Observational data on the association between egg consumption and risk of type 2 diabetes mellitus (DM) have been inconsistent. Because eggs are a good source of protein and micronutrients and are ...inexpensive, it is important to clarify their role in the risk of developing DM.
We conducted a meta-analysis of published prospective cohort studies to evaluate the relation of egg consumption with the risk of DM.
We searched PubMed, Ovid, Cochrane, and Google Scholar (up to October 2015) to retrieve published studies. We used RRs from extreme categories of egg consumption for the main analysis but also evaluated dose response by using cubic splines and generalized least squares regression.
We identified 12 cohorts for a total of 219,979 subjects and 8911 cases of DM. When comparing the highest with the lowest category of egg intake, pooled multivariate RRs of DM were 1.09 (95% CI: 0.99, 1.20) using the fixed-effect model and 1.06 (95% CI: 0.86, 1.30) using the random-effect model. There was evidence for heterogeneity (I(2) = 73.6%, P < 0.001). When stratified by geographic area, there was a 39% higher risk of DM (95% CI: 21%, 60%) comparing highest with lowest egg consumption in US studies (I(2) = 45.4%, P = 0.089) and no elevated risk of DM with egg intake in non-US studies (RR = 0.89; 95% CI: 0.79, 1.02 using the fixed-effect model, P < 0.001 comparing US with non-US studies). In a dose-response assessment using cubic splines, elevated risk of DM was observed in US studies among people consuming ≥3 eggs/wk but not in non-US studies.
Our meta-analysis shows no relation between infrequent egg consumption and DM risk but suggests a modest elevated risk of DM with ≥3 eggs/wk that is restricted to US studies.
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The use of aspirin in the primary prevention of cardiovascular events remains controversial. We aimed to assess the efficacy and safety of aspirin versus placebo in patients with a moderate estimated ...risk of a first cardiovascular event.
ARRIVE is a randomised, double-blind, placebo-controlled, multicentre study done in seven countries. Eligible patients were aged 55 years (men) or 60 years (women) and older and had an average cardiovascular risk, deemed to be moderate on the basis of the number of specific risk factors. We excluded patients at high risk of gastrointestinal bleeding or other bleeding, or diabetes. Patients were randomly assigned (1:1) with a computer-generated randomisation code to receive enteric-coated aspirin tablets (100 mg) or placebo tablets, once daily. Patients, investigators, and others involved in treatment or data analysis were masked to treatment allocation. The primary efficacy endpoint was a composite outcome of time to first occurrence of cardiovascular death, myocardial infarction, unstable angina, stroke, or transient ischaemic attack. Safety endpoints were haemorrhagic events and incidence of other adverse events, and were analysed in the intention-to-treat population. This study is registered with ClinicalTrials.gov, number NCT00501059.
Between July 5, 2007, and Nov 15, 2016, 12 546 patients were enrolled and randomly assigned to receive aspirin (n=6270) or placebo (n=6276) at 501 study sites. Median follow-up was 60 months. In the intention-to-treat analysis, the primary endpoint occurred in 269 (4·29%) patients in the aspirin group versus 281 (4·48%) patients in the placebo group (hazard ratio HR 0·96; 95% CI 0·81–1·13; p=0·6038). Gastrointestinal bleeding events (mostly mild) occurred in 61 (0·97%) patients in the aspirin group versus 29 (0·46%) in the placebo group (HR 2·11; 95% CI 1·36–3·28; p=0·0007). The overall incidence rate of serious adverse events was similar in both treatment groups (n=1266 20·19% in the aspirin group vs n=1311 20·89% in the placebo group. The overall incidence of adverse events was similar in both treatment groups (n=5142 82·01% vs n=5129 81·72% in the placebo group). The overall incidence of treatment-related adverse events was low (n=1050 16·75% vs n=850 13·54% in the placebo group; p<0·0001). There were 321 documented deaths in the intention-to-treat population (n=160 2·55% vs n=161 2·57% of 6276 patients in the placebo group).
