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
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
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
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
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
Plasma lipid levels are important risk factors for cardiovascular disease and are influenced by genetic and environmental factors. Recent genome wide association studies (GWAS) have identified several lipid-associated loci, but these loci have been identified primarily in European populations. In order to identify genetic markers for lipid levels in a Chinese population and analyze the heterogeneity between Europeans and Asians, especially Chinese, we performed a meta-analysis of two genome wide association studies on four common lipid traits including total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL) and high-density lipoprotein cholesterol (HDL) in a Han Chinese population totaling 3,451 healthy subjects. Replication was performed in an additional 8,830 subjects of Han Chinese ethnicity. We replicated eight loci associated with lipid levels previously reported in a European population. The loci genome wide significantly associated with TC were near DOCK7, HMGCR and ABO; those genome wide significantly associated with TG were near APOA1/C3/A4/A5 and LPL; those genome wide significantly associated with LDL were near HMGCR, ABO and TOMM40; and those genome wide significantly associated with HDL were near LPL, LIPC and CETP. In addition, an additive genotype score of eight SNPs representing the eight loci that were found to be associated with lipid levels was associated with higher TC, TG and LDL levels (P = 5.52×10-16, 1.38×10-6 and 5.59×10-9, respectively). These findings suggest the cumulative effects of multiple genetic loci on plasma lipid levels. Comparisons with previous GWAS of lipids highlight heterogeneity in allele frequency and in effect size for some loci between Chinese and European populations. The results from our GWAS provided comprehensive and convincing evidence of the genetic determinants of plasma lipid levels in a Chinese population.
Adiponectin, particularly high-molecular weight adiponectin, and resistin are recently discovered adipokines that may provide a molecular link between adiposity and type 2 diabetes.
To evaluate whether total and high-molecular weight adiponectin and resistin are associated with the future risk for type 2 diabetes, independent of obesity and other known diabetes risk factors.
Prospective, nested case-control study.
1,038 initially healthy women of the Nurses’ Health Study who developed type 2 diabetes after blood sampling (1989–1990) through 2002 and 1,136 matched control subjects.
Plasma concentrations of adipokines were measured by enzyme-linked immunosorbent assays.
In multivariate models adjusting for diabetes risk factors including body-mass index (BMI), both higher total and high-molecular weight adiponectin levels were associated with a substantially lower risk for type 2 diabetes. The odds ratios comparing the highest with the lowest quintiles were 0.17 (95% CI, 0.12–0.25) for total adiponectin and 0.10 (CI, 0.06–0.15) for high-molecular weight adiponectin. In addition, a higher high-molecular weight-to-total adiponectin ratio was associated with a significantly lower risk even after adjusting for total adiponectin (odds ratio, 0.45 [CI, 0.31–0.65]). In the multivariate model adjusting for diabetes risk factors except BMI, high resistin levels were significantly associated with an increased diabetes risk for (odds ratio, 1.68 [CI, 1.25–2.25]). However, after additional adjustment for BMI, this association was no longer statistically significant (odds ratio, 1.28 [CI, 0.93–1.76]).
Residual confounding by imperfectly or unmeasured confounders cannot be excluded.
These results indicate that adiponectin, but not resistin is strongly associated with diabetes risk independent of BMI. The high-molecular weight-to-total adiponectin ratio is related to diabetes risk independent of total adiponectin, suggesting an important role of the relative proportion of high-molecular weight adiponectin in diabetes pathogenesis.
Genome-wide association studies have identified novel type 2 diabetes loci, each of which has a modest impact on risk.
To examine the joint effects of several type 2 diabetes risk variants and their combination with conventional risk factors on type 2 diabetes risk in 2 prospective cohorts.
Nested case–control study.
2809 patients with type 2 diabetes and 3501 healthy control participants of European ancestry from the Health Professionals Follow-up Study and Nurses’ Health Study.
A genetic risk score (GRS) was calculated on the basis of 10 polymorphisms in 9 loci.
After adjustment for age and body mass index (BMI), the odds ratio for type 2 diabetes with each point of GRS, corresponding to 1 risk allele, was 1.19 (95% CI, 1.14 to 1.24) and 1.16 (CI, 1.12 to 1.20) for men and women, respectively. Persons with a BMI of 30 kg/m2 or greater and a GRS in the highest quintile had an odds ratio of 14.06 (CI, 8.90 to 22.18) compared with persons with a BMI less than 25 kg/m2 and a GRS in the lowest quintile after adjustment for age and sex. Persons with a positive family history of diabetes and a GRS in the highest quintile had an odds ratio of 9.20 (CI, 5.50 to 15.40) compared with persons without a family history of diabetes and with a GRS in the lowest quintile. The addition of the GRS to a model of conventional risk factors improved discrimination by 1% (P < 0.001).
