Associations between cooking method of food and type 2 diabetes risk: A prospective analysis focusing on cooking method transitioning.

Cooking process for food significantly impacts household air and increase exposure to endocrine disruptors such as acrylamide and, consequently, affecting human health. In the past 30 years, the transformation of cooking methods to high-temperature thermal processing has occurred widely in China. Yet the transition of cooking methods on the onset of type 2 diabetes (T2D) remains unclear, which may hinder health-based Sustainable Development Goals. We aimed to estimate the associations between dietary intake with different cooking methods and T2D risk. We included 14,745 participants (>20 y) from the China Health and Nutrition Survey (1991-2015). Food consumption was calculated using three consecutive 24-h dietary recalls combined with both individual participant level and household food inventory. Cooking methods, including boiled, steamed, baked, griddled, stir-fried, deep-fried, and raw, were also recorded. The consumption of baked/griddle foods and deep-fried foods are positively associated with 39% and 35% higher of T2D risk by comparing the highest with the lowest categories of food consumption, respectively. The overall unhealthy cooking method for processing foods including baked/griddled and deep-fried foods was attributable for 15 million T2D cases of the total T2D burden in 2011, resulting in a medical cost of $2.7 billion and was expected to be attributable for 39 million T2D cases in 2030, producing a medical cost of $223.8 billion. Replacing one serving of deep-fried foods and baked/griddle foods with boiled/steamed foods was related to 50% and 20% lower risk of T2D, respectively. Our findings support healthy driven cooking methods for daily diet are recommended to nourish sustainable T2D prevention in China.

Habitual Daily Intake of Fried Foods Raises Transgenerational Inheritance Risk of Heart Failure Through NOTCH1-Triggered Apoptosis.

Consumption of fried foods is highly prevalent in the Western dietary pattern. Western diet has been unfavorably linked with high risk of developing cardiovascular diseases. Heart failure (HF) as a cardiovascular disease subtype is a growing global pandemic with high morbidity and mortality. However, the causal relationship between long-term fried food consumption and incident HF remains unclear. Our population-based study revealed that frequent fried food consumption is strongly associated with 15% higher risk of HF. The causal relationship may be ascribed to the dietary acrylamide exposure in fried foods. Further cross-sectional study evidenced that acrylamide exposure is associated with an increased risk of HF. Furthermore, we discover and demonstrate that chronic acrylamide exposure may induce HF in zebrafish and mice. Mechanistically, we reveal that acrylamide induces energy metabolism disturbance in heart due to the mitochondria dysfunction and metabolic remodeling. Moreover, acrylamide exposure induces myocardial apoptosis via inhibiting NOTCH1-phosphatidylinositol 3-kinase/AKT signaling. In addition, acrylamide exposure could affect heart development during early life stage, and the adverse effect of acrylamide exposure is a threat for next generation via epigenetic change evoked by DNA methyltransferase 1 (DNMT1). In this study, we reveal the adverse effects and underlying mechanism of fried foods and acrylamide as a typical food processing contaminant on HF from population-based observations to experimental validation. Collectively, these results both epidemiologically and mechanistically provide strong evidence to unravel the mechanism of acrylamide-triggered HF and highlight the significance of reducing fried food consumption for lower the risk of HF.

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.

Parental exposure to acrylamide disrupts sphingolipid metabolism and impairs transgenerational neurodevelopment in zebrafish (Danio rerio) offspring.

Acrylamide exposure has become an emerging environmental and food safety issue, and its toxicity poses a potential threat to public health worldwide. However, limited studies have paid attention to the detrimental effects of parental exposure to acrylamide on the neurodevelopment in zebrafish offspring. In this study, the embryos were life-cycle exposed to acrylamide (0.125 and 0.25 mM) for 180 days. Subsequently, these zebrafish (F0) were allowed to mate, and their offspring (F1) were collected to culture in clean water from embryos to adults. We employed developmental and morphological observations, behavioral profiles, metabolomics analyses, and transcriptional level examinations to investigate the transgenerational neurotoxicity with parental exposure to acrylamide. Our results showed that parental exposure to acrylamide harms the birth, development, and behavior characterization of the F1 zebrafish larvae, including poor egg quality, increased mortality rates, abnormal heart rates, slowed swimming activity, and heightened anxiety behavior, and continuously disturbs mental health in F1 adult zebrafish. The transcriptional analysis showed that parental chronic exposure to acrylamide deteriorates the neurodevelopment in F1 larvae. In addition, metabolomics analyses revealed that sphingolipid metabolism disruption may be associated with the observed abnormal development and behavioral response in unexposed F1 offspring. Overall, the present study provides pioneer evidence that acrylamide induces transgenerational neurotoxicity via targeting and disrupting sphingolipid metabolism, which reveals intergenerational transmission of acrylamide exposure and unravels its spatiotemporal toxicological effect on neurodevelopment.

