Association between dietary carbohydrate to fiber ratio and metabolic dysfunction associated fatty liver disease in adults: evidence from the NHANES 2017-2020.

This study aimed to explore the association of carbohydrate to fiber ratio (CFR) with metabolic dysfunction-associated fatty liver disease (MAFLD) in adults. In this study, data from the 2 cycles (2017-2018 and 2019-2020) of the NHANES were used. Univariate and multivariate weighted logistic regression analyses were applied to evaluate the association between CFR and MAFLD. Odds ratios (ORs) and 95% confidence levels (CIs) were estimated. Subgroup analysis was further performed in terms of gender, age and comorbidity (diabetes, hypertension). A total of 3180 individuals were included, with 1408 (44.28%) in the non-MAFLD group and 1772 (55.72%) in the MAFLD group. After adjusting different variables, a dietary fiber intake of 11.15-18.40 g was associated with significantly lower odds of MAFLD compared with a fiber intake < 11.15 g (OR = 0.71, 95% CI 0.54-0.93). In contrast to a dietary CFR < 12.58, a CFR > 19.91 was associated with significantly higher odds of MAFLD (OR = 1.57, 95% CI 1.09-2.27). Compared with females with a dietary CFR < 12.58, those with a CFR > 19.91 had significantly increased odds of MAFLD (OR = 1.87, 95% CI 1.29-2.73). Among individuals aged < 65 years, a dietary CFR > 19.91 was associated with higher odds of MAFLD than a dietary CFR < 12.58 (OR = 1.52, 95% CI 1.02-2.25). For participants without diabetes (OR = 1.79, 95% CI 1.26-2.54) or hypertension (OR = 1.93, 95% CI 1.02-3.65), a dietary CFR > 19.91 was associated with elevated odds of MAFLD than a CFR < 12.58. In summary, a higher CFR was associated with significantly greater odds of MAFLD, indicating the negative association between carbohydrate quality and MAFLD. The research would be conducive to metabolic dysfunction-associated fatty liver disease treatment.

The association between glycemic index, glycemic load and total carbohydrate intake and risk of premature coronary artery disease: Iran Premature Coronary Artery Disease Study (IPAD) - A Case-Control Study.

BACKGROUND AND AIMS: The association between glycemic index (GI), glycemic load (GL), total carbohydrate intake, and risk of cardiovascular diseases has been controversial. Premature coronary artery disease (PCAD) is characterized by the age of onset lower than 55 and 65 respectively in men and women. The aim of the current study is to investigate the relationship between GI, GL and carbohydrate levels and the risk of PCAD in Iran. METHODS AND RESULTS: In total, 419 healthy people and 553 patients struggling with PCAD have participated in this case-control study. Dietary GI and GL were calculated using a validated food frequency questionnaire at the baseline. Crude and multivariable logistic regression were used to assess the relationship between GI, GL, and total carbohydrate intake and risk of PCAD. The mean age of participants was 51.13 ± 6.90 and 46 % of them were women. A significant direct relationship was observed between higher carbohydrate intake (OR: 1.74, 95%CI: 1.27-2.38) and GL levels (OR: 1.56, 95 % CI:1.14-2.14) and risk of PCAD. These associations were not significant after adjusting for potential variables. No significant association has been observed between GI and odds of PCAD even after controlling for all covariates. CONCLUSION: We found no significant association between GI, GL, and total carbohydrate intake and risk of premature coronary heart disease. Further observational and clinical trials are required to assess this relationship.

Dietary Macronutrient Intake and Cardiovascular Disease Risk and Mortality: A Systematic Review and Dose-Response Meta-Analysis of Prospective Cohort Studies.

