Chrono-nutrition is an emerging field that examines how the frequency and timing of meals impact health. Previous research shows inconsistency in the relationship between chrono-nutritional components and cardiometabolic health. We investigated cross-sectional associations between these components and cardiometabolic health in 825 Iranian adults aged 20-59 years. Dietary data, including the number of eating occasions (EOs), meal timing, and meal irregularity of energy intake, were collected using three 24-hour dietary recalls. Anthropometric measurements, blood pressure, and laboratory tests (fasting plasma glucose, lipid profile, insulin, uric acid, and c-reactive protein) were conducted. Insulin resistance and sensitivity (HOMA-IR, HOMA-IS), the triglyceride-glucose, the lipid accommodation product and body mass index (BMI) were calculated. The demographic and morning-evening questionnaire (MEQ) was completed. General linear regression was used to assess associations between chrono-nutritional components and outcomes. Interactions with age and BMI were examined in all associations. Chrono-nutrition components were not significantly related to cardiometabolic risk factors in the total population. However, a lower number of EOs was associated with an increased LDL/HDL-C ratio (β (95% CI): 0.26 (0.06–0.48)) among overweight and obese participants. Additionally, less irregularity in breakfast energy intake was associated with a lower total cholesterol/HDL-C ratio (-0.37 (-0.95 to -0.18)) and a lower LDL-C/HDL-C ratio (-0.32 (-0.79 to -0.13)) among participants with a normal BMI (all p < 0.05). The study concluded that more frequent meals, and regular energy intake might enhance cardiometabolic health cross-sectionally, highlighting the need for prospective studies to further investigate these associations and the mediating role of BMI.

In the UK, populations of Black African and Caribbean (BAC) ethnicity suffer higher rates of cardiometabolic disease than White Europeans (WE). Obesity, leading to increased visceral adipose tissue (VAT) and intrahepatic lipid (IHL), has long been associated with cardiometabolic risk, driving insulin resistance and defective fatty acid/lipoprotein metabolism. These defects are compounded by a state of chronic low-grade inflammation, driven by dysfunctional adipose tissue. Emerging evidence has highlighted associations between central complement system components and adipose tissue, fatty acid metabolism and inflammation; it may therefore sit at the intersection of various cardiometabolic disease risk factors. However, increasing evidence suggests an ethnic divergence in pathophysiology, whereby current theories fail to explain the high rates of cardiometabolic disease in BAC populations. Lower fasting and postprandial TAG has been reported in BAC, alongside lower VAT and IHL deposition, which are paradoxical to the high rates of cardiometabolic disease exhibited by this ethnic group. Furthermore, BAC have been shown to exhibit a more anti-inflammatory profile, with lower TNF-α and greater IL-10. In contrast, recent evidence has revealed greater complement activation in BAC compared to WE, suggesting its dysregulation may play a greater role in the high rates of cardiometabolic disease experienced by this population. This review outlines the current theories of how obesity is proposed to drive cardiometabolic disease, before discussing evidence for ethnic differences in disease pathophysiology between BAC and WE populations.

Several studies have examined the association between CD36 rs1761667 polymorphism with cardiometabolic risk factors and metabolic syndrome (MetS). This study aimed to investigate the interactions between rs1761667 polymorphism and dietary patterns on the cardiometabolic risk factors and the risk of MetS in apparently healthy individuals aged 20–70 years. Food consumption data were acquired using a validated semi-quantitative FFQ. Dietary patterns were identified by factor analysis. CD36 rs1761667 was genotyped by PCR-restriction fragment length polymorphism. The gene–diet interaction was detected by the general linear model or logistic regression. Significant or marginally significant interactions were observed between healthy dietary pattern (HDP) and CD36 rs1761667 on weight (P = 0·006), BMI (P = 0·009), waist circumference (P = 0·005), hip circumference (P = 0·06), body muscle percentage (P = 0·02), body fat percentage (P = 0·09), TAG-glucose index (P = 0·057), atherogenic index of plasma (P = 0·07), the risk of MetS (P = 0·02), risk of abdominal obesity (P = 0·02) and elevated blood pressure (P = 0·07). Besides, a gene–diet interaction was detected between the traditional dietary pattern and rs1761667 variants on odds of hypertriglyceridaemia (P = 0·02). The adherence to HDP was associated with a lower weight, BMI and higher odds of HDL-cholesterol only in A-allele carriers. In conclusion, adherence to HDP (a diet with high fibre, fish and dairy products) can be more effective on some cardiometabolic risk factors and risk of MetS components in the A-allele carrier than the GG genotype of rs1761667 polymorphism. However, future studies are required to shed light on this issue.

