Objective: Food security has been suggested to be a risk factor for depression, stress and anxiety. We therefore undertook a systematic review and meta-analysis of available publications to examine these associations further.Design: Relevant studies were identified by searching Web of Science, Embase, Scopus and PubMed databases up to January 2019.Setting: OR was pooled using a random-effects model. Standard methods were used for assessment of heterogeneity and publication bias.Participants: Data were available from nineteen studies with 372 143 individual participants from ten different countries that were pooled for the meta-analysis.Results: The results showed there was a positive relationship between food insecurity (FI) and risk of depression (OR = 1·40; 95 % CI: 1·30, 1·58) and stress (OR = 1·34; 95 % CI: 1·24, 1·44) but not anxiety. Subgroup analysis by age showed that subjects older than ≥65 years exhibited a higher risk of depression (OR = 1·75; 95 % CI: 1·20, 2·56) than younger participants (OR = 1·34; 95 % CI: 1·20, 1·50), as well as a greater risk of depression in men (OR = 1·42; 95 % CI: 1·17, 1·72) than women (OR = 1·30; 95 % CI: 1·16, 1·46). Finally, subgroup analysis according to geographical location illustrated that food insecure households living in North America had the highest risk of stress and anxiety.Conclusions: The evidence from this meta-analysis suggests that FI has a significant effect on the likelihood of being stressed or depressed. This indicates that health care services, which alleviate FI, would also promote holistic well-being in adults.

We performed a systematic review and meta-analysis to examine the relationship between heavy metals (HMs) exposure and the risk of chronic kidney disease (CKD). Databases of Web of Science, Embase, MEDLINE, and Scopus were searched through June 2020 to identify studies assessing the relationships between exposure to HMs (i.e. cadmium, lead, arsenic, mercury) and the risk of CKD, evaluated by decreased estimated glomerular filtration rate (eGFR) and/or increased proteinuria risks in adults (≥18 years). Data were pooled by random-effects models and expressed as weighted mean differences and 95% confidence intervals. The risk of bias was assessed by the Newcastle–Ottawa scale (NOS). Twenty-eight eligible articles (n = 107,539 participants) were included. Unlike eGFR risk (p = 0.10), Cadmium exposure was associated with an increased proteinuria risk (OR = 1.35; 95% CI: 1.13, 1.61; p < 0.001; I² = 79.7%). Lead exposure was associated with decreased eGFR (OR = 1.12; 95%CI: 1.03, 1.22; p = 0.008; I² = 87.8%) and increased proteinuria (OR = 1.25; 95% CI: 1.04, 1.49; p = 0.02; I² = 79.6) risks. Further, arsenic exposure was linked to a decreased eGFR risk (OR = 1.55; 95% CI: 1.05, 2.28; p = 0.03; I² = 89.1%) in contrast to mercury exposure (p = 0.89). Only two studies reported the link between arsenic exposure and proteinuria risk, while no study reported the link between mercury exposure and proteinuria risk. Exposure to cadmium, lead, and arsenic may increase CKD risk in adults, albeit studies were heterogeneous, warranting further investigations. Our observations support the consideration of these associations for preventative, diagnostic, monitoring, and management practices of CKD.

We performed a systematic review and dose–response meta-analysis of observational studies assessing the association between UPF consumption and adult mortality risk. A systematic search was conducted using ISI Web of Science, PubMed/MEDLINE, and Scopus electronic databases from inception to August 2021. Data were extracted from seven cohort studies (totaling 207,291 adults from four countries). Using a random-effects model, hazard ratios (HR) of pooled outcomes were estimated. Our results showed that UPF consumption was related to an enhanced risk of all-cause mortality (HR = 1.21; 95% CI: 1.13, 1.30; I² = 21.9%; p < 0.001), cardiovascular diseases (CVDs)-cause mortality (HR = 1.50; 95% CI: 1.37, 1.63; I² = 0.0%; p < 0.001), and heart-cause mortality (HR = 1.66; 95% CI: 1.50, 1.85; I² = 0.0%; p = 0.022), but not cancer-cause mortality. Furthermore, our findings revealed that each 10% increase in UPF consumption in daily calorie intake was associated with a 15% higher risk of all-cause mortality (OR = 1.15; 95% CI: 1.09, 1.21; I² = 0.0%; p < 0.001). The dose–response analysis revealed a positive linear association between UPF consumption and all-cause mortality (P_nonlinearity = 0.879, P_{dose–response} = p < 0.001), CVDs-cause mortality (P_nonlinearity = 0.868, P_{dose–response} = p < 0.001), and heart-cause mortality (P_nonlinearity = 0.774, P_{dose–response} = p < 0.001). It seems that higher consumption of UPF is significantly associated with an enhanced risk of adult mortality. Despite this, further experimental studies are necessary to draw a more definite conclusion.

(1) Background: Recent individual studies have demonstrated that consumption of ultra-processed food (UPF) may be related to type two diabetes mellitus (T2DM). We aimed to synthesize the results from these individual studies by conducting an updated systematic review and meta-analysis of observational studies evaluating the association between UPF consumption and the risk of T2DM. (2) Methods: A systematic search was conducted using ISI Web of Science, PubMed/MEDLINE and Scopus electronic databases from inception up to August 2021. Data were extracted from five studies (one cross-sectional study and four cohort studies, totaling 230,526 adults from four different countries). Risk ratios (RR) of pooled results were estimated using a random-effects model. (3) Results: Our results revealed that higher UPF consumption was significantly associated with an increased risk of T2DM (RR = 1.74; 95% CI: 1.36, 2.22; I² = 68.9%; p < 0.001; n = 5). Linear dose-response analysis indicated that each 10% increase in UPF consumption (kcal/d) was associated with a 15% higher risk of T2DM (RR = 1.15; 95% CI: 1.06, 1.26; I² = 86.0%; p < 0.001; n = 5) among adults. Non-linear dose-response analysis demonstrated a positive linear association between UPF consumption and T2DM (p_nonlinearity = 0.13, p_{dose-response} < 0.001; n = 5) among adults. (4) Conclusions: A higher intake of UPF was significantly associated with an increased risk of T2DM. However, underlying mechanisms remain unknown and future experimental studies are warranted.