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.

Artificial sweeteners are generally used and recommended to alternate added sugar for health promotion. However, the health effects of artificial sweeteners remain unclear. In this study, we included 6371 participants from the National Health and Nutrition Examination Survey with artificial sweetener intake records. Logistic regression and Cox regression were applied to explore the associations between artificial sweeteners and risks of cardiometabolic disorders and mortality. Mendelian randomisation was performed to verify the causal associations. We observed that participants with higher consumption of artificial sweeteners were more likely to be female and older and have above medium socio-economic status. After multivariable adjustment, frequent consumers presented the OR (95 % CI) for hypertension (1·52 (1·29, 1·80)), hypercholesterolaemia (1·28 (1·10, 1·50)), diabetes (3·74 (3·06, 4·57)), obesity (1·52 (1·29, 1·80)), congestive heart failure (1·89 (1·35, 2·62)) and heart attack (1·51 (1·10, 2·04)). Mendelian randomisation confirmed the increased risks of hypertension and type 2 diabetes. Moreover, an increased risk of diabetic mortality was identified in participants who had artificial sweeteners ≥ 1 daily (HR = 2·62 (1·46, 4·69), P = 0·001). Higher consumption of artificial sweeteners is associated with increased risks of cardiometabolic disorders and diabetic mortality. These results suggest that using artificial sweeteners as sugar substitutes may not be beneficial.

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.

The role of dietary factors in osteoporotic fractures (OFs) in women is not fully elucidated. We investigated the associations between incidence of OF and dietary calcium, magnesium and soy isoflavone intake in a longitudinal study of 48 584 postmenopausal women. Multivariable Cox regression was applied to derive hazard ratios (HRs) and 95 % confidence intervals (CIs) to evaluate associations between dietary intake, based on the averages of two assessments that took place with a median interval of 2⋅4 years, and fracture risk. The average age of study participants is 61⋅4 years (range 43⋅3–76⋅7 years) at study entry. During a median follow-up of 10⋅1 years, 4⋅3 % participants experienced OF. Compared with daily calcium intake ≤400 mg/d, higher calcium intake (>400 mg/d) was significantly associated with about a 40–50 % reduction of OF risk among women with a calcium/magnesium (Ca/Mg) intake ratio ≥1⋅7. Among women with prior fracture history, high soy isoflavone intake was associated with reduced OF risk; the HR was 0⋅72 (95 % CI 0⋅55, 0⋅93) for the highest (>42⋅0 mg/d) v. lowest (<18⋅7 mg/d) quartile intake. This inverse association was more evident among recently menopausal women (<10 years). No significant association between magnesium intake and OF risk was observed. Our findings provide novel information suggesting that the association of OF risk with dietary calcium intake was modified by Ca/Mg ratio, and soy isoflavone intake was modified by history of fractures and time since menopause. Our findings, if confirmed, can help to guide further dietary intervention strategies for OF prevention.

Dairy product intake was suggested to reduce the risk of gastrointestinal cancers. This study investigated the association between dairy product intake and the risk of pancreatic cancer (PAC) using a prospective cohort study and meta-analysis of prospective cohort studies. First, we included 59 774 people aged 40–79 years from the Japan Collaborative Cohort Study (JACC Study). The Cox regression was used to compute the hazard ratios (HR) and 95 % CI of incident PAC for individuals who reported the highest intakes of milk, cheese and yogurt compared with not consuming the corresponding dairy products. Then, we combined our results with those from other four prospective cohort studies that were eligible after searching several databases, in a meta-analysis, using the fixed-effects model before evaluating publication bias and heterogeneity across studies. In the JACC Study, the highest v. no intakes of milk, cheese and yogurt were not associated with the reduced risk of PAC after a median follow-up of 13·4 years: HR (95 % CI) = 0·93 (0·64, 1·33), 0·91 (0·51, 1·62) and 0·68 (0·38, 1·21), respectively. The results did not significantly change in the meta-analysis: 0·95 (0·82, 1·11) for milk, 1·16 (0·87, 1·55) for cheese and 0·91 (0·79, 1·05) for yogurt. The meta-analysis showed no signs of publication bias or heterogeneity across studies. To conclude, consumption of milk, cheese and yogurt was not associated with the risk of PAC either in the JACC Study or the meta-analysis.

