Effects of Long term Stress

Effects of Long term Stress - We have just examined some of the major physiological changes that occur in response to the perception of stress. What do these changes mean? Although the short-term mobilization that occurs in response to stress originally prepared humans to fight or flee, rarely do stressful events requre these kindsof adjustments. Consequently, in response to stress, we often experience the effects of sudden elevations of circulating stress hormones that, in certain respect, do not serve the purpose for which they were originallyintended.

Stress

many thoughts create stress

Over the long term, excessive discharge of epinephine and norepinephrine can lead to suppression of celular immune functions; produce hymodynamic changes,such as increased blood pressure and heart rate; provoke variations in normal heart rhythms, such as ventricular arrhythmias, which may be a precusrsor to sudden death: and produce neurochemichal imbalances that may contribute to the development of psychiatric disorders. The catecholamines may also have effects on lipid levels and free fatty acids, all of which may be important in the development of atherosclerosis.

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Corticosteroids  have immunosuppressive affects, which can compromise the functioning of the immunensystem. Prolonged cortisol secretion has also been related to the destruction of neurons in the hippocampus. This destruction can lead to problems in verbal functioning, memory, and concentration, (Starkman, Giordani, Brenent, Schork & Schreingart, 2001) and may be one of the merchanisms by which the senility that sometimes occurs in old age sets in. Pronounced HPA activation is common in depression, with episodes of cortisol secretion being more frequent and of longer duration among depressed than nondepressed people, although it is not entirely clear whether HPA activation is a cause or an effect of these disorders. Another longterm consequence of the endocrine abnormalities that result from chronic HPA activation is the storage of fat in central visceral areas, rather than to the hips. Accumulation leads to a high waist-to-hip ratio, which is used by some researchers as a maker for chronic stress (Bjorntorp, 1996).

Which of these responses to stress have implications for desease? Several researchers (Dienstbier, 1989; Frankenhaeuser, 1991) have suggested that the health consequences of HPA axis actvation. Sympathetic adrenal in response to stress may not be a pathway for desease; HPA activation may be required as well. Some researchers have sugessted that this reasoning explains why exercise, which produces sympathetic arousal but not HPA activation, is protective for health rather than health compromising.

Stress may also impair the immune system capacity to respond to hormonal signals that terminate inflammation. A study that demonstrates this point compared 50 healthy adults, half of whom were parents of cancer patients and, the other helf, parents of healthy children. Childhood cancer is known to be one of the most stressfulevents that parents encounter. The parents of the cancer patients reported more stress and flatter daily slopes of cortisol secretion than was true for the parents of healthy children. Moreover, the ability to suppress production of a proinflammatory cytokine called IL-6 was diminised among parents of the cancer patients. Because proinflammatory cytokines are implicated in a broad array of desease, these findings suggest that the impaired ability to terminate inflammantion may be another pathway by which stress affects illness outcomes (G. E. Miller, Cohen, & Ritchey, 2002).