Biological limits to reduction in rates of coronary heart disease--论文代写范文精选

最近讨论慢性病与衰老相关的条件,包括心血管疾病(CVD)、骨质疏松症、关节炎、II型糖尿病等。CRP是一个模式，识别分子的先天免疫反应,从而提供早期防御和激活来适应性免疫系统。下面的essay代写范文进行详述。

Abstract 
On both empirical and theoretical grounds we find that a particular form of social hierarchy, here characterized as ‘pathogenic’, can, from the earliest phases of life, exert a formal analog to evolutionary selection pressure, literally writing a permanent image of itselfupon immune function as chronic vascular inflammation and its consequences. The staged nature of resulting disease emerges ‘naturally’ as an analog to punctuated equilibrium in evolutionary theory. Exposure differs according to the social constructs of race, class, and ethnicity, accounting in large measure for observed population-level differences in rates of coronary heart disease affecting industrialized societies. The system of American Apartheid, which enmeshes both majority and minority communities in a construct of pathogenic hierarchy, appears to present a severe biological limit to ultimate possible reductions in rates of coronary heart disease and related disorders for powerful as well as subordinate subgroups. 
Key words: Apartheid, coronary heart disease, hierarchy, immune cognition, punctuated equilibrium, racism, vascular inflammation, wage slavery

Introduction 
The origin of ‘racial’, ‘class’, and ‘ethnic’ disparities in health has recently become the center of some debate in the US, with remedies proposed by mainstream authorities characteristically and predictably focused on individualoriented ‘prevention’ by altered life-style or related medical ‘magic bullet’ interventions. See Link and Phelan [2000] for a comprehensive critique and review. Indeed, for certain US subpopulations, changes in diet, exercise, patterns of smoking and alcohol intake, and so forth, are widely credited with causing marked declines in coronary heart disease (CHD): the age-adjusted national death rate from CHD for white US males fell from about 420 per 100,000 in 1980 to about 240 by 1997, compared to declines from 350 to 235 for Black males [Cooper et al., 2000]. 

Declines for both Black and white females have not been as spectacular, starting from a lower 1980 baseline of about 240, and falling to near 150 by 1997. As Cooper et al. [2000] and Cooper [2001] note, however, the declines have not been uniformly distributed: age-adjusted all-cause heart mortality rates in the US are especially high in black men relative to other race/sex groups: 243 per 100,000 vs. 175 for white males, compared with 156 for Black females vs. 95 for white females (1996 data). Barnett and Halverson [2000] found unexpectedly high rates of premature CHD mortality for African Americans in major metropolitan regions outside the South, despite favorable levels of socioeconomic resources. A recent paper by Fang et al. [1998] finds close correlation of CHD mortality with patterns of racial segregation in NewYork City, one of the world’s most segregated urban centers. Cooper [2001] argues that the intersection of income inequality and residential segregation at the US metropolitan regional level provides an ‘emergent’ phenomenon which drives patterns of cardiovascular disease mortality. More generally, Polednak [1991, 1993, 1996] and Collins and Williams [1995] show that allcause black-white mortality differences are highest in US metropolitan areas with the greatest racial segregation.

Kiecolt-Glaser et al. [2002] discuss how chronic inflammation has recently been linked with a spectrum of conditions associated with aging, including cardiovascular disease (CVD), osteoporosis, arthritis, type II diabetes, certain cancers, and other conditions. The association between CVD and inflammation is mediated by the cytokine IL-6, related to its central role in promoting the production of C-reactive protein (CRP), which Du Clos [2000] and Volanakis [2001] describe as an ancient and highly conserved protein secreted by the liver in response to trauma, inflammation, and infection. 