Epidemiological studies on the association between the low carbohydrate diet (LCD) score and CVD risk factors have limited and inconsistent results. Data are from the baseline survey of Community-based Cohort Study on Nervous System Diseases. A total of 4609 adults aged ≥ 18 years were included in the study. Dietary data were assessed using a validated semi-quantitative FFQ. Multivariable logistic regression analyses were used to estimate relationships of three LCD scores with low HDL-cholesterol, high LDL-cholesterol, hypercholesterolaemia, hypertriacylglycerolaemia, impaired fasting glucose (IFG), high blood pressure and hyperuricaemia after adjusting for potential confounders. A higher LCD score was negatively associated with low HDL-cholesterol (OR: 0·65 (95 % CI 0·50, 0·83), P = 0·0001) and IFG (OR: 0·65 (95 % CI 0·51, 0·81), P = 0·001) after the final adjustment. However, there are sex differences in this result. Males in the highest quintile of the animal-based or plant-based LCD scores showed a decreased risk of low HDL-cholesterol, and females in the highest quintile of the animal-based or plant-based LCD scores showed a decreased risk of IFG than those in the lowest quintile of the LCD scores. These results suggest that sex differences should be considered when using LCD to treat dyslipidaemia and reduce fasting blood glucose.

This study aimed to investigate the association between hyperemesis gravidarum (HG) severity and early enteral tube feeding on cardiometabolic markers in offspring cord blood. We included women admitted for HG, who participated in the MOTHER randomised controlled trial (RCT) and observational cohort. The MOTHER RCT showed that early enteral tube feeding in addition to standard care did not affect symptoms/birth outcomes. Among RCT and cohort participants, we assessed how HG severity affected lipid, c-peptide, glucose and free thyroxine cord blood levels. HG severity measures were severity of vomiting at inclusion and 3 weeks after inclusion, pregnancy weight gain and 24-h energy intake at inclusion, readmissions and duration of hospital admissions. Cord blood measures were also compared between RCT participants allocated to enteral tube feeding and those receiving standard care. Between 2013-2016, 215 women were included: 115 RCT and 100 cohort participants. Eighty-one cord blood samples were available. Univariable not multivariable regression analysis showed that lower maternal weight gain was associated with higher cord blood glucose levels (β: –0·08, 95% CI –0·16, –0·00). Lower maternal weight gain was associated with higher Apo-B cord blood levels in multivariable regression analysis (β: –0·01, 95% CI –0·02, –0·01). No associations were found between other HG severity measures or allocation to enteral tube feeding and cord blood cardiometabolic markers. In conclusion, while lower maternal weight gain was associated with higher Apo-B cord blood levels, no other HG severity measures were linked with cord blood cardiometabolic markers, nor were these markers affected by enteral tube feeding.

Evidence suggests that maternal prepregnancy body mass index (BMI) is associated with offspring cardiometabolic risk factors. This study was aimed at assessing the association of maternal prepregnancy BMI with offspring cardiometabolic risk factors in adolescence and adulthood. We also evaluated whether offspring BMI was a mediator in this association. The study included mother–offspring pairs from three Pelotas birth cohorts. Offspring cardiometabolic risk factors were collected in the last follow-up of each cohort [mean age (in years) 30.2, 22.6, 10.9]. Blood pressure was measured using an automatic device, cholesterol by using an enzymatic colorimetric method, and glucose from fingertip blood, using a portable glucose meter. In a pooled analysis of the cohorts, multiple linear regression was used to control for confounding. Mediation analysis was conducted using G-computation formula. In the adjusted model, mean systolic blood pressure of offspring from overweight and obese mothers was on average 1.25 (95% CI: 0.45; 2.05) and 2.13 (95% CI: 0.66; 3.59) mmHg higher than that of offspring from normal-weight mothers; for diastolic blood pressure, the means were 0.80 (95% CI: 0.26; 1.34) and 2.60 (95% CI: 1.62; 3.59) mmHg higher, respectively. Non-HDL cholesterol was positively associated with maternal BMI, whereas blood glucose was not associated. Mediation analyses showed that offspring BMI explained completely the association of maternal prepregnancy BMI with offspring systolic and diastolic blood pressure, and non-HDL cholesterol. Our findings suggest that maternal prepregnancy BMI is positively associated with offspring blood pressure, and blood lipids, and this association is explained by offspring BMI.

