Whether nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of mortality remains controversial. The present study aimed to clarify this issue. A systematic search of PubMed ...and Embase was conducted through October 2018. Studies providing risk estimates of NAFLD and mortality were included. A random-effects model was employed to calculate summary risk estimates. Subgroup analyses were performed to identify potential effect modifiers. Fourteen studies, involving 498501 subjects and 24234 deaths, were included. Patients with NAFLD were found to be at an elevated risk of all-cause mortality compared with those without hazard ratio (HR) = 1.34; 95% confidence interval (CI) 1.17-1.54). The significantly positive association between NAFLD and all-cause mortality could not be modified by age, sex, follow-up duration, and adjustment for body mass index, diabetes, smoking or hypertension (all P
> 0.05), and remained in sensitivity analyses. No significant associations of NAFLD with CVD (HR = 1.13; 95% CI 0.92-1.38) and cancer (HR = 1.05; 95% CI 0.89-1.25) mortality were found. In conclusion, NAFLD is a predictor of increased all-cause mortality but not CVD and cancer mortality. These findings have important implications for decision making in public health and clinical practice, and highlight the urgency of developing effective treatments for NAFLD.
Abstract
Background
The associations of frailty with all-cause and cause-specific mortality remain unclear. Therefore, we performed this meta-analysis to fill this gap.
Methods
We searched the PubMed ...and Embase databases through June 2022. Prospective cohort studies or clinical trials examining frailty were evaluated, and the multiple adjusted risk estimates of all-cause and cause-specific mortality, such as death from cardiovascular disease (CVD), cancer, respiratory illness, dementia, infection, and coronavirus disease 2019 (COVID-19), were included. A random effects model was used to calculate the summary hazard ratio (HR).
Results
Fifty-eight studies were included for the qualitative systematic review, of which fifty-six studies were eligible for the quantitative meta-analysis, and the studies included a total of 1,852,951 individuals and more than 145,276 deaths. Compared with healthy adults, frail adults had a significantly higher risk of mortality from all causes (HR 2.40; 95% CI 2.17–2.65), CVD (HR 2.64; 95% CI 2.20–3.17), respiratory illness (HR 4.91; 95% CI 2.97–8.12), and cancer (HR 1.97; 95% CI 1.50–2.57). Similar results were found for the association between prefrail adults and mortality risk. In addition, based on the studies that have reported the HRs of the mortality risk per 0.1 and per 0.01 increase in the frailty index, we obtained consistent results.
Conclusions
The present study demonstrated that frailty was not only significantly related to an increased risk of all-cause mortality but was also a strong predictor of cause-specific mortality from CVD, cancer, and respiratory illness in community-dwelling adults. More studies are warranted to clarify the relationship between frailty and cause-specific mortality from dementia, infection, and COVID-19.
Trial registration
PROSPERO (CRD42021276021).
Ultra-processed foods have now become dominant in the global food system. Whether their consumption is associated with cardiovascular mortality remains controversial. Moreover, data on ...ultra-processed foods and cardiovascular outcomes are scarce in the US population. We aimed to examine the association of ultra-processed food consumption with cardiovascular mortality in a US population.
A population-based cohort of 91,891 participants was identified from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary data were collected through a validated 137-item food frequency questionnaire. Ultra-processed foods were defined by the NOVA classification. Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for cardiovascular mortality. Restricted cubic spline regression was used to test nonlinearity. Subgroup analyses were conducted to identify the potential effect modifiers.
