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Cross-sectional nutritional survey data collected in eight countries were used to estimate saturated fatty acid intakes. Our objective was to estimate the proportion of excessive saturated fatty acid intakes (>10 % of total energy intake) that could be avoided if ultra-processed food consumption was reduced to levels observed in the first quintile of each country. Secondary analysis was performed of 24 h dietary recall or food diary/record data collected by the most recently available nationally representative cross-sectional surveys carried out in Brazil (2008–9), Chile (2010), Colombia (2005), Mexico (2012), Australia (2011–12), the UK (2008–16), Canada (2015) and the US (2015–16). Population attributable fractions estimated the impact of reducing ultra-processed food consumption on excessive saturated fatty acid intakes (above 10 % of total energy intake) in each country. Significant relative reductions in the percentage of excessive saturated fatty acid intakes would be observed in all countries if ultra-processed food consumption was reduced to levels observed in the first quintile's consumption. The reductions in excessive intakes ranged from 10⋅0 % (95 % CI 6⋅2–13⋅6 %) in Canada to 35⋅0 % (95 % CI 28⋅7–48⋅0 %) in Mexico. In all eight studied countries, all presenting more than 30 % of intakes with excessive saturated fatty acids, lowering the dietary contribution of ultra-processed foods to attainable, context-specific levels was shown to be a potentially effective way to reduce the percentage of intakes with excessive saturated fatty acids, which may play an important role in the prevention of non-communicable diseases, particularly cardiovascular diseases.
The aim of this study was to systematically assess the association between smoking and cardiovascular disease (CVD) and disease progression among novel coronavirus pneumonia (coronavirus disease 2019 (COVID-19)) cases. PubMed database and Cochrane Library database were searched by computer to seek the epidemiological data of COVID-19 cases and literatures regarding CVDs from 1 Jan to 6 October 2020. Two researchers independently conducted literature screening, data collection and the assessment of the risk of bias of the studies included. RevMan 5.2 software was employed for meta-analysis. Funnel plot was adopted to assess the publication bias. On the whole, 21 studies comprising 7041 COVID-19 cases were included. As revealed from the meta-analysis, 14.0% (984/7027) of cases had a history of smoking, and 9.7% (675/6931) were subject to underlying CVDs. Cases with a history of smoking achieved a higher rate of COVID-19 disease progression as opposed to those having not smoked (OR 1.53, 95% CI 1.29–1.81, P < 0.00001), while no significant association could be found between smoking status and COVID-19 disease progression (OR 1.23, 95% CI 0.93–1.63, P = 0.15). Besides, smoking history elevated the mortality rate by 1.91-fold (OR 1.91, 95% CI 1.35–2.69, P = 0.0002). Moreover, underlying CVD elevated the incidence of severe disease by 2.87-fold (OR 2.87, 95% CI 2.29–3.61, P < 0.00001) and mortality by 3.05-fold (OR 3.05, 95% CI 1.82–5.11, P < 0.0001) in COVID-19 cases. As demonstrated from the current evidence, smoking displays a strong association with COVID-19 disease progression and mortality, and intensive tobacco control is imperative. Moreover, cases with CVD show a significantly elevated risk of disease progression and death when subject to COVID-19. However, the association between COVID-19 and CVD, and the potential effect exerted by smoking in the development of the two still require further verifications by larger and higher quality studies.
Beneficial effects of probiotic, prebiotic and polyphenol-rich interventions on fasting lipid profiles have been reported, with changes in the gut microbiota composition believed to play an important role in lipid regulation. Primary bile acids, which are involved in the digestion of fats and cholesterol metabolism, can be converted by the gut microbiota to secondary bile acids, some species of which are less well reabsorbed and consequently may be excreted in the stool. This can lead to increased hepatic bile acid neo-synthesis, resulting in a net loss of circulating low density lipoprotein. Bile acids may therefore provide a link between the gut microbiota and cardiovascular health. This narrative review presents an overview of bile acid metabolism and the role of probiotics, prebiotics and polyphenol-rich foods in modulating circulating cardiovascular disease (CVD) risk markers and bile acids. Although findings from human studies are inconsistent, there is growing evidence for associations between these dietary components and improved lipid CVD risk markers, attributed to modulation of the gut microbiota and bile acid metabolism. These include increased bile acid neo-synthesis, due to bile sequestering action, bile salt metabolising activity and effects of short chain fatty acids generated through bacterial fermentation of fibres. Animal studies have demonstrated effects on the FXR/FGF-15 axis and hepatic genes involved in bile acid synthesis (CYP7A1) and cholesterol synthesis (SREBP and HMGR). Further human studies are needed to determine the relationship between diet and bile acid metabolism and whether circulating bile acids can be utilised as a potential CVD risk biomarker.
