ObjectiveTo examine and quantify the potential dose-response relation between intake of total, animal, and plant protein and the risk of mortality from all causes, cardiovascular disease, and cancer.DesignSystematic review and meta-analysis of prospective cohort studies.Data sourcesPubMed, Scopus, and ISI Web of Science until December 2019, and references of retrieved relevant articles.Study selectionProspective cohort studies that reported the risk estimates for all cause, cardiovascular, and cancer mortality in adults aged 18 or older.Data synthesisRandom effects models were used to calculate pooled effect sizes and 95% confidence intervals for the highest versus lowest categories of protein intake and to incorporate variation between studies. Linear and non-linear dose-response analyses were done to evaluate the dose-response relations between protein intake and mortality.Results32 prospective cohort studies were included in the systematic review and 31 in the meta-analysis. During the follow-up period of 3.5 to 32 years, 113 039 deaths (16 429 from cardiovascular disease and 22 303 from cancer) occurred among 715 128 participants. Intake of total protein was associated with a lower risk of all cause mortality (pooled effect size 0.94, 95% confidence interval 0.89 to 0.99, I2=58.4%, P<0.001). Intake of plant protein was significantly associated with a lower risk of all cause mortality (pooled effect size 0.92, 95% confidence interval 0.87 to 0.97, I2=57.5%, P=0.003) and cardiovascular disease mortality (pooled hazard ratio 0.88, 95% confidence interval 0.80 to 0.96, I2=63.7%, P=0.001), but not with cancer mortality. Intake of total and animal protein was not significantly associated with risk of cardiovascular disease and cancer mortality. A dose-response analysis showed a significant inverse dose-response association between intake of plant protein and all cause mortality (P=0.05 for non-linearity). An additional 3% energy from plant proteins a day was associated with a 5% lower risk of death from all causes.ConclusionsHigher intake of total protein was associated with a lower risk of all cause mortality, and intake of plant protein was associated with a lower risk of all cause and cardiovascular disease mortality. Replacement of foods high in animal protein with plant protein sources could be associated with longevity.
Objective To examine the associations between dietary intake and tissue biomarkers of alpha linolenic acid (ALA) and risk of mortality from all causes, cardiovascular disease (CVD), and cancer. Design Systematic review and meta-analysis of prospective cohort studies. Data sources PubMed, Scopus, ISI Web of Science, and Google Scholar to 30 April 2021. Study selection Prospective cohort studies that reported the risk estimates for death from all causes, CVD, and cancer. Data synthesis Summary relative risks and 95% confidence intervals were calculated for the highest versus lowest categories of ALA intake using random effects and fixed effects models. Linear and non-linear dose-response analyses were conducted to assess the dose-response associations between ALA intake and mortality. Results 41 articles from prospective cohort studies were included in this systematic review and meta-analysis, totalling 1 197 564 participants. During follow-up ranging from two to 32 years, 198 113 deaths from all causes, 62 773 from CVD, and 65 954 from cancer were recorded. High intake of ALA compared with low intake was significantly associated with a lower risk of deaths from all causes (pooled relative risk 0.90, 95% confidence interval 0.83 to 0.97, I 2 =77.8%, 15 studies), CVD (0.92, 0.86 to 0.99, I 2 =48.2%, n=16), and coronary heart disease (CHD) (0.89, 0.81 to 0.97, I 2 =5.6%, n=9), and a slightly higher risk of cancer mortality (1.06, 1.02 to 1.11, I 2 =3.8%, n=10). In the dose-response analysis, a 1 g/day increase in ALA intake (equivalent to one tablespoon of canola oil or 0.5 ounces of walnut) was associated with a 5% lower risk of all cause (0.95, 0.91 to 0.99, I 2 =76.2%, n=12) and CVD mortality (0.95, 0.91 to 0.98, I 2 =30.7%, n=14). The pooled relative risks for the highest compared with lowest tissue levels of ALA indicated a significant inverse association with all cause mortality (0.95, 0.90 to 0.99, I 2 =8.2%, n=26). Also, based on the dose-response analysis, each 1 standard deviation increment in blood concentrations of ALA was associated with a lower risk of CHD mortality (0.92, 0.86 to 0.98, I 2 =37.1%, n=14). Conclusions The findings show that dietary ALA intake is associated with a reduced risk of mortality from all causes, CVD, and CHD, and a slightly higher risk of cancer mortality, whereas higher blood levels of ALA are associated with a reduced risk of all cause and CHD mortality only. Systematic review registration PROSPERO CRD42021229487.