Low urinary iodine concentration (UIC) is associated with dyslipidaemia in adults but is not well characterised in adolescents. Because dyslipidaemia is a cardiovascular risk factor, identifying such an association in adolescents would allow for the prescription of appropriate measures to maintain cardiovascular health. The present study addresses this question using data in the 2001–2012 National Health and Nutrition Examination Survey for 1692 adolescents aged 12–19 years. Primary outcomes were UIC, cardiometabolic risk factors and dyslipidaemia. Data for subjects categorised by low and normal UIC and by sex were analysed by univariate and multivariate logistic regression. Treating UIC as the independent variable, physical activity level, apoB and lipid profiles differed significantly between subjects with low and normal UIC. Subjects with low UIC had a significantly greater risk of elevated total cholesterol (TC) (95 % CI 1·37, 2·81), elevated non-HDL (95 % CI 1·33, 2·76) and elevated LDL (95 % CI 1·83, 4·19) compared with those with normal UIC. Treating UIC as a dependent variable, the risk of low UIC was significantly greater in those with higher apoB (95 % CI 1·52, 19·08), elevated TC (≥4·4mmol/l) (95 % CI 1·37, 2·81) and elevated non-HDL (≥3·11mmol/l) (95 % CI 1·33, 2·76) than in those with normal UIC. These results show that male and female adolescents with low UIC tend to be at greater risk of dyslipidaemia and abnormal cardiometabolic biomarkers, though the specific abnormal parameters differed between sexes. These results may help to identify youth who would benefit from interventions to improve their cardiometabolic risk.

A population-based cross-sectional study was carried out in the northern neighbourhoods of Ouagadougou (Burkina Faso), to examine the relationship of nutritional deficiencies and cardiometabolic risk factors (CMRF) with lifestyle in adults. We randomly selected 330 households stratified by income tertile. In each income stratum, 110 individuals aged 25–60 years and having lived in Ouagadougou for at least 6 months were randomly selected. We performed anthropometric, dietary intake and physical activity measurements, and blood sample collection. Cluster analysis of dietary intake identified two dietary patterns: ‘urban’ (29 % of subjects) and ‘traditional’ (71 %). The ‘urban’ cluster exhibited a higher intake of fat and sugar, whereas a higher intake of plant protein, complex carbohydrate and fibre was observed in the ‘traditional’ pattern. Female sex, low income and lack of education were associated with the ‘traditional’ cluster, as well as Fe and vitamin A deficiency. CMRF prevalence (abdominal obesity, hypertension, hyperglycaemia, dyslipidaemia) was similar in both clusters. Subjects in the ‘traditional’ cluster spent more time in physical activity and had less sedentary time than those in the ‘urban’ cluster. ‘Traditional’ dietary pattern, low income, female sex and sedentary time were significant contributing factors to the double burden of malnutrition. The rapid nutrition transition is reflected in this co-occurrence of CMRF and nutritional deficiencies. This stresses the need for prevention strategies addressing both ends of the nutrition spectrum.

Many clinical and epidemiological studies have shown that the polyunsaturated n-3 fatty acids EPA and DHA from fish and fish oils, provide cardiovascular protection, particularly in the setting of secondary prevention. n-3 Fatty acids beneficially influence a number of cardiometabolic risk factors including blood pressure, cardiac function, vascular reactivity and lipids, as well as having anti-platelet, anti-inflammatory and anti-oxidative actions. They do not appear to adversely interact with other medications such as statins and other lipid-lowering drugs or antihypertensive medications. n-3 Fatty acids have gained widespread usage by general practitioners and clinicians in a number of clinical settings such as pregnancy and infant development, secondary prevention in CHD patients, treatment of dyslipidaemias and haemodialysis patients. Small doses are achievable with consumption of two to three oily fish meals per week or via purified encapsulated preparations now readily available. n-3 Fatty acids, particularly when consumed as fish, should be considered an important component of a healthy diet. The present paper reviews the effects of n-3 fatty acids on cardiometabolic risk factors, concentrating particularly on the evidence from randomised controlled studies in human subjects.