After an average follow-up of 13.5 years (1,236,049.2 person-years), 5490 cardiovascular deaths were documented, including 3985 heart disease deaths and 1126 cerebrovascular deaths. In the fully adjusted model, participants in the highest vs. the lowest quintiles of ultra-processed food consumption had higher risks of death from cardiovascular disease (HR
, 1.50; 95% CI, 1.36-1.64) and heart disease (HR
, 1.68; 95% CI, 1.50-1.87) but not cerebrovascular disease (HR
, 0.94; 95% CI, 0.76-1.17). A nonlinear dose-response pattern was observed for overall cardiovascular and heart disease mortality (all P
< 0.05), with a threshold effect observed at ultra-processed food consumption of 2.4 servings/day and 2.3 servings/day, respectively; below the thresholds, no significant associations were observed for these two outcomes. Subgroup analyses showed that the increased risks of mortality from ultra-processed foods were significantly higher in women than in men (all P
< 0.05).
High consumption of ultra-processed foods is associated with increased risks of overall cardiovascular and heart disease mortality. These harmful associations may be more pronounced in women. Our findings need to be confirmed in other populations and settings.
Whether ultra‐processed food consumption is associated with the risk of pancreatic cancer has not been determined. We performed a prospective study to fill this gap. A population‐based cohort of 98 ...265 American adults was identified from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Ultra‐processed foods were defined by the NOVA classification. Cox regression was used to estimate hazard ratios (HRs) for pancreatic cancer incidence. Subgroup analysis was performed to identify the potential effect modifiers. During a mean follow‐up of 8.86 years, 387 pancreatic cancer cases occurred. High consumption of ultra‐processed foods was found to be associated with an increased risk of pancreatic cancer (fully adjusted HRquartile 4 vs 1:1.49; 95% confidence interval CI: 1.07‐2.07; Ptrend = .021) in a linear dose‐response manner (Pnonlinearity = .075). Subgroup analysis further found that the positive association of ultra‐processed food consumption with the risk of pancreatic cancer was more pronounced in subjects aged <65 years (HRquartile 4 vs 1:2.17; 95% CI: 1.14‐4.15) than in those aged ≥65 years (HRquartile 4 vs 1:1.32; 95% CI: 0.88‐1.94), though the interaction test failed to achieve the statistical significance (Pinteraction = .061). These findings suggest that reducing ultra‐processed food consumption may be beneficial in decreasing pancreatic cancer incidence.
What's new?
“Ultra‐processed” foods, industrially formulated products consisting of ingredients extracted from foods, but no intact foods, now make up as much as 58.5% of Americans' daily calorie intake. Think frozen meals, hot dogs and packaged snacks. Here, the authors investigate the relationship between ultra‐processed foods and pancreatic cancer in a cohort of 98 265 American adults. High consumption of ultra‐processed foods was associated with increased risk of pancreatic cancer, and the association was more pronounced for those under age 65.
Chronic inflammation plays an important role in primary liver cancer (PLC) etiology and can be influenced by dietary habits. No prospective study has investigated the association of dietary ...inflammatory index (DII) with PLC incidence and mortality. Therefore, we used prospective data from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial to fill this gap. The DII was calculated from a validated 137‐item food frequency questionnaire in a cohort of 103,902 individuals. Cox regression was used to estimate hazard ratios (HRs) for PLC incidence, and competing risk regression was used to estimate subdistribution HRs (SHRs) for PLC mortality. Restricted cubic spline regression was employed to identify the potential dose–response pattern. A total of 120 PLC cases and 102 PLC deaths were observed during follow‐up. Higher DII scores from food and supplement were found to be associated with higher risks of developing PLC (HRTertile 3 vs. 1 2.05; 95% confidence interval CI 1.23–3.41) and death from this disease (SHRTertile 3 vs. 1 1.97; 95% CI 1.13–3.41). Similar results were obtained for DII score from food only. A nonlinear dose–response pattern was identified for the aforementioned associations (all pnonlinearity < 0.05). Overall, a more pro‐inflammatory diet, as suggested by higher DII scores, is associated with higher risks of PLC incidence and mortality. These findings indicate that encouraging intake of more anti‐inflammatory dietary components and reducing intake of pro‐inflammatory components represent an attractive strategy to reduce PLC incidence and mortality.
What's new?