The study focused only on persons of European ancestry; whether GRS is associated with type 2 diabetes in other ethnic groups remains unknown.
Although its discriminatory value is currently limited, a GRS that combines information from multiple genetic variants might be useful for identifying subgroups with a particularly high risk for type 2 diabetes.
The role of weight training in the primary prevention of type 2 diabetes is largely unknown. We examined the association of weight training with risk of type 2 diabetes among U.S. men and assessed the influence of combining weight training and aerobic exercise.
We performed a prospective cohort study among 32,002 men from the Health Professionals Follow-up Study that were followed from 1990 until 2008. Weekly time spent on weight training and aerobic exercise (including brisk walking, jogging, running, bicycling, swimming, tennis, squash, calisthenics/rowing) was obtained from questionnaires at baseline and biennially during follow-up.
During 508,332 person years of follow-up (18 years), we documented 2,278 new cases of type 2 diabetes. In multivariable adjusted models, we observed a dose-response relationship between an increasing amount of time spent on weight training or aerobic exercise and lower risk of diabetes (p for trend<0.001). Engaging in weight training or aerobic exercise of at least 150 min/week was independently associated with a lower risk of diabetes of 34% (95% CI 7 – 54%) and 52% (95% CI 45 – 58%), respectively. Men who engaged in both aerobic exercise and weight training of at least 150 min/week had the greatest reduction in type 2 diabetes risk (59%, 95% CI 39 – 73%).
Weight training was associated with a significantly lower risk of type 2 diabetes, independent of aerobic exercise. The combination of weight training and aerobic exercise conferred a greater benefit.
Type 2 diabetes (T2D) has become a leading health problem throughout the world. It is caused by both environmental and genetic factors and interactions between them. However, until very recently, the T2D susceptibility genes have been poorly understood. During the past 5 years, with the advent of genome-wide association studies (GWAS), a total of 58 T2D susceptibility loci have been associated with T2D risk at a genome-wide significance level (P <5×10−8) and evidence shows that most of these genetic variants influence pancreatic β-cell function. Most novel T2D susceptibility loci were identified through GWAS in European populations and later confirmed in other ethnic groups. Although the recent discovery of novel T2D susceptibility loci has contributed substantially to our understanding of the pathophysiology of the disease, clinical utility of these loci in disease prediction and prognosis is limited. More studies using multiethnic meta-analysis, gene-environment interaction analysis, sequencing analysis, epigenetic analysis, and functional experiments are needed to identify new susceptibility T2D loci and causal variants and to establish biological mechanisms.
Europeans; Genetics; Genome-wide association studies; Type 2 diabetes
Red meat consumption has been associated with an increased risk of chronic diseases. However, its relationship with mortality remains uncertain.
We prospectively followed 37698 men from the Health Professionals Follow-up Study (1986-2008) and 83644 women from the Nurses' Health Study (1980-2008), who were free of cardiovascular disease (CVD) and cancer at baseline. Diet was assessed by validated food-frequency questionnaires and updated every four years.
We documented 23926 deaths (including 5910 CVD and 9464 cancer deaths) during 2.96 million person-years of follow-up. After multivariate adjustment for major lifestyle and dietary risk factors, the pooled hazard ratio (HR) and 95% confidence interval of total mortality was 1.13 (1.07-1.20) for 1-serving per day increase of unprocessed red meat, 1.20 (1.15-1.24) for processed red meat. The corresponding HRs were 1.18 (1.13-1.23) and 1.21 (1.13-1.31) for CVD mortality, 1.10 (1.06-1.14) and 1.16 (1.09-1.23) for cancer mortality. We estimated that substitutions of 1-serving per day of other foods (including fish, poultry, nuts, legumes, low-fat dairy, and whole grains) for 1-serving per day of red meat were associated with a 7%-19% lower mortality risk. We also estimated that 9.3% of deaths in men and 7.6% in women in our cohorts could be prevented at the end of follow-up if all individuals consumed <0.5 serving/d (≈42 g/d) of red meat.
