El respeto al cuerpo en las obras de arte (22-IV-81/26-IV-81)

We all know that life can be difficult, but evolution has provided mechanisms to protect the body during crises. Such protection requires many different changes in many different parts of the body, and, as usual, hormones coordinate these

widespread and diverse efforts. When the crisis is past, ebbing hormone levels signal the all-clear, and the body resumes other interests such as eating, body repair, and reproduction. But if the crisis persists, or if the individual’s perception of crisis persists, hormones continue to drive the body to take

desperate measures, sometimes with disastrous consequences (Sapolsky, 2002).

There is well-established evidence that a variety of social and environmental “toxic” extremes can produce physiological responses that interfere with the capacity for normal behavior and contribute to the persistence or aggravation of existing stress-related illness (Nelson 2005; Barr 2008; Shonkoff, Boyce, and McEwen 2009). Anxiety disorders and

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depression are common stress-related maladies in industrialized countries with a reported lifetime prevalence rate of 26.4 percent in the United States (The WHO World Mental Health Survey Consortium 2004). Approximately 50 percent of individuals who are diagnosed with depression are also diagnosed with an anxiety disorder and the comorbidity of anxiety and depression has been well-established in the elderly demographic (Lenze 2003; Anxiety and Depression Association of America 2014). The incidence of depression is much higher in individuals at the lower end of the socioeconomic scale (McEwen, 2000). The persistence of stress-related aberrant behaviors and physiological disorders after disasters has been observed in vulnerable population subsets (Boman 1979; Norris, Friedman, and Watson 2002; Burton et al. 2009; Holman and Silver 2011).Approximately 8 percent of men and 20 percent of women who have experienced a major psychological trauma, such as a natural disaster, will develop post- traumatic stress disorder (PTSD) (National Center for PTSD 2013). A recent study of 2004 tsunami survivors found that a cohort of community-dwelling elders who remained in the same locale after the disaster were significantly more likely to meet criteria for PTSD than their younger counterparts (Viswanath et al. 2012).

What has become evident in the fields of cognitive neuroscience and behavioral

endocrinology is that there are biological mechanisms that influence and control certain aspects of human behavior and contribute to aberrant responses to stress and result in comorbid

psychological and physiological disorders. Chronic pain conditions, ischemic vascular disorders, gastrointestinal and cognitive disorders can be exacerbated by anxiety and/or depression (Sareen et al; 2003, Roy-Byrne 2008; Anxiety and Depression Association of

America 2014). The inherited response to a variety of stressful stimuli affects human behavior in the form of the classic “fight or flight response”. This is a physiological neuroendocrine reaction

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to environmental and social influence. It is exhibited in the nuanced involuntary behavior of “performance anxiety’ and ranges from the simple act of blushing to the perspiration, rapidity of heart rate, and sense of fear and avoidance when exposed to threatening scenarios. The range of physiological reactions is certainly evident in disaster environments where individual and communal reactions may result in alterations and departures from rational thought. The biological imperative of “fight or flight” is an inherited characteristic shared by all vertebrate species including humans. It is an innate involuntary response to a potential threatening stimulus.

Ehrlich and Ornstein (1989) hypothesize that humans are affected by a lack of natural selection for response to slowly developing threats. Our physiological response capacity to threat is based on the “fight or flight” response to immediate challenge. We are not selectively

conditioned to adequately tolerate prolonged stress. Lumsden (1983) indicates that culturally complex societies with high degrees of social stratification are behaviorally constrained and less capable of adaptive cognitive development than less developed cultures. The inheritance of a physiological stress response from our vertebrate ancestors was designed to deal with the short term immediacy of physical danger. The repetitive prolonged insidious stressors associated with poverty, poor health, lack of access to social support, and limited education can exceed the inherited capacity of this physiological mechanism and result in pathological behavioral effects that are exacerbated in the presence of a natural or technological disaster.