Chronic inflammation can be influenced by dietary habits. It also appears to play an important role in the etiology of primary liver cancer (PLC). Does a pro‐inflammatory diet therefore increase the risk of PLC? In this study, the authors used the “dietary inflammatory index” (DII) and found that the answer is yes, in terms of both PLC incidence and mortality. These results suggest that encouraging the consumption of more anti‐inflammatory dietary components and reducing consumption of pro‐inflammatory components represents an attractive strategy to reduce PLC risk and improve prognosis.
Epidemiological studies on magnesium intake and primary liver cancer (PLC) are scarce, and no prospective studies have examined the associations of magnesium intake with PLC incidence and mortality. ...We sought to clarify whether higher magnesium intake from diet and supplements was associated with lower risks of PLC incidence and mortality in the US population. Magnesium intake from diet and supplements was evaluated through a food frequency questionnaire in a cohort of 104,025 participants. Cox regression was employed to calculate hazard ratios for PLC incidence and competing risk regression was employed to calculate subdistribution hazard ratios for PLC mortality. Restricted cubic spline regression was employed to test nonlinearity. We documented 116 PLC cases during 1,193,513.5 person‐years of follow‐up and 100 PLC deaths during 1,198,021.3 person‐years of follow‐up. Total (diet + supplements) magnesium intake was found to be inversely associated with risks of PLC incidence (hazard ratiotertile 3 vs. 1: 0.44; 95% confidence interval: 0.24, 0.80; ptrend = 0.0065) and mortality (subdistribution hazard ratiotertile 3 vs. 1: 0.37; 95% confidence interval: 0.19, 0.71; ptrend = 0.0008). Similar results were obtained for dietary magnesium intake. Nonlinear inverse dose–response associations with PLC incidence and mortality were observed for both total and dietary magnesium intakes (all pnonlinearity < 0.05). In summary, in the US population, a high magnesium intake is associated with decreased risks of PLC incidence and mortality in a nonlinear dose–response manner. These findings support that increasing the consumption of foods rich in magnesium may be beneficial in reducing PLC incidence and mortality.
What's new?
Magnesium is believed to be involved in cancer pathogenesis, with magnesium intake reducing the risk for a variety of cancers. Epidemiological studies on magnesium intake and primary liver cancer (PLC) remain scarce, however. Using prospective data from the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial, here the authors found that total (diet + supplements) and dietary magnesium intakes were inversely associated with risks of PLC incidence and mortality in a non‐linear dose–response manner. These findings suggest that increasing the consumption of foods rich in magnesium may be beneficial in reducing PLC incidence and mortality in the US population.
Abstract
No epidemiologic studies have been conducted to assess the association of intake of dietary vitamin K with the risk of pancreatic cancer. We used prospective data from the Prostate, Lung, ...Colorectal, and Ovarian Cancer Screening Trial between 1993 and 2009 to fill this gap. A total of 101,695 subjects were identified. Dietary intakes of phylloquinone (vitamin K1), menaquinones (vitamin K2), and dihydrophylloquinone (dihydrovitamin K1) were assessed using a food frequency questionnaire. Cox regression was applied to calculate hazard ratios and 95% confidence intervals. During a mean follow-up of 8.86 years (900,744.57 person-years), 361 cases of pancreatic cancer were documented. In the fully adjusted model, dietary intakes of phylloquinone (for quartile 4 vs. quartile 1, hazard ratio (HR) = 0.57, 95% confidence interval (CI): 0.39, 0.83; P for trend = 0.002) and dihydrophylloquinone (for quartile 4 vs. quartile 1, HR = 0.59; 95% CI: 0.41, 0.85; P for trend = 0.006), but not menaquinones (for quartile 4 vs. quartile 1, HR = 0.93; 95% CI: 0.65, 1.33; P for trend = 0.816), were found to be inversely associated with the risk of pancreatic cancer in a nonlinear dose–response manner (all P values for nonlinearity < 0.05), and this was not modified by predefined stratification factors and remained in sensitivity analyses. In conclusion, dietary intakes of phylloquinone and dihydrophylloquinone, but not menaquinones, confer a lower risk of pancreatic cancer. Future studies should confirm our findings.
