Childhood abuse increases adult risk for morbidity and mortality. Less clear is how this “toxic” stress becomes embedded to influence health decades later, and whether protective factors guard ...against these effects. Early biological embedding is hypothesized to occur through programming of the neural circuitry that influences physiological response patterns to subsequent stress, causing wear and tear across multiple regulatory systems. To examine this hypothesis, we related reports of childhood abuse to a comprehensive 18-biomarker measure of multisystem risk and also examined whether presence of a loving parental figure buffers against the impact of childhood abuse on adult risk. A total of 756 subjects (45.8% white, 42.7% male) participated in this ancillary substudy of the Coronary Artery Risk Development in Young Adults Study. Childhood stress was determined by using the Risky Families Questionnaire, a well-validated retrospective self-report scale. Linear regression models adjusting for age, sex, race, parental education, and oral contraceptive use found a significant positive relationship between reports of childhood abuse and multisystem health risks B (SE) = 0.68 (0.16); P < 0.001. Inversely, higher amounts of reported parental warmth and affection during childhood was associated with lower multisystem health risks B (SE) = −0.40 (0.14); P < 0.005. A significant interaction of abuse and warmth (P < 0.05) was found, such that individuals reporting low levels of love and affection and high levels of abuse in childhood had the highest multisystem risk in adulthood.
In this article, the authors evaluate the possible roles of negative emotions and cognitions in the association between socioeconomic status (SES) and physical health, focusing on the outcomes of ...cardiovascular diseases and all-cause mortality. After reviewing the limited direct evidence, the authors examine indirect evidence showing that (a) SES relates to the targeted health outcomes, (b) SES relates to negative emotions and cognitions, and (c) negative emotions and cognitions relate to the targeted health outcomes. The authors present a general framework for understanding the roles of cognitive-emotional factors, suggesting that low-SES environments are stressful and reduce individuals' reserve capacity to manage stress, thereby increasing vulnerability to negative emotions and cognitions. The article concludes with suggestions for future research to better evaluate the proposed model.
Early menopause is linked to an increased risk of cardiovascular disease mortality; however, the association between early menopause and incidence and timing of cardiovascular disease is unclear. We ...aimed to assess the associations between age at natural menopause and incidence and timing of cardiovascular disease.
We harmonised and pooled individual-level data from 15 observational studies done across five countries and regions (Australia, Scandinavia, the USA, Japan, and the UK) between 1946 and 2013. Women who had reported their menopause status, age at natural menopause (if postmenopausal), and cardiovascular disease status (including coronary heart disease and stroke) were included. We excluded women who had hysterectomy or oophorectomy and women who did not report their age at menopause. The primary endpoint of this study was the occurrence of first non-fatal cardiovascular disease, defined as a composite outcome of incident coronary heart disease (including heart attack and angina) or stroke (including ischaemic stroke or haemorrhagic stroke). We used Cox proportional hazards models to estimate multivariate hazard ratios (HRs) and 95% CIs for the associations between age at menopause and incident cardiovascular disease event. We also adjusted the model to account for smoking status, menopausal hormone therapy status, body-mass index, and education levels. Age at natural menopause was categorised as premenopausal or perimenopausal, younger than 40 years (premature menopause), 40–44 years (early menopause), 45–49 years (relatively early), 50–51 years (reference category), 52–54 years (relatively late), and 55 years or older (late menopause).
Overall, 301 438 women were included in our analysis. Of these 301 438 women, 12 962 (4·3%) had a first non-fatal cardiovascular disease event after menopause, of whom 9369 (3·1%) had coronary heart disease and 4338 (1·4%) had strokes. Compared with women who had menopause at age 50–51 years, the risk of cardiovascular disease was higher in women who had premature menopause (age <40 years; HR 1·55, 95% CI 1·38–1·73; p<0·0001), early menopause (age 40–44 years; 1·30, 1·22–1·39; p<0·0001), and relatively early menopause (age 45–49 years; 1·12, 1·07–1·18; p<0·0001), with a significantly reduced risk of cardiovascular disease following menopause after age 51 years (p<0·0001 for trend). The associations persisted in never smokers, and were strongest before age 60 years for women with premature menopause (HR 1·88, 1·62–2·20; p<0·0001) and early menopause (1·40, 1·27–1·54; p<0·0001), but were attenuated at age 60–69 years, with no significant association observed at age 70 years and older.
