci among ER-positive tumors. Obesity was associated with methylation of genes that function in immune response, cell growth, and DNA repair. Conclusions: Obesity is associated with altered methylation overall, and with hypermethylation among ER-positive tumors in particular, suggesting that obesity may influence the methylation of genes with known relevance to cancer. Some of these differences in methylation by obese status may influence levels of gene expression within breast cells. Impact: If our results are validated, obesity-associated methylation sites could serve as targets for prevention and treatment research. Cancer Epidemiol Biomarkers Prev; 24(3); 580–6. ©2015 AACR.

Where people shop is not associated with the nutrient quality of packaged foods for any racial-ethnic group in the United States

BACKGROUND In the literature, it has been suggested that there are race-ethnic disparities in what Americans eat. In addition, some studies have shown that residents of African American and low-income neighborhoods have less access to grocery stores and supermarkets, which tend to stock healthier foods. However, it is unclear whether differences in food shopping patterns contribute to the poorer nutrient profile of food purchases made by racial-ethnic minorities. OBJECTIVES We examined whether the mix of food stores where people shop (i.e., food-shopping patterns) was associated with the nutrient profile of packaged food purchases (PFPs) and the types of foods and beverages purchased, and we determined whether these associations differ across racial-ethnic groups. DESIGN We used PFPs by US households (Nielsen National Consumer Panel) from 2007 to 2012 and implemented a cluster analysis to categorize households according to their food-shopping patterns. Longitudinal random-effects linear regression models were used to examine the association between food shopping patterns and the nutrient qualities and types of packaged foods and beverages purchased by race-ethnicity in US households. RESULTS Shopping primarily at grocery chains was not associated with a better nutrient profile of household PFPs or the food and beverages that households purchased than was shopping primarily at mass merchandisers (value-oriented stores that sell merchandise lines in multiple departments) or at a combination of large and small stores. These results were consistent across racial-ethnic groups. Regardless of where households shopped, non-Hispanic African American households purchased foods with higher energy, total sugar, and sodium densities than did non-Hispanic white and Hispanic households. CONCLUSION Policy initiatives that focus on increasing physical access to stores or helping stores sell healthier products to encourage healthier purchases may be ineffective because other factors may be more important determinants of food and beverage purchases than where people shop or what is available in the store.

Association of Changes in Neighborhood-Level Racial Residential Segregation With Changes in Blood Pressure Among Black Adults: The CARDIA Study

Importance Despite cross-sectional evidence linking racial residential segregation to hypertension prevalence among non-Hispanic blacks, it remains unclear how changes in exposure to neighborhood segregation may be associated with changes in blood pressure. Objective To examine the association of changes in neighborhood-level racial residential segregation with changes in systolic and diastolic blood pressure over a 25-year period. Design, Setting, and Participants This observational study examined longitudinal data of 2280 black participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study, a prospective investigation of adults aged 18 to 30 years who underwent baseline examinations in field centers in 4 US locations from March 25, 1985, to June 7, 1986, and then were re-examined for the next 25 years. Racial residential segregation was assessed using the Getis-Ord Gi* statistic, a measure of SD between the neighborhood’s racial composition (ie, percentage of black residents) and the surrounding area’s racial composition. Segregation was categorized as high (Gi* >1.96), medium (Gi* 0-1.96), and low (Gi* <0). Fixed-effects linear regression modeling was used to estimate the associations of within-person change in exposure to segregation and within-person change in blood pressure while tightly controlling for time-invariant confounders. Data analyses were performed between August 4, 2016, and February 9, 2017. Main Outcomes and Measures Within-person changes in systolic and diastolic blood pressure across 6 examinations over 25 years. Results Of the 2280 participants at baseline, 974 (42.7%) were men and 1306 (57.3%) were women. Of these, 1861 (81.6%) were living in a high-segregation neighborhood; 278 (12.2%), a medium-segregation neighborhood; and 141 (6.2%), a low-segregation neighborhood. Systolic blood pressure increased by a mean of 0.16 (95% CI, 0.06-0.26) mm Hg with each 1-SD increase in segregation score after adjusting for interactions of time with age, sex, and field center. Of the 1861 participants (81.6%) who lived in high-segregation neighborhoods at baseline, reductions in exposure to segregation were associated with reductions in systolic blood pressure. Mean differences in systolic blood pressure were −1.33 (95% CI, −2.26 to −0.40) mm Hg when comparing high-segregation with medium-segregation neighborhoods and −1.19 (95% CI, −2.08 to −0.31) mm Hg when comparing high-segregation with low-segregation neighborhoods after adjustment for time and interactions of time with baseline age, sex, and field center. Changes in segregation were not associated with changes in diastolic blood pressure. Conclusions and Relevance Decreases in exposure to racial residential segregation are associated with reductions in systolic blood pressure. This study adds to the small but growing body of evidence that policies that reduce segregation may have meaningful health benefits.