We report a new strategy to design carbon-based electrocatalysts containing nitrogen through the co-pyrolysis of blood protein and carbon black support. The results show that the nitrogen in ...electro-catalysts is primarily in the form of pyridinic- and pyrrolic-type nitrogen species. High-temperature pyrolysis processes can transfer a significant amount of pyridinic-N to pyrrolic-N. The electrocatalyst containing a higher amount of the pyrrolic-N configuration exhibits better electrocatalytic activity towards oxygen reduction reaction in terms of onset potential, half-wave potential, and limited current density. It is suggested that the pyrrolic-N configuration may be the electrocatalytically active site and may be responsible for the enhanced ORR performance in alkaline media. The carbon black support also plays an important role in the pyrolysis process, improving the ORR catalytic activity.
The association between chronic obstructive pulmonary disease (COPD), lung function and risk of type 2 diabetes mellitus (T2DM) remains controversial. We performed a meta-analysis to clarify this ...issue.
The PubMed and EMBASE databases were searched. Cohort studies on COPD, lung function and risk of T2DM in adults were included. A random effects model was adopted to calculate the summary risk ratio (RR) and 95% confidence interval (CI). Dose-response analysis was conducted where possible.
A total of 13 eligible cohort studies involving 307,335 incident T2DM cases and 7,683,784 individuals were included. The risk of T2DM was significantly higher in patients with COPD than those without COPD (RR = 1.25, 95% CI 1.16-1.34). Compared to the highest category of percentage forced vital capacity (FVC%), the lowest category of FVC% was associated with a higher risk of T2DM (RR = 1.43, 95% CI 1.33-1.53). Similarly, the summary RR of T2DM for the lowest versus highest category of percentage forced expiratory volume in 1 s (FEV1%) was 1.49 (95% CI 1.39-1.60). Significant linear associations of FVC% and FEV1% with risk of T2DM were found (P
> 0.05); the RR of T2DM was 0.88 (95% CI 0.82-0.95) and 0.87 (95% CI 0.81-0.94) per 10% increase in FVC% and FEV1%, respectively. There was a non-significant relationship between the FEV1/FVC ratio and the risk of T2DM.
Both COPD and impaired lung function, especially restricted ventilation dysfunction, could increase the risk of T2DM. However, these findings should be interpreted with caution due to the limited number of studies, and need to be validated by future studies.
Abstract
We aimed to examine whether type 2 diabetes–prevention diet, a dietary pattern previously developed for reducing type 2 diabetes risk, was associated with mortality in a US population. A ...population-based cohort of 86,633 subjects was identified from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (1993–2015). Dietary information was collected with a food frequency questionnaire. A dietary diabetes risk-reduction score was calculated to reflect adherence to this dietary pattern, with higher scores representing better adherence. Hazard ratios (HRs) and absolute risk differences (ARDs) in mortality rates per 10,000 person-years were calculated. After a mean follow-up of 13.6 years, 17,532 all-cause deaths were observed. Participants with the highest versus the lowest quintiles of dietary diabetes risk-reduction score were observed to have decreased risks of death from all causes (HR = 0.76, 95% CI: 0.72, 0.80; ARD: −81.94, 95% CI: −93.76, −71.12), cardiovascular disease (HR = 0.73, 95% CI: 0.66, 0.81; ARD: −17.82, 95% CI: −24.81, −11.30), and cancer (HR = 0.85, 95% CI: 0.78, 0.94; ARD: −9.92, 95% CI: −15.86, −3.59), which were modified by sex, smoking status, or alcohol consumption in subgroup analyses (P for interaction < 0.05 for all). In conclusion, a type 2 diabetes–prevention diet confers reduced risks of death from all causes, cardiovascular disease, and cancer in this US population.
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