Sedentary behaviour and risk of all-cause, cardiovascular and cancer mortality, and incident type 2 diabetes: a systematic review and dose response meta-analysis

Previous studies link marital status to mortality across diverse populations. This study examines how sex influences its association with all-cause, cardiovascular disease (CVD), and cancer mortality. The search was conducted through PubMed, Scopus, and Google Scholar databases and included related articles up to September 16, 2025. The titles, abstracts, and full texts of the included articles were reviewed, and data were extracted and analyzed. Twelve cohort studies (1,785,857 individuals) were analyzed. Unmarried status was significantly associated with an increased risk of all-cause, CVD, and cancer mortality. Specifically, single individuals showed a higher risk of all-cause (hazard ratio [HR]: 1.55, 95% CI: 1.37-1.74), cancer (HR: 1.14, 95% CI: 1.07-1.22), and CVD mortality (HR: 1.52, 95% CI: 1.28-1.84). Divorced individuals had an increased risk of all-cause (HR: 1.39, 95% CI: 1.12-1.66) and CVD mortality (HR: 1.27, 95% CI: 1.02-1.52). Widowed individuals showed a higher risk of all-cause (HR: 1.43, 95% CI: 1.11-1.74), cancer (HR: 1.13, 95% CI: 1.03-1.23), and CVD mortality (HR: 1.67, 95% CI: 1.23-2.10). Unmarried status is significantly associated with an increased risk of all-cause, cancer, and CVD mortality. The association between marital status and mortality differs by sex and geographic region. For instance, the link between divorced status and all-cause mortality is significantly stronger in men, while the association between single status and cancer mortality is significantly stronger in women. These findings highlight the importance of considering sex and regional differences in public health interventions.

Total, Dietary, and Supplemental Magnesium Intakes and Risk of All-Cause, Cardiovascular, and Cancer Mortality: A Systematic Review and Dose–Response Meta-Analysis of Prospective Cohort Studies

BackgroundImbalanced dietary patterns, sedentary behavior, and other unhealthy lifestyle behaviors are among the potentially modifiable risk factors most consistently linked to all-cause and cardiovascular disease (CVD) mortality. This study aimed to investigate the joint association of antioxidant intakes from diet and supplements and sedentary behavior with all-cause and CVD mortality.MethodsThis retrospective cohort study included 16,019 adults from National Health and Nutrition Examination Survey (NHANES) 2007–2014. All-cause and CVD mortality was ascertained by linkage to National Death Index records through 31 December 2019. Participants were divided into four lifestyle patterns based on their intake of six antioxidants from dietary intakes and supplements and their self-reported sedentary behavior: low-antioxidant diet and prolonged sedentary behavior, low-antioxidant diet and nonprolonged sedentary behavior, high-antioxidant diet and prolonged sedentary behavior, high-antioxidant diet and nonprolonged sedentary behavior. Multivariable Cox proportional hazards models were utilized to evaluate the associations of antioxidant diet and sedentary behavior with regards to all-cause and CVD mortality.ResultsOver an average follow-up of 8.5 years, a total of 1,894 overall deaths and 482 CVD deaths were reported. Compared with the low-antioxidant diet and prolonged sedentary behavior group, participants in the high-antioxidant diet and nonprolonged sedentary behavior group had a significantly lower risk of all-cause (hazard ratio [HR], 0.60; 95% confidence interval [CI], 0.50–0.72) and CVD (0.51; 0.34–0.77) mortality. Similarly, individuals following a low-antioxidant diet and engaging in nonprolonged sedentary behavior also had a reduced risk of all-cause (0.63; 0.52–0.75) and CVD (0.54; 0.38–0.76) mortality. On the other hand, there was no significant reduction in all-cause mortality among individuals in the high-antioxidant diet and prolonged sedentary behavior group (0.83; 0.68–1.03), as well as CVD mortality (0.87; 0.62–1.21). Subgroup and sensitivity analyses yielded results that were consistent with the overall analysis.ConclusionsParticipants with both high-antioxidant diet and nonprolonged sedentary behavior had the lowest all-cause and CVD mortality. Additionally, nonprolonged sedentary behavior can help counteract the harms of low-antioxidant diet, whereas a high-antioxidant diet fails to offset the deleterious effect of prolonged sedentary behavior.