People with bipolar disorder (BPD) are more likely to die prematurely, which is partly attributed to comorbid cardiometabolic traits. Previous studies report cardiometabolic abnormalities in BPD, but their shared aetiology remains poorly understood. This study examined the phenotypic associations and shared genetic aetiology between BPD and various cardiometabolic traits.
In a subset of the UK Biobank sample (N = 61 508) we investigated phenotypic associations between BPD (ncases = 4186) and cardiometabolic traits, represented by biomarkers, anthropometric traits and cardiometabolic diseases. To determine shared genetic aetiology in European ancestry, polygenic risk scores (PRS) and genetic correlations were calculated between BPD and cardiometabolic traits.
Several traits were significantly associated with increased risk for BPD, namely low total cholesterol, low high-density lipoprotein cholesterol, high triglycerides, high glycated haemoglobin, low systolic blood pressure, high body mass index, high waist-to-hip ratio; and stroke, coronary artery disease and type 2 diabetes diagnosis. BPD was associated with higher polygenic risk for triglycerides, waist-to-hip ratio, coronary artery disease and type 2 diabetes. Shared genetic aetiology persisted for coronary artery disease, when correcting PRS associations for cardiometabolic base phenotypes. Associations were not replicated using genetic correlations.
This large study identified increased phenotypic cardiometabolic abnormalities in BPD participants. It is found that the comorbidity of coronary artery disease may be based on shared genetic aetiology. These results motivate hypothesis-driven research to consider individual cardiometabolic traits rather than a composite metabolic syndrome when attempting to disentangle driving mechanisms of cardiometabolic abnormalities in BPD.
Adults who were born preterm are at increased risk of hypertension and cardiovascular disease in later life. Infants born late preterm are the majority of preterm births; however, the effect of late preterm on risk of cardiovascular disease is unclear. The objective of this study was to assess whether vascular health and cardiac autonomic control differ in a group of late preterm newborn infants compared to a group of term-born infants.
A total of 35 healthy late preterm newborn infants, with normal growth (34–36 completed weeks’ gestation) and 139 term-born infants (37–42 weeks’ gestation) were compared in this study. Aortic wall thickening, assessed as aortic intima–media thickness (IMT) by high-resolution ultrasound, and cardiac autonomic control, assessed by heart rate variability, were measured during the first week of life. Postnatal age of full-term and late preterm infants at the time of the study was 5 days (standard deviation [SD] 5) and 4 days (SD 3), respectively.
Infants born late preterm show reduced aortic IMT (574 μm [SD 51] vs. 612 μm [SD 73]) and reduced heart rate variability [log total power 622.3 (606.5) ms2 vs. 1180. 6 (1114.3) ms2], compared to term infants. These associations remained even after adjustment for sex and birth weight.
Infants born late preterm show selective differences in markers of cardiovascular risk, with potentially beneficial differences in aortic wall thickness in contrast to potentially detrimental differences in autonomic control, when compared with term-born control infants. These findings provide pathophysiologic evidence to support an increased risk of hypertension and sudden cardiac death in individuals born late preterm.
This study aimed to determine anthropometric cut-points for screening diabetes and the metabolic syndrome (MetS) in Arab and South Asian ethnic groups in Kuwait and to compare the prevalence of the MetS based on the ethnic-specific waist circumference (WC) cut-point and the International Diabetes Federation (IDF) and American Heart Association/National Heart, Lung, and Blood Institute WC criteria. The national population-based survey data set of diabetes and obesity in Kuwait adults aged 18–60 years was analysed. Age-adjusted logistic regression and receiver operating characteristic (ROC) analyses were conducted to evaluate for 3589 individuals the utility of WC, waist:height ratio (WHtR) and BMI to discriminate both diabetes and ≥3 CVD risk factors. Areas under the ROC curve were similar for WC, WHtR and BMI. In Arab men, WC, WHtR and BMI cut-offs for diabetes were 106 cm, 0·55 and 28 kg/m2 and for ≥3 CVD risk factors, 97 cm, 0·55 and 28 kg/m2, respectively. In Arab women, cut-offs for diabetes were 107 cm, 0·65 and 33 kg/m2 and for ≥3 CVD risk factors, 93 cm, 0·60 and 30 kg/m2, respectively. WC cut-offs were higher for South Asian women than men. IDF-based WC cut-offs corresponded to a higher prevalence of the MetS across sex and ethnic groups, compared with Kuwait-specific cut-offs. Any of the assessed anthropometric indices can be used in screening of diabetes and ≥3 CVD risk factors in Kuwaiti Arab and Asian populations. ROC values were similar. The WC threshold for screening the MetS in Kuwaiti Arabs and South Asians is higher for women.
