The Impact of Dietary Carbohydrates on Inflammation-Related Cardiovascular Disease Risk: The ATTICA Study (2002-2022).

The aim of this study was to evaluate the potential interplay between a carbohydrate diet and inflammation in atherosclerotic cardiovascular disease (ASCVD) development. ATTICA is a prospective observational study of 3042 adults free of cardiovascular disease (CVD) who were recruited in 2002 and followed for 20 years. Baseline data on carbohydrate intake and inflammatory biomarker levels were collected. Participants were stratified by carbohydrate intake (low vs. high: 190 g/day) and carbohydrate quality. At the 20-year follow-up in 2022, 1988 participants had complete data for CVD assessment. The overall quantity and quality of carbohydrate intake did not show a significant association with CVD incidence; inflammatory markers were positively correlated with an increased risk of CVD (p-values < 0.05). Chronic systemic inflammation seems to affect the CVD risk of participants who had a higher carbohydrate intake more substantially, as compared to those with low intake. Additionally, individuals with higher high carbohydrate/low fiber intake experienced a higher risk of inflammation-related CVD, compared to those with high carbohydrate/high fiber intake. The presented findings revealed that the effect of inflammation markers on the CVD risk is influenced both by the amount and quality of carbohydrate intake, irrespective of overall dietary habits and clinical and lifestyle characteristics.

Sex-dependent effects of carbohydrate source and quantity on caspase-1 activity in the mouse central nervous system.

BACKGROUND: Mounting evidence links glucose intolerance and diabetes as aspects of metabolic dysregulation that are associated with an increased risk of developing dementia. Inflammation and inflammasome activation have emerged as a potential link between these disparate pathologies. As diet is a key factor in both the development of metabolic disorders and inflammation, we hypothesize that long term changes in dietary factors can influence nervous system function by regulating inflammasome activity and that this phenotype would be sex-dependent, as sex hormones are known to regulate metabolism and immune processes. METHODS: 5-week-old male and female transgenic mice expressing a caspase-1 bioluminescent reporter underwent cranial window surgeries and were fed control (65% complex carbohydrates, 15% fat), high glycemic index (65% carbohydrates from sucrose, 15% fat), or ketogenic (1% complex carbohydrates, 79% fat) diet from 6 to 26 weeks of age. Glucose regulation was assessed with a glucose tolerance test following a 4-h morning fast. Bioluminescence in the brain was quantified using IVIS in vivo imaging. Blood cytokine levels were measured using cytokine bead array. 16S ribosomal RNA gene amplicon sequencing of mouse feces was performed to assess alterations in the gut microbiome. Behavior associated with these dietary changes was also evaluated. RESULTS: The ketogenic diet caused weight gain and glucose intolerance in both male and female mice. In male mice, the high glycemic diet led to increased caspase-1 biosensor activation over the course of the study, while in females the ketogenic diet drove an increase in biosensor activation compared to their respective controls. These changes correlated with an increase in inflammatory cytokines present in the serum of test mice and the emergence of anxiety-like behavior. The microbiome composition differed significantly between diets; however no significant link between diet, glucose tolerance, or caspase-1 signal was established. CONCLUSIONS: Our findings suggest that diet composition, specifically the source and quantity of carbohydrates, has sex-specific effects on inflammasome activation in the central nervous system and behavior. This phenotype manifested as increased anxiety in male mice, and future studies are needed to determine if this phenotype is linked to alterations in microbiome composition.

[Gastrointestinal symptoms and dietary intake of patients with irritable bowel syndrome following a low FODMAP diet].

INTRODUCTION: High FODMAP (fermentable oligo-, di, monosaccharides and polyols) foods have been linked with worsening symptoms of IBS patients. The aim was to compare gastrointestinal symptoms and dietary intake of patients with irritable bowel syndrome following a low FODMAP diet, with or without individual nutrition therapy. MATERIALS AND METHODS: A total of 54 patients that met Rome IV criteria for IBS were randomized into two groups, guided group (individual nutrition therapy, n=28) and self-management group (learned about low FODMAP diet online, n=26). Both groups followed low FODMAP diet for 4 weeks. Four-day food records were used to assess dietary intake. Symptoms were assessed by the IBS-severity scoring system (ISB-SSS). RESULTS: The number of subjects who did not complete the study was 13, thereof five in the nutrition therapy and eight in the self-management group, leaving 23 and 18 subjects available for analysis, respectively. Symptoms declined from baseline to endpoint in both groups, by 183±101 points on average in the group receiving nutrition therapy (p< 0.001) and 132±110 points in the self-management group (p< 0.001), with no difference between groups. At baseline, about 80% of meals in both groups contained food high in FODMAP's. The corresponding proportion was 9% and 36% in week 3 in the nutrition therapy and self-management group, respectively (p< 0.001). CONCLUSION: Both groups experienced relieve of symptoms, but compliance to the low FODMAP diet was better in the group receiving individual nutrition therapy compared with the group who only received instructions on how to learn about low FODMAP diet online.