Dose–Response Association of Dietary Inflammatory Potential with All-Cause and Cause-Specific Mortality

BackgroundCardiometabolic index (CMI) is a comprehensive clinical parameter which integrates overweight and abnormal lipid metabolism. However, its relationship with all-cause, cardiovascular disease (CVD), and cancer mortality is still obscure. Thus, a large-scale cohort study was conducted to illustrate the causal relation between CMI and CVD, cancer, and all-cause mortality among the common American population.MethodsOur research was performed on the basis of National Health and Nutrition Examination Survey (NHANES) database, involving 40,275 participants ranging from 1999 to 2018. The formula of CMI is [waist circumference (cm) / height (cm)] × [triglyceride (mg/dL) / high-density lipoprotein cholesterol (mg/dL)]. Outcome variables consisted of CVD, cancer, and all-cause mortality, which were identified by the International Classification of Diseases (ICD)-10. The correlation between CMI and mortality outcomes was analyzed utilizing the Kaplan–Meier survival modeling, univariate/multivariate Cox regression analysis, smooth curve fitting analysis, threshold effect analysis, and subgroup analysis. Stratification factors for subgroups included age, race/ethnicity, sex, smoking behavior, drinking behavior, BMI, hypertension, and diabetes.ResultsThe baseline characteristics table includes 4,569 all-cause-induced death cases, 1,113 CVD-induced death cases, and 1,066 cancer-induced death cases. Without adjustment for potential covariates, significantly positive causal correlation existed between CMI and all-cause mortality (HR = 1.03, 95% CI 1.02,1.04, P-value<0.05), CVD mortality (HR = 1.04, 95% CI 1.03, 1.05, P-value<0.05) and cancer mortality(HR = 1.03, 95% CI 1.02, 1.05, P-value<0.05); whereas, after confounding factors were completely adjusted, the relationship lost statistical significance in CMI subgroups (P for trend>0.05). Subgroup analysis found no specific subgroups. Under a fully adjusted model, a threshold effect analysis was performed combined with smooth curve fitting, and the findings suggested an L-shaped nonlinear association within CMI and all-cause mortality (the Inflection point was 0.98); in particular, when the baseline CMI was below 0.98, there existed a negative correlation with all-cause mortality with significance (HR 0.59, 95% CI 0.43, 0.82, P-value<0.05). A nonlinear relation was observed between CMI and CVD mortality. Whereas, the correlation between CMI and cancer mortality was linear.ConclusionsAmong the general American population, baseline CMI levels exhibited an L-shaped nonlinear relationship with all-cause mortality, and the threshold value was 0.98. What’s more, CMI may become an effective indicator for CVD, cancer, and all-cause mortality prediction. Further investigation is essential to confirm our findings.

We examined the association between whole grain and refined grain intake with all-cause, cancer and cardiovascular disease (CVD) mortality using the data from the Guangzhou Biobank Cohort Study. 19,597 participants aged 50+ years were recruited from 2003 to 2006 and followed-up until April 2021. Multivariable Cox regression was used to calculate hazard radios (HRs) and 95% confidence intervals (CIs). Substitution analysis was used to replace a serving (50g/day) of whole grain with a serving of refined grain. During 286,821 person-years of follow-up, 4385 deaths occurred, including 1450 from cancer, 1678 from CVD and 1257 from other causes. Compared with never whole grain intake, the highest intake category of whole grain (> 300g/week) was associated with lower risk of all-cause (HR 0.90, 95% CI 0.82-0.98) and CVD mortality (HR 0.85, 0.74-0.98). Compared with the low-intake category of refined grain (< 500g/day), the highest intake category (> 900g/week) was associated with a lower risk of cancer mortality (HR 0.76, 0.62-0.95), but a higher risk of CVD mortality (HR 1.25, 1.03-1.51). No significant associations were found between whole grain intake and cancer mortality nor refined grain and all-cause mortality. The HRs of all-cause, cancer and CVD mortality substituting a serving of whole grain for refined grain were 0.96 (0.94-0.99), 1.01 (0.99-1.02) and 0.95 (0.90-0.99), respectively. We have first shown that in older Chinese, whole grain intake was associated with lower risk of all-cause and CVD mortality. Our results suggest that intake of whole grain of at least 300g/week and refined grain of ≤ 900g/day might be suitable for older Asian. Substituting 50g/day of whole grain for refined grain was associated with a 4-5% lower risk of all-cause and CVD mortality.

