Quality of parental emotional care and calculated risk for coronary heart disease

Objective: To evaluate associations between perceived quality of parental emotional care and calculated 10-year risk for coronary heart disease (CHD). Little is understood about the role of parental emotional care in contributing to the risk for CHD. Methods: The study sample was composed of 267 participants from the New England Family Study. Quality of parental emotional care was measured, using a validated short version of the Parental Bonding Instrument (PBI) as the average care scores for both parents (range = 0-12), with higher scores indicating greater care. Ten-year CHD risk was calculated, using the validated Framingham Risk Algorithm that incorporates the following prevalent CHD risk factors: age, sex, diabetes, smoking, total cholesterol, high-density lipoprotein cholesterol, and blood pressure. Multiple linear regression assessed associations of PBI with calculated CHD risk after adjusting for childhood socioeconomic status, depressive symptomatology, educational attainment, and body mass index. Results: Among females, a 1-unit increase in the parental emotional care score resulted in a 4.6% (p =.004) decrease in the 10-year CHD risk score, after adjusting for covariates. There was no association between parental emotional care score and calculated CHD risk score in males (p =.22). Conclusion: Quality of parental emotional care was inversely associated with calculated 10-year CHD risk in females, and not males. Although the gender differences need further investigation and these findings require replication, these results suggest that the early childhood psychosocial environment may confer risk for CHD in adulthood

Lifecourse socioeconomic position and ankle-brachial index

G Agha, J M Murabito, J W Lynch, M Abrahamowicz, S B Harper, E B Louck

Promoting brain health through physical activity among adults exposed to early life adversity: Potential mechanisms and theoretical framework

Adverse childhood experiences such as abuse, neglect, and poverty, profoundly alter neurobehavioral development in a manner that negatively impacts health across the lifespan. Adults who have been exposed to such adversities exhibit premature and more severe age-related declines in brain health. Unfortunately, it remains unclear whether the negative effects of early life adversity (ELA) on brain health can be remediated through intervention in adulthood. Physical activity may represent a low-cost behavioral approach to address the long-term consequences of ELA on brain health. However, there has been limited research examining the impact of physical activity on brain health among adults with a history of ELA. Accordingly, the purpose of this review is to (1) review the influence of ELA on brain health in adulthood and (2) highlight evidence for the role of neurotrophic factors, hypothalamic-adrenal-pituitary axis regulation, inflammatory processes, and epigenetic modifications in mediating the effects of both ELA and physical activity on brain health outcomes in adulthood. We then propose a theoretical framework to guide future research in this area

Novel variant in glycophorin c gene protects against ribavirin-induced anemia during chronic hepatitis C treatment

Background: The current use of ribavirin in difficult-to-cure chronic hepatitis C patients (HCV) and patients with severe respiratory infections is constrained by the issue of ribavirin-induced hemolytic anemia that affects 30% of treated patients, requiring dosage modification or discontinuation. Though some genetic variants have been identified predicting this adverse effect, known clinical and genetic factors do not entirely explain the risk of ribavirin-induced anemia. Methods: We assessed the associations of previously identified variants in inosine triphosphatase (ITPA), solute carrier 28A2 (SLC28A2) and vitamin D receptor (VDR) genes with ribavirin-induced anemia defined as hemoglobin decline of ≥30 g/L on treatment, followed by a staged discovery (n = 114), replication (n = 74), and combined (n = 188) genome-wide association study to uncover potential new predictive variants. Results: We identified a novel association in the gene coding glycophorin C (rs6741425; OR:0.12, 95%CI:0.04–0.34, P = 2.94 × 10-6) that predicts protection against ribavirin-induced anemia. We also replicated the associations of ITPA and VDR genetic variants with the development of ribavirin-induced anemia (rs1127354; OR:0.13, 95%CI:0.04–0.41, P = 8.66 ×10-5; and rs1544410; OR:1.65, 95%CI:1.01–2.70, P = 0.0437). Conclusions: GYPC variation affecting erythrocyte membrane strength is important in predicting risk for developing ribavirin-induced anemia. ITPA and VDR genetic variants are also important predictors of this adverse reaction