scholarly journals Early adulthood socioeconomic trajectories contribute to inequalities in adult cardiovascular health, independently of childhood and adulthood socioeconomic position

2021 ◽  
pp. jech-2021-216611
Author(s):  
Eleanor M Winpenny ◽  
Laura D Howe ◽  
Esther M F van Sluijs ◽  
Rebecca Hardy ◽  
Kate Tilling

BackgroundCardiovascular health shows significant socioeconomic inequalities, however there is little understanding of the role of early adulthood in generation of these inequalities. We assessed the contribution of socioeconomic trajectories during early adulthood (16–24 years) to cardiovascular health in mid-adulthood (46 years).MethodsParticipants from the 1970 British Cohort Study with socioeconomic data available in early adulthood were included (n=12 423). Longitudinal latent class analysis identified socioeconomic trajectories, based on patterns of economic activity throughout early adulthood. Cardiometabolic risk factors (46 years) were regressed on socioeconomic trajectory class (16–24 years), testing mediation by adult socioeconomic position (46 years). Models were stratified by sex and adjusted for childhood socioeconomic position (SEP) and adolescent health.ResultsSix early adulthood socioeconomic trajectories were identified: (1) Continued Education (20.2%), (2) Managerial Employment (16.0%), (3) Skilled Non-manual Employment (20.9%), (4) Skilled Manual Employment (18.9%), (5) Partly Skilled Employment (15.8%) and (6) Economically Inactive (8.1%). The ‘Continued Education’ trajectory class showed the best cardiovascular health at age 46 years, with the lowest levels of cardiometabolic risk factors. For example, systolic blood pressure was 128.9 mm Hg (95% CI 127.8 to 130.0) among men in the ‘Continued Education’ class, compared with 131.3 mm Hg (95% CI 130.4 to 132.2) among men in the ‘Skilled Manual’ class. Patterns across classes 2–6 differed by risk factor and sex. The observed associations were largely not mediated by SEP at age 46 years.ConclusionFindings suggest an independent contribution of early adulthood socioeconomic trajectories to development of later life cardiovascular inequalities. Further work is needed to understand mediators of this relationship and potential for interventions to mitigate these pathways.

Author(s):  
Gunn-Helen Moen ◽  
Ben Brumpton ◽  
Cristen Willer ◽  
Bjørn Olav Åsvold ◽  
Kåre Birkeland ◽  
...  

AbstractIntroductionThere is a robust and well-documented observational relationship between lower birthweight and higher risk of cardiometabolic disease in later life. The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that adverse environmental factors in utero or in the early years of life result in increased future risk of cardiometabolic disease. Our aim was to investigate whether there was evidence for causal effects of the intrauterine environment, as proxied by maternal single nucleotide polymorphisms (SNPs) that influence offspring birthweight independent of offspring genotype, on offspring cardiometabolic risk factors such as blood pressure, non-fasting glucose, body mass index (BMI), and lipid levels.MethodsWe investigated whether a genetic risk score of maternal SNPs associated with offspring birthweight was also associated with offspring cardiometabolic risk factors, after controlling for offspring genotypes at the same loci, in up to 26,057 mother-offspring pairs from the Nord-Trøndelag Health (HUNT) Study. We also conducted similar analyses in 19,792 father-offspring pairs from the same study to investigate whether there was evidence that any such causal effects operated through the postnatal, rather than the intrauterine environment. To take account of the considerable cryptic relatedness in HUNT, we implemented a computationally efficient genetic linear mixed model using the OpenMx software package to perform our analyses.ResultsWe found little evidence for a maternal genetic effect of birthweight associated variants on offspring cardiometabolic risk factors after adjusting for offspring genotypes at the same loci. Likewise, we found little evidence for paternal genetic effects on offspring cardiometabolic risk factors performing similar analyses in father-offspring pairs. In contrast, offspring genetic risk scores of birthweight associated variants were strongly related to many cardiometabolic risk factors, even after conditioning on maternal genotypes at the same loci.ConclusionOur results suggest that the maternal intrauterine environment, as proxied by maternal SNPs that influence offspring birthweight, is unlikely to be a major determinant of adverse cardiometabolic outcomes in population based samples of individuals. In contrast, genetic pleiotropy appears to explain some of the observational relationship between offspring birthweight and future cardiometabolic risk.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Gunn-Helen Moen ◽  
Ben Brumpton ◽  
Cristen Willer ◽  
Bjørn Olav Åsvold ◽  
Kåre I. Birkeland ◽  
...  