ContextThe evidence regarding bicarbonate status and mortality among diabetes is scarce.ObjectiveThe purpose of this study was to investigate the associations of bicarbonate concentrations with risk of all-cause, cardiovascular disease (CVD), and cancer mortality among patients with type 2 diabetes (T2D).MethodsThis study included 8163 adult diabetic patients from the National Health and Nutrition Examination Survey (NHANES), 1999 to 2018. Death outcomes were ascertained by linkage to National Death Index records through 31 December 2019. The Cox proportional-risk model was used to estimate hazard ratios (HR) and 95% CIs for mortality from all causes, CVD, and cancer. The mediating effects of 11 metabolic, cardiovascular, and renal biomarkers were evaluated using a logistic regression model within a counterfactual framework.ResultsDuring 8163 person-years of follow-up, 2310 deaths were documented, including 659 CVD deaths and 399 cancer deaths. After multivariate adjustment, lower serum bicarbonate levels were significantly linearly correlated with higher all-cause, CVD, and cancer mortality: The risk of all-cause death increased by 40%, the risk of CVD death increased by 48%, and the risk of cancer death increased by 84% compared with the normal group (all P < .05). Altered levels of estimated glomerular filtration rate explained 12.10% and 16.94% of the relation between serum bicarbonate with all-cause and CVD mortality, respectively. Total cholesterol mediated 4.70% and 10.51% of the associations of all-cause and CVD mortality, respectively.ConclusionLower serum bicarbonate concentrations were significantly associated with higher all-cause, CVD, and cancer mortality. These findings suggest that maintaining adequate bicarbonate status may lower mortality risk in individuals with T2D.

Background/Introduction Evidence regarding the potential health effects of sleep characteristics among individuals with type 2 diabetes (T2D) is limited. Purpose We aimed to examine sleep characteristics in relation to subsequent risk of cardiovascular disease (CVD), including coronary heart disease (CHD), and stroke, and all-cause and cause-specific mortality among individuals with T2D. Methods We prospectively followed 21,902 men and women with T2D at baseline or diagnosed during follow-up (Nurses' Health Study: 1986-2018, Health Professionals Follow-Up Study: 1986-2018). Sleep characteristics, including sleep duration, snoring, sleep apnea, and sleep quality, were repeatedly assessed using self-reported questionnaires at baseline and follow-up. Associations of sleep characteristics with CVD risk and mortality were assessed using Cox proportional hazards models with adjustments for demographic, dietary and lifestyle factors, and medical history. Results During 170,355 and 196,458 person-years of follow-up in participants with T2D, there were 2,486 incident CVD events and 3,922 deaths, respectively. Compared with sleeping for 7-8 h/day, the multivariable-adjusted hazard ratios (HRs) of sleeping for ≤5 h/day were 1.21 (1.02, 1.45) for CVD incidence, 1.24 (1.20, 1.51) for CHD incidence, 1.40 (1.24, 1.58) for total mortality, 1.52 (1.20, 1.92) for CVD mortality, and 1.27 (1.01, 1.61) for other non-CVD and non-cancer mortality, while the HRs of ≥10 h/day were 1.42 (1.21, 1.66) for total mortality, and 1.63 (1.20, 2.10) for other non-CVD and non-cancer mortality. Furthermore, compared with participants without habitual snoring, those with habitual snoring had a 21%, 24%, 18%, and 33% higher risk for CVD incidence, CHD incidence, CVD mortality, and total mortality, respectively. Compared with participants without diagnosed sleep apnea, those with sleep apnea had a 27%-58% higher risk for CVD incidence, CVD mortality, and total mortality. In addition, lower habitual sleep quality, including sleep difficulties and restless sleep, was associated with a substantially higher risk of CVD, CHD, or CVD mortality. No associations were observed between sleep characteristics with risk of stroke and cancer mortality in individuals with T2D. Conclusions Short and long sleep durations as well as habitual snoring, sleep apnea, and lower sleep quality were independently associated with higher risks of CVD incidence and mortality, particularly CVD mortality in individuals with T2D.

