High fried food consumption impacts anxiety and depression due to lipid metabolism disturbance and neuroinflammation.

Western dietary patterns have been unfavorably linked with mental health. However, the long-term effects of habitual fried food consumption on anxiety and depression and underlying mechanisms remain unclear. Our population-based study with 140,728 people revealed that frequent fried food consumption, especially fried potato consumption, is strongly associated with 12% and 7% higher risk of anxiety and depression, respectively. The associations were more pronounced among male and younger consumers. Consistently, long-term exposure to acrylamide, a representative food processing contaminant in fried products, exacerbates scototaxis and thigmotaxis, and further impairs exploration ability and sociality of adult zebrafish, showing anxiety- and depressive-like behaviors. Moreover, treatment with acrylamide significantly down-regulates the gene expression of tjp2a related to the permeability of blood-brain barrier. Multiomics analysis showed that chronic exposure to acrylamide induces cerebral lipid metabolism disturbance and neuroinflammation. PPAR signaling pathway mediates acrylamide-induced lipid metabolism disorder in the brain of zebrafish. Especially, chronic exposure to acrylamide dysregulates sphingolipid and phospholipid metabolism, which plays important roles in the development of anxiety and depression symptoms. In addition, acrylamide promotes lipid peroxidation and oxidation stress, which participate in cerebral neuroinflammation. Acrylamide dramatically increases the markers of lipid peroxidation, including (±)5-HETE, 11(S)-HETE, 5-oxoETE, and up-regulates the expression of proinflammatory lipid mediators such as (±)12-HETE and 14(S)-HDHA, indicating elevated cerebral inflammatory status after chronic exposure to acrylamide. Together, these results both epidemiologically and mechanistically provide strong evidence to unravel the mechanism of acrylamide-triggered anxiety and depression, and highlight the significance of reducing fried food consumption for mental health.

Fruit but not vegetable consumption is beneficial for low prevalence of colorectal polyps in a high-risk population: findings from a Chinese Lanxi Pre-colorectal Cancer Cohort study.

PURPOSE: The available evidence regarding the role of fruit and vegetable consumption in the development of colorectal polyps remains inconclusive, and there is a lack of data on different histopathologic features of polyps. We aimed to evaluate the associations of fruit and vegetable consumption with the prevalence of colorectal polyps and its subtypes in a high-risk population in China. METHODS: We included 6783 Chinese participants aged 40-80 years who were at high risk of colorectal cancer (CRC) in the Lanxi Pre-colorectal Cancer Cohort (LP3C). Dietary information was obtained through a validated food-frequency questionnaire (FFQ), and colonoscopy screening was used to detect colorectal polyps. Dose-response associations of fruit and vegetable intake with the prevalence of polyps were calculated using multivariate-adjusted regression models, which was reported as odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: 2064 cases of colorectal polyps were ascertained in the LP3C during 2018-2019. Upon multivariable adjustments, including the diet quality, fruit consumption was inversely associated with the prevalence of polyps (P trend = 0.02). Participants in the highest tertile of fruit intake had a 25% lower risk (OR: 0.75; 95% CI 0.62‒0.92) compared to non-consumers, while vegetable consumption had no significant association with polyp prevalence (P trend = 0.86). In terms of colorectal histopathology and multiplicity, higher fruit intake was correlated with 24, 23, and 33% lower prevalence of small polyps (OR: 0.76; 95% CI 0.62‒0.94; P trend = 0.05), single polyp (OR: 0.77; 95% CI 0.62‒0.96; P trend = 0.04), and distal colon polyps (OR: 0.67; 95% CI 0.51‒0.87; P trend = 0.003), respectively. CONCLUSIONS: Fresh fruit is suggested as a protective factor to prevent colorectal polyps in individuals at high risk of CRC, and should be underscored in dietary recommendations, particularly for high-risk populations.

Preserved vegetable consumption and its association with mortality among 440,415 people in the China Kadoorie Biobank.