Many epidemiological studies have evaluated the intake of macronutrients and the risk of mortality and cardiovascular disease (CVD). However, current evidence is conflicting and warrants further investigation. Therefore, we carried out an umbrella review to examine and quantify the potential dose-response association of dietary macronutrient intake with CVD morbidity and mortality. Prospective cohort studies from PubMed, Embase, and CENTRAL were reviewed, which reported associations of macronutrients (protein, fat, and carbohydrate) with all-cause, CVD, cancer mortality, or CVD events. Multivariable relative risks (RR) were pooled, and heterogeneity was assessed. The results of 124 prospective cohort studies were included in the systematic review and 101 in the meta-analysis. During the follow-up period from 2.2 to 30 years, 506,086 deaths and 79,585 CVD events occurred among 5,107,821 participants. High total protein intake was associated with low CVD morbidity (RR 0.88, 95% confidence interval 0.82-0.94), while high total carbohydrate intake was associated with high CVD morbidity (1.08, 1.02-1.13). For fats, a high intake of total fat was associated with a decreased all-cause mortality risk (0.92, 0.85-0.99). Saturated fatty acid intake was only associated with cancer mortality (1.10, 1.06-1.14); Both monounsaturated fatty acid (MUFA) and polyunsaturated fatty acids (PUFA) intake was associated with all-cause mortality (MUFA: 0.92, 0.86-0.98; PUFA: 0.91, 0.86-0.96). This meta-analysis supports that protein intake is associated with a decreased risk of CVD morbidity, while carbohydrate intake is associated with an increased risk of CVD morbidity. High total fat intake is associated with a low risk of all-cause mortality, and this effect was different in an analysis stratified by the type of fat.

Effects of a high-fat low-carbohydrate diet under different energy conditions on glucose homeostasis and fatty liver development in rats and on gluconeogenesis in the isolated perfused liver.

The beneficial effects of high-fat low-carbohydrate (HFLC) diets on glucose metabolism have been questioned and their effects on liver metabolism are not totally clear. The aim of this work was to investigate the effects of an HFLC diet under different energy conditions on glucose homeostasis, fatty liver development, and hepatic gluconeogenesis using the isolated perfused rat liver. HFLC diet (79% fat, 19% protein, and 2% carbohydrates in Kcal%) was administered to rats for 4 weeks under three conditions: ad libitum (hypercaloric), isocaloric, and hypocaloric (energy reduction of 20%). Fasting blood glucose levels and total fat in the liver were higher in all HFLC diet rats. Oral glucose tolerance was impaired in isocaloric and hypercaloric groups, although insulin sensitivity was not altered. HFLC diet also caused marked liver metabolic alterations: higher gluconeogenesis rate from lactate and a reduced capacity to metabolize alanine, the latter effect being more intense in the hypocaloric condition. Thus, even when HFLC diets are used for weight loss, our data imply that they can potentially cause harmful consequences for the liver.

A Comprehensive Review of the Effects of Glycemic Carbohydrates on the Neurocognitive Functions Based on Gut Microenvironment Regulation and Glycemic Fluctuation Control.

Improper glycemic carbohydrates (GCs) consumption can be a potential risk factor for metabolic diseases such as obesity and diabetes, which may lead to cognitive impairment. Although several potential mechanisms have been studied, the biological relationship between carbohydrate consumption and neurocognitive impairment is still uncertain. In this review, the main effects and mechanisms of GCs' digestive characteristics on cognitive functions are comprehensively elucidated. Additionally, healthier carbohydrate selection, a reliable research model, and future directions are discussed. Individuals in their early and late lives and patients with metabolic diseases are highly susceptible to dietary-induced cognitive impairment. It is well known that gut function is closely related to dietary patterns. Unhealthy carbohydrate diet-induced gut microenvironment disorders negatively impact cognitive functions through the gut-brain axis. Moreover, severe glycemic fluctuations, due to rapidly digestible carbohydrate consumption or metabolic diseases, can impair neurocognitive functions by disrupting glucose metabolism, dysregulating calcium homeostasis, oxidative stress, inflammatory responses, and accumulating advanced glycation end products. Unstable glycemic status can lead to more severe neurological impairment than persistent hyperglycemia. Slow-digested or resistant carbohydrates might contribute to better neurocognitive functions due to stable glycemic response and healthier gut functions than fully gelatinized starch and nutritive sugars.

Dietary Approach of Patients with Hormone-Related Cancer Based on the Glycemic Index and Glycemic Load Estimates.