The event rate was much lower than expected, which is probably reflective of contemporary risk management strategies, making the study more representative of a low-risk population. The role of aspirin in primary prevention among patients at moderate risk could therefore not be addressed. Nonetheless, the findings with respect to aspirin's effects are consistent with those observed in the previously published low-risk primary prevention studies.
Bayer.
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To estimate the incidence and lifetime risk (LTR) of Parkinson disease (PD) in a large cohort of men.
Age is the strongest risk factor for PD, but whether its incidence continues to increase after ...age 80 years remains unclear.
Prospective cohort of 21,970 US male physicians aged 40-84 years at baseline who did not report PD before study entry. Participants self-reported PD on yearly follow-up questionnaires, and all deaths were confirmed. We calculated incidence rates and cumulative incidence using a modified Kaplan-Meier analysis. LTR was estimated by adjusting cumulative incidence for competing risks of death.
Five hundred sixty-three cases of PD were identified over 23 years of follow-up. The crude incidence rate of PD was 121 cases/100,000 person-years. Age-specific incidence rates increased sharply beginning at age 60 years, peaked in those aged 85-89 years, and declined beginning at age 90 years. Cumulative incidence substantially overestimated the long-term risk of PD, particularly in those aged 80 years and older. Cumulative incidence was 9.9% (95% confidence interval CI 8.48%-11.30%) from ages 45 to 100 years, whereas LTR for the same period was 6.7% (95% CI 6.01%-7.43%). The incidence and LTR of PD decreased with increasing exposure to smoking.
Our study provides evidence that the incidence of Parkinson disease (PD) in men increases through age 89 years. Whether the subsequent decline represents a true decrease in risk remains to be established. A history of smoking substantially decreased the incidence and lifetime risk of PD. Incidence studies that do not adjust for competing risks of death may overestimate the true risk of PD in the elderly.
Background Observational studies suggested that a diet high in fruits and vegetables, both of which are rich with antioxidants, may prevent cancer development. However, findings from randomized ...trials of the association between antioxidant use and cancer risk have been mostly negative. Methods From 8171 women who were randomly assigned in the Women's Antioxidant Cardiovascular Study, a double-blind, placebo-controlled 2 × 2 × 2 factorial trial of vitamin C (500 mg of ascorbic acid daily), natural-source vitamin E (600 IU of α-tocopherol every other day), and beta carotene (50 mg every other day), 7627 women who were free of cancer before random assignment were selected for this study. Diagnoses and deaths from cancer at a specific site were confirmed by use of hospital reports and the National Death Index. Cox proportional hazards regression models were used to assess hazard ratios (represented as relative risks RRs) of common cancers associated with use of antioxidants, either individually or in combination. Subgroup analyses were conducted to determine if duration of use modified the association of supplement use with cancer risk. All statistical tests were two-sided. Results During an average 9.4 years of treatment, 624 women developed incident invasive cancer and 176 women died from cancer. There were no statistically significant effects of use of any antioxidant on total cancer incidence. Compared with the placebo group, the RRs were 1.11 (95% confidence interval CI = 0.95 to 1.30) in the vitamin C group, 0.93 (95% CI = 0.79 to 1.09) in the vitamin E group, and 1.00 (95% CI = 0.85 to 1.17) in the beta carotene group. Similarly, no effects of these antioxidants were observed on cancer mortality. Compared with the placebo group, the RRs were 1.28 (95% CI = 0.95 to 1.73) in the vitamin C group, 0.87 (95% CI = 0.65 to 1.17) in the vitamin E group, and 0.84 (95% CI = 0.62 to 1.13) in the beta carotene group. Duration and combined use of the three antioxidants also had no effect on cancer incidence and cancer death. Conclusions Supplementation with vitamin C, vitamin E, or beta carotene offers no overall benefits in the primary prevention of total cancer incidence or cancer mortality.