A step closer to understanding how a diet high in simple carbohydrates may cause dysbiosis.

The gut microbiota is an integral part of the human metaorganism that is required to shape physiologic host immune responses including host defense against pathogens. Disease-associated gut dysbiosis has been characterized by blooms of pathobionts, which are bacterial species that can drive disease under certain conditions. Pathobionts like Enterobacteriaceae often bloom during flares of inflammatory bowel disease (IBD) and are causally linked with IBD in murine models. In this issue of the JCI, Hecht and colleagues investigated how simple carbohydrates are causally linked to the bloom of the gut pathobiont Klebsiella pneumoniae, which belong to the Enterobacteriaceae family. Notably, the presence of fiber reduced the dissemination of K. pneumoniae into the blood and liver in a colitis model. Their findings provide a diet-related mechanism for gut dysbiosis, which has implications in the management of IBD and other conditions in which gut dysbiosis is an underlying factor.

The association between multiple trajectories of macronutrient intake and the risk of new-onset diabetes in Chinese adults.

BACKGROUND: The association between macronutrient intake and diabetes is unclear. We used data from the China Health and Nutrition Survey to explore the association between macronutrient intake trajectories and diabetes risk in this study. METHODS: We included 6755 participants who did not have diabetes at baseline and participated in at least three surveys. The energy supply ratio of carbohydrate, protein, and fat was further calculated from dietary data; different macronutrient trajectories were determined using multitrajectory models; and multiple Cox regression models were used to evaluate the association between these trajectories and diabetes. RESULTS: We found three multitrajectories: decreased low carbohydrate-increased moderate protein-increased high fat (DLC-IMP-IHF), decreased high carbohydrate-moderate protein-increased low fat (DHC-MP-ILF), and balanced-macronutrients (BM). Compared to the BM trajectory, DHC-MP-ILF trajectories were significantly associated with increased risk of diabetes (hazard ratio [HR]: 3.228, 95% confidence interval [CI]: 1.571-6.632), whereas no association between DLC-IMP-IHF trajectories and diabetes was found in our study (HR: 0.699, 95% CI: 0.351-1.392). CONCLUSIONS: The downward trend of high carbohydrate and the increasing trend of low fat increased the risk of diabetes in Chinese adults.

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.

Glycative stress as a cause of macular degeneration.

People are living longer and rates of age-related diseases such as age-related macular degeneration (AMD) are accelerating, placing enormous burdens on patients and health care systems. The quality of carbohydrate foods consumed by an individual impacts health. The glycemic index (GI) is a kinetic measure of the rate at which glucose arrives in the blood stream after consuming various carbohydrates. Consuming diets that favor slowly digested carbohydrates releases sugar into the bloodstream gradually after consuming a meal (low glycemic index). This is associated with reduced risk for major age-related diseases including AMD, cardiovascular disease, and diabetes. In comparison, consuming the same amounts of different carbohydrates in higher GI diets, releases glucose into the blood rapidly, causing glycative stress as well as accumulation of advanced glycation end products (AGEs). Such AGEs are cytotoxic by virtue of their forming abnormal proteins and protein aggregates, as well as inhibiting proteolytic and other protective pathways that might otherwise selectively recognize and remove toxic species. Using in vitro and animal models of glycative stress, we observed that consuming higher GI diets perturbs metabolism and the microbiome, resulting in a shift to more lipid-rich metabolomic profiles. Interactions between aging, diet, eye phenotypes and physiology were observed. A large body of laboratory animal and human clinical epidemiologic data indicates that consuming lower GI diets, or lower glycemia diets, is protective against features of early AMD (AMDf) in mice and AMD prevalence or AMD progression in humans. Drugs may be optimized to diminish the ravages of higher glycemic diets. Human trials are indicated to determine if AMD progression can be retarded using lower GI diets. Here we summarized the current knowledge regarding the pathological role of glycative stress in retinal dysfunction and how dietary strategies might diminish retinal disease.

High-fat and carbohydrate diet caused chronic kidney damage by disrupting kidney function, caspase-3, oxidative stress and inflammation.