BACKGROUND: Fresh vegetable consumption has been associated with lower incidence of cardiovascular disease (CVD). However, whether preserved vegetable consumption is linked with CVD and mortality remains unclear. This study aimed to assess the associations of preserved vegetable consumption with all-cause and cause-specific mortality. METHODS: A total of 440,415 participants free of major chronic diseases, aged 30-79 years, were enrolled from 10 diverse regions in China between 2004 and 2008 and were followed up for an average of 10 years. Preserved vegetable consumption was assessed using a validated food frequency questionnaire. Cause-specific hazard models with the consideration of competing risk from various deaths were performed to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of mortality. RESULTS: During 4,415,784 person-years of follow-up, we documented 28,625 deaths. After adjustment for major risk factors, preserved vegetable consumption was marginally associated with higher CVD mortality (P = 0.041 for trend and P = 0.025 for non-linearity) but not associated with cancer mortality and total mortality. For specific causes of death, consuming preserved vegetables was associated with higher hemorrhagic stroke mortality. The multivariable-adjusted HRs (95% CIs) of hemorrhagic stroke mortality compared with non-consumers were 1.32 (1.17-1.50) for 1-3 days/week and 1.15 (1.00-1.31) for regular consumers (≥4 days/week) (P = 0.006 for trend and P < 0.001 for non-linearity). In addition, regular preserved vegetable consumption was associated with increased risk of digestive tract cancer mortality [HR (95% CI): 1.13 (1.00-1.28); P = 0.053 for trend] and esophageal cancer mortality [HR (95% CI): 1.45 (1.17-1.81); P = 0.002 for trend]. CONCLUSIONS: Frequent consumption of preserved vegetables was associated with higher risk of mortality from hemorrhagic stroke and esophageal cancer in China. Our findings suggest limiting preserved vegetable consumption might be protective for premature death from hemorrhagic stroke and digestive tract cancer.

Long-term dietary DHA intervention prevents telomere attrition and lipid disturbance in telomerase-deficient male mice.

PURPOSE: Previous evidence indicated anti-ageing potential of docosahexaenoic acid (DHA), but the underlying mechanism remains unclear. We investigated protective effect of DHA on telomere attrition and lipid disturbance in male mice with premature ageing caused by telomerase deficiency. METHODS: Wild-type (WT) and fourth-generation telomerase-deficient (G4 Terc-/-, Terc knockout, KO) male mice (C57BL/6, 2 months old) were fed control diet (WT-C and KO-C groups) or DHA-enriched diet containing 0.80% DHA by weight (WT-DHA and KO-DHA groups) for 10 months. The ageing phenotypes and metabolic level [carbon dioxide emission, oxygen consumption, and respiratory exchange ratio (RER)] were assessed at the end of the experiment. Telomere length in various tissues and the hepatic gene and protein expression for regulating lipid synthesis and lipolysis were measured. Data were tested using one- or two-factor ANOVA. RESULTS: In KO male mice, DHA prevented weight loss, corrected high RER, and reduced fat loss. Telomere shortening was reduced by 22.3%, 25.5%, and 13.5% in heart, liver, and testes of the KO-DHA group compared with those in the KO-C group. The KO-DHA group exhibited higher gene transcription involved in glycerol-3-phosphate pathway [glycerol-3-phosphate acyltransferase (Gpat)], lower gene expression of ß-oxidation [carnitine palmitoyltransferase 1a (Cpt1a)], and upregulation of proteins in lipid synthesis [mammalian target of rapamycin complex 1 (mTORC1) and sterol responsive element binding protein 1 (SREBP1)] in liver than the KO-C group. CONCLUSION: Long-term DHA intervention attenuates telomere attrition and promotes lipid synthesis via the tuberous sclerosis complex 2 (TSC2)-mTORC1-SREBP1 pathway in KO male mice.

Mixed conjugated linoleic acid sex-dependently reverses high-fat diet-induced insulin resistance via the gut-adipose axis.

Conjugated linoleic acid (CLA) may prevent the development of obesity and metabolic disorders. However, the effects of CLA on inflammation and glucose metabolism are controversial. The underlying mechanisms governing the gut microbiota and sexual dimorphisms have also not been elucidated. The present study assessed the effect of CLA on glucose and lipid metabolism in established obesity and examined the mechanism of action based on gut microbiota. Four-week-old C57BL/6J mice were fed a high-fat diet (HFD) for 10 weeks to induce obesity. The diet-induced obese (DIO) mice were fed an HFD supplemented with mixed CLA (50% cis-9, trans-11 isomer and 50% trans-10, cis-12 isomers, 0.2% wt/wt) for 15 weeks. CLA supplementation remarkably reversed body weight in both sexes. CLA favored anti-inflammatory microbiota in male mice, mediating increased short-chain fatty acids and decreased lipopolysaccharide (LPS) production, which alleviated global inflammation and improved insulin sensitivity via inhibition of the TLR4-NF-κB pathway in adipose tissue. CLA promoted the growth of hydrogen sulfide-producing Desulfovibrio and the release of LPS in female mice, which aggravated adipose inflammation and insulin resistance. Although CLA impaired glucose metabolism in females, brown adipose tissue was significantly activated with browning of white adipose tissue in both sexes, which led to enhanced energy expenditure. Fecal transplantation from CLA-treated mice to DIO mice mimicked the sex-dependent phenotype. In conclusion, CLA decreased body weight and increased energy expenditure but sex-dependently modulated insulin resistance via the gut-adipose axis.

Individual SFA intake and risk of overweight/obesity: findings from a population-based nationwide cohort study.