People affected by severe mental health disorders have a greatly reduced life expectancy compared to their non-affected peers. Cardiovascular disease is the main contributor to this early mortality, caused by higher rates of smoking, physical inactivity, unhealthy diet, sleep disturbance, excessive alcohol use or substance abuse and medication side effects. Therefore, we need to take a preventative approach and translate effective interventions for physical health into routine clinical practice. These interventions should be delivered across all stages of mental health disorders and could also have the added benefit of leading to improvements in mental health. Furthermore, we need to advocate to ensure that people affected by severe mental health disorders receive the appropriate medical assessments and treatments when indicated. This themed issue highlights that physical health is now an urgent priority for funding and development in mental health services. The widespread implementation of evidence-based interventions into routine clinical practice is an essential need for consideration by clinicians and policymakers.
Subclinical atherosclerosis in childhood can be evaluated by carotid intima-media thickness, which is considered a surrogate marker for atherosclerotic disease in adulthood. The aims of this study were to evaluate carotid intima-media thickness and, to investigate associated factors.
Cross-sectional study with children and adolescents with congenital heart disease (CHD). Socio-demographic and clinical characteristics were assessed. Subclinical atherosclerosis was evaluated by carotid intima-media thickness. Cardiovascular risk factors, such as physical activity, screen time, passive smoke, systolic and diastolic blood pressure, waist circumference, dietary intake, lipid parameters, glycaemia, and C-reactive protein, were also assessed. Factors associated with carotid intima-media thickness were analysed using multiple logistic regression.
The mean carotid intima-media thickness was 0.518 mm and 46.7% had subclinical atherosclerosis (carotid intima-media thickness ≥ 97th percentile). After adjusting for confounding factors, cyanotic CHD (odds ratio: 0.40; 95% confidence interval: 0.20; 0.78), cardiac surgery (odds ratio: 3.17; 95% confidence interval: 1.35; 7.48), and be hospitalised to treat infections (odds ratio: 1.92; 95% confidence interval: 1.04; 3.54) were associated with subclinical atherosclerosis.
Clinical characteristics related to CHD were associated with subclinical atherosclerosis. This finding suggests that the presence of CHD itself is a risk factor for subclinical atherosclerosis. Therefore, the screen and control of modifiable cardiovascular risk factors should be made early and intensively to prevent atherosclerosis.
Table olives, a product of olive tree (Olea europaea L.), is an important fermented product of the Mediterranean Diet. Agronomical factors, particularly the cultivar, the ripening stage and the processing method employed are the main factors influencing the nutritional and non-nutritional composition of table olives and their organoleptic properties. The important nutritional value of this product is due to its richness in monounsaturated fat (MUFA), mainly oleic acid, fibre and vitamin E together with the presence of several phytochemicals. Among these, hydroxytyrosol (HT) is the major phenolic compound present in all types of table olives. There is a scarcity of in vitro, in vivo and human studies of table olives. This review focused comprehensively on the nutrients and bioactive compound content as well as the health benefits assigned to table olives. The possible health benefits associated with their consumption are thought to be primarily related to effects of MUFA on cardiovascular health, the antioxidant (AO) capacity of vitamin E and its role in protecting the body from oxidative damage and the anti-inflammatory and AO activities of HT. The influence of multiple factors on composition of the end product and the potential innovation in the production of table olives through the reduction of its final salt content was also discussed.
Depression and cardiovascular disease (CVD) are associated with each other but their relationship remains unclear. We aim to determine whether genetic predisposition to depression are causally linked to CVD [including coronary artery disease (CAD), myocardial infarction (MI), stroke and atrial fibrillation (AF)].