Compared with women who had menopause at age 50–51 years, women with premature and early menopause had a substantially increased risk of a non-fatal cardiovascular disease event before the age of 60 years, but not after age 70 years. Women with earlier menopause need close monitoring in clinical practice, and age at menopause might also be considered as an important factor in risk stratification of cardiovascular disease for women.
Australian National Health and Medical Research Council.
The association between socioeconomic status (SES) and physical health is robust. Yet, the psychosocial mediators of SES-health association have been studied in relatively few investigations. In this ...chapter, we summarize and critique the recent literature regarding negative emotions and cognitions, psychological stress, and resources as potential pathways connecting SES and physical health. We discuss the psychosocial origins of the SES-health links and outline how psychosocial factors may lead to persistently low SES. We conclude that psychosocial resources may play a critical mediating role, and the origins of the SES-health connection are apparent in childhood. We offer a blueprint for future research, which we hope contributes to a better understanding of how SES gets under the skin across the life span.
There are distinct racial disparities in cardiovascular disease (CVD) risk, with Black individuals at much greater risk than White individuals. Although many factors contribute to these disparities, ...recent attention has focused on the role of discrimination as a stress‐related factor that contributes to racial disparities in CVD. As such, it is important to understand the mechanisms by which discrimination might affect CVD. Recent studies have examined these mechanisms by focusing on neurobiological mediators of CVD risk. Given this increase in studies, a systematic review of perceived discrimination and neurobiological mediators of CVD risk is warranted. Our review uses a multisystem approach to review studies on the relationship between perceived discrimination and (1) cardiovascular responses to stress, (2) hypothalamic–pituitary–adrenocortical axis function, and (3) the immune system, as well as (4) the brain systems thought to regulate these parameters of peripheral physiology. In addition to summarizing existing evidence, our review integrates these findings into a conceptual model describing multidirectional pathways linking perceived discrimination with a CVD risk.
Our review uses a multi‐system approach to review studies on the relationship between perceived discrimination and (1) cardiovascular responses to stress, (2) hypothalamic–pituitary–adrenocortical axis function, and (3) the immune system, as well as (4) the brain systems thought to regulate these parameters of peripheral physiology. In addition to summarizing existing evidence, our review integrates these findings into a conceptual model describing multidirectional pathways linking perceived discrimination with a cardiovascular disease risk.
This study tested longitudinal associations between cannabis use and cardiometabolic risk factors that underlie the development of cardiovascular diseases.
Participants were men from the youngest ...cohort of the Pittsburgh Youth Study who were followed prospectively from approximately age 7 to 32 years (N = 253). Frequency of cannabis use was assessed yearly from approximately ages 12 to 20 years and again at approximately ages 26, 29, and 32 years. The following cardiometabolic risk factors were assessed during a laboratory visit at approximately age 32 years: body mass index (BMI), waist-hip ratio, high- and low-density lipoprotein cholesterol, triglycerides, fasting glucose, insulin resistance, blood pressure, interleukin 6, and C-reactive protein.
Greater cannabis exposure was associated with relatively lower BMI (β = -0.31, p < .001), smaller waist-hip ratio (β = -0.23, p = .002), better high- (β = 0.14, p = .036) and low-density lipoprotein cholesterol (β = -0.15, p = .026), lower triglycerides (β = -0.17, p = .009), lower fasting glucose (β = -0.15, p < .001) and insulin resistance (β = -0.21, p = .003), lower systolic (β = -0.22, p < .001) and diastolic blood pressure (β = -0.15, p = .028), and fewer metabolic syndrome criteria (β = -0.27, p < .001). With exception of BMI, cannabis users' mean levels on cardiometabolic risk factors were generally below clinical cutoffs for high risk. Most associations between cannabis use and cardiometabolic risk factors remained after adjusting for tobacco use, childhood socioeconomic status, and childhood health. However, after adjusting for adult BMI, these associations were no longer apparent, and mediation tests suggested that cannabis users' relatively lower BMI might explain their lower levels of risk on other cardiometabolic risk factors.
Cannabis use is associated with lower BMI, and lower BMI is related to lower levels of risk on other cardiometabolic risk factors.