The relationship between SFA consumption and the risk of overweight/obesity remains unclear. Epidemiological evidence is lacking among Chinese population. This study aimed to investigate the association between individual dietary SFA intake and the risk of overweight/obesity in Chinese adults. Data from 8465 adults with BMI < 24 kg/m2 at entry in the China Health and Nutrition Survey (1989-2011) were analysed. Three-day 24-h dietary records were used to collect dietary data. Cox proportional hazards regression models were constructed to estimate hazard ratios (HR) and 95 % CI for the risk of developing overweight or obesity. A total of 3171 incident cases of overweight/obesity were identified (1649 for women and 1522 for men) during a median of 11 years of follow-up. Compared with the lowest category, the intake of total SFA (TSFA) showed no significant association with the risk of overweight/obesity. However, an increased risk of overweight/obesity was observed with a higher intake of medium chain SFA (MCSFA) (Ptrend = 0·004), especially decanoic acid (10:0) (HR was 1·25 (95 % CI 1·10, 1·42) comparing the highest category with the reference group; Ptrend < 0·001), whereas an inverse relationship was observed for hexanoic acid (6:0) consumption; compared with non-consumers, 6:0 intake was associated with 32 % lower risk of overweight/obesity (HR: 0·68 (95 % CI 0·56, 0·84); Ptrend < 0·001). Overall, the intake of subtypes of MCSFA but not TSFA was associated with the risk of overweight/obesity. Increasing hexanoic acid (6:0) and limiting decanoic acid (10:0) consumption may be protective for overweight/obesity among Chinese population.

Association of preserved vegetable consumption and prevalence of colorectal polyps: results from the Lanxi Pre-colorectal Cancer Cohort (LP3C).

PURPOSE: Although fresh vegetable consumption has been linked with a lower risk of colorectal polyps, a precursor lesion for colorectal cancer (CRC), the association between preserved vegetable consumption and colorectal polyps is unknown. We aimed to assess the association of preserved vegetable intake with the prevalence of colorectal polyps with the consideration of subsites, sizes and multiplicity of polyps. METHODS: We analyzed the cross-sectional data from 40-80 years Chinese at a high risk of CRC from the Lanxi Pre-colorectal Cancer Cohort (LP3C) baseline survey, which was conducted between March 2018 and December 2019. Dietary information was obtained via a validated food frequency questionnaire. Multivariate logistic regression was employed to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) of preserved vegetable consumption and the prevalence of colorectal polyps. RESULTS: Of 6783 eligible participants in 2018-2019 survey of LP3C, 2064 prevalent colorectal polyp cases were identified. In the multivariable-adjusted model, preserved vegetable consumption was positively associated with the prevalence of colorectal polyps (OR for fourth vs. first quartile: 1.18; 95% CI 1.01-1.36; P trend = 0.02). The similar association was also detected for small polyps [ORQ4 vs Q1 (95% CI): 1.17 (1.00-1.37); P trend = 0.03]. The similar trend was detected for multiple polyps [OR Q4 vs Q1 (95% CI):1.27 (0.98-1.64); P trend = 0.04], proximal colon polyps [ORQ4 vs Q1 (95% CI): 1.12 (0.90-1.38); P trend = 0.07], and single polyp [ORQ4 vs Q1 (95% CI) for 1.15 (0.98-1.35); P trend = 0.06]. No significant association was observed for distal colon [ORQ4 vs Q1 (95% CI) 1.19 (0.98-1.45); P trend = 0.09]. Replacing one serving per day of preserved vegetables with fresh vegetables was related to 20%, 23%, and 37% lower prevalence of overall, small, and multiple polyps, respectively. CONCLUSIONS: Preserved vegetable consumption was associated with a higher prevalence of colorectal polyps in a Chinese population at a high risk of CRC. Replacing preserved vegetables with fresh vegetables may be conducive to lower prevalent colorectal polyps.

Associations of 3-monochloropropane-1,2-diol and glycidol with prevalence of metabolic syndrome: Findings from Lanxi Nutrition and Safety Study.

In this study, we investigated the association of 2,3-dihydroxypropyl mercapturic acid (DHPMA), a urinary biomarker of environmental and dietary exposure to 3-monochloropropane-1,2-diol and glycidol, with prevalent MetS in a Chinese middle-aged and elderly population. The urinary DHPMA concentrations were determined by ultra-high performance liquid chromatography tandem mass spectrometry (UHPLC-MS/MS) analysis and further calibrated by the urinary creatinine content. MetS cases were defined by the Adult Treatment Panel III criteria for Asian-Americans of National Cholesterol Education Program (NCEP/ATPIII). Multivariate-adjusted modified Poisson regression models were used to analyze the associations between the urinary DHPMA concentrations and MetS prevalence. Of the 1613 participants aged 45-75 years, we documented 552 (34.2%) MetS cases. After adjustment for potential risk factors, the relative risks (95% confidence intervals) of MetS prevalence across the increasing quartiles of DHPMA concentrations were 1.14 (0.93-1.39), 1.29 (1.06-1.56), and 1.50 (1.25-1.80), respectively, compared with the lowest quartile. We also observed strong positive association between urinary DHPMA concentrations and hypertriglyceridemia prevalence (P < 0.001 for trend). These positive associations remained unchanged in the subgroups stratified by general demographic, dietary and behavioral risk factors. These results suggested that urinary DHPMA was associated with higher prevalence of MetS among Chinese elderly people.