Using summary statistics from the largest genome-wide association studies (GWAS) or GWAS meta-analysis of depression (primary analysis: n = 500 199), broad depression (help-seeking behavior for problems with nerves, anxiety, tension or depression; secondary analysis: n = 322 580), CAD (n = 184 305), MI (n = 171 875), stroke (n = 446 696) and AF (n = 1 030 836), genetic correlation was tested between two depression phenotypes and CVD [MI, stroke and AF (not CAD as its correlation was previously confirmed)]. Causality was inferred between correlated traits by Mendelian Randomization analyses.
Both depression phenotypes were genetically correlated with MI (depression: rG = 0.169; p = 9.03 × 10−9; broad depression: rG = 0.123; p = 1 × 10−4) and AF (depression: rG = 0.112; p = 7.80 × 10−6; broad depression: rG = 0.126; p = 3.62 × 10−6). Genetically doubling the odds of depression was causally associated with increased risk of CAD (OR = 1.099; 95% CI 1.031–1.170; p = 0.004) and MI (OR = 1.146; 95% CI 1.070–1.228; p = 1.05 × 10−4). Adjustment for blood lipid levels/smoking status attenuated the causality between depression and CAD/MI. Null causal association was observed for CVD on depression. A similar pattern of results was observed in the secondary analysis for broad depression.
Genetic predisposition to depression may have positive causal roles on CAD/MI. Genetic susceptibility to self-awareness of mood problems may be a strong causal risk factor of CAD/MI. Blood lipid levels and smoking may potentially mediate the causal pathway. Prevention and early diagnosis of depression are important in the management of CAD/MI.
We explored the genetic architecture of metabolic risk factors of cardiovascular diseases (CVDs) and their clustering in Chinese boys and girls. Seven metabolic traits (body mass index [BMI], waist circumference [WC], systolic blood pressure [SBP], diastolic blood pressure [DBP], total cholesterol [TC], triglyceride [TG], and uric acid [UA]) were measured in a sample of 1016 twins between 8 and 17 years of age, recruited from the Qingdao Twin Registry. Cholesky, independent pathway, and common pathway models were used to identify the latent genetic structure behind the clustering of these metabolic traits. Genetic architecture of these metabolic traits was largely similar in boys and girls. The highest heritability was found for BMI (a2 = 0.63) in boys and TC (a2 = .69) in girls. Three heritable factors, adiposity (BMI and WC), blood pressure (SBP and DBP), and metabolite factors (TC, TG, and UA), which formed one higher-order latent phenotype, were identified. Latent genetic, common environmental, and unique environmental factors indirectly impacted the three factors through one single latent factor. Our results suggest that there is one latent factor influencing several metabolic traits, which are known risk factors of CVDs in young Chinese twins. Latent genetic, common environmental, and unique environmental factors indirectly imposed on them. These results inform strategies for gene pleiotropic discovery and intervening of CVD risk factors during childhood and adolescence.
Interest exists in identifying the factors that specifically contribute to the increased prevalence of cardiovascular disease observed in psychiatric disease. The apolipoprotein-E (APOE) gene codes for a protein that has a key role in metabolism of cholesterol and triglycerides, with increased levels of apoE found in specific areas of post-mortem schizophrenic brains. This study investigated whether apoE variants influence the prevalence of cardiovascular risk factors (obesity, diabetes and dyslipidaemia), in patients receiving antipsychotic treatment, due to extension of the risk seen in the general population, but also due to the role of the APOE gene in mediating antipsychotic-induced side effects. Seven polymorphisms (rs741780, rs483082, rs429358, rs7412, rs10119, rs439401 and rs405509) were genotyped in 427 American Caucasian patients who were either receiving, or had been prescribed risperidone. Our results support the hypothesis that APOE gene variants influence the prevalence of diabetes and possibly overweight in psychiatric patients. Unfortunately, due to the cross sectional nature of this study, the contribution of antipsychotic treatment was not determined. These associations warrant prospective study to assess interaction between APOE gene variants and the propensity of antipsychotics to induce cardiovascular risk factors.
Improved physical health care is a pressing need for patients with schizophrenia. It can be achieved by means of a multidisciplinary team led by the psychiatrist. Key priorities should include: selection of antipsychotic therapy with a low risk of weight gain and metabolic adverse effects; routine assessment, recording and longitudinal tracking of key physical health parameters, ideally by electronic spreadsheets; and intervention to control CVD risk following the same principles as for the general population. A few simple tools to assess and record key physical parameters, combined with lifestyle intervention and pharmacological treatment as indicated, could significantly improve physical outcomes. Effective implementation of strategies to optimise physical health parameters in patients with severe enduring mental illness requires engagement and communication between psychiatrists and primary care in most health settings.
