Heal the Sick

Kevin Lewis

December 25, 2012

Role Models and the Psychological Characteristics That Buffer Low-Socioeconomic-Status Youth From Cardiovascular Risk

Edith Chen et al.
Child Development, forthcoming

Little is understood about why some youth from low-socioeconomic-status (SES) environments exhibit good health despite adversity. This study tested whether role models and "shift-and-persist" approaches (reframing stressors more benignly while persisting with future optimism) protect low-SES youth from cardiovascular risk. A total of 163 youth, ages 13-16, completed role model interviews and shift-and-persist measures while cholesterol and inflammatory markers, interleukin-6 (IL-6), and C-reactive protein were assessed. Low-SES youth with supportive role models had lower IL-6. Low-SES youth high in shift-and-persist also had lower IL-6. Shift-and-persist partially mediated the interaction of SES and role models on IL-6. Benefits were not found among high-SES youth. Identifying psychological buffers in low-SES youth has implications for health disparities.


Maternal Age and Offspring Adult Health: Evidence From the Health and Retirement Study

Mikko Myrskylä & Andrew Fenelon
Demography, November 2012, Pages 1231-1257

Advanced maternal age is associated with negative offspring health outcomes. This interpretation often relies on physiological processes related to aging, such as decreasing oocyte quality. We use a large, population-based sample of American adults to analyze how selection and lifespan overlap between generations influence the maternal age-offspring adult health association. We find that offspring born to mothers younger than age 25 or older than 35 have worse outcomes with respect to mortality, self-rated health, height, obesity, and the number of diagnosed conditions than those born to mothers aged 25-34. Controls for maternal education and age at which the child lost the mother eliminate the effect for advanced maternal age up to age 45. The association between young maternal age and negative offspring outcomes is robust to these controls. Our findings suggest that the advanced maternal age-offspring adult health association reflects selection and factors related to lifespan overlap. These may include shared frailty or parental investment but are not directly related to the physiological health of the mother during conception, fetal development, or birth. The results for young maternal age add to the evidence suggesting that children born to young mothers might be better off if the parents waited a few years.


Nervous system regulation of the cancer genome

Steven Cole
Brain, Behavior, and Immunity, forthcoming

Genomics-based analyses have provided deep insight into the basic biology of cancer and are now clarifying the molecular pathways by which psychological and social factors can regulate tumor cell gene expression and genome evolution. This review summarizes basic and clinical research on neural and endocrine regulation of the cancer genome and its interactions with the surrounding tumor microenvironment, including the specific types of genes subject to neural and endocrine regulation, the signal transduction pathways that mediate such effects, and therapeutic approaches that might be deployed to mitigate their impact. Beta-adrenergic signaling from the sympathetic nervous system has been found to up-regulate a diverse array of genes that contribute to tumor progression and metastasis, whereas glucocorticoid-regulated genes can inhibit DNA repair and promote cancer cell survival and resistance to chemotherapy. Relationships between socio-environmental risk factors, neural and endocrine signaling to the tumor microenvironment, and transcriptional responses by cancer cells and surrounding stromal cells are providing new mechanistic insights into the social epidemiology of cancer, new therapeutic approaches for protecting the health of cancer patients, and new molecular biomarkers for assessing the impact of behavioral and pharmacologic interventions.


Glucocorticoid excess and the developmental origins of disease: Two decades of testing the hypothesis