Egg and cholesterol consumption and mortality from cardiovascular and different causes in the United States: A population-based cohort study.

BACKGROUND: Whether consumption of egg and cholesterol is detrimental to cardiovascular health and longevity is highly debated. Data from large-scale cohort studies are scarce. This study aimed to examine the associations of egg and cholesterol intakes with mortality from all causes, cardiovascular disease (CVD), and other causes in a US population. METHODS AND FINDINGS: Overall, 521,120 participants (aged 50-71 years, mean age = 62.2 years, 41.2% women, and 91.8% non-Hispanic white) were recruited from 6 states and 2 additional cities in the US between 1995 and 1996 and prospectively followed up until the end of 2011. Intakes of whole eggs, egg whites/substitutes, and cholesterol were assessed by a validated food frequency questionnaire. Cause-specific hazard models considering competing risks were used, with the lowest quintile of energy-adjusted intake (per 2,000 kcal per day) as the reference. There were 129,328 deaths including 38,747 deaths from CVD during a median follow-up of 16 years. Whole egg and cholesterol intakes were both positively associated with all-cause, CVD, and cancer mortality. In multivariable-adjusted models, the hazard ratios (95% confidence intervals) associated with each intake of an additional half of a whole egg per day were 1.07 (1.06-1.08) for all-cause mortality, 1.07 (1.06-1.09) for CVD mortality, and 1.07 (1.06-1.09) for cancer mortality. Each intake of an additional 300 mg of dietary cholesterol per day was associated with 19%, 16%, and 24% higher all-cause, CVD, and cancer mortality, respectively. Mediation models estimated that cholesterol intake contributed to 63.2% (95% CI 49.6%-75.0%), 62.3% (95% CI 39.5%-80.7%), and 49.6% (95% CI 31.9%-67.4%) of all-cause, CVD, and cancer mortality associated with whole egg consumption, respectively. Egg white/substitute consumers had lower all-cause mortality and mortality from stroke, cancer, respiratory disease, and Alzheimer disease compared with non-consumers. Hypothetically, replacing half a whole egg with equivalent amounts of egg whites/substitutes, poultry, fish, dairy products, or nuts/legumes was related to lower all-cause, CVD, cancer, and respiratory disease mortality. Study limitations include its observational nature, reliance on participant self-report, and residual confounding despite extensive adjustment for acknowledged dietary and lifestyle risk factors. CONCLUSIONS: In this study, intakes of eggs and cholesterol were associated with higher all-cause, CVD, and cancer mortality. The increased mortality associated with egg consumption was largely influenced by cholesterol intake. Our findings suggest limiting cholesterol intake and replacing whole eggs with egg whites/substitutes or other alternative protein sources for facilitating cardiovascular health and long-term survival. TRIAL REGISTRATION: ClinicalTrials.gov NCT00340015.

Cooking oil/fat consumption and deaths from cardiometabolic diseases and other causes: prospective analysis of 521,120 individuals.

BACKGROUND: Increasing evidence highlights healthy dietary patterns and links daily cooking oil intake with chronic diseases including cardiovascular disease (CVD) and diabetes. However, food-based evidence supporting the consumption of cooking oils in relation to total and cardiometabolic mortality remains largely absent. We aim to prospectively evaluate the relations of cooking oils with death from cardiometabolic (CVD and diabetes) and other causes. METHODS: We identified and prospectively followed 521,120 participants aged 50-71 years from the National Institutes of Health-American Association of Retired Persons Diet and Health Study. Individual cooking oil/fat consumption was assessed by a validated food frequency questionnaire. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for mortality through the end of 2011. RESULTS: Overall, 129,328 deaths were documented during a median follow-up of 16 years. Intakes of butter and margarine were associated with higher total mortality while intakes of canola oil and olive oil were related to lower total mortality. After multivariate adjustment for major risk factors, the HRs of cardiometabolic mortality for each 1-tablespoon/day increment were 1.08 (95% CI 1.05-1.10) for butter, 1.06 (1.05-1.08) for margarine, 0.99 (0.95-1.03) for corn oil, 0.98 (0.94-1.02) for canola oil, and 0.96 (0.92-0.99) for olive oil. Besides, butter consumption was positively associated with cancer mortality. Substituting corn oil, canola oil, or olive oil for equal amounts of butter and margarine was related to lower all-cause mortality and mortality from certain causes, including CVD, diabetes, cancer, respiratory disease, and Alzheimer's disease. CONCLUSIONS: Consumption of butter and margarine was associated with higher total and cardiometabolic mortality. Replacing butter and margarine with canola oil, corn oil, or olive oil was related to lower total and cardiometabolic mortality. Our findings support shifting the intake from solid fats to non-hydrogenated vegetable oils for cardiometabolic health and longevity.

