The long-term impact of eating duration on the risk of all-cause mortality remains unclear, with limited exploration of how different levels of energy intake and physical activity might influence this impact. To investigate, 24 484 American adults from the National Health and Nutrition Examination Survey spanning 1999–2018 were included. Eating duration was assessed via 24-h dietary recall, and all-cause mortality data were sourced from the National Death Index. The relationship between eating duration and all-cause mortality was analysed using Cox proportional hazards regression models, restricted cubic splines and stratification analysis with complex weighted designs. The median (IQR) of eating duration for participants was 12·5 (11·0, 14·0) h. In this study, 2896 death events were observed, and the median follow-up time (IQR) was 125 (77, 177) months. After multivariable adjustment, compared with Q1, Q2, Q3 and Q4 had reduced risks of all-cause mortality by 17, 15 and 13 %, respectively. Furthermore, each additional hour of eating duration was correlated with a 2 % decrease in the risk of all-cause mortality. Additionally, a non-linear dose–response relationship was observed between eating duration and the risk of all-cause mortality, showing a U-shaped relationship from 8·9 h to 15·3 h (P for non-linearity < 0·05). Interestingly, the non-linear dose–response relationship was observed exclusively among individuals with high energy intake or a lightly active physical activity level. These findings suggest potential health benefits from adjusting eating duration, though further prospective studies are needed for validation.

Previous studies have found direct associations between glycaemic index (GI) and glycaemic load (GL) with chronic diseases. However, this evidence has not been consistent in relation to mortality, and most data regarding this association come from high-income and low-carbohydrate-intake populations. The aim of this study was to evaluate the association between the overall GI and dietary GL and all-cause mortality, CVD and breast cancer mortality in Mexico. Participants from the Mexican Teachers’ Cohort (MTC) study in 2006–2008 were followed for a median of 10 years. Overall GI and dietary GL were calculated from a validated FFQ. Deaths were identified by the cross-linkage of MTC participants with two national mortality registries. Cox proportional hazard models were used to estimate the impact of GI and GL on mortality. We identified 1198 deaths. Comparing the lowest and highest quintile, dietary GI and GL appeared to be marginally associated with all-cause mortality; GI, 1·12 (95 % CI: 0·93, 1·35); GL, 1·12 (95 % CI: 0·87, 1·44). Higher GI and GL were associated with increased risk of CVD mortality, GI, 1·30 (95 % CI: 0·82, 2·08); GL, 1·64 (95 % CI: 0·87, 3·07) and with greater risk of breast cancer mortality; GI, 2·13 (95 % CI: 1·12, 4·06); GL, 2·43 (95 % CI: 0·90, 6·59). It is necessary to continue the improvement of carbohydrate quality indicators to better guide consumer choices and to lead the Mexican population to limit excessive intake of low-quality carbohydrate foods.

We aimed to investigate the association of metabolic obesity phenotypes with all-cause mortality risk in a rural Chinese population. This prospective cohort study enrolled 15 704 Chinese adults (38·86 % men) with a median age of 51·00 (interquartile range: 41·00–60·00) at baseline (2007–2008) and followed up during 2013–2014. Obesity was defined by waist circumference (WC: ≥ 90 cm for men and ≥ 80 cm for women) or waist-to-height ratio (WHtR: ≥ 0·5). The hazard ratio (HR) and 95 % CI for the risk of all-cause mortality related to metabolic obesity phenotypes were calculated using the Cox hazards regression model. During a median follow-up of 6·01 years, 864 deaths were identified. When obesity was defined by WC, the prevalence of participants with metabolically healthy non-obesity (MHNO), metabolically healthy obesity (MHO), metabolically unhealthy non-obesity (MUNO) and metabolically unhealthy obesity (MUO) at baseline was 12·12 %, 2·80 %, 41·93 % and 43·15 %, respectively. After adjusting for age, sex, alcohol drinking, smoking, physical activity and education, the risk of all-cause mortality was higher with both MUNO (HR = 1·20, 95 % CI 1·14, 1·26) and MUO (HR = 1·20, 95 % CI 1·13, 1·27) v. MHNO, but the risk was not statistically significant with MHO (HR = 0·99, 95 % CI 0·89, 1·10). This result remained consistent when stratified by sex. Defining obesity by WHtR gave similar results. MHO does not suggest a greater risk of all-cause mortality compared to MHNO, but participants with metabolic abnormality, with or without obesity, have a higher risk of all-cause mortality. These results should be cautiously interpreted as the representation of MHO is small.

