Sarcopenia is a geriatric condition featured by a progressive loss of muscle mass and function and associated with various adverse health outcomes. In this review, we aimed to summarize the epidemiological features of sarcopenia as well as consequences and risk factors of the disease. We performed a systematic review of meta-analysis on sarcopenia to collect data. The prevalence of sarcopenia varied between studies and depending on definition used. Sarcopenia was estimated to influence 10 %-16 % of the elderly worldwide. The prevalence of sarcopenia was higher among patients compared to general populations. The prevalence of sarcopenia ranged from 18 % in diabetic patients to 66 % in patients with unresectable esophageal cancer. Sarcopenia is associated with a high risk of a wide range of adverse health outcomes, including poor overall and disease-progression free survival rate, postoperative complications, and longer hospitalization in patients with different medical situations as well as falls and fracture, metabolic disorders, cognitive impairment, and mortality in general populations. Physical inactivity, malnutrition, smoking, extreme sleep duration, and diabetes were associated with an increased risk of sarcopenia. However, these associations were mainly based on non-cohort observational studies and need confirmation. High-quality cohort, omics, and Mendelian randomization studies are needed to deeply understand the etiological basis of sarcopenia.

Large-scale genome-wide association studies conducted over the last decade have uncovered numerous genetic variants associated with cardiometabolic traits and risk factors. These discoveries have enabled the Mendelian randomization (MR) design, which uses genetic variation as a natural experiment to improve causal inferences from observational data. By analogy with the random assignment of treatment in randomized controlled trials, the random segregation of genetic alleles when DNA is transmitted from parents to offspring at gamete formation is expected to reduce confounding in genetic associations. Mendelian randomization analyses make a set of assumptions that must hold for valid results. Provided that the assumptions are well justified for the genetic variants that are employed as instrumental variables, MR studies can inform on whether a putative risk factor likely has a causal effect on the disease or not. Mendelian randomization has been increasingly applied over recent years to predict the efficacy and safety of existing and novel drugs targeting cardiovascular risk factors and to explore the repurposing potential of available drugs. This review article describes the principles of the MR design and some applications in cardiovascular epidemiology.

Background: Diabetes has been associated with an increased risk of colorectal cancer in most, but not all, studies. Findings have also been inconclusive with regard to sex and subsite in the colorectum. To resolve these inconsistencies, we conducted a meta-analysis of published data on the association between diabetes and the incidence and mortality of colorectal cancer. Methods: We identified studies by a literature search of Medline from January 1, 1966, through July 31, 2005, and by searching the reference lists of pertinent articles. Summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated with a random-effects model. All statistical tests were two-sided. Results: Analysis of 15 studies (six case–control and nine cohort studies), including 2 593 935 participants, found that diabetes was associated with an increased risk of colorectal cancer, compared with no diabetes (summary RR of colorectal cancer incidence = 1.30, 95% CI = 1.20 to 1.40), without heterogeneity between studies ( P_{heterogeneity} = .21). These results were consistent between case–control and cohort studies and between studies conducted in the United States and in Europe. The association between diabetes and colorectal cancer incidence did not differ statistically significantly by sex (summary RR among women = 1.33, 95% CI = 1.23 to 1.44; summary RR among men = 1.29, 95% CI = 1.15 to 1.44; P_{heterogeneity} = .26) or by cancer subsite (summary RR for colon = 1.43, 95% CI = 1.28 to 1.60; summary RR for rectum = 1.33, 95% CI = 1.14 to 1.54; P_{heterogeneity} = .42). Diabetes was positively associated with colorectal cancer mortality (summary RR = 1.26, 95% CI = 1.05 to 1.50), but there was evidence for heterogeneity between studies ( P_{heterogeneity} = .04). Conclusions: Our findings strongly support a relationship between diabetes and increased risk of colon and rectal cancer in both women and men.

Increasing evidence from animal and in vitro studies indicates that n−3 fatty acids, especially the long-chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, present in fatty fish and fish oils inhibit carcinogenesis. The epidemiologic data on the association between fish consumption, as a surrogate marker for n−3 fatty acid intake, and cancer risk are, however, somewhat less consistent. This review highlights current knowledge of the potential mechanisms of the anticarcinogenic actions of n−3 fatty acids. Moreover, a possible explanation of why some epidemiologic studies failed to find an association between n−3 fatty acid intake and cancer risk is provided. Several molecular mechanisms whereby n−3 fatty acids may modify the carcinogenic process have been proposed. These include suppression of arachidonic acid-derived eicosanoid biosynthesis; influences on transcription factor activity, gene expression, and signal transduction pathways; alteration of estrogen metabolism; increased or decreased production of free radicals and reactive oxygen species; and mechanisms involving insulin sensitivity and membrane fluidity. Further studies are needed to evaluate and verify these mechanisms in humans to gain more understanding of the effects of n−3 fatty acid intake on cancer risk.

Background: Whereas obesity has been associated with an increased risk of colon cancer in men, a weak or no association has been observed in women. Results for rectal cancer have also been inconsistent. Objective: The objective was to perform a meta-analysis to summarize the available evidence from prospective studies on the associations of overall and abdominal obesity with the risk of colon and rectal cancer. Design: We searched MEDLINE (1966–April 2007) and the references of the retrieved articles. Study-specific relative risks (RRs) were pooled by using a random-effects model. Results: Thirty prospective studies were included in the meta-analysis of body mass index (BMI; in kg/m²). Overall, a 5-unit increase in BMI was related to an increased risk of colon cancer in both men (RR: 1.30; 95% CI: 1.25, 1.35) and women (RR: 1.12; 95% CI: 1.07, 1.18), but the association was stronger in men (P < 0.001). BMI was positively associated with rectal cancer in men (RR: 1.12; 95% CI: 1.09, 1.16) but not in women (RR: 1.03; 95% CI: 0.99, 1.08). The difference in RRs between cancer sites was statistically significant (P < 0.001 in men and P = 0.04 in women). Colon cancer risk increased with increasing waist circumference (per 10-cm increase) in both men (RR: 1.33; 95% CI: 1.19, 1.49) and women (RR: 1.16; 95% CI: 1.09, 1.23) and with increasing waist-hip ratio (per 0.1-unit increase) in both men (RR: 1.43; 95% CI: 1.19, 1.71) and women (RR: 1.20; 95% CI: 1.08, 1.33). Conclusions: The association between obesity and colon and rectal cancer risk varies by sex and cancer site.