The relationship between ultra-processed food (UPF) intake and mortality is unknown in Asian countries, yet the intake of UPF is on the rise in these countries. This study examined the association of UPF intake with all-cause, cancer and cardiovascular disease (CVD) mortality. Participants were 113,576 adults who responded to a 106-item food frequency questionnaire during recruitment of the 2004–2013 Health Examinees (HEXA) study, a prospective cohort study in Korea. UPF were defined using the NOVA classification and evaluated as quartiles of the proportion of UPF in the diet (% total food weight). Multivariable Cox regression and restricted cubic spline models were used to examine the association of UPF intake with all-cause and cause specific mortality. A total of 3456 deaths were recorded during a median follow-up of 10.6 (interquartile range, 9.5–11.9) years. There was no evidence of an association of UPF intake with all-cause, cancer or CVD mortality comparing the highest with the lowest quartiles of UPF intake (all-cause mortality, men: hazard ratio [HR] 1.08, 95% confidence interval [CI] 0.95–1.22; women: HR 0.95, 95% CI 0.81–1.11; cancer mortality, men: HR 1.02, 95% confidence interval [CI] 0.84–1.22; women: HR 1.02, 95% CI 0.83–1.26; CVD mortality, men: HR 0.88, 95% CI 0.64–1.22; women: HR 0.80, 95% CI 0.53–1.19). However, the risk of all-cause mortality increased in both men and women with high consumption of ultra-processed red meat and fish (men, HR 1.26, 95% CI 1.11–1.43); women, HR 1.22 95% CI 1.05–1.43); and in men with high consumption of ultra-processed milk (HR 1.13, 95% CI 1.01–1.26); and soymilk drink (HR 1.12, 95% CI 1.00–1.25). We found no evidence of an association between total UPF intake and all-cause, cancer or CVD mortality, but ultra-processed red meat and fish in both sexes, and milk and soymilk drinks in men were positively associated with all-cause mortality.

The relationship between ultra-processed food (UPF) intake and mortality is unknown in Asian countries, yet the intake of UPF is on the rise in these countries. This study examined the association of UPF intake with all-cause, cancer and cardiovascular disease (CVD) mortality. Participants were 113,576 adults who responded to a 106-item food frequency questionnaire during recruitment of the 2004-2013 Health Examinees (HEXA) study, a prospective cohort study in Korea. UPF were defined using the NOVA classification and evaluated as quartiles of the proportion of UPF in the diet (% total food weight). Multivariable Cox regression and restricted cubic spline models were used to examine the association of UPF intake with all-cause and cause specific mortality. A total of 3456 deaths were recorded during a median follow-up of 10.6 (interquartile range, 9.5-11.9) years. There was no evidence of an association of UPF intake with all-cause, cancer or CVD mortality comparing the highest with the lowest quartiles of UPF intake (all-cause mortality, men: hazard ratio [HR] 1.08, 95% confidence interval [CI] 0.95-1.22; women: HR 0.95, 95% CI 0.81-1.11; cancer mortality, men: HR 1.02, 95% confidence interval [CI] 0.84-1.22; women: HR 1.02, 95% CI 0.83-1.26; CVD mortality, men: HR 0.88, 95% CI 0.64-1.22; women: HR 0.80, 95% CI 0.53-1.19). However, the risk of all-cause mortality increased in both men and women with high consumption of ultra-processed red meat and fish (men, HR 1.26, 95% CI 1.11-1.43); women, HR 1.22 95% CI 1.05-1.43); and in men with high consumption of ultra-processed milk (HR 1.13, 95% CI 1.01-1.26); and soymilk drink (HR 1.12, 95% CI 1.00-1.25). We found no evidence of an association between total UPF intake and all-cause, cancer or CVD mortality, but ultra-processed red meat and fish in both sexes, and milk and soymilk drinks in men were positively associated with all-cause mortality.