Psychological stress is a well-recognized correlate of exposure to a variety of hazardous environments (Bland et al. 2005; Reacher et al. 2004). Prolonged psychological stress has been associated with physiological changes in endocrine function resulting in memory deficit and structural change in the brain’s limbic system and the function of the hypothalamic-pituitary axis (Vanitallie, 2002. Dawood, 2004). The evidence strongly suggests a positive correlation between

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exposure to negative social environments and the potential for biochemical induced cognitive dysfunction. This conclusion is based on a physiologic mechanism for irrational behavior during prolonged stress scenarios. The physiological response to stress is varied and our particular concern is directed to the role and effects of the hypothalamus, pituitary, and adrenal glands in the innate response to the challenge of a perceived or actual stressor. The adrenal glands control the release of several hormones including dehydroepiandosterone (DHEA), epinephrine, and cortisol. The innate response of “fight or flight” is a result of the body’s release of adrenal hormones in response to stimulus from the hypothalamus and pituitary gland in the brain when triggered by a stressful event. Epinephrine and cortisol are secreted with a resultant increase in heart rate, blood pressure and the mobilization of stored energy. A concomitant increased sense of awareness and altered inflammatory response is experienced in the normal response to acute stress. This allows the body to deal with the immediate threat before it. However, extreme prolonged exposure to stress events may have a deleterious effect on the body due to continued demand for secretion of adrenal hormones and the effects of those same hormones on normal physiology. Excessive release of adrenal hormones is associated with cognitive mental dysfunction and a host of metabolic abnormalities including diabetes, thyroid disorders, and gastrointestinal distress. McEwen (2000) describes these chemical imbalances as an “allostatic load” that can accelerate a variety of disease processes.

The initial response to acute or intermittent stress results in an increased release of cortisol. Prolonged stress leads to the detrimental effects of excess cortisol secretion. In severe cases, such as those seen in post-traumatic stress disorder, the hypothalamic-pituitary stimulus mechanism exhausts adrenal capacity and results in a decrease in cortisol level and an increase in the pituitary secretion of adrenocorticotropic (ACTH) hormone which has been correlated with

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exacerbation of auto-immune disease and increased fear avoidance response in susceptible individuals (Kenyon, 2000). Kenyon has indicated that it has been suspected for some time that cortisol released from the adrenal cortex during stress has adverse effects on cognitive functions such as learning and memory (2000). Selye’s (1946) work on General Adaptation Syndrome supported a neuroendocrine role for dysfunctional behavior in response to stress. Further

analysis by Kristenson (2004) and McEwen (2008) suggest a cycle of negative outcomes, loss of coping ability, and chronic stress secondary to psychobiological mechanisms associated with the challenges of the socioeconomically impaired. The aberrant response to prolonged or extreme stressful stimuli leads to abnormalities in circulating levels of biochemical inflammatory mediators and contributes to the development of anxiety and depressive disorders and a variety of comorbid somatic, gastrointestinal, immunological, vascular, and cognitive maladies

(Grachev, Fredickson, and Apkarian. 2001;Davidson et al. 2004; O’Keefe et al. 2004;Reacher et al. 2004; Foa, Stein, and McFarlane 2006).

An estimated 25 percent of individuals, 65 and older, are estimated to suffer from mental health disorders and the prevalence of depressive symptoms is greater amongst low income, extreme elderly (>75) and rural populations (Gamm, Stone and Pittman 2003; Pleis, Lucas and Ward 2009). However, concerns regarding anonymity and the social stigma that is associated with mental illness in rural areas may prevent elderly individuals from acknowledging the need for formal behavioral health services for anxiety or depressive disorders (Fox et al. 1999; Letvak 2001). These findings support the dissertation emphasis on the physiological and psychological outcomes of disaster affected individuals in socioeconomically and culturally marginalized rural communities that may have differential access to federal resources. The subjective and objective determinants of the Stafford Act related to the demographics of age, income, health status,

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insurance status, and prior exposure to damages indicate that this policy was formulated with an awareness of the uneven recovery outcomes that may be experienced by individuals who are already burdened by varied socioeconomic stressors. This dissertation considers the presence of multiple stress-related physiological disorders that have well-established comorbid presentations with anxiety and depression as a marker of equitable recovery in presidential disaster declared and denied areas of Illinois after the 2008 flood events.

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