Increasing evidence suggests that high-sensitivity C-reactive protein (hs-CRP) is associated with cardiometabolic risk factors (CMRF) while being also related to micronutrient deficiencies. As part of a project on the double burden of under- and overnutrition in sub-Saharan Africa, we assessed the relationship between hs-CRP and both CMRF and micronutrient deficiencies in a population-based cross-sectional study carried out in the Northern district of Ouagadougou, the capital city of Burkina Faso. We randomly selected 330 households stratified by income tertile. In each income stratum, 110 individuals aged 25–60 years and having lived in Ouagadougou for at least 6 months were randomly selected, and underwent anthropometric measurements and blood sample collection. The prevalence of high hs-CRP was 39·4 %, with no sex difference. Vitamin A-deficient subjects (12·7 %) exhibited significant risk of elevated hs-CRP (OR 2·5; P= 0·015). Serum ferritin was positively correlated with log hs-CRP (r 0·194; P= 0·002). The risk of elevated hs-CRP was significant in subjects with BMI ≥ 25 kg/m2 (OR 6·9; 95 % CI 3·6, 13·3), abdominal obesity (OR 4·6; 95 % CI 2·2, 7·3) and high body fat (OR 10·2; 95 % CI 5·1, 20·3) (P< 0·001, respectively). Independent predictors of hs-CRP in linear regression models were waist circumference (β = 0·306; P= 0·018) and serum TAG (β = 0·158; P= 0·027). In this sub-Saharan population, hs-CRP was consistently associated with adiposity. Assuming that plasma hs-CRP reflects future risk of cardiovascular events, intervention which reduces CRP, or chronic and acute nutrition conditions associated with it, could be effective in preventing their occurrence particularly in sub-Saharan Africa.

Inflammation is a hallmark of the metabolic syndrome, which also contributes to a pro-atherogenic state. NF-κB activation, a critical step in regulating inflammatory reactions, can be inhibited by polyphenol (PF) extracts, at least in vitro. In the present study, we set out to study whether a PF-rich extract could attenuate the chronic inflammatory state and/or an acute immune response in vivo in subjects with clustered metabolic risk factors. A commercially available, PF-rich extract (500 mg daily) or placebo was administered for 4 weeks to thirty-four subjects with two or more metabolic risk factors using a randomised, double-blind, cross-over design. During the final study visit, an acute inflammatory challenge (lipopolysaccharide (LPS) 1 ng/kg body weight) was administered to a random subgroup of subjects (PF-rich extract (n 12) and placebo (n 12)). The PF-rich extract modestly reduced the inflammatory chemokines monocyte chemoattractant protein 1 (MCP-1) and macrophage migration inhibitory factor (MIF) (MCP-1 − 6·5 % (PF, median 116 (interquartile range 97–136) pg/ml v. placebo, median 124 (interquartile range 105–153) pg/ml; P < 0·05); MIF − 10·8 % (PF, median 2512 (interquartile range 1898–3972) pg/ml v. placebo, median 2814·5 (interquartile range 2296–3852) pg/ml; P < 0·05); however, other measured markers of inflammation and cardiometabolic disease, such as C-reactive protein, IL-6, HDL-cholesterol, adiponectin and oxidised LDL, remained unaffected. Following the LPS challenge, we found a statistically significant 48 % reduction of MCP-1 production in the PF-rich extract group (n 12) v. placebo (n 12) over 6 h (PF 766 (sd 155) v. placebo 1466 (sd 989) ng/ml; P < 0·05, area under the curve). In conclusion, short-term oral administration of the PF-rich extract caused a modest anti-inflammatory effect in subjects with clustered metabolic risk factors. Further dose-ranging studies are needed to evaluate whether and to what extent PF-rich extracts can be used to reduce the pro-inflammatory state in subjects with metabolic diseases at increased cardiovascular risk.