BackgroundOxidatively induced DNA damage, an important factor in cancer etiology, is repaired by oxyguanine glycosylase 1 (OGG1). The lower repair capacity genotype (homozygote Cys326Cys) in the OGG1-rs1052133 (Ser326Cys) polymorphism has been associated with cancer risk. However, no information is available in relation to cancer mortality, other causes of death, and modulation by diet. ObjectiveOur aim was to evaluate the association of the OGG1-rs1052133 with total, cancer, and cardiovascular disease (CVD) mortality and to analyze its modulation by the Mediterranean diet, focusing especially on total vegetable intake as one of the main characteristics of this diet. DesignSecondary analysis in the PREDIMED (Prevención con Dieta Mediterránea) trial is a randomized, controlled trial conducted in Spain from 2003 to 2010. Participants/settingStudy participants (n=7,170) were at high risk for CVD and were aged 55 to 80 years. InterventionParticipants were randomly allocated to two groups with a Mediterranean diet intervention or a control diet. Vegetable intake was measured at baseline. Main outcome measuresMain outcomes were all-cause, cancer, and CVD mortality after a median follow-up of 4.8 years. Statistical analysesMultivariable-adjusted Cox regression models were fitted. ResultsThree hundred eighteen deaths were detected (cancer, n=127; CVD, n=81; and other, n=110). Cys326Cys individuals (prevalence 4.2%) presented higher total mortality rates than Ser326-carriers (P=0.009). The multivariable-adjusted hazard ratio for Cys326Cys vs Ser326-carriers was 1.69 (95% CI 1.09 to 2.62; P=0.018). This association was greater for CVD mortality (P=0.001). No relationship was detected for cancer mortality in the whole population (hazard ratio 1.07; 95% CI 0.47 to 2.45; P=0.867), but a significant age interaction (P=0.048) was observed, as Cys326Cys was associated with cancer mortality in participants <66.5 years (P=0.029). Recessive effects limited our ability to investigate Cys326Cys×diet interactions for cancer mortality. No statistically significant interactions for total or CVD mortality were found for the Mediterranean diet intervention. However, significant protective interactions for CVD mortality were found for vegetable intake (hazard ratio interaction per standard deviation 0.42; 95% CI 0.18 to 0.98; P=0.046). ConclusionsIn this population, the Cys326Cys-OGG1 genotype was associated with all-cause mortality, mainly CVD instead of cancer mortality. Additional studies are needed to provide further evidence on its dietary modulation.

Total sugar, added sugar, fructose, and sucrose intake and all-cause, cardiovascular, and cancer mortality: A systematic review and dose-response meta-analysis of prospective cohort studies

BackgroundStress hyperglycemia ratio (SHR) has emerged as an innovative biomarker for stress-induced hyperglycemia and various disease prognosis, yet its relationship with mortality in patients with type 2 diabetes and obesity (termed as diabesity) remains unclear. Accelerated biological aging increases susceptibility to chronic diseases and death. This study sought to examine the association between SHR and mortality in type 2 diabetes and obesity, and also investigate the potential mediating effects of accelerated biological aging in this relationship.MethodsWe analyzed 4253 individuals with type 2 diabetes and obesity from National Health and Nutritional Examination Survey, with mortality outcomes ascertained through linkage to the National Death Index (NDI). Two accelerated biological aging (PhenoAgeAccel and KDMAgeAccel) were calculated using chronological age and blood biomarkers. The clinical endpoints encompassed all-cause mortality, cardiovascular disease (CVD) mortality, and cancer mortality. We visualized survival differences through Kaplan–Meier methodology. We employed multivariable Cox regression, restricted cubic spline (RCS) analysis, and general linear regression models to evaluate the relationships. Mediation analysis was performed to quantify the accelerated biological aging’ contribution to the SHR-mortality link. Subgroup and sensitivity assessments were applied to verify the robustness of findings.ResultsOver a median follow-up period of 110.00 months (interquartile range, 40.00–152.00 months), we recorded 1139 all-cause deaths (26.78%), including 318 CVD deaths (7.48%), and 215 cancer death (5.06%). Kaplan–Meier curves showed higher SHR levels were associated with reduced survival (P < 0.001). After full adjustment for covariates, participants in the highest SHR tertile exhibited significantly elevated hazard ratios (HRs) compared to the reference tertile, with adjusted HRs of 1.32 for all-cause mortality, 1.38 for CVD mortality, and 1.61 for cancer mortality (all P < 0.001). RCS analysis revealed U-shaped relationships for all-cause and CVD mortality, while cancer mortality showed a linear positive correlation with SHR. Both two aging metrics exhibited linear relationships with the mortalities, with SHR positively correlated with KDMAgeAccel and PhenoAgeAccel (β = 5.00 and 1.15, respectively, both P < 0.01). Mediation analysis indicated KDMAgeAccel mediated 10.31%, 12.81%, and 3.65% of SHR’s effects on all-cause, CVD, and cancer mortality, respectively (all P < 0.05), while PhenoAgeAccel showed the suppression effect of SHR on all-cause and CVD mortality, as well as exacerbated SHR’s effect on cancer mortality. These findings remained consistent across all subgroup and sensitivity analyses.ConclusionBoth SHR and accelerated biological aging independently predict higher all-cause, CVD, and cancer mortality in patients with type 2 diabetes and obesity. Furthermore, KDMAgeAccel could significantly mediates these associations, while PhenoAgeAccel could potentially suppress the direct effect of SHR on all-cause and CVD mortality, and exacerbate SHR’s direct effect on cancer mortality. Interventions targeting both stress hyperglycemia and aging-related pathways may reduce mortality risks in patients with type 2 diabetes and obesity.Graphical abstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s12933-025-02931-1.