Red meat consumption is associated with an increased risk of total, CVD and cancer mortality. Substitution of other healthy protein sources for red meat is associated with a lower mortality risk.
cardiovascular disease risk factors; China; diabetes mellitus type 2; diet; Editorials; nutrition
Epidemiological studies have repeatedly investigated the association between depression and metabolic syndrome (MetS). However, the results have been inconsistent. This meta-analysis aimed to summarize the current evidence from cross-sectional and prospective cohort studies that evaluated this association.
RESEARCH DESIGN AND METHODS
MEDLINE, EMBASE, and PsycINFO databases were searched for articles published up to January 2012. Cross-sectional and cohort studies that reported an association between the two conditions in adults were included. Data on prevalence, incidence, unadjusted or adjusted odds ratio (OR), and 95% CI were extracted or provided by the authors. The pooled OR was calculated separately for cross-sectional and cohort studies using random-effects models. The I2 statistic was used to assess heterogeneity.
The search yielded 29 cross-sectional studies (n = 155,333): 27 studies reported unadjusted OR with a pooled estimate of 1.42 (95% CI 1.28–1.57; I2 = 55.1%); 11 studies reported adjusted OR with depression as the outcome (1.27 [1.07–1.57]; I2 = 60.9%), and 12 studies reported adjusted OR with MetS as the outcome (1.34 [1.18–1.51]; I2 = 0%). Eleven cohort studies were found (2 studies reported both directions): 9 studies (n = 26,936 with 2,316 new-onset depression case subjects) reported adjusted OR with depression as the outcome (1.49 [1.19–1.87]; I2 = 56.8%), 4 studies (n = 3,834 with 350 MetS case subjects) reported adjusted OR with MetS as the outcome (1.52 [1.20–1.91]; I2 = 0%).
Our results indicate a bidirectional association between depression and MetS. These results support early detection and management of depression among patients with MetS and vice versa.
Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes. Few studies have tested for a relationship with coronary heart disease (CHD), or intermediate biomarkers. The role of artificially sweetened beverages is also unclear.
Methods and Results
We performed an analysis of the Health Professionals Follow-up study, a prospective cohort study including 42 883 men. Associations of cumulatively averaged sugar-sweetened (e.g. sodas) and artificially sweetened (e.g. diet sodas) beverage intake with incident fatal and non-fatal CHD (myocardial infarction) were examined using proportional hazard models. There were 3683 CHD cases over 22 years of follow-up. Participants in the top quartile of sugar-sweetened beverage intake had a 20% higher relative risk of CHD than those in the bottom quartile (RR=1.20, 95% CI: 1.09, 1.33, p for trend < 0.01) after adjusting for age, smoking, physical activity, alcohol, multivitamins, family history, diet quality, energy intake, BMI, pre-enrollment weight change and dieting. Artificially sweetened beverage consumption was not significantly associated with CHD (multivariate RR=1.02, 95% CI: 0.93, 1.12, p for trend = 0.28). Adjustment for self-reported high cholesterol, high triglycerides, high blood pressure and diagnosed type 2 diabetes slightly attenuated these associations. Intake of sugar-sweetened but not artificially sweetened beverages was significantly associated with increased triglycerides, CRP, IL6, TNFr1, TNFr2, decreased HDL, Lp(a), and leptin (p values < 0.02).
Consumption of sugar-sweetened beverages was associated with increased risk of CHD and some adverse changes in lipids, inflammatory factors, and leptin. Artificially sweetened beverage intake was not associated with CHD risk or biomarkers.
nutrition; myocardial infarction; inflammation; lipids; epidemiology
Although it has been hypothesized that the depression-obesity relation is bidirectional, few studies have addressed this hypothesis in a prospective setting. We aimed to examine the bidirectional relationship in middle-aged and elderly women.
A total of 65,955 women aged 54–79 years in the Nurses’ Health Study were prospective followed from 1996 to 2006 with updated information on body weight, depression status and various covariates every two years. Depression was defined as self-report of physician-diagnosed depression and/or antidepressant use. Obesity was defined as a body mass index ≥30.0 kg/m2. The first three waves (1996–2000) were used as the baseline period, and the last three waves (2002–2006) were used as the follow-up period.
