Background The extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain.
Methods We calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual–participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies.
Results For people born between 1900 and 1960, mean adult height increased 0.5–1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96–0.99) for death from any cause, 0.94 (0.93–0.96) for death from vascular causes, 1.04 (1.03–1.06) for death from cancer and 0.92 (0.90–0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12–1.42) for risk of melanoma death to 0.84 (0.80–0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators.
Conclusion Adult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.
Height; cardiovascular disease; cancer; cause-specific mortality; epidemiological study; meta-analysis
Considerable controversy exists regarding the association between coffee consumption and cardiovascular disease (CVD) risk. A meta-analysis was performed to assess the dose-response relationship of long-term coffee consumption with CVD risk.
Methods and Results
Pubmed and EMBASE were searched for prospective cohort studies of the relationship between coffee consumption and CVD risk, which included coronary heart disease, stroke, heart failure, and CVD mortality. Thirty-six studies were included with 1,279,804 participants and 36,352 CVD cases. A non-linear relationship of coffee consumption with CVD risk was identified (P for heterogeneity = 0.09, P for trend < 0.001, P for non-linearity < 0.001). Compared with the lowest category of coffee consumption (median: 0 cups/d), the relative risk of CVD was 0.95 (95% CI, 0.87 to 1.03) for the highest (median: 5 cups/d) category, 0.85 (0.80 to 0.90) for the second highest (median: 3.5 cups/d), and 0.89 (0.84 to 0.94) for the third highest category (median: 1.5 cups/d). Looking at separate outcomes, coffee consumption was non-linearly associated with both CHD (P for heterogeneity = 0.001, P for trend < 0.001, P for non-linearity < 0.001) and stroke risks (P for heterogeneity = 0.07, P for trend < 0.001, P for non-linearity< 0.001) (P for trend differences > 0.05).
A non-linear association between coffee consumption with CVD risk was observed in this meta-analysis. Moderate coffee consumption was inversely significantly associated with CVD risk, with the lowest CVD risk at 3 to 5 cups/d, and heavy coffee consumption was not associated with elevated CVD risk.
coffee; cardiovascular disease; meta-analysis
Prolonged television (TV) viewing is the most prevalent and pervasive sedentary behavior in industrialized countries and has been associated with morbidity and mortality. However, a systematic and quantitative assessment of published studies is not available.
To perform a meta-analysis of all prospective cohort studies to determine the association between TV viewing and risk of type 2 diabetes, fatal or nonfatal cardiovascular disease, and all-cause mortality.
Data Sources and Study Selection
Relevant studies were identified by searches of the MEDLINE database from 1970 to March 2011 and the EMBASE database from 1974 to March 2011 without restrictions and by reviewing reference lists from retrieved articles. Cohort studies that reported relative risk estimates with 95% confidence intervals (CIs) for the associations of interest were included.
Data were extracted independently by each author and summary estimates of association were obtained using a random-effects model.
Of the 8 studies included, 4 reported results on type 2 diabetes (175 938 individuals; 6428 incident cases during 1.1 million person-years of follow-up), 4 reported on fatal or nonfatal cardiovascular disease (34 253 individuals; 1052 incident cases), and 3 reported on all-cause mortality (26 509 individuals; 1879 deaths during 202 353 person-years of follow-up). The pooled relative risks per 2 hours of TV viewing per day were 1.20 (95% CI, 1.14-1.27) for type 2 diabetes, 1.15 (95% CI, 1.06-1.23) for fatal or nonfatal cardiovascular disease, and 1.13 (95% CI, 1.07-1.18) for all-cause mortality. While the associations between time spent viewing TV and risk of type 2 diabetes and cardiovascular disease were linear, the risk of all-cause mortality appeared to increase with TV viewing duration of greater than 3 hours per day. The estimated absolute risk differences per every 2 hours of TV viewing per day were 176 cases of type 2 diabetes per 100 000 individuals per year, 38 cases of fatal cardiovascular disease per 100 000 individuals per year, and 104 deaths for all-cause mortality per 100 000 individuals per year.
Prolonged TV viewing was associated with increased risk of type 2 diabetes, cardiovascular disease, and all-cause mortality.