CONTEXT Multivitamin preparations are the most common dietary supplement, taken by at least one-third of all US adults. Observational studies have not provided evidence regarding associations of ...multivitamin use with total and site-specific cancer incidence or mortality. OBJECTIVE To determine whether long-term multivitamin supplementation decreases the risk of total and site-specific cancer events among men. DESIGN, SETTING, AND PARTICIPANTS A large-scale, randomized, double-blind, placebo-controlled trial (Physicians' Health Study II) of 14 641 male US physicians initially aged 50 years or older (mean SD age, 64.3 9.2 years), including 1312 men with a history of cancer at randomization, enrolled in a common multivitamin study that began in 1997 with treatment and follow-up through June 1, 2011. INTERVENTION Daily multivitamin or placebo. MAIN OUTCOME MEASURES Total cancer (excluding nonmelanoma skin cancer), with prostate, colorectal, and other site-specific cancers among the secondary end points. RESULTS During a median (interquartile range) follow-up of 11.2 (10.7-13.3) years, there were 2669 men with confirmed cancer, including 1373 cases of prostate cancer and 210 cases of colorectal cancer. Compared with placebo, men taking a daily multivitamin had a statistically significant reduction in the incidence of total cancer (multivitamin and placebo groups, 17.0 and 18.3 events, respectively, per 1000 person-years; hazard ratio HR, 0.92; 95% CI, 0.86-0.998; P = .04). There was no significant effect of a daily multivitamin on prostate cancer (multivitamin and placebo groups, 9.1 and 9.2 events, respectively, per 1000 person-years; HR, 0.98; 95% CI, 0.88-1.09; P = .76), colorectal cancer (multivitamin and placebo groups, 1.2 and 1.4 events, respectively, per 1000 person-years; HR, 0.89; 95% CI, 0.68-1.17; P = .39), or other site-specific cancers. There was no significant difference in the risk of cancer mortality (multivitamin and placebo groups, 4.9 and 5.6 events, respectively, per 1000 person-years; HR, 0.88; 95% CI, 0.77-1.01; P = .07). Daily multivitamin use was associated with a reduction in total cancer among 1312 men with a baseline history of cancer (HR, 0.73; 95% CI, 0.56-0.96; P = .02), but this did not differ significantly from that among 13 329 men initially without cancer (HR, 0.94; 95% CI, 0.87-1.02; P = .15; P for interaction = .07). CONCLUSION In this large prevention trial of male physicians, daily multivitamin supplementation modestly but significantly reduced the risk of total cancer. TRIAL REGISTRATION clinicaltrials.gov Identifier: NCT00270647.
Elevated body mass index (BMI; weight in kilograms divided by height in meters squared) in the obese range (> or =30 kg/m(2)) is associated with an excess risk of heart failure (HF). However, the ...impact of overweight or preobese (BMI, 25 to 29.9 kg/m(2)) status and physical activity on HF risk is unclear.
In a prospective cohort of 21,094 men (mean age, 53 years) without known coronary heart disease at baseline in the Physicians' Health Study, we examined the individual and combined effects of BMI and vigorous physical activity (exercise to the point of breaking a sweat) on HF incidence from 1982 to 2007. We evaluated BMI as both a continuous (per 1-kg/m(2) increment) and a categorical (lean, <25 kg/m(2); overweight, 25 to 29.9 kg/m(2); and obese, > or =30 kg/m(2)) variable; we evaluated vigorous physical activity primarily as a dichotomous variable (inactive rarely/never versus active > or =1 to 3 times a month). During follow-up (mean, 20.5 years), 1109 participants developed new-onset HF. In multivariable analyses, every 1-kg/m(2) increase in BMI was associated with an 11% (95% confidence interval CI, 9 to 13) increase in HF risk. Compared with lean participants, overweight participants had a 49% (95% CI, 32 to 69) and obese participants had a 180% (95% CI, 124 to 250) increase in HF risk. Vigorous physical activity conferred an 18% (95% CI, 4 to 30) decrease in HF risk. No interaction was found between BMI and vigorous physical activity and HF risk (P=0.96). Lean active men had the lowest and obese inactive men had the highest risk of HF. Compared with lean active men, the hazard ratios were 1.19 (95% CI, 0.94 to 1.51), 1.49 (95% CI, 1.30 to 1.71), 1.78 (95% CI, 1.43 to 2.23), 2.68 (95% CI, 2.08 to 3.45), and 3.93 (95% CI, 2.60 to 5.96) in lean inactive, overweight active, overweight inactive, obese active, and obese inactive men, respectively.
