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      Association Between Residential Greenness and Cardiovascular Disease Risk

      research-article
      , PhD 1 , 2 , , MS 1 , 2 , 3 , , PhD 9 , , MD 4 , , PhD 10 , , PhD 1 , 2 , , PhD 1 , 2 , , PhD 11 , , PhD 1 , 2 , , PhD 1 , 2 , , MD, PhD 5 , , MD 6 , , PhD 1 , 2 , , MS 1 , , PhD 1 , 2 , , MD 1 , 7 , , PhD 3 , 8 , , MD 5 , , PhD 1 , 2 ,
      Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
      John Wiley and Sons Inc.
      cardiovascular disease risk factors, catecholamine, endothelial progenitor cells, environment, greenness, normalized difference vegetation index, oxidative stress, Angiogenesis, Biomarkers, Mechanisms, Cardiovascular Disease

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          Abstract

          Background

          Exposure to green vegetation has been linked to positive health, but the pathophysiological processes affected by exposure to vegetation remain unclear. To study the relationship between greenness and cardiovascular disease, we examined the association between residential greenness and biomarkers of cardiovascular injury and disease risk in susceptible individuals.

          Methods and Results

          In this cross‐sectional study of 408 individuals recruited from a preventive cardiology clinic, we measured biomarkers of cardiovascular injury and risk in participant blood and urine. We estimated greenness from satellite‐derived normalized difference vegetation index ( NDVI) in zones with radii of 250 m and 1 km surrounding the participants’ residences. We used generalized estimating equations to examine associations between greenness and cardiovascular disease biomarkers. We adjusted for residential clustering, demographic, clinical, and environmental variables. In fully adjusted models, contemporaneous NDVI within 250 m of participant residence was inversely associated with urinary levels of epinephrine (−6.9%; 95% confidence interval, −11.5, −2.0/0.1 NDVI) and F2‐isoprostane (−9.0%; 95% confidence interval, −15.1, −2.5/0.1 NDVI). We found stronger associations between NDVI and urinary epinephrine in women, those not on β‐blockers, and those who had not previously experienced a myocardial infarction. Of the 15 subtypes of circulating angiogenic cells examined, 11 were inversely associated (8.0–15.6% decrease/0.1 NDVI), whereas 2 were positively associated (37.6–45.8% increase/0.1 NDVI) with contemporaneous NDVI.

          Conclusions

          Independent of age, sex, race, smoking status, neighborhood deprivation, statin use, and roadway exposure, residential greenness is associated with lower levels of sympathetic activation, reduced oxidative stress, and higher angiogenic capacity.

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          Most cited references49

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          A Review of the Health Benefits of Greenness.

          Researchers are increasingly exploring how neighborhood greenness, or vegetation, may affect health behaviors and outcomes. Greenness may influence health by promoting physical activity and social contact; decreasing stress; and mitigating air pollution, noise, and heat exposure. Greenness is generally measured using satellite-based vegetation indices or land-use databases linked to participants' addresses. In this review, we found fairly strong evidence for a positive association between greenness and physical activity, and a less consistent negative association between greenness and body weight. Research suggests greenness is protective against adverse mental health outcomes, cardiovascular disease, and mortality, though most studies were limited by cross-sectional or ecological design. There is consistent evidence that greenness exposure during pregnancy is positively associated with birth weight, though findings for other birth outcomes are less conclusive. Future research should follow subjects prospectively, differentiate between greenness quantity and quality, and identify mediators and effect modifiers of greenness-health associations.
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            Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress.

            The stress system coordinates the adaptive responses of the organism to stressors of any kind.(1). The main components of the stress system are the corticotropin-releasing hormone (CRH) and locus ceruleus-norepinephrine (LC/NE)-autonomic systems and their peripheral effectors, the pituitary-adrenal axis, and the limbs of the autonomic system. Activation of the stress system leads to behavioral and peripheral changes that improve the ability of the organism to adjust homeostasis and increase its chances for survival. The CRH and LC/NE systems stimulate arousal and attention, as well as the mesocorticolimbic dopaminergic system, which is involved in anticipatory and reward phenomena, and the hypothalamic beta-endorphin system, which suppresses pain sensation and, hence, increases analgesia. CRH inhibits appetite and activates thermogenesis via the catecholaminergic system. Also, reciprocal interactions exist between the amygdala and the hippocampus and the stress system, which stimulates these elements and is regulated by them. CRH plays an important role in inhibiting GnRH secretion during stress, while, via somatostatin, it also inhibits GH, TRH and TSH secretion, suppressing, thus, the reproductive, growth and thyroid functions. Interestingly, all three of these functions receive and depend on positive catecholaminergic input. The end-hormones of the hypothalamic-pituitary-adrenal (HPA) axis, glucocorticoids, on the other hand, have multiple roles. They simultaneously inhibit the CRH, LC/NE and beta-endorphin systems and stimulate the mesocorticolimbic dopaminergic system and the CRH peptidergic central nucleus of the amygdala. In addition, they directly inhibit pituitary gonadotropin, GH and TSH secretion, render the target tissues of sex steroids and growth factors resistant to these substances and suppress the 5' deiodinase, which converts the relatively inactive tetraiodothyronine (T(4)) to triiodothyronine (T(3)), contributing further to the suppression of reproductive, growth and thyroid functions. They also have direct as well as insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension (metabolic syndrome X) and direct effects on the bone, causing "low turnover" osteoporosis. Central CRH, via glucocorticoids and catecholamines, inhibits the inflammatory reaction, while directly secreted by peripheral nerves CRH stimulates local inflammation (immune CRH). CRH antagonists may be useful in human pathologic states, such as melancholic depression and chronic anxiety, associated with chronic hyperactivity of the stress system, along with predictable behavioral, neuroendocrine, metabolic and immune changes, based on the interrelations outlined above. Conversely, potentiators of CRH secretion/action may be useful to treat atypical depression, postpartum depression and the fibromyalgia/chronic fatigue syndromes, all characterized by low HPA axis and LC/NE activity, fatigue, depressive symptomatology, hyperalgesia and increased immune/inflammatory responses to stimuli.
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              Circadian misalignment increases cardiovascular disease risk factors in humans.