After adjusting for baseline age, physical activity, comorbidities, body mass index (BMI) and other covariates, depression at the baseline period was associated with an increased risk of obesity at the follow-up period in all women (multivariate-adjusted odds ratio [OR], 1.38; 95% CI, 1.24–1.53) and baseline non-obese women (OR, 1.51; 95% CI, 1.36–1.67). In the opposite direction, after adjusting for baseline age, physical activity, comorbidities, depression status and other covariates, obese women at baseline had a moderately increased risk of depression at the follow-up period compared with normal weight women (OR, 1.11; 95% CI, 1.03–1.18); and this association was similar for new onset of depression (OR for obese vs. normal weight women, 1.10; 95% CI, 1.02–1.20).
Our results suggest a bidirectional association between depression and obesity in middle-aged and elderly women. Future studies are needed to confirm our findings in different populations, and investigate the potential mechanisms underlying this association. Our results underscore the importance of early detection and proper behavioral modifications to lower the burden of both conditions.
obesity; depression; prospective cohort study
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
Women with a history of gestational diabetes mellitus (GDM) are at higher risk of developing type 2 diabetes (T2DM); however, little is known about the association between other common pregnancy complications (eg, preterm birth, macrosomia) and T2DM risk. We examined the associations between first-pregnancy preterm, postterm birth, low birth weight, and macrosomia with subsequent risk of T2DM.
We conducted a prospective cohort study of Nurses’ Health Study II (NHSII) participants; 51,728 women in the study had a single live birth and complete pregnancy history. NHSII confirmed incident diabetes mellitus through supplemental questionnaires. Participants were followed from year of first birth until 2005. We defined gestational age as very preterm (20 to ≤32 weeks), moderate preterm (33 to ≤37 weeks), term (38 to ≤42 weeks), and postterm (≥43 weeks). We defined low birth weight as an infant born at term weighing less than 5.5 pounds, and we defined macrosomia as an infant born at term weighing 10 pounds or more. We used Cox proportional hazards models, adjusting for potential confounders.
Women with a very preterm birth (2%) had an increased T2DM risk (adjusted hazard ratio, 1.34; 95% confidence interval [CI], 1.05–1.71). This increased risk emerged in the decade following pregnancy. Macrosomia (1.5%) was associated with a 1.61 increased T2DM risk, after adjusting for risk factors, including GDM (95% CI, 1.24–2.08). This association was apparent within the first 5 years after pregnancy. Moderate preterm and term low birth weight did not significantly increase the risk of T2DM over the 35-year follow-up time.
Women who experienced a very preterm birth or had an infant that weighed 10 pounds or more may benefit from lifestyle intervention to reduce T2DM risk. If replicated, these findings could lead to a reduced risk of T2DM through improved primary care for women experiencing a preterm birth or an infant of nonnormal birth weight.
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.
Several studies have suggested that depression is associated with an increased risk of stroke; however, the results are inconsistent.
To conduct a systematic review and meta-analysis of prospective studies assessing the association between depression and risk of developing stroke in adults.
A search of MEDLINE, EMBASE, and PsychINFO databases (to May 2011) was supplemented by manual searches of bibliographies of key retrieved articles and relevant reviews.
We included prospective cohort studies that reported risk estimates of stroke morbidity or mortality by baseline or updated depression status assessed by self-reported scales or clinician diagnosis.
Two independent reviewers extracted data on depression status at baseline, risk estimates of stroke, study quality, and methods used to assess depression and stroke. Hazard ratios (HRs) were pooled using fixed-effect or random-effects models when appropriate. Associations were tested in subgroups representing different participant and study characteristics. Publication bias was evaluated with funnel plots and Begg test.
The search yielded 28 prospective cohort studies (n = 317540 participants) that reported 8478 stroke cases (morbidity and mortality) during a follow-up period ranging from 2 to 29 years. The pooled adjusted HRs were 1.45 (95% confidence interval [CI], 1.29–1.63; P-for-heterogeneity <0.001; random-effects model) for total stroke, 1.55 (1.25–1.93; P-for-heterogeneity = 0.31; fixed-effects model) for fatal stroke (8 studies), and 1.25 (1.11–1.40; P-for-heterogeneity = 0.34; fixed-effects model) for ischemic stroke (6 studies). The estimated absolute risk differences associated with depression were 106 cases for total stroke, 53 cases for ischemic stroke, and 22 cases for fatal stroke per 100 000 individuals per year. The increased risk of total stroke associated with depression was consistent across most subgroups.
Depression is associated with a significantly increased risk of stroke morbidity and mortality.