In this cohort of men, elevated BMI, even in the preobese range, was associated with an increased risk of HF, and vigorous physical activity was associated with a decreased risk. Public health measures to curtail excess weight, to maintain optimal weight, and to promote physical activity may limit the scourge of HF.
Infectious disease was a major concern, and the most common causes of death in the US and in many parts of the world at the time were pneumonia and tuberculosis. Today, most individuals die of ...cardiovascular disease or cancer. Despite the many advances in preventive medicine and treatment that reduced cardiovascular disease, the new stage of the epidemiologic transition, the age of obesity and inactivity, emerged to threaten the progress made in postponing illness and death to later in adult life spans. Here, Gaziano addresses the risk factors such as smoking, hypertension, and dyslipidemia that are threatened by the obesity epidemic.
Obesity and diabetes are associated with an increased liver cancer risk. However, most studies have examined all primary liver cancers or hepatocellular carcinoma, with few studies evaluating ...intrahepatic cholangiocarcinoma (ICC), the second most common type of liver cancer. Thus, we examined the association between obesity and diabetes and ICC risk in a pooled analysis and conducted a systematic review/meta-analysis of the literature.
For the pooled analysis, we utilized the Liver Cancer Pooling Project, a consortium of 13 US-based, prospective cohort studies with data from 1,541,143 individuals (ICC cases n = 414). In our systematic review, we identified 14 additional studies. We then conducted a meta-analysis, combining the results from LCPP with results from the 5 prospective studies identified through September 2017.
In the LCPP, obesity and diabetes were associated with a 62% Hazard Ratio (HR) = 1.62, 95% Confidence Interval (CI): 1.24-2.12 and an 81% (HR = 1.81, 95% CI: 1.33-2.46) increased ICC risk, respectively. In the meta-analysis of prospectively ascertained cohorts and nested case-control studies, obesity was associated with a 49% increased ICC risk Relative Risk (RR) = 1.49, 95% CI: 1.32-1.70; n = 4 studies; I
= 0%. Diabetes was associated with a 53% increased ICC risk (RR = 1.53, 95% CI: 1.31-1.78; n = 6 studies). While we noted heterogeneity between studies (I
= 67%) for diabetes, results were consistent in subgroup analyses. Results from hospital-based case-control studies (n = 9) were mostly consistent, but these studies are potentially subject to reverse causation.
These findings suggest that obesity and diabetes are associated with increased ICC risk, highlighting similar etiologies of hepatocellular carcinoma and intrahepatic cholangiocarcinoma. However, additional prospective studies are needed to verify these associations.