Second-generation antipsychotics (SGA) are being used more often than ever before in children and adolescents with psychotic and a wide range of non-psychotic disorders. Several SGA have received regulatory approval for some paediatric indications in various countries, but off-label use is still frequent. The aim of this paper was to perform a systematic review and critically evaluate the literature on cardiometabolic and endocrine side-effects of SGA in children and adolescents through a Medline/Pubmed/Google Scholar search of randomized, placebo controlled trials of antipsychotics in children and adolescents (<18 years old) until February 2010. In total, 31 randomized, controlled studies including 3595 paediatric patients were identified. A review of these data confirmed that SGA are associated with relevant cardiometabolic and endocrine side-effects, and that children and adolescents have a high liability to experience antipsychotic induced hyperprolactinaemia, weight gain and associated metabolic disturbances. Only weight change data were sufficiently reported to conduct a formal meta-analysis. In 24 trials of 3048 paediatric patients with varying ages and diagnoses, ziprasidone was associated with the lowest weight gain (−0.04 kg, 95% confidence interval [CI]: −0.38 to +0.30), followed by aripiprazole (0.79 kg, 95% CI: 0.54 to 1.04], quetiapine (1.43 kg, 95% CI: 1.17 to 1.69) and risperidone (1.76 kg, 95% CI: 1.27 to 2.25) were intermediate, and olanzapine was associated with weight gain the most (3.45 kg, 95% CI: 2.93 to 3.97). Significant weight gain appeared to be more prevalent in patients with autistic disorder who were also younger and likely less exposed to antipsychotics previously. These data clearly suggest that close screening and monitoring of metabolic side effects is warranted and that the least cardiometabolically problematic agents should be used first whenever possible. A good collaboration between child- and adolescent psychiatrists, general practitioners and paediatricians is essential to maximize overall outcomes and to reduce the likelihood of premature cardiovascular morbidity and mortality.
This international meeting discussed the management of physical health in patients with schizophrenia in several countries including France, Spain, Germany, the UK and Italy. Physical health parameters, including weight, blood pressure, blood glucose, lipids and standard biochemical assessments are measured in many patients at the first hospital consultation. These reveal physical disorders such as obesity, hypertension, dyslipidaemia, the metabolic syndrome, substance abuse, cardiovascular disease, extrapyramidal symptoms, sexual dysfunction and diabetes in substantial proportions of patients. Psychiatrists consider switching antipsychotic therapy if excessive sedation, extrapyramidal symptoms, unacceptable weight gain, hyperglycaemia or dyslipidaemia occur. In general, switching is more likely to be considered for symptomatic adverse events than for laboratory abnormalities. Switching is discouraged by limited knowledge of protocols, the absence of guidelines and fears of relapse or reduced treatment adherence. The physical health of patients with schizophrenia receives much less attention in the community setting than in the hospital setting. Improved guidelines, protocols, resources and support are needed to improve the physical health of patients in the community.
Affective disorders are associated with an increased risk of cardiovascular disease, which, at least partly, appears to be independent of psychopharmacological treatments used to manage these disorders. Reduced heart rate variability (SDNN) and a low Omega-3 Index have been shown to be associated with increased risk for death after myocardial infarction. Therefore, we set out to investigate heart rate variability and the Omega-3 Index in euthymic patients with bipolar disorders.
We assessed heart rate variability (SDNN) and the Omega-3 Index in 90 euthymic, mostly medicated patients with bipolar disorders (Bipolar-I, Bipolar-II) on stable psychotropic medication, free of significant medical comorbidity and in 62 healthy controls. Heart rate variability was measured from electrocardiography under a standardized 30 minutes resting state condition. Age, sex, BMI, smoking, alcohol consumption and caffeine consumption as potential confounders were also assessed.
Heart rate variability (SDNN) was significantly lower in patients with bipolar disorders compared to healthy controls (35.4 msec versus 60.7 msec; P < 0.0001), whereas the Omega-3 Index did not differ significantly between the groups (5.2% versus 5.3%). In a linear regression model, only group membership (patients with bipolar disorders versus healthy controls) and age significantly predicted heart rate variability (SDNN).
Heart rate variability (SDNN) may provide a useful tool to study the impact of interventions aimed at reducing the increased risk of cardiovascular disease in euthymic patients with bipolar disorders. The difference in SDNN between cases and controls cannot be explained by a difference in the Omega-3 Index.