Hormone-related cancers, namely breast, endometrial, cervical, prostate, testicular, and thyroid, constitute a specific group of cancers dependent on hormone levels that play an essential role in cancer growth. In addition to the traditional risk factors, diet seems to be an important environmental factor that partially explains the steadily increased prevalence of this group of cancer. The composition of food, the dietary patterns, the endocrine-disrupting chemicals, and the way of food processing and preparation related to dietary advanced glycation end-product formation are all related to cancer. However, it remains unclear which specific dietary components mediate this relationship. Carbohydrates seem to be a risk factor for cancer in general and hormone-related cancers, in particular, with a difference between simple and complex carbohydrates. Glycemic index and glycemic load estimates reflect the effect of dietary carbohydrates on postprandial glucose concentrations. Several studies have investigated the relationship between the dietary glycemic index and glycemic load estimates with the natural course of cancer and, more specifically, hormone-related cancers. High glycemic index and glycemic load diets are associated with cancer development and worse prognosis, partially explained by the adverse effects on insulin metabolism, causing hyperinsulinemia and insulin resistance, and also by inflammation and oxidative stress induction. Herein, we review the existing data on the effect of diets focusing on the glycemic index and glycemic load estimates on hormone-related cancers.

Associations of dietary sugar types with coronary heart disease risk: a prospective cohort study.

BACKGROUND: Higher intake of total sugar has been linked with coronary heart disease (CHD) risk, but the role of individual sugars, particularly fructose, is uncertain. OBJECTIVES: This study aimed to investigate the associations of individual dietary sugars with CHD risk. METHODS: In prospective cohort studies, we followed 76,815 women (Nurses' Health Study, 1980-2020) and 38,878 men (Health Professionals Follow-up Study, 1986-2016). Sugar and carbohydrate intake, including total fructose equivalents ([TFE] from fructose monosaccharides and sucrose), total glucose equivalents ([TGE] from glucose monosaccharides, disaccharides, and starch), and other sugar types, was measured every 2 to 4 y by semiquantitative food frequency questionnaires. RESULTS: We documented 9,723 incident CHD cases over 40 years. In isocaloric substitution models with total fat as a comparison nutrient, comparing extreme quintiles of intake, hazard ratios (HRs), 95% confidence interval [CI]) for CHD risk were 1.31 (1.20 to 1.42; Ptrend < 0.001) for TGE and 1.03 (0.94 to 1.11; Ptrend = 0.25) for TFE. TFE from fruits and vegetables was not associated with CHD risk (Ptrend = 0.70), but TFE from added sugar and juice was associated with CHD risk (HR: 1.12, 95% CI: 1.04 to 1.20; Ptrend < 0.01). Intakes of total sugars and added sugar were positively associated with CHD risk (HRs: 1.16, 95% CI: 1.07 to 1.26, Ptrend < 0.001; 1.08, 95% CI: 0.99 to 1.16, Ptrend = 0.04). CONCLUSIONS: Intakes of TGE, total sugar, added sugar, and fructose from added sugar and juice were associated with higher CHD risk, but TFE and fructose from fruits and vegetables were not.

Dietary carbohydrate quality index (CQI), cardio-metabolic risk factors and insulin resistance among adults with obesity.

BACKGROUND: Metabolic syndrome (MetS), as a cluster of cardiometabolic risk factors, is a global public health concern due to its increasing prevalence. Considering the previous evidence of the association between carbohydrate quality and cardiometabolic risk factors, our study was aimed to evaluate any possible association between carbohydrate quality index (CQI) and cardiometabolic risk factors among obese adults. METHODS: In this cross-sectional study, 336 apparently healthy individuals with obesity were participated. Dietary intake was assessed by a semi-quantitative Food Frequency Questionnaire (FFQ), including 168 food items validated for the Iranian population. CQI was calculated with three components of solid carbohydrates to total carbohydrates ratio, dietary fiber intake, and dietary glycemic index (GI). Body composition was determined by bioelectrical impedance analysis (BIA). Blood pressure was measured by sphygmomanometer and enzymatic methods were used to evaluate serum lipid, glucose, and insulin concentrations. RESULTS: Subjects in the third quartile of CQI had significantly lower systolic blood pressure (SBP) (P = 0.03) and diastolic blood pressure (DBP) (P = 0.01). Participants in the higher quartiles of CQI had more intake of energy, carbohydrates, fat, saturated fatty acid (SFA), and mono-saturated fatty acid (MUFA) (P < 0.05). Moreover, the homeostasis model assessment of insulin resistance (HOMA-IR) was decreased in the second quartile of CQI [odds ratio (OR) = 0.146, P = 0.01) after adjustment for age, body mass index (BMI), sex, physical activity, socioeconomic status (SES) and energy intake. CONCLUSION: According to our findings, a higher quality of dietary carbohydrates, determined by CQI, could be associated with a lower risk of hypertension.