Rebecca Reynolds
Psychoneuroendocrinology, January 2013, Pages 1-11

Low birthweight, a marker of an adverse in utero environment, is associated with cardiometabolic disease and brain disorders in adulthood. The adaptive changes made by the fetus in response to the intra-uterine environment result in permanent changes in physiology, structure and metabolism, a phenomenon termed early life programming. One of the key hypotheses to explain programming, namely over exposure of the developing fetus to glucocorticoids, was proposed nearly two decades ago, following the observation that the fetus was protected from high glucocorticoid levels in the mother by the actions of the placental barrier enzyme, 11β-hydroxysteroid dehydrogenase, which converts active glucocorticoids into inactive products. Numerous mechanistic studies in animal models have been carried out to test this hypothesis using manipulations to increase maternal glucocorticoids. Overall, these have resulted in offspring of lower birthweight, with an activated hypothalamic-pituitary-adrenal (HPA) axis and an adverse metabolic profile and behavioural phenotype in adulthood. Altered glucocorticoid activity or action is a good candidate mechanism in humans to link low birthweight with cardiometabolic and brain disorders. We have carried out detailed studies in men and women showing that high levels of endogenous glucocorticoids, or treatment with exogenous glucocorticoids, is associated with an adverse metabolic profile, increased cardiovascular disease and altered mood and cognitive decline. Our laboratory carried out the first translational studies in humans to test the glucocorticoid hypothesis, firstly demonstrating in studies of adult men and women, that low birthweight was associated with high fasting cortisol levels. We went on to dissect the mechanisms underlying the high fasting cortisol, demonstrating activation of the HPA axis, with increased cortisol responses to stimulation with exogenous adrenocorticotrophin hormone, lack of habituation to the stress of venepuncture, and increased cortisol responses to psychosocial stress. We have developed new dynamic tests to dissect the mechanisms regulating HPA axis central negative feedback sensitivity in humans, and demonstrated that this may be altered in obesity, one component of the metabolic syndrome. There are now studies in humans demonstrating that high circulating levels of maternal cortisol during pregnancy correlate negatively with birthweight, suggesting that excess glucocorticoids can by-pass the placental barrier. Deficiencies in the barrier enzyme, potentially increasing fetal glucocorticoid exposure, can also arise in association with maternal stress, malnutrition and disease, and can be inhibited by consumption of liquorice, which contains glycyrrhizin, an HSD inhibitor. Importantly, studies in humans have now demonstrated that high maternal cortisol in pregnancy and/or inhibition of HSD2 are associated with programmed outcomes in childhood including higher blood pressure, behavioural disorders as well as altered brain structure. We are investigating this further, using novel magnetic resonance imaging techniques to study the developing fetal brain in utero. The translational studies in support of the glucocorticoid hypothesis, and demonstrating that glucocorticoids are both mediators and targets of programming, are exciting and raise the question of whether this information can be used to identify those individuals most at risk of later life disease. In a recent study we showed that alterations in DNA methylation at genes important in regulating cortisol levels, tissue glucocorticoid action, blood pressure and fetal growth, are present in adulthood in association with both early life parameters and cardiometabolic risk factors. These preliminary data add to the limited literature in humans indicating a persisting epigenetic link between early life events and subsequent disease risk. Such findings open novel avenues for further exploration of the contribution of glucocorticoids to later life disease.


Increasing autism prevalence in metropolitan New Jersey

Walter Zahorodny et al.
Autism, forthcoming

High baseline autism spectrum disorder prevalence estimates in New Jersey led to a follow-up surveillance. The objectives were to determine autism spectrum disorder prevalence in the year 2006 in New Jersey and to identify changes in the prevalence of autism spectrum disorder or in the characteristics of the children with autism spectrum disorder, between 2002 and 2006. The cohorts included 30,570 children, born in 1998 and 28,936 children, born in 1994, residing in Essex, Hudson, Union, and Ocean counties, New Jersey. Point prevalence estimates by sex, ethnicity, autism spectrum disorder subtype, and previous autism spectrum disorder diagnosis were determined. For 2006, a total of 533 children with autism spectrum disorder were identified, consistent with prevalence of 17.4 per 1000 (95% confidence interval = 15.9-18.9), indicating a significant increase in the autism spectrum disorder prevalence (p < 0.001), between 2002 (10.6 per 1000) and 2006. The rise in autism spectrum disorder was broad, affecting major demographic groups and subtypes. Boys with autism spectrum disorder outnumbered girls by nearly 5:1. Autism spectrum disorder prevalence was higher among White children than children of other ethnicities. Additional studies are needed to specify the influence of better awareness of autism spectrum disorder prevalence estimates and to identify possible autism spectrum disorder risk factors. More resources are necessary to address the needs of individuals affected by autism spectrum disorder.