The benefits of moderate alcohol consumption for type 2 diabetes have been postulated to involve a mechanism of improved insulin sensitivity. Fetuin-A, which is known to inhibit insulin signalling, has emerged as a biomarker for diabetes risk. Alcohol consumption may influence circulating fetuin-A concentrations and subsequently diabetes risk by altering the insulin signal. We therefore hypothesised that moderate alcohol consumption would be associated with lower fetuin-A concentration and that fetuin-A would partly explain the association between alcohol consumption and incident type 2 diabetes.
Among diabetes-free female participants in the Nurses’ Health Study (n=1331), multiple linear regression was conducted to assess the association between alcohol consumption and plasma fetuin-A. Least-squares means (lsmeans) of fetuin-A were estimated in categories of alcohol consumption (0, 0.1-4.9, 5-14.9 and ≥15 g/day). The proportion of alcohol consumption and diabetes association explained by baseline fetuin-A was assessed in 470 matched incident diabetes case–control pairs with follow-up 2000-2006.
Higher alcohol consumption was associated with lower plasma fetuin-A (p for trend=0.009): lsmean±SE 476.5±5.9 μg/ml for abstainers, 468.9±5.2 μg/ml for 0.1-4.9 g/day consumers, 455.9±7.0 μg/ml for 5.0-14.9 g/day consumers, and 450.0±9.4 μg/ml for ≥15.0 g/day consumers. Fetuin-A and fasting insulin explained 18.4% and 54.8%, respectively, of the inverse association between alcohol consumption and diabetes after multiple adjustment (both p for contribution <0.04).
Moderate alcohol consumption is associated with lower plasma fetuin-A in diabetes-free women. Fetuin-A and insulin explain a significant proportion of the association between alcohol consumption and incident type 2 diabetes. Further studies are needed to examine potential biological mechanisms underlying this association.
Alcohol; Fetuin-A; Insulin sensitivity; Type 2 diabetes
Insomnia complaints are common in older adults and may be associated with mortality risk. However, evidence regarding this association is mixed. We thus prospectively examined whether men with insomnia symptoms had an increased risk of mortality during 6 years of follow-up.
Methods and Results
A prospective cohort study of 23,447 US men participating in the Health Professionals Follow-up Study and free of cancer, reported on insomnia symptoms in 2004 were followed through 2010. Deaths were identified from state vital statistic records, the National Death Index, family reports, and the postal system. We documented 2025 deaths during 6 years of follow-up (2004-2010). The multivariable-adjusted hazard ratios (HRs) of total mortality were 1.25 (95% confidence interval (CI):1.04-1.50) for difficulty initiating sleep, 1.09 (95%CI:0.97-1.24) for difficulty maintaining sleep, 1.04 (95%CI:0.88-1.22) for early-morning awakenings, and 1.24 (95%CI:1.05-1.46) for non-restorative sleep, comparing men with those symptoms most of the time to men without those symptoms, after adjusting for age, lifestyle factors and presence of common chronic conditions. Men with difficulty initiating sleep and non-restorative sleep most of the time had a 55% (HR:1.55; 95% CI:1.19-2.04; P-trend= 0.01) and 32% (HR:1.32; 95% CI:1.02-1.72; P-trend=0.002) increased risk of CVD mortality, respectively, relative to men without those symptoms.
Some insomnia symptoms, especially difficulty initiating asleep and non-restorative sleep, are associated with a modestly higher risk of mortality.
Mortality; Sleep Disorders; Cardiovascular Outcomes; Insomnia
diet; cardiovascular disease prevention; diabetes mellitus; nutrition; epidemiology; nuts; grains; cocoa; coffee; legumes
Red meat consumption has been consistently associated with an increased risk of type 2 diabetes. However, whether changes in red meat intake are related to subsequent type 2 diabetes risk remains unknown.
We evaluated the association between changes in red meat consumption during a 4-year period and subsequent 4-year risk of type 2 diabetes in US adults.
Design, setting and participants
We followed 26,357 men in the Health Professionals Follow-up Study (HPFS, 1986–2006), 48,709 women in the Nurses’ Health Study (NHS, 1986–2006) and 74,077 women in NHS II (1991–2007). Diet was assessed by validated food frequency questionnaires and updated every 4 years. Time-dependent Cox proportional hazard models were used to calculate hazard ratios (HRs) with adjustment for age, family history, race, marital status, initial red meat consumption, initial and changes in other lifestyle factors (physical activity, smoking status, alcohol intake, energy intake, and dietary quality). Results across cohorts were pooled by inverse-variance-weighted fixed-effect meta-analyses.