Type 1 diabetes and low carbohydrate diets-Defining the degree of nutritional ketosis.

AIMS: Adopting a low- or very low-carbohydrate (LCD or VLCD) diet in type 1 diabetes mellitus (T1D) is a controversial intervention. The main fear is that these diets may increase the risk of diabetic ketoacidosis. However, there is little data about the ketoacidosis risk and the level of physiological nutritional ketosis in individuals following these diets. We aimed to define the level of ketosis in those with T1D following carbohydrate restricted diets in a real-world observational study. METHODS: Patients with T1D who had self-selected dietary carbohydrate restriction were enrolled from local clinics and were compared to those following an unrestricted regular carbohydrate control diet (RCCD). Participants completed a 3-day diary, documenting food intake, ketones, and blood/interstitial glucose concentrations. RESULTS: Participants were divided into three groups according to mean carbohydrate intake: VLCD (<50 g carbohydrates/day) n = 6, LCD (50-130 g carbohydrates/day) n = 6, and RCCD (>130 g carbohydrates/day) n = 3. Mean beta-hydroxybutyrate (BOHB) concentrations were 1.2 mmol/l (SD 0.14), 0.3 mmol/l (SD 0.12) and 0.1mmol/l (SD 0.05) in the VLCD, LCD and RCCD groups, respectively (p = 0.02). Post hoc Dunn test demonstrated this reached statistical significance between the VLCD and RCCD groups (p = 0.02). CONCLUSION: Carbohydrate restricted diets, in particular VLCDs, are associated with a higher BOHB level. However, the degree of ketosis seen is much lower than we expected, and significantly lower than the level typically associated with diabetic ketoacidosis. This may suggest the risk of ketoacidosis is lower than feared, although safety will need to be evaluated further in large scale randomised trials.

Effect of high-refined carbohydrate diet on intestinal integrity.

OBJECTIVES: One of the leading causes of obesity is the consumption of excess nutrients. Obesity is characterized by adipose tissue expansion, chronic low-grade inflammation, and metabolic alterations. Although consumption of a high-fat diet has been demonstrated to be a diet-induced obesity model associated with gut disorders, the same effect is not well explored in a mild-obesity model induced by high-refined carbohydrate (HC) diet intake. The intestinal tract barrier comprises mucus, epithelial cells, tight junctions, immune cells, and gut microbiota. This system is susceptible to dysfunction by excess dietary components that could increase intestinal permeability and bacterial translocation. The aim of this study was to evaluate whether an HC diet and the alterations resulting from its intake are linked to small intestine changes. METHODS: Male BALB/c mice were fed a chow or an HC diet for 8 wk. RESULTS: Although differences in body weight gain were not observed between the groups, mice fed the HC diet showed increased adiposity associated with metabolic alterations. The interferon-γ expression and myeloperoxidase levels were increased in the small intestine in mice fed an HC diet. However, the intestinal villi length, the expression of tight junctions (zonula occludens-1 and claudin-4) and tumor necrosis factor-α cytokine, and the percentage of intraepithelial lymphocytes did not differ in the jejunum or ileum between the groups. We did not observe differences in intestinal permeability and bacterial translocation. CONCLUSION: Metabolic alterations caused by consumption of an HC diet lead to a mild obesity state that does not necessarily involve significant changes in intestinal integrity.

Different carbohydrate exposures and weight gain-results from a pooled analysis of three population-based studies.

BACKGROUND: The role of carbohydrate quantity and quality in weight gain remains unsolved, and research on carbohydrate subcategories is scarce. We examined total carbohydrates, dietary fiber, total sugar, and sucrose intake in relation to the risk of weight gain in Finnish adults. METHODS: Our data comprised 8327 adults aged 25-70 years in three population-based prospective cohorts. Diet was assessed by a validated food frequency questionnaire and nutrient intakes were calculated utilizing the Finnish Food Composition Database. Anthropometric measurements were collected according to standard protocols. Two-staged pooling was applied to derive relative risks across cohorts for weight gain of at least 5% by exposure variable intake quintiles in a 7-year follow-up. Linear trends were examined based on a Wald test. RESULTS: No association was observed between intakes of total carbohydrate, dietary fiber, total sugar or sucrose and the risk of weight gain of at least 5%. Yet, total sugar intake had a borderline protective association with the risk of weight gain in participants with obesity (RR 0.63; 95% CI 0.40-1.00 for highest vs. lowest quintile) and sucrose intake in participants with ≥10% decrease in carbohydrate intake during the follow-up (RR 0.78; 95% CI 0.61-1.00) after adjustments for sex, age, baseline weight, education, smoking, physical activity, and energy intake. Further adjustment for fruit consumption strengthened the associations. CONCLUSIONS: Our findings do not support an association between carbohydrate intake and weight gain. However, the results suggested that concurrent changes in carbohydrate intake might be an important determinant of weight change and should be further examined in future studies.