Spatial clusters of autism births and diagnoses point to contextual drivers of increased prevalence

Soumya Mazumdar et al.
Social Science & Medicine, forthcoming

Autism prevalence has risen dramatically over the past two decades in California. Although often suggested to have been crucial to the rise of autism, environmental and social contextual drivers of diagnosis have not been extensively examined. Identifying the spatial patterning of autism cases at birth and at diagnosis can help clarify which contextual drivers are affecting autism's rising prevalence. Children with autism not co-morbid with mental retardation served by the California Department of Developmental Services during the period 1992 to 2005 were matched to California's Birth Master Files. We search for spatial clusters of autism at time of birth and at time of diagnosis using a spatial scan approach that controls for key individual-level risk factors. We then test whether indicators of neighborhood-level diagnostic resources are associated with the diagnostic clusters and assess the extent of clustering by autism symptom severity through a multivariate scan. Finally, we test whether children who move into neighborhoods with higher levels of resources are more likely to receive an autism diagnosis relative to those who do not move with regard to resources. Significant birth and diagnostic clusters of autism are observed independent of key individual-level risk factors. While the clusters overlap, there is a strong positive association between the diagnostic clusters and neighborhood-level diagnostic resources. In addition, children with autism who are higher functioning are more likely to be diagnosed within a cluster than children with autism who are lower functioning. Most importantly, children who move into a neighborhood with more diagnostic resources than their previous residence are more likely to subsequently receive an autism diagnosis than children whose neighborhood resources do not change. We identify birth and diagnostic clusters of autism in California that are independent of individual-level autism risk factors. Our findings implicate a causal relationship between neighborhood-level diagnostic resources and spatial patterns of autism incidence but do not rule out the possibility that environmental toxicants have also contributed to autism risk.


The Long-Term Effects of Military Conscription on Mortality: Estimates From the Vietnam-Era Draft Lottery

Dalton Conley & Jennifer Heerwig
Demography, August 2012, Pages 841-855

Research on the effects of Vietnam military service suggests that Vietnam veterans experienced significantly higher mortality than the civilian population at large. These results, however, may be biased by nonrandom selection into the military if unobserved background differences between veterans and nonveterans affect mortality directly. To generate unbiased estimates of exposure to conscription on mortality, the present study compares the observed proportion of draft-eligible male decedents born 1950-1952 to the (1) expected proportion of draft-eligible male decedents given Vietnam draft-eligibility cutoffs; and (2) observed proportion of draft-eligible decedent women. The results demonstrate no effect of draft exposure on mortality, including for cause-specific death rates. When we examine population subgroups - including splits by race, educational attainment, nativity, and marital status - we find weak evidence for an interaction between education and draft eligibility. This interaction works in the opposite direction of putative education-enhancing, mortality-reducing effects of conscription that have, in the past, led to concern about a potential exclusion restriction violation in instrumental variable (IV) regression models. We suggest that previous research, which has shown that Vietnam-era veterans experienced significantly higher mortality than nonveterans, might be biased by nonrandom selection into the military and should be further investigated.


Early Life Health Interventions and Academic Achievement

Prashant Bharadwaj, Katrine Vellesen Løken & Christopher Neilson
American Economic Review, forthcoming

This paper studies the effect of improved neonatal health care on mortality and long run academic achievement in school. We use the idea that medical treatments often follow rules of thumb for assigning care to patients, such as the classification of Very Low Birth Weight (VLBW), which assigns infants special care at a specific birth weight cutoff. Using detailed administrative data on schooling and birth records from Chile and Norway, we establish that children who receive extra medical care at birth have lower mortality rates and higher test scores and grades in school. These gains are in the order of 0.15-0.22 standard deviations.


Broke, Ill, and Obese: Is There an Effect of Household Debt on Health?