Main Outcome Measure
Incident T2D cases validated by supplementary questionnaires.
During 1,965,824 person-years of follow-up, we documented 7,540 incident type 2 diabetes cases. In the multivariate-adjusted models, increasing red meat intake during a 4-year interval was associated with an elevated risk of type 2 diabetes over the subsequent four years in each cohort (all P-trend <0.001): compared with the reference group of no change in red meat intake, increasing red meat intake of >0.5 serving/d was associated with a 48% (pooled HR, 1.48; 95% CI, 1.37–1.59) elevated risk in the subsequent 4-year period, and the association was modestly attenuated after further adjustment for initial body mass index and concurrent weight gain (1.30; 95% CI, 1.21–1.41). A reduction of red meat consumption of >0.5 serving/day from baseline to the first four years of follow-up was associated with a 14% (95% CI, 7%–20%) lower risk during subsequent follow-up through 2006/2007.
Increasing red meat consumption over time is associated with an elevated subsequent risk of type 2 diabetes, and the association is partly mediated by body weight. Our results add further evidence that limiting red meat consumption over time confers benefits for diabetes prevention.
red meat; diabetes; prospective cohort study
Obesity, a major public health concern, is a multifactorial disease caused by both environmental and genetic factors. Although recent genome-wide association studies have identified many loci related to obesity or body mass index, the identified variants explain only a small proportion of the heritability of obesity. Better understanding of the interplay between genetic and environmental factors is the basis for developing effective personalized obesity prevention and management strategies. This article reviews recent advances in identifying gene-environment interactions related to obesity and describes epidemiological designs and newly developed statistical approaches to characterizing and discovering gene-environment interactions on obesity risk.
Excess body weight and adiposity cause insulin resistance, inflammation, and numerous other alterations in metabolic and hormonal factors that promote atherosclerosis, tumorigenesis, neurodegeneration, and aging. Studies in both animals and humans have demonstrated a beneficial role of dietary restriction and leanness in promoting health and longevity. Epidemiological studies have found strong direct associations between increasing body mass index (BMI) and risks of developing type 2 diabetes, cardiovascular disease, and several types of cancer, beginning from BMI of 20–21 kg m−2. Although a recent meta-analysis suggests that overweight individuals have significantly lower overall mortality than normal-weight individuals, these data are likely to be an artifact produced by serious methodological problems, especially confounding by smoking, reverse causation due to existing chronic disease, and nonspecific loss of lean mass and function in the frail elderly. From a clinical and public health point of view, maintaining a healthy weight through diet and physical activity should remain the cornerstone in the prevention of chronic diseases and the promotion of healthy aging.
body mass index; calorie intake; disease prevention; health; obesity
Previous studies found normal weight compared to overweight/obese adults with type 2 diabetes had a higher mortality risk, and body-mass index (BMI)–mortality studies do not typically account for baseline diabetes status.
To determine if diabetes influences the BMI–mortality relationship.
Using a prospective study design, we analyzed data from a nationally representative sample of US adults participating in the National Health Interview Survey from 1997 to 2002, and followed for mortality through 2006.
Excluding those with heart disease or cancer, our final analytic sample included 74,710 (34,805 never smoker) adults.
BMI was calculated from self-reported height and weight. Diabetes status was based on self-reported diagnosis from a health professional. We used direct age standardization to calculate all-cause mortality rates and adjusted Cox models for all-cause mortality hazard ratios by BMI quintile; this was done separately for adults with diabetes and without diabetes.
Among never smokers, mean age was 50.1 years and 43 % were men. Mean BMI was 27.4 kg/m2, 26 % were obese, and 2,035 (5 %) reported diagnosed diabetes. After 9 years, there were 4,355 deaths (754 of 4,740 with diabetes; 3,601 of 69,970 without) among 74,710 participants, and 1,238 (247 of 2,035 with diabetes; 991 of 32,770 without) among 34,805 never smokers. We observed a qualitative interaction with diabetes on the BMI–mortality relationship (p = 0.002). Death rates were substantially higher among participants with diabetes compared to those without diabetes across all BMI quintiles. However, death rates in participants with diabetes fell with increasing BMI quintile, while rates followed a J-shaped curve among those without diabetes. In adjusted Cox models, BMI was positively associated with mortality in adults without diabetes, but inversely associated with mortality among participants with diabetes.