This study aims to systematically investigate the associations of varying volumes of vigorous-intensity physical activity (VPA) and its proportion to moderate-to-vigorous intensity physical activity (MVPA) with all-cause, cardiovascular disease (CVD), and cancer mortality. The review was registered in the PROSPERO (CRD42024525067). Web of Science, Embase, and PubMed were searched from inception to March 22, 2024. Empirical studies that investigated the effects of VPA compared to light-to-moderate intensity physical activities (LMPA) on all-cause, CVD, and cancer mortality were included. Additionally, studies that reported the effects of the proportion of VPA (relative to MVPA) on these mortality risks were also included. In total, 20 studies were included in the analyses. A curvilinear inverse dose-response relationship was observed between the volume of VPA and all-cause, CVD, and cancer mortality. Engaging in 180 minutes of VPA per week was associated with a substantial reduction in mortality risk: 22% for all-cause mortality, 23% for CVD mortality, and 14% for cancer mortality, compared to LMPA. Further increases in VPA volume yielded only modest additional benefits. Furthermore, a U-shaped inverse dose-response relationship was observed between the proportion of VPA (relative to MVPA) and all-cause as well as CVD mortality. Compared to 0% VPA, a 37.5% VPA (relative to MVPA) was associated with the greatest reduction in all-cause mortality (HR = 0.90, 95% CI [0.88-0.93]) and CVD mortality (HR = 0.88, 95% CI [0.83-0.94]) risk, and the size of the reduction remained stable when VPA constituted 30-60% of MVPA. Engaging in more than 180 minutes of VPA per week is associated with a substantial reduction in risks of all-cause, CVD, and cancer mortality. Maintaining VPA at 30-60% of total MVPA appears to be associated with maximal reduction in all-cause and CVD mortality risks.

We aimed to summarize the associations between food sources of fructose and cardiovascular diseases (CVD), cancer, and all-cause mortality risk using a systematic review and meta-analysis. We searched PubMed, Scopus, and Web of Science up to November 2020. We included cohort studies that investigated the relationship between mortality risk (all-cause, CVD, specific CVD, and total and site-specific cancers) and intake of ≥1 food source of fructose (fruit, fruit juice, breakfast cereals, sugar-sweetened beverages (SSBs), sweets, and yogurt) in general adult population. Summary hazard ratios and 95% CIs were estimated using a random-effects model for linear and nonlinear relationships. Findings indicated that each 100 g/d increase in fruit intake was associated with 8-13% lower risk of CVDs, stroke, gastrointestinal, and lung cancer mortality. For all-cause mortality, there was a beneficial relationship up to 200 g/d fruit, and then plateaued. For ischemic heart disease and cancer mortality, there was a beneficial relationship up to 300 g/d followed by a slight increase. Ingestion of breakfast cereals and sweets was also associated with lower risk of all-cause mortality. For yogurt, a non-linear marginal decrease in all-cause mortality was found. Ingestion of each 200 g/d yogurt was associated with a 14% lower risk of CVD mortality. Every 60 g/d increase in sweet intake was linked to a 5% lower risk of all-cause mortality. Contrariwise, every 250 g/d increase in SSBs intake was associated with 7–10% higher risk of all-cause and CVD mortality. In conclusion, beneficial associations were found between fruit, breakfast cereals, sweets, and yogurt with all-cause and/or CVD mortality risk. Fruit intake had also an inverse link with cancer mortality. Conversely, SSBs had a harmful relationship with all-cause and CVD mortality. Registry number: CRD42019144956