The study aimed to compare the effects of a diet rich in fat, carbohydrates and protein on rat kidneys. The study was conducted on 40 Wistar albino rats bred at Inönü University Faculty of Medicine after the approval of the ethics committee. Rats were randomly divided into 4 groups: Control group, and the groups where the animals were fed with high carbohydrate, fat and protein rich feed. After the applications, the rat kidney tissues were removed by laparoscopy under anesthesia and blood samples were collected. 13 weeks long fat-rich and carbohydrate feed application had negative effects on oxidant-antioxidant balance, oxidative stress index, inflammation markers, kidney functions tests, histopathology and immunohistochemistry caspase-3 findings in rat kidney tissues, especially in the carbohydrate group when compared to the controls. Protein-rich feed, there were no significant difference in biochemical and histopathology compared to the control group. Fat and carbohydrate rich feed led to an increase in oxidative stress in rat kidney tissues. Oxidative stress led to nephrotoxicity, which in turn led to chronic kidney tissue damages. A more balanced and protein-rich diet instead of excessive sugar and fatty food intake could be suggested to prevent chronic kidney damage.

Consumption of foods and beverages rich in added sugar associated with incident metabolic syndrome: the Coronary Artery Risk Development in Young Adults (CARDIA) study.

AIMS: Numerous studies report positive associations between total carbohydrate (CHO) intake and incident metabolic syndrome (MetS), but few differentiate quality or type of CHO relative to MetS. We examined source of CHO intake, including added sugar (AS), AS-rich CHO foods, and sugar-sweetened beverages (SSBs) associated with incident MetS in adults enrolled in the Coronary Artery Risk Development in Young Adults (CARDIA) study. METHODS AND RESULTS: Among 3154 Black American and White American women and men aged 18-30 years at baseline, dietary intake was assessed by diet history three times over 20 years. Sources of AS-rich CHO foods and beverages include sugar-rich refined grain products, candy, sugar products, and SSBs. Incident MetS was created according to standard criteria. Time-dependent Cox proportional hazards regression analysis evaluated the associations of incident MetS across quintiles of cumulative intakes of AS-rich CHO foods and beverages, AS, and SSBs adjusted for potential confounding factors over 30 years of follow-up. The associations of AS-rich CHO foods and beverages, AS, and SSB intakes with incident MetS were consistent. Compared with the lowest intake, the greatest intakes of AS-rich CHOs, AS, and SSBs were associated with 59% (Ptrend < 0.001), 44% (Ptrend = 0.01), and 34% (Ptrend = 0.03) higher risk of developing MetS, respectively. As expected, diet quality was lower across increasing quintiles of AS-rich CHO foods and beverages, AS, and SSBs (all Ptrend < 0.001). CONCLUSION: Our study findings are consistent with an elevated risk of developing MetS with greater consumption of AS, AS-rich CHO foods, and SSBs, which support consuming fewer AS-rich CHO foods and SSBs.

Metabolic syndrome (MetS) is a condition consisting of three out of five heart disease risk factors. Researchers have found that the risk of developing MetS increases as carbohydrate (CHO) intake also increases. However, how this risk is related to the type and quality of CHO has not been well studied. To study this, we used data from 3154 African American and White American women and men aged 18­30 years old at baseline (1985­86). Information was collected about their health and what they ate. This allowed us to find out if MetS occurred over time if it ever did. We determined how much added sugar (AS), sugar-sweetened beverages (SSBs), and AS-rich CHO foods and beverages they ate. Added sugar­rich foods and beverages contain sugars, syrups, and caloric sweeteners added to them during production or preparation. Carbohydrate foods containing AS include refined grain breads, rolls, bakery products, candy, and jellies. We found that people with the greatest intake of AS, SSBs, and AS-rich CHO foods and beverages had a higher risk of developing MetS compared with those with the lowest intake. These results align with US Dietary Guidelines as well as European guidelines to consume less AS and, therefore, to consume fewer AS-rich CHO foods and SSBs.

Dietary insulin indices and low-carbohydrate diet and the odds of colorectal cancer: a case-control study.

BACKGROUND: Regarding the role of insulin and insulin-inducing dietary factors in some cancers' etiology, we hypothesized that the risk of colorectal cancer may be lessened by following a lower carbohydrate and insulinogenic diet. Therefore, we performed this study to explore the association between a low-carbohydrate diet and insulin indices and the odds of colorectal cancer. METHOD: This hospital-based case-control study was conducted on 150 newly diagnosed colorectal cancer patients and 300 healthy age- and sex-matched hospitalized controls. A valid and reliable food frequency questionnaire was used to calculate the insulin indices and low-carbohydrate diet score. Multivariate logistic regression was used to estimate the association between insulin indices and low-carbohydrate diet and the odds of colorectal cancer. RESULT: After adjusting for potential confounders, individuals in the highest tertile of insulin indices had a higher risk of colorectal cancer (OR insulin index  = 3.46; 95% CI, 2.00-5.96; OR insulin load  = 2; 95% CI, 1.17-3.41). No association was found between a low-carbohydrate diet and colorectal cancer (OR = 1.55; 95% CI, 0.85-2.84). CONCLUSION: Current results demonstrated that a high insulinemic diet was associated with a higher risk of colorectal cancer.

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.

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 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.

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.