This study aimed to investigate the association between individual and combinations of macronutrients with premature death, CVD and dementia. Sex differences were investigated. Data were utilised from a prospective cohort of 120 963 individuals (57 % women) within the UK Biobank, who completed ≥ two 24-h diet recalls. The associations of macronutrients, as percentages of total energy intake, with outcomes were investigated. Combinations of macronutrients were defined using k-means cluster analysis, with clusters explored in association with outcomes. There was a higher risk of death with high carbohydrate intake (hazard ratios (HR), 95 % CI upper v. lowest third 1·13 (1·03, 1·23)), yet a lower risk with higher intakes of protein (upper v. lowest third 0·82 (0·76, 0·89)). There was a lower risk of CVD with moderate intakes (middle v. lowest third) of energy and protein (sub distribution HR (SHR), 0·87 (0·79, 0·97) and 0·87 (0·79, 0·96), respectively). There was a lower risk of dementia with moderate energy intake (SHR 0·71 (0·52, 0·96)). Sex differences were identified. The dietary cluster characterised by low carbohydrate, low fat and high protein was associated with a lower risk of death (HR 0·84 (0·76, 0·93)) compared with the reference cluster and a lower risk of CVD for men (SHR 0·83 (0·71, 0·97)). Given that associations were evident, both as single macronutrients and for combinations with other macronutrients for death, and for CVD in men, we suggest that the biggest benefit from diet-related policy and interventions will be when combinations of macronutrients are targeted.

Healthy Nordic diet has been beneficially associated with CHD risk factors, but few studies have investigated risk of developing CHD. We investigated the associations of healthy Nordic diet with major CHD risk factors, carotid atherosclerosis and incident CHD in middle-aged and older men from eastern Finland. A total of 1981 men aged 42–60 years and free of CHD at baseline in 1984–1989 were investigated. Diet was assessed with 4-d food recording and the healthy Nordic diet score was calculated based on the Baltic Sea Diet Score. Carotid atherosclerosis was assessed by ultrasonography of the common carotid artery intima–media thickness in 1053 men. ANCOVA and Cox proportional hazards regression analyses were used for analyses. Healthy Nordic diet score was associated with lower serum C-reactive protein (CRP) concentrations (multivariable-adjusted extreme-quartile difference 0·66 mg/l, 95 % CI 0·11, 1·21 mg/l) but not with serum lipid concentrations, blood pressure or carotid atherosclerosis. During the average follow-up of 21·6 years (sd 8·3 years), 407 men had a CHD event, of which 277 were fatal. The multivariable-adjusted hazard ratios in the lowest v. the highest quartile of the healthy Nordic diet score were 1·15 (95 % CI 0·87, 1·51) for any CHD event (P trend 0·361) and 1·44 (95 % CI 0·99, 2·08) (P trend 0·087) for fatal CHD event. We did not find evidence that adherence to a healthy Nordic diet would be associated with a lower risk of CHD or with carotid atherosclerosis or major CHD risk factors, except for an inverse association with serum CRP concentrations.

According to World Cancer Research Fund International/American Institute for Cancer Research, it is ‘probable’ that dairy products decrease the risk of colorectal cancer (CRC). However, meta-analyses restricted to women have not shown associations between milk intake and risk of CRC. The aim of this study was to examine the association between milk intake and risk of CRC, colon cancer and rectal cancer among women. Data from 81 675 participants in the Norwegian Women and Cancer Cohort Study were included, and multivariable Cox proportional hazard regression models were used to investigate milk intake using two different analytical approaches: one that included repeated measurements and one that included baseline measurements only (872 and 1084 CRC cases, respectively). A weak inverse association between milk intake and risk of colon cancer may be indicated both in repeated measurements analyses and in baseline data analyses. Hazard ratios (HR) for colon cancer of 0·80 (95 % CI 0·62, 1·03, Ptrend 0·07) and 0·81 (95 % CI 0·64, 1·01, Ptrend 0·03) and HR for rectal cancer of 0·97 (95 % CI 0·67, 1·42, Ptrend 0·92) and 0·71 (95 % CI 0·50, 1·01, Ptrend 0·03) were found when comparing the high with the no/seldom milk intake group in energy-adjusted multivariable models. Our study indicates that there may be a weak inverse association between milk intake and risk of colon cancer among women. The two analytical approaches yielded different results for rectal cancer and hence CRC. Our study indicates that the use of single or repeated measurements in analyses may influence the results.