Mortality increased with increasing BMI in adults without diabetes, but decreased with increasing BMI among their counterparts with diabetes. Future studies need to be better designed to answer the question of whether normal weight adults with diabetes have a higher risk of mortality, by minimizing the possibility of reverse causation. Future studies should also account for prevalent diabetes in all investigations of the BMI–mortality relationship.
Electronic supplementary material
The online version of this article (doi:10.1007/s11606-013-2553-7) contains supplementary material, which is available to authorized users.
diabetes; body mass index; mortality
Fetuin-A, a protein secreted primarily by the liver, has been associated with non-alcoholic fatty liver disease and insulin resistance. In a recent study, higher circulating fetuin-A was associated with cardiovascular events, particularly ischemic stroke. However, these data have not been replicated.
A nested case-control design was utilized to examine the relationship between fetuin-A and ischemic stroke among female participants of the Nurses’ Health Study. Fetuin-A was measured in blood samples collected and stored between 1989–1990. A total of 459 incident cases of ischemic stroke were identified and confirmed by medical records according to the National Survey of Stroke criteria between 1990–2006 and matched to 459 controls by age, menopausal status, postmenopausal hormone use, and smoking status. The association between fetuin-A and ischemic stroke was modeled using conditional logistic regression.
Circulating Fetuin-A was higher in women (P<0.01), who reported increased body mass index (BMI≥25 kg/m2), total cholesterol ≥200 mg/dL, high-sensitivity C-reactive protein ≥3 mg/L and current hormone use at baseline. Significant partial Spearman correlations (P<0.001), adjusted for matching factors, were found between measured concentrations of fetuin-A and triglycerides (r=0.20), C-reactive protein (r=0.14), and BMI (r=0.15). Fetuin-A quartiles were not significantly associated with increased risk of incident ischemic stroke when adjusted for matching factors (RR=1.03; 95% CI: 0.69–1.54, extreme quartiles); additional adjustment for lifestyle factors or CVD risk factors and biomarkers did not alter results.
In this sample of women, fetuin-A was not significantly associated with risk of ischemic stroke. Further research is needed to explore this association.
Ischemic stroke; fetuin-A; α2-Heremans-Schmid glycoprotein
Very long-chain saturated fatty acids (VLSFAs) are saturated fatty acids with 20 or more carbons. In contrast to the more abundant saturated fatty acids, such as palmitic acid, there is growing evidence that circulating VLSFAs may have beneficial biological properties. Whether genetic factors influence circulating levels of VLSFAs is not known. We investigated the association of common genetic variation with plasma phospholipid/erythrocyte levels of three VLSFAs by performing genome-wide association studies in seven population-based cohorts comprising 10,129 subjects of European ancestry. We observed associations of circulating VLSFA concentrations with common variants in two genes, serine palmitoyl-transferase long-chain base subunit 3 (SPTLC3), a gene involved in the rate-limiting step of de novo sphingolipid synthesis, and ceramide synthase 4 (CERS4). The SPTLC3 variant at rs680379 was associated with higher arachidic acid (20:0 , P = 5.81 × 10−13). The CERS4 variant at rs2100944 was associated with higher levels of 20:0 (P = 2.65 × 10−40) and in analyses that adjusted for 20:0, with lower levels of behenic acid (P = 4.22 × 10−26) and lignoceric acid (P = 3.20 × 10−21). These novel associations suggest an inter-relationship of circulating VLSFAs and sphingolipid synthesis.
arachidic acid; behenic acid; lignoceric acid; sphingolipids
Dietary factors are known to influence colorectal cancer (CRC) risk, however, their association with CRC survival is unclear. Therefore, we prospectively examined the association between diet quality scores, dietary patterns and colorectal cancer (CRC) survival.
1201 women diagnosed with stage I–III CRC between 1986 and 2008, were followed through 2010. Diet was assessed via a food frequency questionnaire administered at least 6 months after diagnosis. We computed the Alternate Healthy Eating Index-2010 (AHEI-2010), alternate Mediterranean Diet score (aMED) and Dietary Approaches to Stop Hypertension score (DASH) and derived two dietary patterns, Western (unhealthy) and prudent (healthy), by principal component analysis for each woman.
