Dietary Mn intake may have a beneficial effect in reducing cancer risk; however, its association with thyroid cancer (TC) risk remains inadequately understood. Additionally, Mn was associated with inflammation markers. Thus, we examined whether dietary Mn intake emerges a protective role against TC and whether this preventative effect has an interaction with IL1 receptor type 1 (IL1R1) rs3917225. The prospective study was designed at National Cancer Center in Korea between October 2007 and December 2020 including 17 754 participants. We identified TC cases by following participants until December 2020. Mn intake was collected using a semiquantitative food frequency questionnaire (SQFFQ). Genotyping was performed to determine IL1R1 rs3917225. The hazard ratios (HR) and 95 % confidence interval (CI) were calculated with a Cox proportional hazards model. We ascertained 108 incident TC cases throughout follow-up duration. Dietary Mn intake was found to be inversely associated with TC risk (HR (95 % CI)=0·64 (0·44, 0·95)). However, IL1R1 rs3917225 seemed to modify this association; the protective effect was limited to G-allele carriers (HR = 0·30 (0·11, 0·86), P interaction=0·028). A higher dietary Mn was suggested to be a protective factor against TC. Additionally, we drew a potential biological interaction between Mn intake and IL1R1 rs3917225 with a greater effect among individuals with a minor allele. This implies that when considering the cancer-preventive role of Mn, it is important to account for the influence of inflammatory gene participation.

Folate metabolism is involved in the development and progression of various cancers. We investigated the association of single nucleotide polymorphisms (SNP) in folate-metabolising genes and their interactions with serum folate concentrations with overall survival (OS) and liver cancer-specific survival (LCSS) of newly diagnosed hepatocellular carcinoma (HCC) patients. We detected the genotypes of six SNP in three genes related to folate metabolism: methylenetetrahydrofolate reductase (MTHFR), 5-methyltetrahydrofolate-homocysteine methyltransferase reductase (MTRR) and 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR). Cox proportional hazard models were used to calculate multivariable-adjusted hazard ratios (HR) and 95 % CI. This analysis included 970 HCC patients with genotypes of six SNP, and 864 of them had serum folate measurements. During a median follow-up of 722 d, 393 deaths occurred, with 360 attributed to HCC. In the fully-adjusted models, the MTRR rs1801394 polymorphism was significantly associated with OS in additive (per G allele: HR = 0·84, 95 % CI: 0·71, 0·99), co-dominant (AG v. AA: HR = 0·77; 95 % CI: 0·62, 0·96) and dominant (AG + GG v. AA: HR = 0·78; 95 % CI: 0·63, 0·96) models. Carrying increasing numbers of protective alleles was linked to better LCSS (HR10–12 v. 2–6 = 0·70; 95 % CI: 0·49, 1·00) and OS (HR10–12 v. 2–6 = 0·67; 95 % CI: 0·47, 0·95). Furthermore, we observed significant interactions on both multiplicative and additive scales between serum folate levels and MTRR rs1801394 polymorphism. Carrying the variant G allele of the MTRR rs1801394 is associated with better HCC prognosis and may enhance the favourable association between higher serum folate levels and improved survival among HCC patients.

Epidemiological and clinical trial evidence indicates that n-6 polyunsaturated fatty acid (PUFA) intake is cardioprotective. Nevertheless, claims that n-6 PUFA intake promotes inflammation and oxidative stress prevail. This narrative review aims to provide health professionals with an up-to-date evidence overview to provide the requisite background to address patient/client concerns about oils containing predominantly unsaturated fatty acids (UFA), including MUFA and PUFA. Edible plant oils, commonly termed vegetable oils, are derived from vegetables, nuts, seeds, fruits and cereal grains. Substantial variation exists in the fatty acid composition of these oils; however, all are high in UFA, while being relatively low in saturated fatty acids (SFA), except for tropical oils. Epidemiological evidence indicates that higher PUFA intake is associated with lower risk of incident CVD and type 2 diabetes mellitus (T2DM). Additionally, replacement of SFA with PUFA is associated with reduced risk of CVD and T2DM. Clinical trials show higher intake of UFA from plant sources improves major CVD risk factors, including reducing levels of atherogenic lipids and lipoproteins. Importantly, clinical trials show that increased n-6 PUFA (linoleic acid) intake does not increase markers of inflammation or oxidative stress. Evidence-based guidelines from authoritative health and scientific organisations recommend intake of non-tropical vegetable oils, which contain MUFA and n-6 PUFA, as part of healthful dietary patterns. Specifically, vegetable oils rich in UFA should be consumed instead of rich sources of SFA, including butter, tallow, lard, palm and coconut oils.