We aimed to examine the association between the Alternative Healthy Eating Index updated in 2010 (AHEI-2010), the Dietary Inflammatory Index (DIITM) and risk of mortality in the Whitehall II study. We also conducted a meta-analysis on the DII-based results from previous studies to summarise the overall evidence. Data on dietary behaviour assessed by self-administered repeated FFQ and on mortality status were available for 7627 participants from the Whitehall II cohort. Cox proportional hazards regression models were performed to assess the association between cumulative average of AHEI-2010 and DII scores and mortality risk. During 22 years of follow-up, 1001 participants died (450 from cancer, 264 from CVD). Both AHEI-2010 (mean=48·7 (sd 10·0)) and DII (mean=0·37 (sd 1·41)) were associated with all-cause mortality. The fully adjusted hazard ratio (HR) per sd, were 0·82; 95 % CI 0·76, 0·88 for AHEI-2010 and 1·18; 95 % CI 1·08, 1·29 for DII. Significant associations were also observed with cardiovascular and cancer mortality risk. For DII, a meta-analysis (using fixed effects) from this and four previous studies showed a positive association of DII score with all-cause (HR=1·04; 95 % CI 1·03, 1·05, 28 891deaths), cardiovascular (HR=1·05; 95 % CI 1·03, 1·07, 10 424 deaths) and cancer mortality (HR=1·05; 95 % CI 1·03, 1·07, n 8269).The present study confirms the validity to assess overall diet through AHEI-2010 and DII in the Whitehall II cohort and highlights the importance of considering diet indices related to inflammation when evaluating all-cause, cardiovascular and cancer mortality risk.

Knowledge regarding association of dietary branched-chain amino acid (BCAA) and type 2 diabetes (T2D), and the contribution of BCAA from meat to the risk of T2D are scarce. We evaluated associations between dietary BCAA intake, meat intake, interaction between BCAA and meat intake and risk of T2D. Data analyses were performed for 74 155 participants aged 50−79 years at baseline from the Women’s Health Initiative for up to 15 years of follow-up. We excluded from analysis participants with treated T2D, and factors potentially associated with T2D or missing covariate data. The BCAA and total meat intake was estimated from FFQ. Using Cox proportional hazards models, we assessed the relationship between BCAA intake, meat intake, and T2D, adjusting for confounders. A 20 % increment in total BCAA intake (g/d and %energy) was associated with a 7 % higher risk for T2D (hazard ratio (HR) 1·07; 95 % CI 1·05, 1·09). For total meat intake, a 20 % increment was associated with a 4 % higher risk of T2D (HR 1·04; 95 % CI 1·03, 1·05). The associations between BCAA intake and T2D were attenuated but remained significant after adjustment for total meat intake. These relations did not materially differ with or without adjustment for BMI. Our results suggest that dietary BCAA and meat intake are positively associated with T2D among postmenopausal women. The association of BCAA and diabetes risk was attenuated but remained positive after adjustment for meat intake suggesting that BCAA intake in part but not in full is contributing to the association of meat with T2D risk.

The dietary inflammatory indexTM (DII) has been shown to correlate with concentrations of several inflammatory markers and a variety of chronic disease endpoints, including cancers of various anatomic sites. We investigated whether the DII was associated with the risk for death among women with breast cancer (BrCa). This retrospective cohort study included 1453 women with BrCa, diagnosed between 1990 and 1994, and previously enrolled in a case–control study in northern Italy. With a median follow-up of 12·6 years, we observed 503 deaths, among which 398 were due to BrCa. The usual diet was assessed at BrCa diagnosis using a validated FFQ. DII scores were calculated using thirty-one foods/nutrients. Hazard ratios (HR) of death from all causes or from BrCa, with corresponding 95 % CI, were calculated using the Cox models, adjusted for age at diagnosis, tumour stage, oestrogen/progesterone receptor status and other potential confounders. The median DII score of the study women was −1·23, with a relatively narrow range (interquartile range −2·24 to −0·11), indicating a mainly anti-inflammatory diet. There was no difference in survival according to DII tertiles, neither considering all-cause mortality (HRtertile III v. I 1·00; 95 % CI 0·78, 1·28) nor BrCa-specific mortality (HRtertile III v. I 0·97; 95 % CI 0·73, 1·27). Study findings did not suggest an association between the inflammatory potential of diet, measured by the DII, and the survival of BrCa women. However, further studies are needed in populations reporting higher DII scores and a broader range of variability in the scores.

Prospective studies on the association between soft drink consumption and incident risk of the metabolic syndrome (MetS) have not been carried out in Asians. We explored the sex-specific association between soft drink consumption and incident risk of the MetS in Korean adults during 10 years of follow-up. A total of 5797 subjects who were free of the MetS at baseline were studied. Soft drink consumption was assessed using a semi-quantitative FFQ. Time-dependent Cox proportional hazard model was used to examine hazard ratios (HR) of incidence of the MetS and its components in relation to soft drink consumption. In women, the multivariable-adjusted HR for developing the MetS was 1·8-fold higher in frequent consumers of soft drinks (≥4 servings/week) compared with rare consumers (95 % CI 1·23, 2·64). The adjusted HR for elevated blood pressure increased by 2-fold (95 % CI 1·24, 3·14) and for hypertriacylglycerolaemia by 1·9-fold (95 % CI 1·19, 2·88) in frequent consumers of soft drinks compared with rare consumers. However, in men, there was no association between soft drink consumption and incident risk of the MetS or its components. Frequent soft drink consumption was associated with increased risk of developing the MetS and its components only in middle-aged Korean women, suggesting sex differences for the risk of the MetS related to diet.

