scholarly journals Maternal prenatal anxiety and depression and trajectories of cardiometabolic risk factors across childhood and adolescence: a prospective cohort study

2021 ◽  
Author(s):  
Karen Matvienko-Sikar ◽  
Kate N O’ Neill ◽  
Abigail Fraser ◽  
Catherine Hayes ◽  
Laura D Howe ◽  
...  
Keyword(s):  
Risk Factors ◽  
High Density Lipoprotein ◽  
Fat Mass ◽  
High Density Lipoprotein Cholesterol ◽  
Cardiometabolic Risk ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Anxiety And Depression ◽  
Cardiometabolic Health ◽  
Prenatal Anxiety

AbstractBackgroundQuantifying long-term offspring cardiometabolic health risks associated with maternal prenatal anxiety and depression can guide cardiometabolic risk prevention. This study examines associations between maternal prenatal anxiety and depression, and offspring cardiometabolic risk from birth to 18 years.MethodsParticipants were 526-8,606 mother-offspring pairs from the Avon Longitudinal Study of Parents and Children (ALSPAC). Exposures were anxiety (Crown-Crisp Inventory score) and depression (Edinburgh Postnatal Depression Scale score) measured at 18 and 32 weeks gestation. Outcomes were trajectories of offspring body mass index; fat mass; lean mass; pulse rate; glucose, diastolic and systolic blood pressure; triglycerides, high-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol, and insulin from birth/early childhood to 18 years. Exposures were analysed categorically using clinically relevant, cut-offs and continuously to examine associations across the distribution of prenatal anxiety and depression.ResultsWe found no strong evidence of associations between maternal anxiety and depression, and offspring trajectories of any cardiometabolic risk factors, except for small, inconsistent associations with fat mass trajectories that attenuated upon confounder adjustment. For instance, in unadjusted analyses, anxiety at both 18 and 32 weeks was associated with a 1.8% (95% Confidence Interval (CI), 0.29,3.33) higher mean BMI, which spanned the null (difference (95% CI): 0.7% (−0.76,2.13) after adjustment for confounders.ConclusionsThis is the first examination of maternal prenatal anxiety and depression and trajectories of offspring cardiometabolic risk. Our findings suggest that prevention of maternal prenatal anxiety and depression may have limited impact on offspring cardiometabolic health across the first two decades of life.

scholarly journals Maternal prenatal anxiety and depression and trajectories of cardiometabolic risk factors across childhood and adolescence: a prospective cohort study

BMJ Open ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. e051681
Author(s):  
Karen Matvienko-Sikar ◽  
Kate O' Neill ◽  
Abigail Fraser ◽  
Catherine Hayes ◽  
Laura Howe ◽  
...  
Keyword(s):  
Risk Factors ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Cardiometabolic Risk ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
Anxiety And Depression ◽  
Cardiometabolic Health ◽  
Prenatal Anxiety

ObjectivesQuantifying long-term offspring cardiometabolic health risks associated with maternal prenatal anxiety and depression can guide cardiometabolic risk prevention. This study examines associations between maternal prenatal anxiety and depression, and offspring cardiometabolic risk from birth to 18 years.DesignThis study uses data from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort.ParticipantsParticipants were 526–8606 mother–offspring pairs from the ALSPAC cohort.SettingBritish birth cohort set, Bristol, UK.Primary and secondary outcomesExposures were anxiety (Crown-Crisp Inventory score) and depression (Edinburgh Postnatal Depression Scale score) measured at 18 and 32 weeks gestation. Outcomes were trajectories of offspring body mass index; fat mass; lean mass; pulse rate; glucose, diastolic and systolic blood pressure (SBP); triglycerides, high-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol and insulin from birth/early childhood to 18 years. Exposures were analysed categorically using clinically relevant, cut-offs and continuously to examine associations across the distribution of prenatal anxiety and depression.ResultsWe found no strong evidence of associations between maternal anxiety and depression and offspring trajectories of cardiometabolic risk factors. Depression at 18 weeks was associated with higher SBP at age 18 (1.62 mm Hg (95% CI 0.17 to 3.07). Anxiety at 18 weeks was also associated with higher diastolic blood pressure at 7 years in unadjusted analyses (0.70 mm Hg (95% CI 0.02 to 1.38)); this difference persisted at age 18 years (difference at 18 years; 0.89 mm Hg (95% CI 0.05 to 1.73). No associations were observed for body mass index; fat mass; lean mass; pulse rate; glucose; triglycerides, high-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol and insulin.ConclusionsThis is the first examination of maternal prenatal anxiety and depression and trajectories of offspring cardiometabolic risk. Our findings suggest that prevention of maternal prenatal anxiety and depression may have limited impact on offspring cardiometabolic health across the first two decades of life.

scholarly journals Genetically Predicted Insomnia in Relation to 14 Cardiovascular Conditions and 17 Cardiometabolic Risk Factors: A Mendelian Randomization Study

2021 ◽  
Author(s):  
Xinhui Liu ◽  
Chuanbao Li ◽  
Xiaoru Sun ◽  
Yuanyuan Yu ◽  
Shucheng Si ◽  
...  
Keyword(s):  
Risk Factors ◽  
Body Mass Index ◽  
High Density Lipoprotein ◽  
Body Mass ◽  
High Density Lipoprotein Cholesterol ◽  
Cardiometabolic Risk ◽  
Mendelian Randomization ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol