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.

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.

Circulating fatty acids, genetic risk, and incident coronary artery disease: A prospective, longitudinal cohort study.

The role of fatty acids (FAs) in primary prevention of coronary artery disease (CAD) is highly debated, and the modification effect by genetic risk profiles remains unclear. Here, we report the prospective associations of circulating FAs and genetic predisposition with CAD development in 101,367 U.K. Biobank participants. A total of 3719 CAD cases occurred during a mean follow-up of 11.5 years. Plasma monounsaturated FAs (MUFAs) were positively associated with risk of CAD, whereas the risk was significantly lower with higher n-3 polyunsaturated FAs (PUFAs) and more reductions in risk were detected among TT carriers of rs174547. Furthermore, increased plasma saturated FAs (SFAs) and linoleic acid were related to a significant increase in CAD risk among participants with high genetic risk (genetic risk score > 90%). These findings suggest that individuals with high genetic risk need to reduce plasma SFAs levels for CAD prevention. Supplementation of n-3 PUFAs for CAD prevention may consider individuals' genetic makeup.

Healthy dietary patterns and risk of cardiovascular disease in diabetic patients: a prospective cohort study.

Purpose: Evidence is limited regarding the associations of different dietary patterns with cardiovascular disease (CVD) risk among the population with diabetes. Thus, we aimed to explore the associations between three dietary patterns and CVD incidence among the population with diabetes. Materials and methods: We prospectively followed 22 473 diabetic patients from the UK Biobank at the baseline. The healthy dietary pattern was derived from a food frequency questionnaire; meanwhile, the Alternate Mediterranean Diet (AMED) and the Dietary Approaches to Stop Hypertension (DASH) diet were assessed based on the Oxford WebQ online 24 h dietary questionnaire. Results: During an average of 10.8 years of follow-up, 5209 incident CVD cases, including 3552 coronary heart disease (CHD) events and 881 strokes, were documented. After multivariate adjustment, a higher healthy diet score was negatively associated with CVD, CHD, and stroke incidence. The hazard ratios and 95% confidence intervals across increasing quintiles of healthy diet score were 0.86 (0.79-0.95), 0.83 (0.75-0.93), and 0.71 (0.57-0.88) for CVD, CHD, and stroke, respectively. A similar protective association with CVD incidence was found for the AMED but not the DASH diet. Conclusions: Adherence to healthy dietary patterns is related to a lower risk of developing CVD among diabetic patients. Our findings further provide vigorous evidence for formulating dietary adherence guidelines for diabetic patients to reduce the burden of CVD complications.

Association of Fish Oil Supplementation with Risk of Coronary Heart Disease in Individuals with Diabetes and Prediabetes: A Prospective Study in the UK Biobank.

This study aimed to explore the association between habitual intake of fish oil supplementation and the risk of developing CHD in patients with prediabetes and diabetes. Habitual use of fish oil was assessed by repeated questionnaires. Cox proportional hazard models were applied to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Over a median follow-up of 11.6 years, 4304 and 3294 CHD cases were documented among 47,663 individuals with prediabetes and 22,146 patients with diabetes in the UK Biobank, respectively. After multivariable adjustment, the HRs (95% CI) of CHD were 0.91 (0.85-0.98) and 0.87 (0.80-0.95) for individuals utilizing fish oil supplementation compared with non-users among the participants with prediabetes and diabetes, respectively. Furthermore, we identified an inverse relationship between fish oil use and CHD incidence, which was significantly mediated by serum C-reactive protein (CRP) levels in individuals with prediabetes and by very-low-density lipoprotein cholesterol (VLDL-C) in patients with diabetes at baseline. The inverse associations were consistent in the analyses stratified by potential confounders. In conclusion, the consumption of fish oil supplements was linked to decreased serum CRP and VLDL-C levels and subsequent CHD risk among adults with prediabetes and diabetes. Our findings highlight the important role of the habitual intake of fish oil supplements in preventing CHD in individuals with impaired glucose metabolism.

Associations of specific dietary unsaturated fatty acids with risk of overweight/obesity: population-based cohort study.