              Shift work is a risk factor for hypertension, inflammation, and cardiovascular disease. This increased risk cannot be fully explained by classic risk factors. One of the key features of shift workers is that their behavioral and environmental cycles are typically misaligned relative to their endogenous circadian system. However, there is little information on the impact of acute circadian misalignment on cardiovascular disease risk in humans. Here we show-by using two 8-d laboratory protocols-that short-term circadian misalignment (12-h inverted behavioral and environmental cycles for three days) adversely affects cardiovascular risk factors in healthy adults. Circadian misalignment increased 24-h systolic blood pressure (SBP) and diastolic blood pressure (DBP) by 3.0 mmHg and 1.5 mmHg, respectively. These results were primarily explained by an increase in blood pressure during sleep opportunities (SBP, +5.6 mmHg; DBP, +1.9 mmHg) and, to a lesser extent, by raised blood pressure during wake periods (SBP, +1.6 mmHg; DBP, +1.4 mmHg). Circadian misalignment decreased wake cardiac vagal modulation by 8-15%, as determined by heart rate variability analysis, and decreased 24-h urinary epinephrine excretion rate by 7%, without a significant effect on 24-h urinary norepinephrine excretion rate. Circadian misalignment increased 24-h serum interleukin-6, C-reactive protein, resistin, and tumor necrosis factor-α levels by 3-29%. We demonstrate that circadian misalignment per se increases blood pressure and inflammatory markers. Our findings may help explain why shift work increases hypertension, inflammation, and cardiovascular disease risk.
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                Author and article information

                Contributors
                aruni@louisville.edu
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                05 December 2018
                18 December 2018
                : 7
                : 24 ( doiID: 10.1002/jah3.2018.7.issue-24 )
                : e009117
                Affiliations
                [ 1 ] Envirome Institute University of Louisville Louisville KY
                [ 2 ] Superfund Research Center University of Louisville Louisville KY
                [ 3 ] Department of Bioinformatics and Biostatistics University of Louisville Louisville KY
                [ 4 ] Department of Environmental and Occupational Health Sciences University of Louisville Louisville KY
                [ 5 ] Department of Pediatrics University of Louisville Louisville KY
                [ 6 ] Division of Endocrinology, Metabolism & Diabetes University of Louisville Louisville KY
                [ 7 ] Division of Cardiovascular Medicine University of Louisville Louisville KY
                [ 8 ] Biostatistics and Bioinformatics Shared Facility James Graham Brown Cancer Center University of Louisville Louisville KY
                [ 9 ] Center for Public Health Policy American Public Health Association Washington D.C.
                [ 10 ] Department of Geography Indiana University ‐ Purdue University Indianapolis Indianapolis IN
                [ 11 ] Beckman Coulter Fort Collins CO
                Author notes
                [*] [* ] Correspondence to: Aruni Bhatnagar, PhD, Diabetes and Obesity Center, University of Louisville, Delia Baxter Building, 580 S. Preston Street, Rm 421F, Louisville, KY 40202. E‐mail: aruni@ 123456louisville.edu
                Article
                JAH33662
                10.1161/JAHA.118.009117
                6405613
                30561265
                1d5f2f34-8b6f-4fbf-ad2e-1dcc5a07219c
                © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 12 March 2018
                : 16 October 2018
                Page count
                Figures: 5, Tables: 1, Pages: 12, Words: 8429
                Funding
                Funded by: WellPoint Foundation
                Funded by: National Institute of Environmental Health Sciences
                Award ID: ES19217
                Award ID: ES023716
                Award ID: ES029846
                Categories
                Original Research
                Original Research
                Epidemiology
                Custom metadata
                2.0
                jah33662
                18 December 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.4 mode:remove_FC converted:18.12.2018

                Cardiovascular Medicine
                cardiovascular disease risk factors,catecholamine,endothelial progenitor cells,environment,greenness,normalized difference vegetation index,oxidative stress,angiogenesis,biomarkers,mechanisms,cardiovascular disease

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