During follow-up, we documented 435 deaths, including 162 from CRC. After adjusting for potential confounders, only a higher AHEI-2010 score was significantly associated with lower overall mortality (HR comparing extreme quintiles = 0.71, 95% CI 0.52–0.98, p trend = 0.01) as well as borderline significantly with lower risk of CRC mortality by the trend test (HR Q5 vs Q1 = 0.72, 95% CI = 0.43–1.21, p trend = 0.07). When AHEI-2010 components were examined separately, inverse associations for overall mortality were primarily accounted for by moderate alcohol intake (HR comparing abstainers vs 5–15 g/d = 1.30, 95%CI = 1.05–1.61) and lower intake of sugar sweetened beverages and fruit juices combined (HR for each additional serving = 1.11, 95% CI = 1.01–1.23). No other diet quality score or dietary pattern was associated with overall or CRC-specific mortality.
Higher AHEI-2010 score may be associated with lower overall mortality, moderate alcohol consumption and lower consumption of sugar sweetened beverages and juices combined appeared to account for most of the observed associations.
Little is known about the long-term effects of dietary energy density (ED) on weight gain.
We conducted a prospective study of 50,026 women (mean age: 36.5; SD: 4.6) in the Nurses' Health Study II followed from 1991 to 1999. Dietary ED and body weight were ascertained in 1991, 1995, and 1999. Total dietary ED was calculated by dividing each subject's daily energy intake (kcal) by the reported weight (g) of all foods consumed.
Dietary ED was positively correlated with saturated fat (r=0.16), trans fat (r=0.15), and the glycemic index (r=0.16), but inversely correlated with vegetable protein (r=−0.30), vegetables (r=−0.27), and fruits (r=−0.17). ED was not significantly correlated with total fat intake (r=0.08). Women who increased their dietary ED during follow-up the most (5th quintile) had a statistical significant greater multivariate-adjusted weight gain as compared with those who decreased their dietary ED most (1st quintile) (in the 8-y time period: 6.42 kg versus 4.57 kg; p for trend < 0.001). However, the amount of weight change over time varied considerably according to the ED of individual foods and beverages.
Increases in total dietary ED were associated with long-term weight gain among younger and middle-aged women. However, public health recommendations cannot be made simply based on ED values of individual foods and beverages only. Reducing consumption of foods high in saturated and trans fats and refined carbohydrates and increasing consumption of fruits and vegetables may help to reduce dietary ED and prevent weight gain.
To examine the long-term relationship between changes in water and beverage intake and weight change.
Prospective cohort studies of 50 013 women aged 40-64 in the Nurses’ Health Study (NHS, 1986-2006), 52 987 women aged 27-44 in the NHS II (1991-2007), and 21 988 men aged 40-64 in the Health Professionals Follow-up Study (1986-2006) without obesity and chronic diseases at baseline.
We assessed the association of weight change within each 4-year interval with changes in beverage intakes and other lifestyle behaviors during the same period. Multivariate linear regression with robust variance and accounting for within-person repeated measures were used to evaluate the association. Results across the three cohorts were pooled by an inverse-variance-weighted meta-analysis.
Participants gained an average of 1.45 kg (5th to 95th percentile, −1.87 to 5.46) within each 4-year period. After controlling for age, baseline body mass index, and changes in other lifestyle behaviors (diet, smoking habits, exercise, alcohol, sleep duration, TV watching), each 1-cup/d increment of water intake was inversely associated with weight gain within each 4-year period (−0.13 kg; 95% CI: −0.17, −0.08). The associations for other beverages were: SSBs (0.36 kg; 0.24, 0.48), fruit juice (0.22 kg; 0.15, 0.28), coffee (−0.14 kg; −0.19, −0.09), tea (−0.03 kg; −0.05, −0.01), diet beverages (−0.10 kg; −0.14, −0.06), low-fat milk (0.02 kg; −0.04, 0.09), and whole milk (0.02 kg; −0.06, 0.10). We estimated that replacement of 1 serving/d of SSBs by 1 cup/d of water was associated with 0.49 kg (95% CI: 0.32, 0.65) less weight gain over each 4-year period, and the replacement estimate of fruit juices by water was 0.35 kg (95% CI: 0.23, 0.46). Substitution of SSBs or fruit juices by other beverages (coffee, tea, diet beverages, low-fat and whole milk) were all significantly and inversely associated with weight gain.