Dietary Fats in Relation to Total and Cause-Specific Mortality in a Prospective Cohort of 521 120 Individuals With 16 Years of Follow-Up.

RATIONALE: Evidence linking saturated fat intake with cardiovascular health is controversial. The associations of unsaturated fats with total and cardiovascular disease (CVD) mortality remain inconsistent, and data about non-CVD mortality are limited. OBJECTIVE: To assess dietary fat intake in relation to total and cause-specific mortality. METHODS AND RESULTS: We analyzed data of 521 120 participants aged 50 to 71 years from the National Institutes of Health-American Association of Retired Persons Diet and Health Study with 16 years of follow-up. Intakes of saturated fatty acids (SFAs), trans-fatty acids, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) were assessed via food frequency questionnaires. Hazard ratios and 95%CIs were estimated using the Cox proportional hazards model. Overall, 129 328 deaths were documented during 7.3 million person-years of follow-up. In the replacement of carbohydrates, multivariable-adjusted hazard ratios of total mortality comparing extreme quintiles were 1.29 (95% CI, 1.25-1.33) for SFAs, 1.03 (1.00-1.05) for trans-fatty acids, 0.98 (0.94-1.02) for MUFAs, 1.09 (1.06-1.13) for animal MUFAs, 0.94 (0.91-0.97) for plant MUFAs, 0.93 (0.91-0.95) for PUFAs, 0.92 (0.90-0.94) for marine omega-3 PUFAs, 1.06 (1.03-1.09) for α-linolenic acid, 0.88 (0.86-0.91) for linoleic acid, and 1.10 (1.08-1.13) for arachidonic acid. CVD mortality was inversely associated with marine omega-3 PUFA intake ( P trend <0.0001), whereas it was positively associated with SFA, trans-fatty acid, and arachidonic acid intake. Isocalorically replacing 5% of the energy from SFAs with plant MUFAs was associated with 15%, 10%, 11%, and 30% lower total mortality, CVD, cancer, and respiratory disease mortality, respectively. Isocaloric replacement of SFA with linoleic acid (2%) was associated with lower total (8%), CVD (6%), cancer (8%), respiratory disease (11%), and diabetes mellitus (9%) mortality. CONCLUSIONS: Intakes of SFAs, trans-fatty acids, animal MUFAs, α-linolenic acid, and arachidonic acid were associated with higher mortality. Dietary intake of marine omega-3 PUFAs and replacing SFAs with plant MUFAs or linoleic acid were associated with lower total, CVD, and certain cause-specific mortality. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov . Unique identifier: NCT00340015.

Nontargeted metabolomics-based mapping urinary metabolic fingerprints after exposure to acrylamide.

Acrylamide classified as a probable carcinogen to humans is a high production volume chemical in industrial applications released to aquatic and environmental ecosystems, and also widely found in the thermal processing of starch-rich foods. To gain insight into the urinary metabolomics that may induce physiological responses stimulated by acrylamide, rats were orally administered with a single dose of 13C3-acrylamide (10 mg/kg bw) in the treatment group and urine samples were continuously collected every 2 h during the first 18 h and every 3 h during the period from 18 h to 36 h. A reliable nontargeted screening method for the analysis of urinary metabolomics in rats was developed using ultra-high performance liquid chromatography coupled to quadrupole-Orbitrap high-resolution mass spectrometry. All metabolites in urine of rats receiving isotope-labeled acrylamide were screened by validated orthogonal partial least squares-discriminant analyses compared to the animals in the control group, while exposure biomarkers were further confirmed according to the characteristic fragmentation rules and time-dependent profiles. Here we identified 2 new specific exposure biomarkers, named N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine-sulfoxide and N-acetyl-S-(2-carboxyl)-L-cysteine, compared to 4 currently acknowledged mercapturic acid adducts of acrylamide. In addition, our findings on analysis of acrylamide metabolic pathway and identification of exposure biomarkers confirmed that acrylamide could significantly affect energy metabolism and amino acid metabolism by the Kyoto Encyclopedia of Genes and Genomes pathway analysis for key metabolites. Homocysteine thiolactone and hypoxanthine may be potential biomarkers for the cardiotoxicity, while methionine sulfoxide, hippuric acid and melatonin may be specifically related to the neurotoxicity. Thus, the current study provided new evidence on the identification of emerging exposure biomarkers and specific signature metabolites related to the toxicity of acrylamide, and shed light on how acrylamide affected energy and amino acid metabolism by further mapping urinary metabolic fingerprints.