Prospective studies assessing the association between fibre intake or fibre-rich food consumption and the risk of CVD have often been limited by baseline assessment of diet. Thus far, no study has used yearly repeated measurements of dietary changes during follow-up. Moreover, previous studies included healthy and selected participants who did not represent subjects at high cardiovascular risk. We used yearly repeated measurements of diet to investigate the association between fibre intake and CVD in a Mediterranean cohort of elderly adults at high cardiovascular risk. We followed-up 7216 men (55–80 years) and women (60–80 years) initially free of CVD for up to 7 years in the PREvención con DIeta MEDiterránea study (registered as ISRCTN35739639). A 137-item validated FFQ was repeated yearly to assess diet. The primary end point, confirmed by a blinded ad hoc Event Adjudication Committee, was a composite of cardiovascular death, myocardial infarction and stroke. Time-dependent Cox’s regression models were used to estimate the risk of CVD according to baseline dietary exposures and to their yearly updated changes. We found a significant inverse association for fibre (Pfor trend=0·020) and fruits (Pfor trend=0·024) in age-sex adjusted models, but the statistical significance was lost in fully adjusted models. However, we found a significant inverse association with CVD incidence for the sum of fruit and vegetable consumption. Participants who consumed in total nine or more servings/d of fruits plus vegetables had a hazard ratio 0·60 (95 % CI 0·40, 0·96) of CVD in comparison with those consuming <5 servings/d.

Exclusive breast-feeding (EBF) for 6 months supports optimal infant growth, health and development. This paper examined whether maternal HIV status was associated with EBF and other infant feeding practices. Pregnant women were enrolled after HIV counselling, and their babies were followed up for up to 1 year. Data on household socio-economics and demographics, maternal characteristics and infants’ daily diet were available for 482 infants and their mothers (150 HIV-positive (HIV-P), 170 HIV-negative (HIV-N) and 162 HIV-unknown (HIV-U)). Survival analyses estimated median EBF duration and time to introduction of liquids and foods; hazards ratios (HR) used data from 1–365 and 1–183 d, adjusting for covariates. Logistic regression estimated the probability of EBF for 6 months. Being HIV-P was associated with a shorter EBF duration (139 d) compared with HIV-N (163 d) and HIV-U (165 d) (P=0·004). Compared with HIV-N, being HIV-P was associated with about a 40 % higher risk of stopping EBF at any time point (HR 1·39; 95 % CI 1·06, 1·84; P=0·018) and less than half as likely to complete 6 months of EBF (adjusted OR 0·42; 95 % CI 0·22, 0·81; P=0·01). Being HIV-P tended to be or was associated with a higher risk of introducing non-milk liquids (HR 1·34; 95 % CI 0·98, 1·83; P=0·068), animal milks (HR 2·37; 95 % CI 1·32, 4·24; P=0·004) and solids (HR 1·56; 95 % CI 1·10, 2·22; P=0·011) during the first 6 months. Weight-for-age Z-score was associated with EBF and introducing formula. Different factors (ethnicity, food insecurity, HIV testing strategy) were associated with the various feeding behaviours, suggesting that diverse interventions are needed to promote optimal infant feeding.

This research describes the onset of 13 health conditions and death among 38 adults with spinal cord injuries (SCIs) and 149 adults with traumatic brain injuries (TBIs) compared to adults without disabilities in the same primary care setting, using a retrospective cohort design. The subjects were accrued from an urban and a rural practice, both affiliated with a university family medicine department. Survival analyses, using Cox proportional hazard models, were used to model the onset of each of the health conditions. The results indicated adults with SCI had an increased risk for onset of chronic obstructive pulmonary disease and depression. Individuals with TBIs had an increased risk for onset of anxiety, chronic obstructive pulmonary disease, dementia, depression, and seizures. Neither group had increased risk for asthma, cancer, coronary artery disease, congestive heart failure, diabetes, hypertension, obesity, or transient ischaemic attack. The only conditions with increased risk were those previously identified as secondary to traumatic injury. The other conditions including death did not have higher incidence among the study group, during 7–9 years of retrospective follow-up.