50 research outputs found

    Neighborhood crime is differentially associated with cardiovascular risk factors as a function of race and sex

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    Background: Neighborhood crime may be an important factor contributing to cardiovascular health disparities, and these relations may vary by race and sex. The present investigation evaluated (a) potential differential associations between neighborhood crime and cardiovascular disease (CVD) risk factors within subgroups of African American (AA) and White men and women, and (b) potential mediation by negative affect. Design and Methods: Participants were 1,718 AAs and Whites (58% AA; 54% female; 59% above poverty; ages 30-64 years) living in Baltimore, Maryland who completed the first wave of the Healthy Aging in Neighborhoods of Diversity across the Life Span study from 2004-2009. CVD risk factors included body mass index, total serum cholesterol, glucose, and systolic and diastolic blood pressure. A negative affect composite was comprised of self-reported depression, anxiety, anger, vigilance, and perceived stress. Hierarchical multiple regression analyses were used to examine associations between per capita overall and violent crime rates, negative affect, and CVD risk factors. Results: There were significant associations of greater overall crime rate with higher fasting glucose (b=.192, P<0.05), and greater violent crime rate with higher systolic (b=86.50, P<0.05) and diastolic (b=60.12, P<0.05) blood pressure in AA women, but not men. These associations were not explained by negative affect. In Whites, there were no significant associations of overall or violent crime rates with cardiovascular risk factors. Conclusions: AA women may be particularly vulnerable to the negative impact of crime on cardiovascular risk. Preventative efforts aimed toward this group may help to deter the detrimental effects that living in a high crime area may have on one’s cardiovascular health

    Lifetime Racial/Ethnic Discrimination and Ambulatory Blood Pressure: The Moderating Effect of Age

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    Objective To determine if the relationships of lifetime discrimination to ambulatory blood pressure (ABP) varied as a function of age in a sample of Black and Latino(a) adults ages 19 – 65. Methods Participants were 607 Black (n = 318) and Latino(a) (n = 289) adults (49% female) who completed the Perceived Ethnic Discrimination Questionnaire-Community Version (PEDQ-CV), which assesses lifetime exposure to racism/ethnic discrimination. They were outfitted with an ABP monitor to assess systolic and diastolic blood pressure (SBP, DBP) across a 24-hour period. Mixed-level modeling was conducted to examine potential interactive effects of lifetime discrimination and age to 24-hour, daytime, and nighttime ABP after adjustment for demographic, socioeconomic, personality and life stress characteristics, and substance consumption covariates (e.g., smoking, alcohol). Results There were significant interactions of Age × Lifetime Discrimination on 24-hour and daytime DBP (ps ≤ .04), and in particular significant interactions for the Social Exclusion component of Lifetime Discrimination. Post-hoc probing of the interactions revealed the effects of Lifetime Discrimination on DBP were seen for older, but not younger participants. Lifetime discrimination was significantly positively associated with nocturnal SBP, and these effects were not moderated by age. All associations of Lifetime Discrimination to ABP remained significant controlling for recent exposure to discrimination as well as all other covariates. Conclusions Exposure to racial/ethnic discrimination across the life course is associated with elevated ABP in middle to older aged Black and Latino(a) adults. Further research is needed to understand the mechanisms linking discrimination to ABP over the life course

    Helicobacter pylori, persistent infection burden and structural brain imaging markers

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    Persistent infections, whether viral, bacterial or parasitic, including Helicobacter pylori infection, have been implicated in non-communicable diseases, including dementia and other neurodegenerative diseases. In this cross-sectional study, data on 635 cognitively normal participants from the UK Biobank study (2006–21, age range: 40–70 years) were used to examine whether H. pylori seropositivity (e.g. presence of antibodies), serointensities of five H. pylori antigens and a measure of total persistent infection burden were associated with selected brain volumetric structural MRI (total, white, grey matter, frontal grey matter (left/right), white matter hyperintensity as percent intracranial volume and bi-lateral sub-cortical volumes) and diffusion-weighted MRI measures (global and tract-specific bi-lateral fractional anisotropy and mean diffusivity), after an average 9–10 years of lag time. Persistent infection burden was calculated as a cumulative score of seropositivity for over 20 different pathogens. Multivariable-adjusted linear regression analyses were conducted, whereby selected potential confounders (all measures) and intracranial volume (sub-cortical volumes) were adjusted, with stratification by Alzheimer’s disease polygenic risk score tertile when exposures were H. pylori antigen serointensities. Type I error was adjusted to 0.007. We report little evidence of an association between H. pylori seropositivity and persistent infection burden with various volumetric outcomes (P > 0.007, from multivariable regression models), unlike previously reported in past research. However, H. pylori antigen serointensities, particularly immunoglobulin G against the vacuolating cytotoxin A, GroEL and outer membrane protein antigens, were associated with poorer tract-specific white matter integrity (P < 0.007), with outer membrane protein serointensity linked to worse outcomes in cognition-related tracts such as the external capsule, the anterior limb of the internal capsule and the cingulum, specifically at low Alzheimer’s disease polygenic risk. Vacuolating cytotoxin A serointensity was associated with greater white matter hyperintensity volume among individuals with mid-level Alzheimer’s disease polygenic risk, while among individuals with the highest Alzheimer’s disease polygenic risk, the urease serointensity was consistently associated with reduced bi-lateral caudate volumes and the vacuolating cytotoxin A serointensity was linked to reduced right putamen volume (P < 0.007). Outer membrane protein and urease were associated with larger sub-cortical volumes (e.g. left putamen and right nucleus accumbens) at middle Alzheimer’s disease polygenic risk levels (P < 0.007). Our results shed light on the relationship between H. pylori seropositivity, H. pylori antigen levels and persistent infection burden with brain volumetric structural measures. These data are important given the links between infectious agents and neurodegenerative diseases, including Alzheimer’s disease, and can be used for the development of drugs and preventive interventions that would reduce the burden of those diseases