Type 2 diabetes (T2D) and CVD are major causes of mortality and chronic morbidity. Whilst mortality from CVD has decreased they remain the largest cause of death in Europe and the prevalence of T2D is increasing rapidly. A consistent component of public health advice is to reduce intake of SFA to reduce CVD in particular, which implies limiting dairy food consumption. The prospective studies and randomised controlled trials included in this review show that for dairy foods at least, SFA are not consistently associated with CVD or T2D risk. For CVD the association with dairy foods is generally neutral despite dairy foods being the major source of SFA in many diets. This creates considerable doubt, at least for dairy foods, concerning the validity of the traditional diet-heart hypothesis which positively relates SFA intake to increased serum LDL-cholesterol and subsequent increased CVD. There is now emerging evidence to explain this which is highly relevant to dairy foods. These include the potentially counterbalancing effect of SFA-stimulated HDL-cholesterol and specific food matrix factors. In addition, SFA are associated with the less atherogenic large buoyant LDL particles and possible counterbalancing hypotensive effects of dairy proteins. Overall, dairy foods have either a neutral or beneficial association with CVD and T2D. Beneficial associations are seen for blood pressure and the reduced T2D risk linked to yoghurt consumption, a subject that needs urgent attention given the sharp rise in T2D prevalence in many countries.

The association between dietary Cu intake and mortality risk remains uncertain. We aimed to investigate the relationship of dietary Cu intake with all-cause mortality among Chinese adults. A total of 17 310 participants from the China Health and Nutrition Survey, a national ongoing open cohort of Chinese participants, were included in the analysis. Dietary intake was measured by three consecutive 24-h dietary recalls in combination with a weighing inventory over the same 3 d. The average intakes of the 3-d dietary macronutrients and micronutrients were calculated. The study outcome was all-cause mortality. During a median follow-up of 9·0 years, 1324 (7·6 %) participants died. After adjusting for sex, age, BMI, ever alcohol drinking, ever smoking, education levels, occupations, urban or rural residents, systolic blood pressure, diastolic blood pressure and the intakes of fat, protein and carbohydrate, the association between dietary Cu intake and all-cause mortality followed a J-shape (P for nonlinearity = 0·047). When dietary Cu intake was assessed as quartiles, compared with those in the first quartile (<1·60 mg/d), the adjusted hazard ratios for all-cause mortality were 0·87 (95 % CI (0·71, 1·07)), 0·98 (95 % CI (0·79, 1·21)) and 1·49 (95 % CI (1·19, 1·86)), respectively, in participants in the second (1·60–<1·83 mg/d), third (1·83–<2·09 mg/d) and fourth (≥2·09 mg/d) quartiles. A series of subgroup analyses and sensitivity analyses showed similar results. Overall, our findings emphasised the importance of maintaining optimal dietary Cu intake levels for prevention of premature death.