Background: The role of specific unsaturated fatty acids (FAs) in the development of overweight/obesity remains unclear in the general population. Here, we aimed to explore the associations of different types of unsaturated FAs with overweight/obesity risk among the Chinese population. Methods: Eight thousand seven hundred forty-two subjects free of overweight/obesity at entry in the China Health and Nutrition Survey (CHNS) were followed up until 2015. Dietary unsaturated FAs were assessed by 3-day 24-h recalls with a weighing method in each wave. Cox regression models were used to obtain the hazard ratios (HRs) and 95% confidence intervals (CIs) for overweight/obesity risk associated with unsaturated FAs. Results: During a median follow-up of 7 years, 2,753 subjects (1,350 males and 1,403 females) developed overweight/obesity. Consuming more monounsaturated FAs (MUFAs) was associated with a lower risk of overweight/obesity (highest vs. lowest quartile: HR 0.80, 95% CI 0.67-0.96; P-trend = 0.010). Similar inverse associations were observed for plant-MUFAs (HRQ4vsQ1 0.83, 95% CI: 0.73-0.94; P-trend = 0.003) and animal-MUFAs (HRQ4vsQ1 0.77, 95% CI: 0.64-0.94; P-trend = 0.004), total dietary oleic acid (OA) (HRQ4vsQ1 0.66, 95% CI: 0.55-0.79; P-trend <0.001), plant-OA (HRQ4vsQ1 0.73, 95% CI: 0.64-0.83; P-trend <0.001) and animal-OA (HRQ4vsQ1 0.68, 95% CI: 0.55-0.84; P-trend <0.001). In addition, the intakes of n-3 polyunsaturated FAs (PUFAs) (HRQ4vsQ1 1.24, 95% CI: 1.09-1.42; P-trend = 0.017) and α-linolenic acid (ALA) (HRQ4vsQ1 1.22, 95% CI: 1.07-1.39; P-trend = 0.039) but not marine n-3 PUFAs were positively linked to overweight/obesity risk. Consumption of n-6 PUFAs (HRQ4vsQ1 1.13, 95% CI: 0.99-1.28; P-trend = 0.014) and linoleic acid (LA) (HRQ4vsQ1 1.11, 95% CI: 0.98-1.26; P-trend = 0.020) had marginal and positive relationships with the incidence of overweight/obesity. N-6/n-3 PUFA ratio ranging from 5.7 to 12.6 was related to higher risk of overweight/obesity. Conclusion: Higher dietary intake of MUFAs was associated with lower overweight/obesity risk, which was mainly driven by dietary OA from either plant or animal sources. Intakes of ALA, n-6 PUFAs and LA were related to higher risk of overweight/obesity. These results support consuming more MUFAs for maintaining a healthy body weight among the Chinese population.

Potato consumption, polygenic scores, and incident type 2 diabetes: An observational study.

Whether the consumption of different processed potatoes is detrimental to type 2 diabetes (T2D) is highly debated. This study aimed to assess the relations between potato consumption and the risk of T2D and whether the relationship was modified by the genetic predisposition to T2D. We included 174,665 participants from the UK Biobank at baseline. Potato consumption was evaluated using the 24-hour dietary questionnaire. The genetic risk score (GRS) was calculated based on 424 variants associated with T2D. After adjustment for demographic, lifestyle, and dietary factors, the consumption of total potatoes was significantly and positively associated with T2D risk [hazard ratio (HR) comparing two or more servings/day with non-consumers was 1.28 (95% CI: 1.13-1.45)]. HRs (95% CIs) of T2D for each 1-SD increment in boiled/baked potatoes, mashed potatoes, and fried potatoes were 1.02 (0.99-1.05), 1.05 (1.02-1.08), and 1.05 (1.02-1.09), respectively. There were no significant interactions between the consumption of total or different processed potatoes and overall GRS on T2D risk. Theoretically, replacing one serving/day of total potatoes with the same amount of non-starchy vegetables was related to a 12% (95% CI: 0.84-0.91) lower T2D risk. These results showed the positive associations of the consumption of total potatoes, mashed potatoes or fried potatoes and genetic risk with higher incident T2D. An unhealthy potato-based diet is associated with higher diabetes risk regardless of genetic risk.

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.

The sulfur microbial diet and increased risk of obesity: Findings from a population-based prospective cohort study.