The Effect of a Moderately Restricted Carbohydrate Diet on Cardiometabolic Risk Factors in Overweight and Obese Women With Metabolic Syndrome: A Randomized Controlled Trial.

PURPOSE: Metabolic syndrome (MetS) is a major public health concern that increases the risk of cardiovascular disease and mortality. In previous studies of MetS management, low-carbohydrate diets have been strongly emphasized, despite the fact that many apparently healthy individuals have difficulties adhering to these diets on a long-term basis. The purpose of the present study was to elucidate the effects of a moderately restricted carbohydrate diet (MRCD) on cardiometabolic risk factors in women with MetS. METHODS: This parallel 3-month, single-blind randomized controlled trial was conducted in Tehran, Iran, among 70 women with overweight or obesity aged 20 to 50 years with MetS. Patients were randomly allocated to receive either MRCD (42%-45% carbohydrates and 35%-40% fats) (n = 35) or a normal weight loss diet (NWLD) (52%-55% carbohydrates and 25%-30% fats) (n = 35). Both diets contained the same quantity of protein, which accounted for 15% to 17% of total energy. Anthropometric measurements, blood pressure, lipid profile, and glycemic indices were all assessed before and after the intervention. FINDINGS: Compared with the NWLD group, following an MRCD significantly decreased weight (-4.82 vs -2.40 kg; P = 0.01), body mass index (-1.88 vs -0.94 kg/m2; P = 0.01), waist circumference (-5.34 vs -2.75 cm; P = 0.01), hip circumference (-2.58 vs -1.11 cm; P = 0.01), serum triglyceride (-26.8 vs -7.19 mg/dL; P = 0.01), and increased serum HDL-C levels (1.89 vs. 0.24 mg/dL; P = 0.01). There was no significant difference between the 2 diets in waist-to-hip ratio, serum total cholesterol, serum LDL-C, systolic and diastolic blood pressure, fasting blood glucose, insulin levels, or the homeostasis model assessment for insulin resistance. IMPLICATIONS: Moderate carbohydrate replacement with dietary fats significantly improved weight, body mass index, waist circumference, hip circumference, serum triglyceride, and HDL-C levels among women with MetS. Iranian Registry of Clinical Trials identifier: IRCT20210307050621N1.

Carbohydrate Intakes Below Recommendations With a High Intake of Fat Are Associated With Higher Prevalence of Metabolic Syndrome.

BACKGROUND: More than one-third of adults in the United States have metabolic syndrome, and dietary carbohydrate intake may modify the likelihood of developing this condition. Currently, there is a lack of consistent evidence demonstrating the relationship between carbohydrate intake that falls below recommendations and metabolic syndrome. Not accounting for the differences in fatty acid classes of these dietary patterns may be a reason for inconsistent findings. OBJECTIVE: This study evaluated the association between a carbohydrate intake below recommendations and metabolic syndrome stratified by fat quantity and fatty acid classes in a nationally representative sample of US adults. DESIGN: This cross-sectional study acquired data on food and nutrient intake and markers of metabolic syndrome from respondents in the National Health and Nutrition Examination Survey 1999-2018. PARTICIPANTS/SETTING: This study included 19,078 respondents who were aged 20 years or older, had reliable and complete data on food and nutrient intake and markers of metabolic syndrome, and were not pregnant or breastfeeding. MAIN OUTCOME MEASURES: The main outcome was prevalence of metabolic syndrome. STATISTICAL ANALYSES PERFORMED: Usual dietary intake was estimated using the National Cancer Institute's usual intake methodology. Multivariable logistic regression models assessed the relative odds of prevalent metabolic syndrome between those who had a carbohydrate intake below recommendations and those who met carbohydrate recommendations. RESULTS: Those who had a carbohydrate intake below recommendations had 1.067 (95% CI 1.063 to 1.071) times greater odds of having metabolic syndrome compared with those who met carbohydrate recommendations (P < 0.001). High intake of fat of any class was associated with higher odds of metabolic syndrome (total fat: 1.271, 95% CI 1.256 to 1.286; saturated fatty acid: 1.072, 95% CI 1.060 to 1.085; monounsaturated fatty acid: 1.317, 95% CI 1.300 to 1.333; polyunsaturated fatty acid: 1.056, 95% CI 1.047 to 1.066; P < 0.001 for all comparisons) in those who had a carbohydrate intake below recommendations. CONCLUSIONS: The odds of prevalent metabolic syndrome were higher among individuals who had a carbohydrate intake below recommendations compared with individuals who met carbohydrate recommendations.