Sleep duration and obesity among adolescents transitioning to adulthood: Do results differ by sex?

OBJECTIVES To examine the association between short sleep duration and obesity among adolescents (mean age 16 years) transitioning into young adulthood (mean age 21 years) in the National Longitudinal Study of Adolescent Health (N = 10,076). STUDY DESIGN Self-reported sleep duration was categorized as <6, 6-8, or >8 hours. Obesity status, using measured height and weight, was defined as body mass index ≥95th percentile in adolescence and body mass index ≥30 kg/m(2) in young adulthood. RESULTS Cross-sectionally, short sleep duration was associated with obesity in adolescent males (prevalence ratio 1.8 [95% CI, 1.3-2.4]) but not in females (prevalence ratio 1.0 [95% CI, 0.7-1.4]). In longitudinal analyses, short sleep duration in adolescence was associated with incident obesity in both males and females (risk ratio 1.2 [95% CI, 1.0-1.6]) in young adulthood. No interactions by sex were noted. CONCLUSIONS Analyzing the association of sleep duration and obesity longitudinally resolved sex discrepancies observed in earlier cross-sectional analyses. Optimizing sleep duration during adolescence may be an effective intervention to prevent excess weight gain in young adults.

Trends in Inpatient and Outpatient Hysterectomy and Oophorectomy Rates Among Commercially Insured Women in the United States, 2000-2014.

Trends in Inpatient and Outpatient Hysterectomy and Oophorectomy Rates Among Commercially Insured Women in the United States, 2000-2014 A hysterectomy is the second most common surgical procedure among women in the United States, with approximately 600 000 performed annually for benign gynecologic conditions.1 Trends in hysterectomy rates are an important marker for innovation and quality in gynecology as treatment alternatives increase and as evidence of the underuse of these treatment alternatives emerges.2 The accurate identification of a hysterectomy requires capturing data from both inpatient and outpatient services, given the shifting setting of care over recent years. Yet, the highest-quality national trend estimates have been significantly limited by the exclusion of data on outpatient procedures due to the use of databases restricted to inpatient settings.3,4 Prior studies that included inpatient and outpatient settings have focused on small geographic areas only, limiting their generalizability.5 The lack of national outpatient data is a critical gap because the rapid dissemination of robotic surgery has likely shifted the proportion of hysterectomies that are performed in outpatient settings. The same shifting pattern may also be true for an oophorectomy, another common procedure among US women. As with hysterectomy rates, the ability to analyze trends in oophorectomy rates is limited by the use of data restricted to inpatient settings.

Selection bias: A missing factor in the obesity paradox debate

Dear Drs. Ravussin and Ryan: The September issue of Obesity featured articles by Tobias and Hu (1) and Flegal and KalantarZadeh (2) that explored the observation that, in clinical populations, such as individuals with heart failure, chronic kidney disease, or diabetes, those with higher BMI often have lower mortality rates than leaner individuals. The articles disagree whether this phenomenon, known as the obesity paradox, is a true causal effect. Flegal and KalantarZadeh assert that the research on the obesity paradox is consistent with greater BMI conferring “modest survival advantages” (2). Tobias and Hu disagree, arguing that the obesity paradox is likely an “artifact of methodological limitations” (1).