BACKGROUND & AIMS: Gut-produced hydrogen sulfide (H2S) has been associated with increased gut permeability and inflammation, which may be related to higher obesity risk. We investigated the association of sulfur microbial diet, a dietary index associated with 43 sulfur-metabolizing bacteria, with the incident obesity and whether the relationship was modified by the genetic predisposition to obesity. METHODS: We included 27,429 participants with available body mass index (BMI) data from the UK Biobank. The sulfur microbial diet score was assessed using the 24-h dietary assessment method. Obesity and abdominal obesity were defined according to the World Health Organization criteria. Body fat percentage was assessed using a body composition analyzer. The genetic risk score (GRS) was calculated by 940 BMI-related variants. RESULTS: We documented 1472 and 2893 cases of obesity and abdominal obesity during a mean follow-up of 8.1 years. After multivariable adjustment, the sulfur microbial diet score was positively associated with obesity (HRQ4vsQ1 = 1.63; 95% CI = 1.40-1.89, P-trend = 0.001) and abdominal obesity risk (HRQ4vsQ1 = 1.17; 95% CI = 1.05-1.30, P-trend = 0.002). We also observed that increased sulfur microbial diet score was positively related to several adiposity indicators, including a 5% increase in BMI, WC, and body fat percentage. Moreover, the sulfur microbial diet had no significant interactions with genetic risk on obesity incidence. CONCLUSIONS: Our results emphasized the significance of avoiding the sulfur microbial diet for obesity prevention across all levels of genetic risk.

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.

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.

Association of egg consumption with colorectal polyp prevalence: findings from the Lanxi Pre-Colorectal Cancer Cohort (LP3C) in China.

Eggs contain high-quality protein, lavish vitamins and other bioactive nutrients but are rich in cholesterol. Our study is designed to assess the association of egg intake with polyp prevalence. A total of 7068 participants at a high risk of CRC from the Lanxi Pre-Colorectal Cancer Cohort Study (LP3C) were recruited. A food frequency questionnaire (FFQ) was utilized to obtain dietary data through a face-to-face interview. Cases of colorectal polyps were identified by electronic colonoscopy. The logistic regression model was exploited to achieve odds ratios (ORs) and 95% confidence intervals (CIs). Overall 2064 cases of colorectal polyps were identified in the 2018-2019 survey of LP3C. A positive association of egg consumption with colorectal polyp prevalence was found after the multivariable adjustment [ORQ4 vs. Q1 (95% CI): 1.23 (1.05-1.44); Ptrend = 0.01]. However, a positive relationship disappeared after further adjustment for dietary cholesterol (Ptrend = 0.37), which explained that the harmful role of eggs could be ascribed to the high content of dietary cholesterol. Besides, a positive trend was found between dietary cholesterol and polyp prevalence [OR (95% CI): 1.21 (0.99-1.47); Ptrend = 0.04]. Furthermore, replacing 1 egg (50 g d-1) with an equal amount of total dairy products was related to 11% lower colorectal polyp prevalence [OR (95% CI): 0.89 (0.80-0.99); P = 0.03]. In summary, higher egg consumption was correlated with a higher polyp prevalence among the Chinese population at a high risk of CRC, which was ascribed to the high content of dietary cholesterol in eggs. Besides, individuals with the highest dietary cholesterol tended to have a higher polyp prevalence. Reducing the consumption of eggs and replacing eggs with total dairy products as alternative protein sources may prevent the occurrence of polyps in China.

Advancing metabolic networks and mapping updated urinary metabolic fingerprints after exposure to typical carcinogenic heterocyclic aromatic amines.

Heterocyclic aromatic amines (HAAs) were not only present in cooked foods and cigarette smoke, but also measured in airborne particles and diesel-exhaust particles. Typical HAAs have been reported to induce carcinogenicity and metabolic disturbances, but how these hazardous compounds interfere with metabolic networks by regulating metabolic pathways and fingerprinting signature metabolites as biomarkers remains ambiguous. We developed an advanced strategy that adopted chemical isotope labeling ultrahigh-performance liquid chromatography coupled to quadrupole-Orbitrap high-resolution mass spectrometry for urinary nontargeted metabolomics analysis to gain new insight into in vivo physiological responses stimulated by exposure to typical HAAs. Rats were orally administered with a single dose of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) or 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) (1 and 10 mg/kg bw) and their D3-isotopic compounds, respectively, and urine samples were then continuously collected within 36 h. Metabolomics data were acquired and processed by classical multivariate statistical analysis, while urinary metabolites were further identified and characterized according to mass spectrometric fragmentation rules, time- and dose-dependent profiles, and calibration of synthesized standards. We monitored 23 and 37 urinary metabolites as the biotransformation products of PhIP and MeIQx, respectively, and first identified demethylated metabolites of PhIP, tentatively named 2-amino-6-phenylimidazo[4,5-b]pyridine, and dihydroxylation products of classical HAAs as short-term biomarkers of exposure to further unravel the metabolic networks. In addition, our findings revealed that both HAAs significantly disturb histidine metabolism, arginine and proline metabolism, tryptophan metabolism, pyrimidine metabolism, tricarboxylic acid cycle, etc. Furthermore, we found that histamine, methionine, alanine, and 4-guanidinobutanoic acid could be considered potential characteristic biomarkers for the oncogenicity or carcinogenicity of both PhIP and MeIQx and screened their specific key pivotal metabolites. The current metabolomics approach is applicable in mapping updated urinary metabolic fingerprints and identifying potential specific biomarkers for HAAs-induced early tumorigenesis.