Our results suggest that increasing water intake in place of SSBs or fruit juices is associated with lower long-term weight gain.
water; beverage; body weight; prospective cohort study
Systems epidemiology applied to the field of nutrition has potential to provide new insight into underlying mechanisms and ways to study the health effects of specific foods more comprehensively. Human intervention and population-based studies have identified i) common genetic factors associated with several nutrition-related traits and ii) dietary factors altering the expression of genes and levels of proteins and metabolites related to inflammation, lipid metabolism and/or gut microbial metabolism, results of high relevance to metabolic disease. System-level tools applied type 2 diabetes and related conditions have revealed new pathways that are potentially modified by diet and thus offer additional opportunities for nutritional investigations. Moving forward, harnessing the resources of existing large prospective studies within which biological samples have been archived and diet and lifestyle have been measured repeatedly within individual will enable systems-level data to be integrated, the outcome of which will be improved personalized optimal nutrition for prevention and treatment of disease.
nutrition; systems; genomics; transcriptomics; proteomics; metabolomics; type 2 diabetes; obesity; metabolic disease; epidemiology; populations; diet; network; nutrigenetics; nutrigenomics
Few prospective studies have examined separate forms of screen time in relation to adiposity. Our objective was to assess independent relations of television, electronic games (video/computer), and digital versatile disc (DVD)/videos and total screen time with change in adolescent BMI.
Using data from the 2004, 2006, and 2008 waves of the ongoing Growing up Today Study II, we assessed baseline and 2-year change in reported screen time in relation to concurrent change in BMI among 4287 girls and 3505 boys aged 9 to 16 years in 2004. Gender-specific models adjusted for previous BMI, age, race/ethnicity, growth/development, months between questionnaires, and physical activity.
Among girls and boys, each hour per day increase in reported television viewing was associated with a 0.09 increase in BMI (Ps < .001), and each hour per day increase in total screen time was associated with a 0.07 increase among girls and 0.05 increase among boys (Ps < .001). Among girls only, greater baseline television, games, and total screen time and change in DVDs/videos were associated with gains in BMI (Ps < .05). BMI gains associated with change in television and total screen time were stronger among overweight girls than lean girls (Ps-heterogeneity < .001).
Television, which remains the steadiest source of food advertising, was most consistently associated with BMI gains. Among girls, electronic games and DVDs/videos were also related to increased BMI, possibly due to influences of product placements and advergames on diet and/or distracted eating. Adolescents, especially overweight adolescents, may benefit from reduced time with multiple types of media.
television; video games; sedentary lifestyle; BMI; body weight; adolescent; adiposity; longitudinal studies
Obesity is a major public health issue and is associated with increased risk of several cancers, currently a leading cause of mortality. Obese patients undergoing bariatric surgery may allow for evaluation of the effect of intentional excess weight loss on subsequent risk of cancer. We aim to evaluate cancer risk, incidence, and mortality following bariatric surgery.
A comprehensive literature search was conducted using PubMed / MEDLINE and Embase from the inception of both databases to January 2012. Inclusion criteria incorporated all human studies examining oncologic outcomes following bariatric surgery. Two authors independently reviewed selected studies and relevant articles from their bibliographies for data extraction, quality appraisal, and meta-analysis.
Six observational studies (N = 51,740) comparing relative risk (RR) of cancer in obese patients undergoing bariatric surgery versus obese controls were analyzed. Overall, the RR of cancer in obese patients after undergoing bariatric surgery is 0.55 [95% CI: 0.41–0.73, P < 0.0001, I2 = 83%]. The effect of bariatric surgery on cancer risk is modified by gender (P = 0.021). The pooled RR in females is 0.68 [95% CI: 0.60–0.77, P < 0.0001, I2 < 0.1%] while in males is 0.99 [95% CI: 0.74–1.32, P = 0.937, I2 < 0.1%].
Our results suggest that bariatric surgery reduces cancer risk and mortality in formerly obese patients. When stratifying our meta-analysis by gender, the effect of bariatric surgery on oncologic outcomes is protective in women but not in men.
Bariatric; Surgery; Cancer; Oncology; Meta-Analysis
The relation between consumption of different types of dairy and risk of type 2 diabetes (T2D) remains uncertain. Therefore, we aimed to evaluate the association between total dairy and individual types of dairy consumptions and incident T2D in US adults.