    Neuropsychology of Cardiovascular Disease

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    Cardiovascular disease, the leading cause of morbidity and mortality in the United States and many other countries, confers substantial risk for cerebrovascular events, such as stroke and vascular dementia. The neuropsychological sequelae of such conditions are well documented and can have a devastating impact on individuals\u27 quality of life. However, prior to the development of overt cerebrovascular complications, persons with cardiovascular disease or its risk factors may display mild to severe neuropsychological difficulties. Medical and surgical treatments for cardiovascular disease have also been found to affect neuropsychological function. This landmark volume offers the first comprehensive overview of the neuropsychological consequences of cardiovascular disease, tracking its natural history, epidemiology, and treatments. It encourages researchers and clinicians to consider all relevant facets of vascular disease processes in their evaluation, study, and treatment of affected patients and indicates a need for primary and secondary prevention efforts. Neuropsychology of Cardiovascular Disease will be welcomed as an invaluable resource by neuropsychologists, specialists in behavioral medicine, neurologists, cardiologists, epidemiologists, gerontologists, and many other health professionals whose work brings them into contact with these challenging patients.https://digitalcommons.library.umaine.edu/fac_monographs/1193/thumbnail.jp

    Neuropsychology of Cardiovascular Disease

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    Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the United States and most westernized nations. Both CVDs and their risk factors confer substantial risk for stroke and dementia, but are also associated with more subtle changes in brain structure and function and cognitive performance prior to such devastating clinical outcomes. It has been suggested that there exists a continuum of brain abnormalities and cognitive difficulties associated with increasingly severe manifestations of cardiovascular risk factors and diseases that precede vascular cognitive impairment and may ultimately culminate in stroke or dementia. This second edition examines the relations of a host of behavioral and biomedical risk factors, in addition to subclinical and clinical CVDs, to brain and cognitive function. Associations with dementia and pre-dementia cognitive performance are reported, described, and discussed with a focus on underlying brain mechanisms. Future research agendas are suggested, and clinical implications are considered.https://digitalcommons.library.umaine.edu/fac_monographs/1201/thumbnail.jp

    Central and autonomic nervous system integration in emotion.

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    Abstract Emotions involve physiological responses that are regulated by the brain. The present paper reviews the empirical literature on central nervous system (CNS) and autonomic nervous system (ANS) concomitants of emotional states, with a focus on studies that simultaneously assessed CNS and ANS activity. The reviewed data support two primary conclusions: (1) numerous cortical and subcortical regions show co-occurring activity with ANS responses in emotion, and (2) there may be reversed asymmetries on cortical and subcortical levels with respect to CNS/ANS interrelations. These observations are interpreted in terms of a model of neurovisceral integration in emotion, and directions for future research are presented

    Depression And Lipoprotein Lipids In Healthy, Postmenopausal Women: The Moderating Effects Of Hormone Replacement Therapy

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    Objective Naturally occurring low cholesterol levels have been related to increased depressive symptoms in studies conducted predominantly in men. However, depression is more common among women, may increase during the menopause, and may be impacted by hormone replacement therapy (HRT). We therefore examined the potential interactive relation of depressive symptoms and HRT status to lipoprotein lipids among postmenopausal women. Methods Seventy healthy, postmenopausal women (ages 50-70; 36% receiving HRT) completed the Center for Epidemiological Studies Depression Scale and provided two fasting blood samples for assessment of lipoprotein lipids. Results Following statistical adjustment for age, body mass index (BMI), HRT status, and depressive symptoms, the interaction of depression and HRT explained 16% variance in total cholesterol and 17% variance in low-density lipoprotein cholesterol (Ps\u3c.01). Greater levels of depressive symptoms were associated with lower cholesterol levels only among women who were not taking HRT. Conclusion These findings suggest that HRT may buffer associations between naturally occurring low cholesterol levels and increased symptoms of depression in postmenopausal women. © 2004 Elsevier Inc. All rights reserved
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