The contribution of dietary saturated fatty acids (SFA) to cardiovascular disease (CVD) and mortality remains debated after decades of research. Few previous studies had repeated dietary assessments and power to assess mortality. Evidence for individual SFA is limited. In this large population-based cohort study, we investigated associations between intake of total and individual SFA and risk of total and CVD mortality. Adult residents (mean 41·1 years at baseline) in three Norwegian counties were invited to repeated health screenings between 1974 and 1988 (> 80 % attendance). We calculated cumulative average intakes of macronutrients from semi-quantitative FFQ. Median (interquartile range) intake of SFA was 14·6 % (12·8–16·6 %) of total energy (E%). Hazard ratios (HR) and 95 % CI were estimated using multivariable Cox regression models to assess total, CVD, ischaemic heart disease (IHD) and acute myocardial infarction (AMI) mortality. Among 78 725 participants, 28 555 deaths occurred during a median follow-up of 33·5 years, with 9318 deaths due to CVD. Higher intake of SFA (replacing carbohydrates) was positively associated with all mortality endpoints, including total (HR per 5 E% increment, 1·18; 95 % CI 1·13, 1·23) and CVD mortality (1·16; 95 % CI 1·07, 1·25). Theoretical isoenergetic substitution of SFA with carbohydrates or MUFA was associated with lower risk. Of individual SFA, myristic (14:0) and palmitic acid (16:0) were positively associated with mortality. In summary, dietary SFA intake was strongly associated with higher total and CVD mortality in this long-term cohort study. This supports policies implemented to reduce SFA consumption in favour of carbohydrates and unsaturated fats.

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.

Previous studies revealed that consuming spicy food reduced mortality from CVD and lowered stroke risk. However, no studies reported the relationship between spicy food consumption, stroke types and dose–response. This study aimed to further explore the association between the frequency of spicy food intake and the risk of stroke in a large prospective cohort study. In this study, 50 174 participants aged 30–79 years were recruited. Spicy food consumption data were collected via a baseline survey questionnaire. Outcomes were incidence of any stroke, ischaemic stroke (IS) and haemorrhagic stroke (HS). Multivariable-adjusted Cox proportional hazard models estimated the association between the consumption of spicy food and incident stroke. Restricted cubic spline analysis was used to examine the dose–response relationship. During the median 10·7-year follow-up, 3967 strokes were recorded, including 3494 IS and 516 HS. Compared with those who never/rarely consumed spicy food, those who consumed spicy food monthly, 1–2 d/week and 3–5 d/week had hazard ratio (HR) of 0·914 (95 % CI 0·841, 0·995), 0·869 (95 % CI 0·758, 0·995) and 0·826 (95 % CI 0·714, 0·956) for overall stroke, respectively. For IS, the corresponding HR) were 0·909 (95 % CI 0·832, 0·994), 0·831 (95 % CI 0·718, 0·962) and 0·813 (95 % CI 0·696, 0·951), respectively. This protective effect showed a U-shaped dose–response relationship. For obese participants, consuming spicy food ≥ 3 d/week was negatively associated with the risk of IS. We found the consumption of spicy food was negatively associated with the risk of IS and had a U-shaped dose–response relationship with risk of IS. Individuals who consumed spicy food 3–5 d/week had a significantly lowest risk of IS.