Abstract There is a robust observational relationship between lower birthweight and higher risk of cardiometabolic disease in later life. The Developmental Origins of Health and Disease (DOHaD) hypothesis posits that adverse environmental factors in utero increase future risk of cardiometabolic disease. Here, we explore if a genetic risk score (GRS) of maternal SNPs associated with offspring birthweight is also associated with offspring cardiometabolic risk factors, after controlling for offspring GRS, in up to 26,057 mother–offspring pairs (and 19,792 father–offspring pairs) from the Nord-Trøndelag Health (HUNT) Study. We find little evidence for a maternal (or paternal) genetic effect of birthweight associated variants on offspring cardiometabolic risk factors after adjusting for offspring GRS. In contrast, offspring GRS is strongly related to many cardiometabolic risk factors, even after conditioning on maternal GRS. Our results suggest that the maternal intrauterine environment, as proxied by maternal SNPs that influence offspring birthweight, is unlikely to be a major determinant of adverse cardiometabolic outcomes in population based samples of individuals.


2019 ◽  
Vol 66 (4) ◽  
pp. 366-376
Author(s):  
Akinwumi Ayodeji Akinbodewa ◽  
Ademola Oluseyi Adejumo ◽  
Oluwakemi Abiola Lamidi ◽  
Ogunleye Adeyemi

Abstract Background Clustering of cardiometabolic risk factors is rapidly becoming prevalent among children and adolescents with grave implications for their cardiovascular health. We set out to determine prevalence and pattern of clustering of risk factors and, identify factors (if any) that determine their clustering. Methods A cross-sectional study of children (3–9 years) and adolescents (10–17 years) in a rural, agrarian community. Their blood pressure, body mass index and lipids were measured. Data was analyzed with SPSS 20. Results A total of 114 (M : F, 1 : 1.1) subjects were studied. The mean age of children and adolescents were 5.6 ± 2.1 and 12.9 ± 2.2 years respectively. The most prevalent cardiometabolic risk factors were elevated non-high density lipoprotein-cholesterol (HDL-c; 39.5%), low HDL-c (33.3%), prehypertension (12.3%) and overweight (9.6%). The prevalence of hypertension was higher among females (11.9% vs. 1.8%, p = 0.024) and adolescents (13.2% vs. 1.6%, p = 0.037). Serum levels of non-HDL-c was higher among adolescents than children (50.9% vs. 29.5%, p = 0.013). At least one risk factor was present in 68.4% of the subjects. Clustering of two and three risk factors were present in 18.4% and 6.1%. The presence of prehypertension (χ2 23.93, p < .001), hypertension (χ2 12.19, p = 0.002), high serum non-HDL-c (χ2 6.336, p = 0.011) and high serum total cholesterol (TC; χ2 8.810, p < 0.001) were associated with clustering of cardiometabolic risk factors. Conclusion The burden of cardiometabolic risk factors among children and adolescents is high. Identified determinants of risk factor clustering were prehypertension, hypertension, non-HDL-c and TC.


2019 ◽  
Vol 121 (09) ◽  
pp. 1039-1048
Author(s):  
Xiaoxia Wang ◽  
Tongzhang Xian ◽  
Lina Zhang ◽  
Xiaofan Jia ◽  
Fuli Man ◽  
...  

AbstractLow 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.


Author(s):  
Sanem Kayhan ◽  
Nazli Gulsoy Kirnap ◽  
Mercan Tastemur

Abstract. Vitamin B12 deficiency may have indirect cardiovascular effects in addition to hematological and neuropsychiatric symptoms. It was shown that the monocyte count-to-high density lipoprotein cholesterol (HDL-C) ratio (MHR) is a novel cardiovascular marker. In this study, the aim was to evaluate whether MHR was high in patients with vitamin B12 deficiency and its relationship with cardiometabolic risk factors. The study included 128 patients diagnosed with vitamin B12 deficiency and 93 healthy controls. Patients with vitamin B12 deficiency had significantly higher systolic blood pressure (SBP), diastolic blood pressure (DBP), MHR, C-reactive protein (CRP) and uric acid levels compared with the controls (median 139 vs 115 mmHg, p < 0.001; 80 vs 70 mmHg, p < 0.001; 14.2 vs 9.5, p < 0.001; 10.2 vs 4 mg/dl p < 0.001; 6.68 vs 4.8 mg/dl, p < 0.001 respectively). The prevalence of left ventricular hypertrophy was higher in vitamin B12 deficiency group (43.8%) than the control group (8.6%) (p < 0.001). In vitamin B12 deficiency group, a positive correlation was detected between MHR and SBP, CRP and uric acid (p < 0.001 r:0.34, p < 0.001 r:0.30, p < 0.001 r:0.5, respectively) and a significant negative correlation was detected between MHR and T-CHOL, LDL, HDL and B12 (p < 0.001 r: −0.39, p < 0.001 r: −0.34, p < 0.001 r: −0.57, p < 0.04 r: −0.17, respectively). MHR was high in vitamin B12 deficiency group, and correlated with the cardiometabolic risk factors in this group, which were SBP, CRP, uric acid and HDL. In conclusion, MRH, which can be easily calculated in clinical practice, can be a useful marker to assess cardiovascular risk in patients with vitamin B12 deficiency.


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