Associations between types and sources of dietary carbohydrates and cardiovascular disease risk: a prospective cohort study of UK Biobank participants.

BACKGROUND: Recent studies have reported that the associations between dietary carbohydrates and cardiovascular disease (CVD) may depend on the quality, rather than the quantity, of carbohydrates consumed. This study aimed to assess the associations between types and sources of dietary carbohydrates and CVD incidence. A secondary aim was to examine the associations of carbohydrate intakes with triglycerides within lipoprotein subclasses. METHODS: A total of 110,497 UK Biobank participants with ≥ two (maximum five) 24-h dietary assessments who were free from CVD and diabetes at baseline were included. Multivariable-adjusted Cox regressions were used to estimate risks of incident total CVD (4188 cases), ischaemic heart disease (IHD; 3138) and stroke (1124) by carbohydrate intakes over a median follow-up time of 9.4 years, and the effect of modelled dietary substitutions. The associations of carbohydrate intakes with plasma triglycerides within lipoprotein subclasses as measured by nuclear magnetic resonance (NMR) spectroscopy were examined in 26,095 participants with baseline NMR spectroscopy measurements. RESULTS: Total carbohydrate intake was not associated with CVD outcomes. Free sugar intake was positively associated with total CVD (HR; 95% CI per 5% of energy, 1.07;1.03-1.10), IHD (1.06;1.02-1.10), and stroke (1.10;1.04-1.17). Fibre intake was inversely associated with total CVD (HR; 95% CI per 5 g/d, 0.96;0.93-0.99). Modelled isoenergetic substitution of 5% of energy from refined grain starch with wholegrain starch was inversely associated with total CVD (0.94;0.91-0.98) and IHD (0.94;0.90-0.98), and substitution of free sugars with non-free sugars was inversely associated with total CVD (0.95;0.92-0.98) and stroke (0.91;0.86-0.97). Free sugar intake was positively associated with triglycerides within all lipoproteins. CONCLUSIONS: Higher free sugar intake was associated with higher CVD incidence and higher triglyceride concentrations within all lipoproteins. Higher fibre intake and replacement of refined grain starch and free sugars with wholegrain starch and non-free sugars, respectively, may be protective for incident CVD.

Dietary treatment of type 1 diabetes: Beyond carbohydrate counting to fight cardiovascular risk.

AIMS: Type 1 diabetes (T1D) is tied to an increased risk of cardiovascular morbidity and mortality. Dietary treatment would be an elective therapeutic strategy to fight this risk. However, it is not known what the best dietary approach is. We revisited the currently available literature on the nutritional treatment of T1D in the light of their potential comprehensive effects on the management of cardio-metabolic risk factors (body weight, fasting and postprandial glucose and lipid metabolism). DATA SYNTHESIS: Nutritional research in T1D is mainly focused on blood glucose control, with most of the trials aiming at evaluating the acute effects of nutrients on postprandial glycemic response. The effects of the quantity and quality of nutrients and some specific foods on other metabolic risk factors have been explored mainly in cross-sectional analysis. Very few well-designed nutritional trials evaluated the best dietary approach to comprehensively manage cardiovascular risk by targeting along with blood glucose control, overweight, fasting and postprandial dyslipidemia. Therefore, the current best practice guidance for the dietary management of cardiovascular risk in T1D is generally based on evidence from patients with type 2 diabetes. CONCLUSIONS: Well-conducted nutritional trials specifically designed for T1D are needed to identify the best dietary treatment to fight cardiovascular risk in these patients.