Data on the association of nut intake with risk of cancer and its mortality are conflicting. Although previous meta-analyses summarized available findings in this regard, some limitations may distort their findings. Moreover, none of these meta-analyses examined the dose-response associations of total nut intake with the risk of specific cancers as well as associations between specific types of nuts and cancer mortality. Therefore, this study aimed to summarize available findings on the associations of total nut (tree nuts and peanuts), tree nut (walnuts, pistachios, macadamia nuts, pecans, cashews, almonds, hazelnuts, and Brazil nuts), peanut (whole peanuts without considering peanut butter), and peanut butter consumption with risk of cancer and its mortality by considering the above-mentioned points. We searched the online databases until March 2020 to identify eligible articles. In total, 43 articles on cancer risk and 9 articles on cancer mortality were included in the current systematic review and meta-analysis. The summary effect size (ES) for risk of cancer, comparing the highest with lowest intakes of total nuts, was 0.86 (95% CI: 0.81, 0.92, P < 0.001, I2 = 58.1%; P < 0.01), indicating a significant inverse association. Such a significant inverse association was also seen for tree nut intake (pooled ES: 0.87, 95% CI: 0.78–0.96, P < 0.01, I2 = 15.8%; P = 0.28). Based on the dose-response analysis, a 5-g/d increase in total nut intake was associated with 3%, 6%, and 25% lower risks of overall, pancreatic, and colon cancers, respectively. In terms of cancer mortality, we found 13%, 18%, and 8% risk reductions with higher intakes of total nuts, tree nuts, and peanuts, respectively. In addition, a 5-g/d increase in total nut intake was associated with a 4% lower risk of cancer mortality. In conclusion, our findings support the protective association between total nut and tree nut intake and the risk of cancer and its mortality.
Background Inflammation and sleep disturbances increase the risk of multiple diseases, including cardiovascular disease, type 2 diabetes and dementia. Since diet plays a significant role in inflammatory responses and sleep quality, this study aimed to investigate the association of a plant‐based diet index (PDI) with sleep quality and inflammatory markers in overweight and obese women. Methods 390 overweight and obese women aged 18‐48 years participated in this cross‐sectional study. A validated food frequency questionnaire (FFQ) was used to create an overall PDI, healthful plant‐based diet index (hPDI) and unhealthful plant‐based diet index (uPDI). Sleep quality was assessed by Pittsburgh Sleep Quality Index (PSQI). Higher scores on the PSQI were indicative of poor sleep. Anthropometric measurements and serum concentrations of high‐sensitivity C‐reactive protein (hs‐CRP), interleukin 1 beta (IL‐1β) and transforming growth factor‐beta (TGF‐β) were evaluated. Linear regression models were used to determine the association between exposure and outcomes. Results After taking potential confounders into account, we found a significant inverse association between adherence to hPDI and hs‐CRP (β = −0.14, 95% confidence interval [CI]: −0.22,0.06, P = .001) and a significant positive association between uPDI and hs‐CRP (β = 0.13, 95% CI: 0.05,0.21, P = .001). Overall, PDI was significantly associated with TGF‐β (β = 2.04, 95% CI: 0.54,3.55, P = .008). No association was detected between PDI indices and IL‐1β. Higher adherence to uPDI was significantly associated with higher PSQI score (lower sleep quality) (β= 0.20, 95% CI:0.007,0.40, P = .04). A significant positive association was found between TGF‐β (β = 0.05, 95% CI:0.005,0.10, P = .03) and hs‐CRP (β = 0.32, 95% CI:0.02,0.62, P = .03) with PSQI. Conclusion Our findings indicated a significant association between adherence to a plant‐based diet with inflammation and sleep quality in obese and overweight females. What is already known about this topic? Sleep is an essential part of life, and sleep quality has a significant impact on individual well‐being and performance. There is a bidirectional relationship between disturbed sleep and elevated levels of inflammatory markers. Diet plays a major part in sleep quality and its related health consequences. Plant‐based diets are associated with lower risk of chronic diseases such as coronary artery disease (CAD), type 2 diabetes, obesity and reduced level of inflammation. What does this article add? Adherence to a healthful plant‐based diet is associated with lower level of hs‐CRP, while adherence to an unhealthful plant‐based diet is associated with higher concentrations of hs‐CRP. Adherence to an unhealthful plant‐based diet is associated with lower sleep quality.
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