Lifelong docosahexaenoic acid intervention ameliorates aging in the telomere-DNA-mitochondria axis in telomerase-deficient mice.

The health benefits of n-3 polyunsaturated fatty acids (PUFAs) in multiple age-related diseases are associated with telomere length. Telomerase is intimately related to inflammation and oxidative stress, but whether the underlying function of n-3 PUFAs on telomere maintenance is based on telomerase activation or related mechanisms remains unclear. Herein, we utilized late-generation (G4) telomerase-deficient (Terc-/-) mice to perform a lifelong docosahexaenoic acid (DHA) intervention to determine the potential of DHA in telomere maintenance and health promotion. Unfortunately, DHA failed to prolong mouse longevity in either intrinsic or premature aging. However, intriguingly, lifelong dietary DHA intervention slowed the aging phenotypes and profoundly attenuated telomere attrition in blood leukocytes and multiple tissues, consistent with decreased ß-galactosidase activity and other senescence hallmarks with no observed sex differences. Notably, DHA intervention alleviated telomere attrition-induced γ-H2AX accumulation dependent on poly (ADP-ribose) polymerase 1 (PARP1) recruitment, and further regulated mitochondrial dysfunction critically involved in the DNA damage response. Together with the improvement of mitochondria function, the blocked reactive oxygen species (ROS) accumulation and suppression of the nuclear factor-κB (NF-κB)/nucleotide-binding domain-like receptor protein 3 (NLRP3)/caspase-1 pathways partially indicated anti-oxidative and anti-inflammatory effects of DHA. These data revealed a regulatory paradigm involving DHA in the telomere-DNA-mitochondria feedback loop mediated by DNA damage response and inflammation in alleviating senescence, which may hold potential as a translatable intervention in telomere-related diseases during aging.

Machine learning prediction of exposure to acrylamide based on modelling of association between dietary exposure and internal biomarkers.

The ubiquitous occurrence of acrylamide in various thermal processing food products poses a potential health risk for the public. An accurate exposure assessment is crucial to the risk evaluation of acrylamide. Machine learning emerging as a powerful computational tool for prediction was employed to establish the association between internal exposure and dietary exposure to acrylamide among a Chinese cohort of middle-aged and elderly population (n = 1,272). Five machine learning regression models were constructed and compared to predict the daily dietary acrylamide exposure based on urinary biomarkers including N-acetyl-S-(2-carbamoylethyl)-L-cysteine (AAMA), N-acetyl-S-(2-carbamoylethyl)-L-cysteine-sulfoxide (AAMA-sul), N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine (GAMA), and N-acetyl-S-(1-carbamoyl-2-hydroxyethyl)-L-cysteine (iso-GAMA). Other important covariates such as age, gender, physical activities, and total energy intake were also considered as predictors in the models. Average dietary intake of acrylamide among Chinese elderly participants was 8.9 µg/day, while average urinary contents of AAMA, AAMA-sul, GAMA, and iso-GAMA were 52.2, 19.1, 4.4, and 1.7 nmol/g Ucr (urine creatinine), respectively. Support vector regression (SVR) model showed the best prediction performance with a R of 0.415, followed by light gradient boosting machine (LightGBM) model (R = 0.396), adjusted multiple linear regression (MLR) model (R = 0.378), neural networks (NN) model (R = 0.365), MLR model (R = 0.363), and extreme gradient boosting (XGBoost) model (R = 0.337). The present study firstly correlated dietary exposure with internal exposure to acrylamide among Chinese elderly population, providing an innovative perspective for the exposure assessment of acrylamide.