One potential mechanism by which diet and lifestyle may affect chronic disease risk and subsequent mortality is through chronic systemic inflammation. In this study, we investigated whether the inflammatory potentials of diet and lifestyle, separately and combined, were associated with all-cause, all-CVD and all-cancer mortality risk. We analysed data on 18 484 (of whom 4103 died during follow-up) Black and White men and women aged ≥45 years from the prospective REasons for Geographic and Racial Differences in Stroke study. Using baseline (2003–2007) Block 98 FFQ and lifestyle questionnaire data, we constructed the previously validated inflammation biomarker panel-weighted, 19-component dietary inflammation score (DIS) and 4-component lifestyle inflammation score (LIS) to reflect the overall inflammatory potential of diet and lifestyle. From multivariable Cox proportional hazards models, the hazards ratios (HR) and their 95 % CI for the DIS–all-cause mortality and LIS–all-cause mortality risk associations were 1·32 (95 % CI (1·18, 1·47); P for trend < 0·01) and 1·25 (95 % CI (1·12, 1·38); P for trend < 0·01), respectively, among those in the highest relative to the lowest quintiles. The findings were similar by sex and race and for all-cancer mortality, but weaker for all-CVD mortality. The joint HR for all-cause mortality among those in the highest relative to the lowest quintiles of both the DIS and LIS was 1·91 (95 % CI 1·57, 2·33) (P for interaction < 0·01). Diet and lifestyle, via their contributions to systemic inflammation, separately, but perhaps especially jointly, may be associated with higher mortality risk among men and women.

Diet and physical activity (PA) have been studied extensively in epidemiology as single or combined lifestyle factors; however, their interaction has not been studied thoroughly. Studying potential synergisms between lifestyle components with a comprehensive interaction analysis, including additive measures of interaction, provides key insights into the nature of their joint effect and helps target interventions more effectively. First, a comprehensive review was conducted to assess the potential research gap regarding reported interaction analyses conducted in studies assessing the Mediterranean diet (MedDiet) in combination with PA on all-cause mortality. Thereafter, we prospectively assessed the joint association of the MedDiet with PA on all-cause mortality in the Seguimiento Universidad de Navarra (SUN) cohort, followed by both multiplicative and additive interaction analyses. The conjoint effect of low adherence to the MedDiet and low PA observed an increased risk greater than the individual risk factors, suggesting a potential additive interaction or synergism between both exposures, with relative risk due to interaction (RERI) and (95 % confidence interval (95 % CI)) = 0·46 (–0·83 to 1·75) and attributable proportion (95 % CI) due to interaction of 36 % (–0·62, 1·34). No multiplicative interaction was detected. Studying interactions between lifestyle factors, such as the MedDiet and PA, is particularly relevant given the current research gaps in studying the complexities of combined aspects of lifestyle in comparison with isolated behaviours. Our findings underline the important public health message of adhering to both the MedDiet and PA for the prevention of premature mortality.

Recent studies found positive associations between intake of red meat and processed meat and total mortality; however, substitution of red meat with poultry and fish has been poorly investigated. We aimed to investigate associations for substitutions of red meat (unprocessed/processed) and total mortality and deaths due to cancer or CVD. We used data from the Danish Diet, Cancer and Health cohort, including 57 053 participants aged 50–64 years at baseline. Information on diet was collected through a validated 192-item FFQ. Information regarding total mortality, deaths due to cancer and deaths due to CVD was obtained by record linkage. Cox proportional hazards models were used to estimate the hazard ratio (HR) of 150 g/week substitutions of red meat with poultry or fish. During a follow-up (mean 16·1 years), 8840 deaths occurred (4567 were due to cancer; 1816 due to CVD). The adjusted HR for total death when substituting 150 g/week total red meat with poultry was 0·96 (95 % CI 0·95, 1·00) and with fish 0·99 (95 % CI 0·97, 1·01). Corresponding HR for cancer death or CVD death were similar. Substitution of processed red meat with fish or poultry was more consistently associated with a lower mortality than substitution of unprocessed red meat. For example, the adjusted HR for total death when substituting 150 g/week processed red meat with poultry was 0·95 (95 % CI 0·92, 0·98). We found that replacing processed red meat with poultry or fish was associated with a lower risk of total mortality and deaths due to cancer, but not deaths due to CVD.