It is uncertain whether dietary intake of mushrooms rich in dietary fibre and several antioxidants is associated with a lower risk of dementia. We sought to examine prospectively the association between mushroom intake and the risk of disabling dementia. We performed a prospective study involving 3750 people aged 40 to 64 years residing in three communities who participated in an annual cardiovascular risk survey from 1985 to 1999. Cases of incident disabling dementia were surveyed from 1999 to 2020. We calculated the hazard ratios (HR) and 95 % CI for incident total dementia according to mushroom intake among participants with or without a history of stroke. During a mean 16·0 years’ follow-up in 3739 eligible participants, 670 people developed disabling dementia. For women, mushroom intake was inversely associated with the risk of total dementia and the association was confined to dementia without a history of stroke. The multivariable HR (95 % CI) for total dementia in women were 0·81 (0·62, 1·06) for mushroom intake of 0·1–14·9 g/d and 0·56 (0·42, 0·75) for mushroom intake above 15·0 g/d (Pfor trend = 0·003) compared with no intake. The corresponding HR (95 % CI) for dementia without a history of stroke were 0·66 (0·47, 0·93) and 0·55 (0·38, 0·79) (Pfor trend = 0·01). In men, no associations were observed between mushroom intake and the risk of disabling dementia. Among Japanese women, dietary mushroom intake was associated with a lower risk of disabling dementia.

Epidemiological studies on the potential health effects of dietary polyamines are scarce. The present study aimed to estimate habitual intake of polyamines (putrescine, spermidine and spermine) and examine whether spermidine intake is inversely associated with all-cause and cause-specific mortality in a population-based cohort study in Japan. The study included 13 355 men and 15 724 women aged 35 years and older. Diet was assessed via a validated FFQ at the baseline in 1992. The intake of polyamines was estimated mainly using databases of polyamine content in foods consumed among Japanese population. Sex-specific hazard ratios (HR) and 95 % CI for all-cause and cause-specific mortality were estimated according to polyamine quartiles. During 16 years of follow-up, 2901 deaths in men and 2438 in women occurred. The intake of any polyamine was not significantly associated with all-cause or cause-specific mortality after controlling for covariates in men and women. There was a suggestive positive association between spermidine intake and cancer mortality in women: HR for the highest v. lowest quartile were 1·38 (95 % CI (0·99, 1·93); Ptrend = 0·02). Our results did not provide support for the notion that dietary spermidine has beneficial effects on mortality. Further studies on dietary polyamines and longevity, as well as the morbidity of specific diseases, including cancer, are needed across populations with different dietary habits.

Nordic Nutrition Recommendations recommend reducing red and processed meat and increasing fish consumption, but the impact of this replacement on mortality is understudied. This study investigated the replacement of red and processed meat with fish in relation to mortality. Of 83 304 women in the Norwegian Women and Cancer Study (NOWAC) study, 9420 died during a median of 21·0 years of follow-up. The hazard ratios (HR) for mortality were estimated using Cox proportional hazards regression with analyses stratified on red and processed meat intake due to non-linearity. Higher processed meat (> 30 g/d), red and processed meat (> 50 g/d), and fatty fish consumption were associated with higher mortality, while red meat and lean fish consumption were neutral or beneficial. Among women with higher processed meat intake (> 30 g/d), replacing 20 g/d with lean fish was associated with lower all-cause (HR 0·92, 95 % CI 0·89, 0·96), cancer (HR 0·92, 95 % CI 0·88, 0·97) and CVD mortality (HR 0·82, 95 % CI 0·74, 0·90), while replacing with fatty fish was associated with lower CVD mortality (HR 0·87, 95 % CI 0·77, 0·97), but not with all-cause or cancer mortality. Replacing processed meat with fish among women with lower processed meat intake (≤ 30 g/d) or replacing red meat with fish was not associated with mortality. Replacing processed meat with lean or fatty fish may lower the risk of premature deaths in Norwegian women, but only in women with high intake of processed meat. These findings suggest that interventions to reduce processed meat intake should target high consumers.