Preeclampsia (PE) is now recognised as a cardiovascular risk factor for women. Emerging evidence suggests that children exposed to PE in utero may also be at increased risk of cardiovascular disease (CVD) in later life. Individuals exposed to PE in utero have higher systolic and diastolic blood pressure and higher body mass index (BMI) compared to those not exposed to PE in utero. The aim of this review is to discuss the potential mechanisms driving the relationship between PE and offspring CVD. Exposure to an adverse intrauterine environment as a consequence of the pathophysiological changes that occur during a pregnancy complicated by PE is proposed as one mechanism that programs the fetus for future CVD risk. Consistent with this hypothesis, animal models of PE where progeny have been studied demonstrate causality for programming of offspring cardiovascular health by the preeclamptic environment. Shared alleles between mother and offspring, and shared lifestyle factors between mother and offspring provide alternate pathways explaining associations between PE and offspring CVD risk. In addition, adverse lifestyle habits can also act as second hits for those programmed for increased CVD risk. PE and CVD are both multifactorial diseases and, hence, identifying the relative contribution of PE to offspring risk for CVD is a very complex task. However, considering the emerging strong association between PE and CVD, those exposed to PE in utero may benefit from targeted primary CVD preventive strategies.
The mechanisms linking cardiovascular disease (CVD) and depression are still not established. We investigated the impact of mental vulnerability on the relationship between CVD and depression.
A total of 19,856 individuals from five cohorts of random samples of the background population in Copenhagen were followed from baseline (1983–2011) until 2017 in Danish registries. Additive hazard and Cox proportional hazard models were used to analyze the effects of confounding by mental vulnerability as well as interactions between mental vulnerability and CVD on the risk of depression.
During follow-up, 15.3% developed CVD, while 18.1% experienced depression. A strong positive association between CVD and depression (hazard ratio: 3.60 [95% confidence intervals (CI): 3.30; 3.92]) corresponding to 35.4 (95% CI: 31.7; 39.1) additional cases per 1,000 person-years was only slightly attenuated after adjustment for mental vulnerability in addition to other confounders. Synergistic interaction between CVD and mental vulnerability was identified in the additive hazard model. Due to interaction between CVD and mental vulnerability, CVD was associated with 50.9 more cases of depression per 1,000 person-years among individuals with high mental vulnerability compared with individuals with low mental vulnerability.
Mental vulnerability did not explain the strong relationship between CVD and depression. CVD was associated with additional cases of depression among individuals with higher mental vulnerability indicating that this group holds the greatest potential for intervention, for example, in rehabilitation settings.
Gestational diabetes mellitus (GDM) is a pregnancy complication that affects one in seven pregnancies. Emerging evidence demonstrates that children born of pregnancies complicated by GDM may be at increased risk of cardiovascular disease (CVD) in adulthood. Therefore, the aim of this study was to determine cardiovascular risk factors in offspring exposed to GDM in utero. PubMed, CINAHL, SCOPUS, and EMBASE databases were searched. Information was extracted on established CVD risk factors including blood pressure, lipids, blood glucose, fasting insulin, body mass index (BMI), and endothelial/microvascular function. The review protocol is registered in PROSPERO (CRD42018094983). Prospective and retrospective studies comparing offspring exposed to GDM compared to controls (non-GDM pregnancies) were considered. We included studies that defined GDM based on the International Association of Diabetes and Pregnancy Study Groups (IADPSG) definition, or prior definitions. The PRISMA guidelines were followed in conducting this systematic review. Methodological quality was assessed using the Newcastle–Ottawa Quality Assessment Scale. Study selection, data extraction, and quality assessment were done by two independent reviewers. The data were pooled using a random-effects model. Of 59 eligible studies, 24 were included in the meta-analysis. Offspring exposed to GDM had higher systolic blood pressure (mean difference (MD): 1.75 mmHg, 95% CI 0.57–2.94; eight studies, 7264 participants), BMI z-score (MD 0.11, 95% CI 0.02–0.20; nine studies, 8759 participants), and glucose (standard MD 0.43, 95% CI 0.08–0.77; 11 studies, 6423 participants) than control participants. In conclusion, offspring exposed to GDM have elevated systolic blood pressure, BMI, and glucose. Those exposed to GDM in utero may benefit from early childhood blood pressure measurements.