In the 2011 "Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents," several medical conditions among youth were identified that predispose to ...accelerated atherosclerosis and early cardiovascular disease (CVD), and risk stratification and management strategies for youth with these conditions were elaborated. Major depressive disorder (MDD) and bipolar disorder (BD) among youth satisfy the criteria set for, and therefore merit inclusion among, Expert Panel tier II moderate-risk conditions. The combined prevalence of MDD and BD among adolescents in the United States is ≈10%, at least 10 times greater than the prevalence of the existing moderate-risk conditions combined. The high prevalence of MDD and BD underscores the importance of positioning these diseases alongside other pediatric diseases previously identified as moderate risk for CVD. The overall objective of this statement is to increase awareness and recognition of MDD and BD among youth as moderate-risk conditions for early CVD. To achieve this objective, the primary specific aims of this statement are to (1) summarize evidence that MDD and BD are tier II moderate-risk conditions associated with accelerated atherosclerosis and early CVD and (2) position MDD and BD as tier II moderate-risk conditions that require the application of risk stratification and management strategies in accordance with Expert Panel recommendations. In this scientific statement, there is an integration of the various factors that putatively underlie the association of MDD and BD with CVD, including pathophysiological mechanisms, traditional CVD risk factors, behavioral and environmental factors, and psychiatric medications.
To compare estimates of sleep duration defined by polysomnography (PSG), actigraphy, daily diary, and retrospective questionnaire and to identify characteristics associated with differences between ...measures.
Cross-sectional.
Community sample.
The sample consisted of 223 Black, White, and Asian middle- to older-aged men and women residing in the Pittsburgh, PA area.
Not applicable.
Two nights of in-home PSG; 9 nights of wrist actigraphy and sleep diaries; retrospective sleep questionnaires; and measures of sociodemographic, psychosocial, and adiposity characteristics.
All measures of sleep duration differed significantly, with modest associations between PSG-assessed and retrospective questionnaire-assessed sleep duration. Individuals estimated their habitual sleep duration about 20-30 minutes longer by questionnaire and their prospective sleep diaries compared with both PSG- and actigraphy-assessed sleep duration. Persons reporting higher hostility had smaller associations between PSG-assessed sleep duration and other methods compared with those with lower hostility; those reporting more depressive symptoms and poorer overall health had smaller associations between actigraphy-assessed sleep duration and questionnaire and diary measures. Apnea-hypopnea index was not related to differences among estimates of sleep duration.
PSG, actigraphy, diary, and retrospective questionnaire assessments yield different estimates of sleep duration. Hostility, depressive symptoms, and perceptions of poor health were associated with the magnitude of differences among some estimates. These findings may be useful in understanding the health consequences of short or long self-reported sleep duration and for guiding investigator decisions about choices of measures in specific populations.
We examined temporal associations between objectively-measured physical activity (PA) during the day and in the evening, and sleep quantity and quality.
PA and sleep were measured by actigraphs for ...an average of one week in an epidemiological cohort study of 275 eight-year-old children.
For each one standard deviation (SD) unit of increased PA during the day, sleep duration was decreased by 0.30, sleep efficiency by 0.16, and sleep fragmentation increased by 0.08 SD units that night. For each one SD unit increase in sleep duration and efficiency the preceding night, PA the following day decreased by 0.09 and 0.16 SD units, respectively. When we contrasted days with a high amount of moderate to vigorous activity during the day or in the evening to days with a more sedentary profile, the results were essentially similar. However, moderate to vigorous PA in the evening shortened sleep latency.
The relationship between a higher level of PA and poorer sleep is bidirectional. These within-person findings challenge epidemiological findings showing that more active people report better sleep. Since only a few studies using objective measurements of both PA and sleep have been conducted in children, further studies are needed to confirm/refute these results.
Poor sleep may play a role in insulin resistance and diabetes risk. Yet few studies of sleep and insulin resistance have focused on the important developmental period of adolescence. To address this ...gap, we examined the association of sleep and insulin resistance in healthy adolescents.
Cross-sectional.
Community setting in one high school.
245 (137 African Americans, 116 males) high school students.
Participants provided a fasting blood draw and kept a sleep log and wore a wrist actigraph for one week during the school year. Participants' families were from low to middle class based on family Hollingshead scores. Total sleep time across the week averaged 7.4 h by diary and 6.4 h by actigraph; homeostatic model assessment of insulin resistance (HOMA-IR unadjusted) averaged 4.13. Linear regression analyses adjusted for age, race, gender, body mass index, and waist circumference showed that the shorter the sleep, the higher the HOMA-IR, primarily due to sleep duration during the week. No evidence was found for long sleep being associated with elevated HOMA-IR. Fragmented sleep was not associated with HOMA-IR but was associated with glucose levels.
Reduced sleep duration is associated with HOMA-IR in adolescence. Long sleep duration is not associated. Interventions to extend sleep duration may reduce diabetes risk in youth.
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