Background This Mendelian randomization study aims to investigate causal associations between genetically predicted insomnia and 14 cardiovascular diseases (CVDs) as well as the potential mediator role of 17 cardiometabolic risk factors. Methods and Results Using genetic association estimates from large genome‐wide association studies and UK Biobank, we performed a 2‐sample Mendelian randomization analysis to estimate the associations of insomnia with 14 CVD conditions in the primary analysis. Then mediation analysis was conducted to explore the potential mediator role of 17 cardiometabolic risk factors using a network Mendelian randomization design. After correcting for multiple testing, genetically predicted insomnia was consistent significantly positively associated with 9 of 14 CVDs, those odds ratios ranged from 1.13 (95% CI, 1.08–1.18) for atrial fibrillation to 1.24 (95% CI, 1.16–1.32) for heart failure. Moreover, genetically predicted insomnia was consistently associated with higher body mass index, triglycerides, and lower high‐density lipoprotein cholesterol, each of which may act as a mediator in the causal pathway from insomnia to several CVD outcomes. Additionally, we found very little evidence to support a causal link between insomnia with abdominal aortic aneurysm, thoracic aortic aneurysm, total cholesterol, low‐density lipoprotein cholesterol, glycemic traits, renal function, and heart rate increase during exercise. Finally, we found no evidence of causal associations of genetically predicted body mass index, high‐density lipoprotein cholesterol, or triglycerides on insomnia. Conclusions This study provides evidence that insomnia is associated with 9 of 14 CVD outcomes, some of which may be partially mediated by 1 or more of higher body mass index, triglycerides, and lower high‐density lipoprotein cholesterol.

scholarly journals Association between rs1421085 and rs9939609 Polymorphisms of Fat Mass and Obesity-Associated Gene with High-Density Lipoprotein Cholesterol and Triglyceride in Obese Turkish Children and Adolescents

2020 ◽  
Author(s):  
Nihal Inandiklioğlu ◽  
Adem Yaşar
Keyword(s):  
High Density Lipoprotein ◽  
Fat Mass ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
Healthy Children ◽  
Obese Children ◽  
Fto Gene ◽  
Turkish Children

AbstractSeveral studies have shown that rs9939609 and rs1421085 in fat mass and obesity-associated (FTO) gene rs17782313 and rs12970134 in melanocortin-4 receptor (MC4R) gene influence obesity. In the present study, we aimed to determine association between rs9939609, rs1421085, rs17782313, and rs12970134 polymorphism, and their relation with body mass index (BMI), glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR) and lipid values in obese children. We included 100 newly diagnosed obese children and 100 healthy children. The rs1421085 (CC/CT) (p = 0.019) and rs9939609 (AA/AT) (p = 0.002) polymorphism regions were higher in the obese group. Additionally, we found that both the rs1421085 (CC/CT) and rs9939609 (AA/AT) polymorphism associated with high-density lipoprotein cholesterol (p = 0.011 and p = 0.003) and triglycerides (p = 0.01 and p = 0.004) level, respectively. Further, the rs9939609 and rs1421085 variants of FTO gene associated with HDL-cholesterol and triglycerides levels in obese children; however, updated studies with a large sample size are required to establish strong links with genetic variants and risk factors in childhood obesity.

Comparison of atherogenic risk factors among poorly controlled and well-controlled adolescent phenylketonuria patients

2015 ◽  
Vol 26 (5) ◽  
pp. 901-908 ◽  
Author(s):  
Mehmet Gündüz ◽  
Sevim Çakar ◽  
Pınar Kuyum ◽  
Balahan Makay ◽  
Nur Arslan
Keyword(s):  
Risk Factors ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
Platelet Volume ◽  
Cholesterol Levels ◽  
The Mean ◽  
Serum Phenylalanine

AbstractBackgroundPrevious studies investigating the known risk factors of atherosclerosis in phenylketonuria patients have shown conflicting results. The primary aim of our study was to investigate the serum atherogenic markers in adolescent classical phenylketonuria patients and compare these parameters with healthy peers. The secondary aim was to compare these atherogenic markers in well-controlled and poorly controlled patients.MethodsA total of 59 patients (median age: 12.6 years, range: 11–17 years) and 44 healthy controls (median age: 12.0 years, range: 11–15 years) were enrolled in our study. Phenylketonuria patients were divided into two groups: well-controlled (serum phenylalanine levels below 360 µmol/L; 24 patients) and poorly controlled patients (serum phenylalanine levels higher than 360 µmol/L).ResultsThe mean high-density lipoprotein cholesterol levels of well-controlled patients (1.0±0.2 mmol/L) were significantly lower compared with poorly controlled patients and controls (1.1±0.2 mmol/L, p=0.011 and 1.4±0.2 mmol/L, p<0.001, respectively). Poorly controlled patients had lower high-density lipoprotein cholesterol levels than healthy controls (p=0.003). Homocysteine levels of both well-controlled (9.8±6.4 µmol/L) and poorly controlled (9.2±5.6 µmol/L) patients were higher compared with controls (5.8±1.8 µmol/L, p<0.01). The mean platelet volume of well-controlled patients (9.5±1.1 fL) was higher than that of poorly controlled patients and controls (8.9±0.8 fL, p=0.024 and 7.7±0.6 fL, p<0.001, respectively).ConclusionLower high-density lipoprotein cholesterol and higher homocysteine and mean platelet volume levels were detected in phenylketonuria patients. In particular, these changes were more prominent in well-controlled patients. We conclude that phenylketonuria patients might be at risk for atherosclerosis, and therefore screening for atherosclerotic risk factors should be included in the phenylketonuria therapy and follow-up in addition to other parameters.

Sign in / Sign up

Export Citation Format

Share Document