Matthias Keese & Hendrik Schmitz
Review of Income and Wealth, forthcoming

We analyze the association between household indebtedness and different health outcomes using data from the German Socio-Economic Panel from 1999 to 2009. We control for unobserved heterogeneity by applying fixed-effects methods and furthermore use a subsample of constantly employed individuals plus lagged debt variables to reduce problems of reverse causality. We apply different measures of household indebtedness, such as the percentage shares of household income spent on consumer credit and home loan repayments (which indicate the severity of household indebtedness) and a binary variable of relative overindebtedness (which indicates a precarious debt situation). We find all debt measures to be strongly correlated with health satisfaction, mental health, and obesity. This relationship vanishes for obesity after controlling for unobserved heterogeneity while it stays significant with respect to worse physical and mental health.


Has Scotland always been the ‘sick man' of Europe? An observational study from 1855 to 2006

Gerry McCartney et al.
European Journal of Public Health, December 2012, Pages 756-760

Background: Scotland has been dubbed ‘the sick man of Europe' on account of its higher mortality rates compared with other western European countries. It is not clear the length of time for which Scotland has had higher mortality rates. The root causes of the higher mortality in Scotland remain elusive.

Methods: Life expectancy data from the Human Mortality Database were tabulated and graphed for a selection of wealthy, mainly European countries from around 1850 onwards.

Results: Scotland had a life expectancy in the mid-range of countries included in the Human Mortality Database from the mid-19th century until around 1950. After 1950, Scottish life expectancy improved at a slower rate than in comparably wealthy nations before further faltering during the last 30 years. Scottish life expectancy now lies between that of western European and eastern European nations. The USA also displays a marked faltering in its life expectancy trend after 1981. There is an inverse association between life expectancy and the Index of Economic Freedom such that greater neoliberalism is associated with a smaller increase, or a decrease, in life expectancy.

Conclusion: Life expectancy in Scotland has only been relatively low since around 1950. From 1980, life expectancy in Scotland, the USA and, to a greater extent, the former USSR displays a further relative faltering. It has been suggested that Scotland suffered disproportionately from the adoption of neoliberalism across the nations of the UK, and the evidence here both supports this suggestion and highlights other countries which may have suffered similarly.


Education and Dementia Risk: Results From the Aging Demographics and Memory Study

Rashmita Basu
Research on Aging, January 2013, Pages 7-31

This study examined importance of education on dementia risk among older adults. It explored to what extent this relationship represents an independent effect of education on dementia risk. A cross-sectional sample of adults age 70 years or older was selected from the Aging Demographics and Memory Study, a supplement to the Health and Retirement Study, to examine the association between education and dementia risk and to mitigate the possibility of self-selection bias (unobserved variable bias) in explaining this correlation. An identification strategy using parental and sibling characteristics as instrumental variables for education was used to remove bias from the estimate of education parameter's effect on dementia risk. The association between education and dementia risk was observed after accounting for self-selection bias. Results from the two-stage ordered logit model suggest that the impact of education on dementia risk is not an artifact but rather the observed association between education and dementia incidence has a causal component.


Does Information on Health Status Lead to a Healthier Lifestyle? Evidence from China on the Effect of Hypertension Diagnosis on Food Consumption

Meng Zhao, Yoshifumi Konishi & Paul Glewwe
Journal of Health Economics, forthcoming

We examine the role of information in understanding the differential effects of income on the demand for health. In the health capital framework of Grossman (JPE, 1972), we derive the testable hypotheses that individuals adjust their diet in a healthier direction upon receiving negative health information, and that the effect is greater for richer individuals. Based on unique Chinese longitudinal data and a regression discontinuity design that exploits the exogenous cutoff of systolic blood pressure in the diagnosis of hypertension, we find that, upon receiving hypertension diagnosis, individuals reduce fat intake significantly, and richer individuals reduce more. Our results also indicate that among the rich, hypertension diagnosis is more effective for individuals with lower education.

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