High fibre intake is associated with reduced mortality risk in both general and chronic kidney disease populations. However, in dialysis patients, such data are limited. Therefore, the association between dietary fibre intake (DFI) and the risk of all-cause and CVD mortality was examined in this study. A total of 1044 maintenance haemodialysis (MHD) patients from eight outpatient dialysis centres in China were included in this study. Data on DFI were collected using 24-h dietary recalls for 3 d in a week and were normalised to actual dry weight. The study outcomes included all-cause and CVD mortality. Over a median of 46 months of follow-up, 354 deaths were recorded, of which 210 (59 %) were due to CVD. On assessing DFI as tertiles, the CVD mortality risk was significantly lower in patients in tertiles 2–3 (≥0·13 g/kg per d; hazard ratio (HR) 0·71; 95 % CI 0·51, 0·97) compared with those in tertile 1 (<0·13 g/kg per d). A similar but non-significant trend was found for the association between DFI (tertiles 2–3 v. tertile 1; HR 0·83; 95 % CI 0·64, 1·07) and all-cause mortality. In summary, higher DFI was associated with lower CVD mortality risk among Chinese MHD patients. This study emphasises the significance of DFI in MHD patients and provides information that is critical for the improvement of dietary guidelines for dialysis patients.

Excessive Ca intakes have been proposed to associate with vascular calcification and a higher risk of prostate cancer. We investigated the associations of supplemental and dietary Ca intake with mortality using data from 497 828 UK Biobank participants. The average follow-up was 4·2 years and 14 255 participants died, 8297 from cancer, 2959 from CVD and 572 from respiratory disease. The use of Ca supplements and milk consumption were associated with differences in mortality in younger (≤65 years) but not in older participants (>65 years, Pinteraction ≤ 0·04 for all comparisons). Among participants <65 years, there was an inverse association between Ca supplementation (OR 0·91, 95 % CI 0·83, 0·99) and milk consumption (OR 0·93, 95 % CI 0·86, 1·00) with respect to all-cause mortality. In the same age group, milk drinkers had lower odds of cancer mortality (OR 0·89, 95 % CI 0·80, 0·98) but Ca supplement use was associated with increased odds of respiratory mortality (OR 1·69, 95 % CI 1·16, 2·74). All associations in participants aged ≥65 years were null after full adjustment. In sensitivity analyses stratified by hormone replacement therapy, Ca supplement use was associated with decreased odds of cancer mortality in users but increased risk in other women (OR 0·81, 95 % CI 0·69, 0·94 v. OR 1·17, 95 % CI 1·01, 1·35, respectively). To conclude, we saw little evidence for harm with dietary or supplemental Ca. Further studies are required to confirm the proposed interaction with hormone replacement therapy and to exclude reverse causation as a determinant in the association between Ca supplements and increased risk of respiratory diseases.

Maintenance haemodialysis (MHD) is the use of a machine to filter wastes, salts and fluid from blood for at least 3 months to prolong the life of patients with advanced kidney failure. Although low dietary energy intake (DEI) has been observed in MHD patients, few studies have related DEI to the risk of mortality. To explore this relationship, a study included 1039 MHD patients from eight centres was conducted. DEI was assessed by three 24-h diet recalls and was normalised to ideal body weight (IBW). All-cause mortality and CVD mortality were the primary and secondary outcomes, respectively. During a median follow-up of 28 months, a U-shaped relationship was observed between DEI and all-cause or CVD mortality. The risk of all-cause mortality decreased significantly with the increase of DEI in participants with DEI <167·4 kJ/kg IBW per d (hazard ratio (HR) 0·98; 95 % CI 0·96, 1·00) and increased significantly with the increase of DEI in those with DEI ≥167·4 kJ/kg IBW per d (HR 1·12; 95 % CI 1·04, 1·20). Similarly, the risk of CVD mortality decreased with the increase of DEI in participants with DEI <152·7 kJ/kg IBW per d (HR 0·96; 95 % CI 0·93, 0·99) and increased with the increase of DEI in participants with DEI ≥152·7 kJ/kg IBW per d (HR 1·11; 95 % CI 1·04, 1·18). In summary, there was a U-shaped association between DEI and all-cause or CVD mortality, with a turning point at about 167·4 and 152·7 kJ/kg IBW per d, respectively, in MHD patients.