The association between the consumption of dairy products and risk of CVD has been inconsistent. There is a lack of studies in populations with high intakes of dairy products. We aimed to examine the association between intake of dairy products and risk of incident major adverse coronary events and stroke in the Swedish Malmö Diet and Cancer cohort study. We included 26 190 participants without prevalent CVD or diabetes. Dietary habits were obtained from a modified diet history, and endpoint data were extracted from registers. Over an average of 19 years of follow-up, 3633 major adverse coronary events cases and 2643 stroke cases were reported. After adjusting for potential confounders, very high intakes of non-fermented milk (>1000 g/d) compared with low intakes (<200 g/d) were associated with 35 % (95 % CI (8, 69)) higher risk of major adverse coronary events. In contrast, moderate intakes of fermented milk (100–300 g/d) were associated with a lower risk of major adverse coronary events compared with no consumption. Intakes of cheese (only in women) and butter were inversely associated with the risk of major adverse coronary events. We observed no clear associations between any of the dairy products and stroke risk. These results highlight the importance of studying different dairy foods separately. Further studies in populations with high dairy consumption are warranted.

The objective was to evaluate the association between serum carotenoid levels and respiratory morbidity and mortality in a nationally representative sample of US adults. We assessed the association of serum carotenoid levels with respiratory morbidity and mortality using logistic regression and proportional hazards regression models. Meanwhile, a series of confounders were controlled in regression models and restricted cubic spline, which included age, sex, race, marriage, education, income, drinking, smoking, regular exercise, BMI, daily energy intake, vitamin E, vitamin C, fruit intake, vegetable intake, diabetes, hypertension, asthma, emphysema and chronic bronchitis. Compared with participants in the lowest tertiles, participants in the highest tertiles of serum total carotenoids, β-cryptoxanthin and lutein/zeaxanthin levels had a significantly lower prevalence of emphysema (ORtotal carotenoids = 0·61, 95% CI: 0·41–0·89, ORβ-cryptoxanthin = 0·67, 95% CI: 0·49–0·92), chronic bronchitis (ORβ-cryptoxanthin = 0·66, 95% CI: 0·50–0·87) and asthma (Q2: ORlutein/zeaxanthin = 0·78, 95% CI: 0·62–0·97); participants in the highest tertiles of total carotenoids, α-carotene, lutein/zeaxanthin and lycopene had a lower risk of respiratory mortality (hazard ratio (HR)total carotenoids = 0·62, 95% CI: 0·42–0·90, HRα-carotene = 0·54, 95% CI: 0·36–0·82, HRlutein/zeaxanthin = 0·48, 95% CI: 0·33–0·71, HRlycopene = 0·66, 95% CI: 0·45–0·96) than those in the lowest tertiles. Higher serum total carotenoids and β-cryptoxanthin levels is associated with decreased prevalence of emphysema and chronic bronchitis, and higher serum total carotenoids, α-carotene, lutein/zeaxanthin and lycopene levels had a lower mortality of respiratory disease.

According to the World Cancer Research Fund International, vitamin D might decrease the risk of colorectal cancer (CRC). However, less is known about the association with cancers in different subsites of the colon and in the rectum. The aim of this study was to examine associations between pre-diagnostic intake of vitamin D and risk of CRC by anatomical subsites. Data from 95 416 participants in the Norwegian Women and Cancer Cohort Study was included, and vitamin D intake was estimated from two repeated FFQ. Associations between vitamin D intake and incidence of CRC were assessed using multivariable Cox regression. During follow-up, there were 1774 incident cases of CRC. A small but borderline significant inverse association was found for a 5-µg increase in vitamin D intake and risk of CRC (hazard ratio (HR) = 0·97; 95 % CI 0·93, 1·01) and colon cancer (HR = 0·96; 95 % CI 0·91, 1·01). High (≥ 20 µg) compared with low (< 10 µg) vitamin D intake was associated with 17 % borderline significant reduced risk of CRC (HR = 0·83; 95 % CI 0·68, 1·02). Medium (10–19 µg) v. low intake (< 10 µg) was associated with 27 % reduced risk of proximal colon cancer (HR = 0·73; 95 % CI 0·57, 0·94). No significant associations were observed between vitamin D intake and risk of distal colon or rectal cancer. Our study indicates that vitamin D may be differently associated with subsites of the colon. The association between vitamin D intake and proximal colon cancer is novel.