Abstract Galectin-3 is an emerging biomarker of myocardial fibrosis, inflammation, and immune response. We sought to examine the relation of plasma galectin-3 with cardiovascular (CVD) mortality, ...all-cause mortality and incident heart failure. We performed a literature search for all relevant publications using Ovid MEDLINE, Google Scholar and other databases up to January 2016. Two reviewers independently extracted data and assessed risk of bias. We extracted hazard ratios from regression models that adjusted for age, sex, race, body mass index, smoking, hypertension, hyperlipidemia, diabetes, natriuretic peptides, and renal function, when available. A total of 18 studies with 32,350 participants (323,090 person-years of follow-up) met criteria for analysis. The mean age was 57.3 years and 47.2% of participants were women, with a follow-up duration median of 5 years, IQR: 2.9-10 years. Of the 18 studies, 13 (72%) adjusted for NT-proBNP and renal function in the multivariable adjusted models. Using a random effects meta-analysis, we found a HR of 1.10 (95% CI: 1.05-1.14) for all-cause mortality, 1.22 (95% CI: 1.05-1.39) for CVD mortality, and 1.12 (95% CI: 1.04-1.21) for heart failure risk for each one standard deviation increase in galectin-3 level. In a subgroup analysis of CVD mortality, the HR was 1.44 (1.09-1.79) for patients with heart failure, and 1.09 (0.91-1.27) for the general population. In conclusion, our results suggest that elevated plasma galectin-3 is associated with a higher risk of all-cause mortality, CVD mortality and heart failure. It may add prognostic value beyond that provided by traditional CVD risk factors.
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A one-dose-fits-all approach to use of aspirin has yielded only modest benefits in long-term prevention of cardiovascular events, possibly due to underdosing in patients of large body size and excess ...dosing in patients of small body size, which might also affect other outcomes.
Using individual patient data, we analysed the modifying effects of bodyweight (10 kg bands) and height (10 cm bands) on the effects of low doses (≤100 mg) and higher doses (300–325 mg or ≥500 mg) of aspirin in randomised trials of aspirin in primary prevention of cardiovascular events. We stratified the findings by age, sex, and vascular risk factors, and validated them in trials of aspirin in secondary prevention of stroke. Additionally, we assessed whether any weight or height dependence was evident for the effect of aspirin on 20-year risk of colorectal cancer or any in-trial cancer.
Among ten eligible trials of aspirin in primary prevention (including 117 279 participants), bodyweight varied four-fold and trial median weight ranged from 60·0 kg to 81·2 kg (p<0·0001). The ability of 75–100 mg aspirin to reduce cardiovascular events decreased with increasing weight (pinteraction=0·0072), with benefit seen in people weighing 50–69 kg (hazard ratio HR 0·75 95% CI 0·65–0·85) but not in those weighing 70 kg or more (0·95 0·86–1·04; 1·09 0·93–1·29 for vascular death). Furthermore, the case fatality of a first cardiovascular event was increased by low-dose aspirin in people weighing 70 kg or more (odds ratio 1·33 95% CI 1·08–1·64, p=0·0082). Higher doses of aspirin (≥325 mg) had the opposite interaction with bodyweight (difference pinteraction=0·0013), reducing cardiovascular events only at higher weight (pinteraction=0·017). Findings were similar in men and women, in people with diabetes, in trials of aspirin in secondary prevention, and in relation to height (pinteraction=0·0025 for cardiovascular events). Aspirin-mediated reductions in long-term risk of colorectal cancer were also weight dependent (pinteraction=0·038). Stratification by body size also revealed harms due to excess dosing: risk of sudden death was increased by aspirin in people at low weight for dose (pinteraction=0·0018) and risk of all-cause death was increased in people weighing less than 50 kg who were receiving 75–100 mg aspirin (HR 1·52 95% CI 1·04–2·21, p=0·031). In participants aged 70 years or older, the 3-year risk of cancer was also increased by aspirin (1·20 1·03–1·47, p=0·02), particularly in those weighing less than 70 kg (1·31 1·07–1·61, p=0·009) and consequently in women (1·44 1·11–1·87, p=0·0069).
Low doses of aspirin (75–100 mg) were only effective in preventing vascular events in patients weighing less than 70 kg, and had no benefit in the 80% of men and nearly 50% of all women weighing 70 kg or more. By contrast, higher doses of aspirin were only effective in patients weighing 70 kg or more. Given that aspirin's effects on other outcomes, including cancer, also showed interactions with body size, a one-dose-fits-all approach to aspirin is unlikely to be optimal, and a more tailored strategy is required.
Wellcome Trust and National Institute for Health Research Oxford Biomedical Research Centre.
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