We followed 41,436 men in the Health Professionals Follow-Up Study (1986 to 2010), 67,138 women in the Nurses’ Health Study (1980 to 2010), and 85,884 women in the Nurses’ Health Study II (1991 to 2009). Diet was assessed by validated food-frequency questionnaires, and data were updated every four years. Incident T2D was confirmed by a validated supplementary questionnaire.
During 3,984,203 person-years of follow-up, we documented 15,156 incident T2D cases. After adjustment for age, body mass index (BMI) and other lifestyle and dietary risk factors, total dairy consumption was not associated with T2D risk and the pooled hazard ratio (HR) (95% confidence interval (CI)) of T2D for one serving/day increase in total dairy was 0.99 (0.98, 1.01). Among different types of dairy products, neither low-fat nor high-fat dairy intake was appreciably associated with risk of T2D. However, yogurt intake was consistently and inversely associated with T2D risk across the three cohorts with the pooled HR of 0.83 (0.75, 0.92) for one serving/day increment (P for trend <0.001). We conducted a meta-analysis of 14 prospective cohorts with 459,790 participants and 35,863 incident T2D cases; the pooled relative risks (RRs) (95% CIs) were 0.98 (0.96, 1.01) and 0.82 (0.70, 0.96) for one serving total dairy/day and one serving yogurt/day, respectively.
Higher intake of yogurt is associated with a reduced risk of T2D, whereas other dairy foods and consumption of total dairy are not appreciably associated with incidence of T2D.
Electronic supplementary material
The online version of this article (doi:10.1186/s12916-014-0215-1) contains supplementary material, which is available to authorized users.
dairy; type 2 diabetes; cohort; meta-analysis
There is indisputable evidence from epidemiologic and clinical studies that being overweight and obese elevates the risk of developing debilitating and costly chronic diseases, including hypertension, hypercholesterolemia, type 2 diabetes, cardiovascular diseases (CVD), and cancer (1). Nonetheless, the relationship between body mass index (BMI) and mortality remains the subject of much debate. A recent meta-analysis concluded that compared to those of normal weight (BMI<25.0), overweight individuals (BMI 25.0–29.9) had a significantly lower mortality risk (2). Even Class 1 obesity (BMI 30–34.9) was associated with marginally reduced mortality. In this Perspective, we discuss why this finding is likely to be an artifact of methodological limitations and what the clinical and public health implications may be.
Obesity; overweight; mortality; reverse causation; chronic disease; body mass index
Background: Health concerns have been raised about rice consumption, which may significantly contribute to arsenic exposure. However, little is known regarding whether habitual rice consumption is associated with cardiovascular disease (CVD) risk.
Objective: We examined prospectively the association of white rice and brown rice consumption with CVD risk.
Design: We followed a total of 207,556 women and men [73,228 women from the Nurses’ Health Study (1984–2010), 92,158 women from the Nurses’ Health Study II (1991–2011), and 42,170 men from the Health Professionals Follow-Up Study (1986–2010)] who were free of CVD and cancer at baseline. Validated semiquantitative food-frequency questionnaires were used to assess consumption of white rice, brown rice, and other food items. Fatal and nonfatal CVD (coronary artery disease and stroke) was confirmed by medical records or self-reports.
Results: During 4,393,130 person-years of follow-up, 12,391 cases of CVD were identified. After adjustment for major CVD risk factors, including demographics, lifestyle, and other dietary intakes, rice consumption was not associated with CVD risk. The multivariable-adjuted HR of developing CVD comparing ≥5 servings/wk with <1 serving/wk was 0.98 (95% CI: 0.84, 1.14) for white rice, 1.01 (0.79, 1.28) for brown rice, and 0.99 (0.90, 1.08) for total rice. To minimize the potential impact of racial difference in rice consumption, we restricted the analyses to whites only and obtained similar results: the HRs of CVD for ≥5 servings/wk compared with <1 serving/wk were 1.04 (95% CI: 0.88, 1.22) for white rice and 1.01 (0.78, 1.31) for brown rice.
Conclusions: Greater habitual consumption of white rice or brown rice is not associated with CVD risk. These findings suggest that rice consumption may not pose a significant CVD risk among the U.S. population when consumed at current amounts. More prospective studies are needed to explore these associations in other populations.
cardiovascular disease; coronary artery disease; longitudinal study; rice; stroke
Emerging in vitro and animal evidence suggests that methylmercury could increase type 2 diabetes, but little evidence exists in humans. We aimed to prospectively determine associations of mercury exposure, as assessed by biomarker measurement, with incident diabetes.