This study is designed to explore the association between dietary betaine intake and risk of all-cause and cardiovascular death in patients with coronary artery diseases (CAD). In this cohort study, 1292 patients with CAD were followed up for a median of 9·2 years. Baseline dietary betaine intake was collected using a paper-based semi-quantitative FFQ and assessed according to the US Department of Agriculture (USDA) database and the data of betaine in common foods. Cox proportional hazards regression models were used to analyse the association between dietary betaine intake and risks of all-cause and cardiovascular mortality. During the follow-up periods, 259 deaths recorded in 1292 participants, of which 167 died of CVD. Patients in the highest tertile of dietary betaine intake had a lower risk of all-cause (P = 0·007) and cardiovascular death (P < 0·001) than those in the lowest tertile after adjusting for age and sex, traditional cardiovascular risk factors and other potential confounders. After further adjusting for plasma methionine metabolites and vitamins, hazard ratio across tertiles of dietary betaine intake were 1·00, 0·84 and 0·72 for all-cause mortality (P for trend = 0·124), and 1·00, 0·77 and 0·55 for cardiovascular mortality (P for trend = 0·021). Higher dietary betaine intake was associated with a decreased risk of cardiovascular death after fully adjustment for cardiovascular risk factors, other potential confounders and plasma methionine metabolites and vitamins. However, the association between dietary betaine intake and risk of all-cause mortality was not statistically significant after further adjusting for plasma methionine metabolites and vitamins.

Whether starchy and non-starchy vegetables have distinct impacts on health remains unknown. We prospectively investigated the intake of starchy and non-starchy vegetables in relation to mortality risk in a nationwide cohort. Diet was assessed using 24-h dietary recalls. Deaths were identified via the record linkage to the National Death Index. Hazard ratios (HR) and 95 % CI were calculated using Cox regression. During a median follow-up of 7·8 years, 4904 deaths were documented among 40 074 participants aged 18 years or older. Compared to those with no consumption, participants with daily consumption of ≥ 1 serving of non-starchy vegetables had a lower risk of mortality (HR = 0·76, 95 % CI 0·66, 0·88, Ptrend = 0·001). Dark-green and deep-yellow vegetables (HR = 0·79, 95 % CI 0·63, 0·99, Ptrend = 0·023) and other non-starchy vegetables (HR = 0·80, 95 % CI 0·70, 0·92, Ptrend = 0·004) showed similar results. Total starchy vegetable intake exhibited a marginally weak inverse association with mortality risk (HR = 0·89, 95 % CI 0·80, 1·00, Ptrend = 0·048), while potatoes showed a null association (HR = 0·93, 95 % CI 0·82, 1·06, Ptrend = 0·186). Restricted cubic spline analysis suggested a linear dose–response relationship between vegetable intake and death risk, with a plateau at over 300 and 200 g/d for total and non-starchy vegetables, respectively. Compared with starchy vegetables, non-starchy vegetables might be more beneficial to health, although both showed a protective association with mortality risk. The risk reduction in mortality plateaued at approximately 200 g/d for non-starchy vegetables and 300 g/d for total vegetables.