Cooking Oil Consumption Is Positively Associated with Risk of Type 2 Diabetes in a Chinese Nationwide Cohort Study.

BACKGROUND: Evidence suggests that the relations between intakes of individual fatty acids and risk of type 2 diabetes (T2D) vary. However, associations between intakes of different cooking oils as sources of fatty acids and incident T2D remain largely unknown. OBJECTIVES: We aimed to evaluate relations between intakes of individual cooking oils and incident T2D in a nationwide Chinese cohort. METHODS: Overall 15,022 Chinese adults aged ≥20 y from the China Health and Nutrition Survey (CHNS) without self-reported T2D at entry in the 1997, 2000, 2004, 2006, or 2009 rounds were followed up until 2011. Consumption of various cooking oils/fats including lard, peanut oil, soybean oil, canola oil, sesame oil, and refined blended plant oil was assessed using 3-d 24-h records in each survey and the cumulative mean intake was calculated. Multivariable-adjusted Cox proportional hazards regression models were constructed to estimate the HRs of T2D. RESULTS: A total of 1014 cases were recorded after a median follow-up of 14 y. The intakes of animal and plant cooking oils/fats were both associated with higher T2D risk. Compared with nonconsumers, multivariable-adjusted HRs and 95% CIs for the highest tertiles were 1.31 (1.03, 1.67) for lard, 1.36 (1.10, 1.66) for peanut oil, 1.14 (0.91, 1.43) for soybean oil, 1.11 (0.87, 1.43) for canola oil, 1.02 (0.79, 1.32) for sesame oil, and 1.42 (1.12, 1.82) for refined blended plant oil. Substituting 1 tablespoon/d (8 g · 2000 kcal-1 · d-1) of soybean oil for the sum of lard, peanut oil, refined blended plant oil, and other plant oils was associated with a 3% (HR: 0.97; 95% CI: 0.95, 0.99) lower risk of T2D. CONCLUSIONS: Intakes of lard, peanut oil, and refined blended plant oil but not soybean oil, canola oil, and sesame oil are associated with higher T2D risk. Reducing the consumption of cooking oils in general may be protective against T2D among the Chinese population.This trial was registered at clinicaltrials.gov as NCT03259321.

The association between consumption of monounsaturated fats from animal- v. plant-based foods and the risk of type 2 diabetes: a prospective nationwide cohort study.

Although higher dietary intake of MUFA has been shown to improve glycaemic control and lipid profiles, whether MUFA consumption from different sources is linked to the development of type 2 diabetes (T2D) remains unclear. We aimed to prospectively assess the associations of plant-derived MUFA (P-MUFA) and animal-derived MUFA (A-MUFA) intakes with T2D risk in a nationwide oriental cohort. Overall, 15 022 Chinese adults, aged ≥20 years, from the China Health and Nutrition Survey (CHNS 1997-2011) were prospectively followed up for a median of 14 years. Consumption of MUFA from plant and animal sources was assessed using 3-d 24-h recalls in each survey, and the cumulative average of intake was calculated. Multivariable-adjusted Cox models were constructed to estimate the hazard ratios (HR) of T2D according to quartiles of MUFA intake. P-MUFA were mainly consumed from cooked vegetable oils, fried bread sticks and rice, while A-MUFA were mainly consumed from pork, lard and eggs. Intake of P-MUFA was associated with a higher risk of T2D (HRQ4 v. Q1 1·50 (95 % CI 1·18, 1·90); Ptrend = 0·0013), whereas A-MUFA showed no significant association (HRQ4 v. Q1 0·84 (95 % CI 0·59, 1·20); Ptrend = 0·30). When further considering the cooking method of food sources, consumption of P-MUFA from fried foods was positively associated with T2D risk (HRQ4 v. Q1 1·60 (95 % CI 1·26, 2·02); Ptrend = 0·0006), whereas non-fried P-MUFA were not associated. Intake of MUFA from fried plant-based foods may elevate T2D risk among the Chinese population.

Plant-sourced and animal-sourced monounsaturated fatty acid intakes in relation to mortality: a prospective nationwide cohort study.