RESEARCH DESIGN AND METHODS
We used neutron activation analysis to measure toenail mercury, an objective biomarker of methylmercury exposure, in 9,267 adults free of diabetes at baseline in two separate U.S. prospective cohorts. Incident diabetes was identified from biennial questionnaires and confirmed by validated supplementary questionnaire using symptoms, diagnostic tests, and medical therapy. Associations of mercury exposure with incident diabetes were assessed using Cox proportional hazards.
During mean ± SD follow-up of 19.7 ± 7.0 years, 1,010 new cases of diabetes were diagnosed. The 95th percentile of toenail mercury was 1.32 μg/g in men and 0.76 μg/g in women, corresponding to exposures ∼3.5-fold and 2-fold higher than the U.S. Environmental Protection Agency reference dose. In multivariable analyses, toenail mercury concentrations were not associated with higher incidence of diabetes in women, men, or both cohorts combined. Comparing the highest to lowest quintile of exposure, the hazard ratio (95% CI) for incident diabetes was 0.86 (0.66–1.11) in women, 0.69 (0.42–1.15) in men, and 0.77 (0.61–0.98) in the combined cohorts. Findings were similar when more extreme categories (deciles) of mercury were compared, and in analyses stratified by fish or omega-3 consumption, BMI, and age.
These findings from two separate large prospective cohorts do not support adverse effects of methylmercury on development of diabetes in men or women at usual levels of exposure seen in these populations.
To examine racial differences in sleep duration and its relationship with diabetes.
RESEARCH DESIGN AND METHODS
We used data from a nationally representative sample of U.S. adults (n = 130,943) participating in the National Health Interview Survey from 2004 to 2011. Usual sleep duration was self-reported and categorized as <7 h (short), 7 h (optimal), and >7 h (long). Diabetes status was based on self-reported diagnosis from a health professional.
Participants’ mean age was 50.6 years, 49% were men, and 13% were black. Compared with whites, blacks were more likely to report short sleep (37 vs. 28%) and less likely to get 7 h of sleep (24 vs. 33%). Diabetes (9,643 cases [9%] in whites and 3,612 cases [15%] in blacks) had a U-shaped distribution with sleep in whites (10, 7, and 9%, for short, optimal, and long sleep, respectively) and blacks (16, 13, and 15%). Suboptimal sleep duration was more strongly associated with diabetes in whites than in blacks among short (prevalence ratio 1.49 [95% CI 1.40–1.58] vs. 1.21 [1.09–1.34]) and long (1.32 [1.25–1.40] vs. 1.11 [1.00–1.23]) sleepers on the relative scale. Adjustment for socioeconomic status (SES) attenuated the short sleep–diabetes association in blacks (1.15 [1.02–1.29]), and the racial/ethnic difference in the short sleep–diabetes association became nonsignificant after SES adjustments.
Suboptimal sleep duration was positively associated with diabetes in blacks and whites, although diabetes prevalence was higher at any level of sleep in blacks. Socioeconomic factors appear to partly explain the association for short sleep in blacks as well as disparity between racial groups.
Many confirmed genetic loci for obesity are expressed in regions of the brain that regulate energy intake and reward-seeking behavior. Whether these loci contribute to the development of specific eating behaviors has not been investigated. We examined the relationship between a genetic susceptibility to obesity and cognitive restraint, uncontrolled and emotional eating.
Design and Methods
Eating behavior and body mass index (BMI) were determined by questionnaires for 1471 men and 2381 women from two U.S cohorts. Genotypes were extracted from genome-wide scans and a genetic-risk score (GRS) derived from 32 obesity-loci was calculated.
The GRS was positively associated with emotional and uncontrolled eating(P<0.002). In exploratory analysis, BMI-increasing variants of MTCH2, TNNI3K and ZC3H4 were positively associated with emotional eating and those of TNNI3K and ZC3H4 were positively associated with uncontrolled eating. The BMI-increasing variant of FTO was positively and those of LRP1B and TFAP2B were inversely associated with cognitive restraint. These associations for single SNPs were independent of BMI but were not significant after multiple-testing correction.
An overall genetic susceptibility to obesity may also extend to eating behaviors. The link between specific loci and obesity may be mediated by eating behavior but larger studies are warranted to confirm these results.
obesity; emotional eating; uncontrolled eating; cognitive restraint; genotype; population