The present study elucidates the association of intrinsic sugars and free sugars (FS) from all relevant sources with all-cause mortality in the prospective UK Biobank cohort. Sugar intake was assessed in 186 811 UK Biobank participants who completed at least one web-based 24-h dietary recall (Oxford WebQ). Cox proportional hazard regression models for all-cause mortality were used with sugar intake from different sources included as penalised cubic splines to allow non-linear predictor effects. Over a mean follow-up of 12·3 years, 8576 (4·6 %) deaths occurred. FS but not intrinsic sugars were significantly and dose-dependently associated with hazard ratio (HR) for all-cause mortality. The association with all-cause mortality was significant and dose dependent for FS in beverages, but not in solids with the mean (CI) HR at 50 g/d v. 0 g/d consumption at 1·10, 95 % CI (1·07, 1·14) and 1·01, 95 % CI (0·98, 1·03), respectively. Within the beverages subcategories, a significant dose-dependent association with mortality was detected for FS in soda/fruit drinks and milk-based drinks whereas this relation was NS for FS in pure juice and tea/coffee. FS in four different subtypes of solids, i.e. treats, cereals, toppings and sauces, were not positively associated with all-cause mortality. Major findings were robust in sensitivity analyses. In conclusion, only some FS sources were associated with all-cause mortality. Interventions targeting FS subtypes might be most effective concerning mortality if focused on the reduction of soda/fruit drinks and milk-based sugary drinks; however, the present results need to be confirmed by independent studies.

It has been suggested that added sugar intake is associated with non-alcoholic fatty liver disease (NAFLD). However, previous studies only focused on sugar-sweetened beverages; the evidence for associations with total added sugars and their sources is scarce. This study aimed to examine the associations of total added sugars, their physical forms (liquid v. solid) and food sources with risk of NAFLD among adults in Tianjin, China. We used data from 15 538 participants, free of NAFLD, other liver diseases, CVD, cancer or diabetes at baseline (2013–2018 years). Added sugar intake was estimated from a validated 100-item FFQ. NAFLD was diagnosed by ultrasonography after exclusion of other causes of liver diseases. Multivariable Cox proportional hazards models were fitted to calculate hazard ratios (HR) and corresponding 95 % CI for NAFLD risk with added sugar intake. During a median follow-up of 4·2 years, 3476 incident NAFLD cases were documented. After adjusting for age, sex, BMI and its change from baseline to follow-up, lifestyle factors, personal and family medical history and overall diet quality, the multivariable HR of NAFLD risk were 1·18 (95 % CI 1·06, 1·32) for total added sugars, 1·20 (95 % CI 1·08, 1·33) for liquid added sugars and 0·96 (95 % CI 0·86, 1·07) for solid added sugars when comparing the highest quartiles of intake with the lowest quartiles of intake. In this prospective cohort of Chinese adults, higher intakes of total added sugars and liquid added sugars, but not solid added sugars, were associated with a higher risk of NAFLD.

Hyperhomocysteinaemia (HHcy) is associated with all-cause mortality in some disease states. However, the correlation between HHcy and the risk of mortality in the general population has rarely been researched. We aimed to evaluate the association between HHcy and all-cause and cause-specific mortality among adults in the USA. This study analysed data from the National Health and Nutrition Examination Survey database (1999–2002 survey cycle). A multivariable Cox regression model was built to evaluate the correlation between HHcy and all-cause and cause-specific mortality. Smooth curve fitting was used to analyse their dose-dependent relationship. A total of 8442 adults aged 18–70 years were included in this study. After a median follow-up period of 14·7 years, 1007 (11·9 %) deaths occurred including 197 CVD-related deaths, 255 cancer-related deaths and fifty-eight respiratory disease deaths. The participants with HHcy had a 93 % increased risk of all-cause mortality (hazard ratio (HR) 1·93; 95 % CI (1·48, 2·51)), 160 % increased risk of CVD mortality (HR 2·60; 95 % CI (1·52, 4·45)) and 82 % increased risk of cancer mortality (HR 1·82; 95 % CI (1·03, 3·21)) compared with those without HHcy. For unmeasured confounding, E-value analysis proved to be robust. In conclusion, HHcy was associated with high risk of all-cause and cause-specific (CVD, cancer) mortality among adults aged below 70 years.