PURPOSE: Monounsaturated fatty acids (MUFAs) are typical components of various plant-sourced and animal-sourced foods. However, the associations of MUFA consumption from different sources with mortality remain unclear. This study aimed to investigate the relationships between MUFA intakes from plant and animal sources and mortality. METHODS: A total of 14,305 participants from China Health and Nutrition Survey were prospectively followed up for 14 years. Dietary intake of MUFAs was assessed by 3-day 24-h dietary records in each round. Cox proportional hazards regression models were used to compute hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: A total of 1006 deaths occurred during 199,091 person-years of follow-up. Intake of total MUFAs was not associated with mortality (P-trend = 0.17). The plant-sourced MUFA intake was strongly associated with lower mortality [HRQ4vsQ1 (95% CI) 0.72 (0.58-0.89); P-trend = 0.008], whereas animal-sourced MUFA intake showed no significant association. Likewise, oleic acid (OA) and palmitoleic acid (PA) intakes from plant sources were also inversely associated with mortality [HRQ4vsQ1 (95% CI) 0.66 (0.52-0.84) for OA and 0.73 (0.59-0.91) for PA], while animal-sourced OA and PA were not related to mortality. Theoretically replacing saturated fatty acids (SFAs) (5% of total energy) with isocaloric plant-sourced MUFAs was associated with 15% (95% CI 5-25%) lower mortality. In addition, 18% (95% CI 10-26%) lower mortality was observed when theoretically replacing the sum of SFAs and animal-sourced MUFAs with isocaloric plant-sourced MUFAs. CONCLUSIONS: Intakes of MUFAs, including OA and PA, from plant but not animal sources were associated with lower total mortality. These findings suggested the importance of consuming MUFAs from plant-based foods for overall health.

Saturated Fatty Acid Intake Is Associated with Total Mortality in a Nationwide Cohort Study.

Background: Dietary intakes of total and specific types of saturated fatty acids (SFAs) in relation to total mortality remain largely unknown in China. Objective: We assessed the associations of total and individual SFA intakes with total mortality in a Chinese nationwide population. Methods: This prospective analysis included 7888 women and 6495 men, aged >20 y, from the China Health and Nutrition Survey (1989-2011). Cumulative mean of SFA intake was calculated based on 3 d of 24-h records in each round of the survey. Multivariable Cox proportional hazard models were used to estimate HR and 95% CI. Results: There were 1011 deaths during a median of 14 y of follow-up. In isocaloric nutrient density models that replace total carbohydrates, intakes of total SFAs and even-chain SFAs were associated with higher total mortality in women but not in men. Compared with the lowest quartiles, the HRs (95% CIs) in the highest quartiles were 1.65 (1.03, 2.62) for total SFAs (P-trend = 0.042) and 1.83 (1.13, 2.94) for even-chain SFAs (P-trend = 0.016) in women. Intake of odd-chain SFAs was associated with lower total mortality both in men [HR (95% CI): 0.64 (0.47, 0.87); P-trend = 0.01] and in women [HR (95% CI): 0.59 (0.42, 0.84); P-trend = 0.0013]. Moreover, intake of medium-chain SFAs was linked with lower total mortality in men [HR (95% CI): 0.64 (0.44, 0.93); P-trend = 0.013]. However, isocalorically replacing 1% of energy from unsaturated fatty acids with even-chain SFAs was associated with higher total mortality in men [HRs (95% CIs): 1.08 (0.97, 1.20) and 1.39 (1.20, 1.60) for replacing PUFAs and MUFAs, respectively]. Conclusions: Total SFA and even-chain SFA intake was associated with higher total mortality in women, whereas intake of odd-chain SFAs was related to lower total mortality in both sexes. This analysis of cohort was registered at clinicaltrials.gov as NCT03281512.

Arachidonic acid sex-dependently affects obesity through linking gut microbiota-driven inflammation to hypothalamus-adipose-liver axis.

Unraveling the role of dietary lipids is beneficial to treat obesity and metabolic dysfunction. Nonetheless, how dietary lipids affect existing obesity remains unknown. Arachidonic acid (AA), a derivative of linoleic acid, is one of the crucial n-6 fatty acids. The aim of this study was to investigate whether AA affects obesity through associating microbiota-driven inflammation with hypothalamus-adipose-liver axis. Four-week old C57BL/6J mice were fed with a high-fat diet (HFD, 45% fat) for 10weeks to induce obesity, and then fed a HFD enriched with 10g/kg of AA or a continuous HFD in the following 15weeks. Systemic adiposity and inflammation, metabolic profiles, gut microbiota composition, short-chain fatty acids production, hypothalamic feeding regulators, browning process of adipocytes, hepatosteatosis, and insulin resistance in adipose were investigated. The results indicated that AA aggravates obesity for both genders whereas sex-dependently affects gut microbiota composition. Also, AA favors pro-inflammatory microbiota and reduces butyrate production and circulating serotonin, which augments global inflammation and triggers hypothalamic leptin resistance via microglia accumulation in male. AA exacerbates non-alcoholic steatohepatitis along with amplified inflammation through TLR4-NF-κB pathway and induces insulin resistance. Reversely, AA alleviates obesity-related disorders via rescuing anti-inflammatory and butyrate-producing microbiota, up-regulating GPR41 and GPR109A and controlling hypothalamic inflammation in female. Nevertheless, AA modifies adipocyte browning and promotes lipid mobilization for both genders. We show that AA affects obesity likely through a gut-hypothalamus-adipose-liver axis. Our findings formulate recommendations of n-6 fatty acids like AA from dietary intake for obese subjects preferably in a sexually dimorphic way.