Dietary carbohydrate quantity and quality and risk of cardiovascular disease, all-cause, cardiovascular and cancer mortality: A systematic review and meta-analysis.

BACKGROUND & AIMS: Evidence remains conflicted on the association between dietary carbohydrate quantity and quality and risk of cardiovascular disease, all-cause, cardiovascular and cancer mortality, and such meta-analyses are lacking. The study aimed to conduct a systematic review and meta-analysis to synthesize the knowledge about their associations and to explore the dose-response relations. METHODS: We comprehensively searched PubMed, EMBASE, and Web of Science up to March 2022 for observational studies investigating the associations in adults. Random effect model was used to estimate the summary relative risks (RRs) and 95% confidence intervals (CIs) and the dose-response association was explored by restricted cubic splines. RESULTS: We obtained the data from 41 eligible studies. Compared with participants with lowest dietary carbohydrate intake, those with highest intake had an RR of 1.10 (95% CI 1.03-1.17, I2 = 52.8%) for cardiovascular disease, 1.10 (0.98-1.24, I2 = 65.5%) for coronary heart disease (CHD), 1.20 (1.08-1.34, I2 = 0) for stroke, 1.07 (1.00-1.14, I2 = 61.9%) for all-cause mortality, 1.02 (0.92-1.14, I2 = 51.3%) for cardiovascular mortality, and 1.01 (0.89-1.13, I2 = 56.7%) for cancer mortality. For each 5 %E increase in dietary carbohydrate intake, the summary RR was 1.02 (1.00-1.04, I2 = 66.8%) for cardiovascular disease, 1.04 (1.01-1.06, I2 = 0) for stroke but not significant for other outcomes. Restricted cubic splines showed linear associations with risk of cardiovascular disease (Pnon-linearity = 0.143), CHD (Pnon-linearity = 0.508), stroke (Pnon-linearity = 0.654) and non-linear associations with all-cause mortality (Pnon-linearity = 0.008) and cardiovascular mortality (Pnon-linearity = 0.055). Limited studies were found on the association of cardiovascular disease and mortality with dietary carbohydrate quality using a multidimensional and integrated indicator. CONCLUSIONS: Increased consumption of dietary carbohydrate intake is associated with increased risk of cardiovascular disease, stroke, and all-cause mortality. Linear relation was found for cardiovascular disease and stroke but non-linear relation for all-cause mortality. More studies are warranted to investigate the association of dietary carbohydrate quality using a combined indicator and cardiovascular disease and mortality.

The Association of Glycemic Index, Glycemic Load, and Daily Carbohydrates Intake with the Risk of Hepatocellular Carcinoma: A Systematic Review and Meta-Analysis.

Background: Glycemic index (GI), glycemic load (GL) and daily carbohydrates intake have been associated with a variety of cancers, but their implications in hepatocellular carcinoma (HCC) remain controversial. The purpose of our study is to investigate the association of GI, GL and daily carbohydrates intake with the risk of HCC. Methods: Systematic searches were conducted in PubMed, Embase and Web of Science until November 2020. According to the degree of heterogeneity, random effect model or fixed effect model was chosen to obtain the pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs). Results: Four cohort studies and three case-control studies were eventually included. The pooled results showed no significant association of GI (RR = 1.11, 95% CI = 0.80-1.53), GL (RR = 1.09, 95% CI = 0.76-1.55), and daily carbohydrates intake (RR = 1.09, 95% CI = 0.84-1.32) with the risk of HCC in the general population. Subgroup analysis revealed that in hepatitis B virus (HBV) or/and hepatitis C virus (HCV)-positive group, GI was irrelevant to the risk of HCC (RR = 0.65, 95% CI = 0.32-1.32), while a high GL diet was associated with a higher risk of HCC (RR = 1.52, 95% CI = 1.04-2.23). In contrast, in HBV and HCV-negative group, both GI (RR = 1.23, 95% CI = 0.88-1.70) and GL (RR = 1.17, 95% CI = 0.83-1.64) were not associated with the risk of HCC. Conclusion: A high GL diet increases the risk of HCC in those with viral hepatitis. A low GL diet is recommended for them to reduce the risk of HCC.