CRP is a pattern-recognition molecule of the innate immune response keyed to surveillance for altered self and certain pathogens, thus providing early defense and activation of the humoral, adaptive, immune system. It is increasingly seen as a linkage between the two forms of immune response. Inflammation has recently become central to understanding the etiology of CHD, including its staging as a chronic disease. To paraphrase Blake and Ridker [2001], from initial stages of leukocyte recruitment to diseased endothelium, to plaque rupture, inflammatory mechanisms mediate key steps in atherogenesis and its complications. Thus the key to CHD is now seen in the complex basic biology of plaque formation and dynamics rather than in a passive and rather bland lipid storage. 

Triggers for inflammation in atherogenesis include hypertension, diabetes, and obesity. Obesity “not only predisposes to insulin resistance and diabetes, but also contributes to atherogenic dyslipidemia...obesity itself promotes in- flammation and potentiates atherogenesis independent of effects on insulin resistance or lipoproteins” [Libbey et al., 2002]. Libbey et al. [2002] conclude that atherothrombosis is more than a disease of lipid accumulation, rather it is a disorder characterized by low-grade vascular inflammation, often associated with traditional risk factors such as central obesity and body mass index. Data implicate inflammatory pathways in all stages of disease, from early atherogenesis, to the progression of lesions, and finally in the thrombotic complications of the disease. 

As Ridker [2002] states, risk factors for atherosclerosis and adult-onset diabetes closely overlap and the two disorders may derive from similar antecedents, a mutual inflammatory or genetic basis. Recent studies suggest that baseline levels of IL-6 and CRP which were previously shown to predict onset of atherothrombosis, also predict onset of type II diabetes, even after adjustment for body mass index. Ridker [2002] has the grace to note the limits of a strict biochemical approach: “[T]he clinical hypothesis that an enhanced immune response results in increased plaque vulnerability begs the question as to why a population distribution of inflammation exists in the first place and what the underlying determinants of this distribution might be.” This question is, precisely, the principal focus of our analysis.

Indeed, larger hypotheses are not lacking in the literature, and the newlyrecognized cortisol-leptin cycle is worthy of some comment here: Leptin, the ‘fat hormone’, increases Th1 and suppresses Th2 cytokine production [Lord et al., 1998] and also stimulates proliferation and activation of circulating monocytes, and may play a direct role in inflammatory processes [Santos-Alvarez et al., 1999]. Leptin and cortisol have, however, a complex relation. Cortisol, an adrenal stress hormone, and leptin alternate their plasma peaks as part of the normal circadian cycle [Bornstein et al., 1998]. 

Cortisol increases can trigger answering leptin increases [Newcomer et al., 1988]. Glucocorticoid levels also influence plasma leptin levels [Eliman et al., 1998]. Thus leptin and the adrenal hormones regulate each other: patterns of stress thus influence weight change, disease resistance, and inflammatory response. Th1/Th2 balance may be heavily influenced, in turn, by the adrenal hormone/leptin balance. Stress imposed on pregnant women may result in changes to fetal immune and metabolic processes, with implications for birth weight, fat metabolism and risk for cardiovascular disease and allergenic susceptibility over the life course [Wallace, Wallace and Fullilove, 2002]. 

These inferences are strengthened by the results of Singhal et al. [2002] who found that elevation in leptin was associated with impaired vascular function independent of metabolic and inflammatory disturbances associated with obesity. A long series of articles by Barker and co-workers [e.g. Barker, 2002; Barker et al., 2001, Osmond and Barker, 2000; Godfrey and Barker, 2001] is consistent with such mechanisms, suggesting that those who develop CHD grow differently from others both in utero and during childhood. Slow growth during fetal life and infancy is followed by accelerated weight gain in childhood, setting a life history trajectory for CHD, type II diabetes, and hyper-tension. Barker [2002] concludes that slow fetal growth might also heighten the body’s stress responses and increase vulnerability to poor living conditions in later life. Thus, in his view, CHD is a developmental disorder that originates through two widespread biological phenomena, developmental plasticity and compensatory growth, a speculation consistent with the work of Smith et al. [1998] who found that deprivation in childhood influences risk of mortality from CHD in adulthood, although an additive influence of adulthood circumstances is seen in such cases.（essay代写)

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