Fried food consumption, genetic risk, and incident obesity: a prospective study.

Background and aims: Genetic and dietary factors contribute to adiposity risk, but little evidence supports genetic personalization of fried food intake recommendations for the management of obesity. This study aimed to assess the associations between fried food consumption and adiposity incidence and whether the associations were modified by an individual's genotype. Methods: We included 27 427 participants who had dietary data assessed by a validated 24 h dietary recall and available anthropometric information from the UK Biobank study. The genetic risk score (GRS) was calculated using 940 BMI associated variants. Results: With an average of 8.1 years of follow-up, 1472 and 2893 participants were defined as having overall obesity and abdominal obesity, respectively. Individuals in the highest categories of fried food consumption were positively associated with the risk of obesity (HR = 1.31; 95% CI 1.10-1.56) and abdominal obesity (HR = 1.27; 95% CI 1.12-1.45) compared with the lowest categories. Moreover, fried food consumption had a significant interatction with obesity GRS for abdominal obesity risk (P interaction = 0.016). Fried food intake was associated with a higher abdominal obesity risk (HR = 1.59, 95% CI: 1.25-2.00) among participants with a lower genetic risk. Conclusions: Our findings indicated that fried food consumption had a higher abdominal obesity risk among individuals with a lower genetic risk, suggesting the restriction of fried food intake for this group of people.

Fish oil supplementation and risk of dementia among diabetic patients: a prospective study of 16,061 older patients.

BACKGROUND: Although n-3 Polyunsaturated fatty acids (PUFAs) may benefit cognitive performance, the association of n-3 PUFA intake with dementia risk under dysglycemia has not been examined. We aimed to evaluate the relationship between fish oil supplement use or fish consumption and dementia risk among older patients with diabetes. METHOD: A total of 16,061 diabetic patients aged over 60 years were followed up in the UK Biobank. Fish oil supplements use (yes or no) was collected by the touch screen questionnaire. The diagnosis of dementia was ascertained by the UK Biobank Outcome Adjudication Group. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) were estimated using Cox proportional hazards models. RESULTS: A total of 337 cases of dementia were confirmed after a mean duration of 7.7 years (123,486 person-years) of follow-up. Habitual use of fish oil supplements showed a 24% lower dementia risk among older diabetic patients [HRs (95% CIs): 0.76 (0.60-0.98) (P = 0.031)] compared with non-users. Such inverse association was not modified by the APOE ε4 genotype. However, the consumption of both oily fish (≥2 times/week) and non-oily fish (≥2 times/week) had no significant association with dementia risk (p-trend = 0.271 and p-trend = 0.065) compared with non-consumers. CONCLUSION: In summary, fish oil supplementation may play a protective role in cognitive function across all APOE genotypes, while non-oily fish and oily fish consumption have no protective association among older diabetic patients.

Association of soy intake and cooking methods with colorectal polyp and adenoma prevalence: findings from the extended Lanxi pre-colorectal cancer cohort (LP3C).

Background: Limited research has explored the association between dietary soy products and colorectal polyps and adenomas, with insufficient attention given to cooking methods and subtypes of polyps. This study aimed to comprehensively assess the relationship between soy intake, its cooking methods, and the risk of colorectal polyps and adenomas within a high-incidence population of colorectal cancer (CRC) in China. Methods: Data were derived from 14,903 participants aged 40-80 years, enrolled in the extended Lanxi Pre-colorectal Cancer Cohort (LP3C) between March 2018 and December 2022. This cross-sectional study is based on the participants' baseline information. Long-term dietary information was collected through a validated food frequency questionnaire (FFQ), and colorectal polyps and adenomas were identified through electronic colonoscopy. Employing multivariate logistic regression, results were expressed as odds ratios (ORs) with their corresponding 95% confidence intervals (95% CIs). Results: 4,942 cases of colorectal polyps and 2,678 cases of adenomas were ascertained. A significant positive association was found between total soy intake and the occurrence of polyps/adenomas. Considering cooking methods, a notable increase in polyp risk was associated with the consumption of fried soys while no association was detected for boiled or marinated soys. Furthermore, total soy intake demonstrated associations with large and multiple polyps, polyps Yamade-typed less than II, and polyps across all anatomical subsites. Conclusion: Within the high-risk CRC population in China, increased soy product intake was linked to a higher risk of polyps, primarily attributed to the consumption of fried soys. This suggests that modifying cooking methods to avoid fried soys may serve as a preventive strategy for colorectal polyps.