Theories of Environmental Illness.
The clinical ecology literature discusses a variety of theories and concepts to explain both the etiology and pathogenesis of environmental illness. Initially Randolphproposed a theory that failure of the human body to adapt to industrial synthetic chemicals produces a condition of hypersensitivity to these chemicals. This theory does not explain the mechanism of the hypersensitivity, and there has been no evidence up to now to support it.
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A variety of immunologic mechanisms has been proposed to explain IEI. In general, these theories are made under the presumption that environmental chemicals function as haptens to induce formation of IgG antibodies, IgE antibodies, or specifically sensitized T cells. However, the pattern of illness and the absence of any objective evidence of inflammation or organ dysfunction do not support immunologic hypersensitivity in IEI. Furthermore, there has been no evidence of a quantitative or qualitative abnormality of either specific antibodies or a cellular immune response to any of the numerous environmental agents that these patients identify as a cause of their illness. There is an autoimmune theory derived from an unconfirmed report of circulating immune complexes or autoantibodies in some patients with IEI. Disturbance of the normal intrinsic regulation of the immune response is another theory of disease causation, but there is no evidence to support this theory, nor is there evidence of abnormal immune function or immune deficiency.
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These theories subsume additional concepts that are unique to the field of clinical ecology: total body load, chemical overload, masked food sensitivity, and spreading phenomenon. They are employed to explain the lack of a consistent dose-response relationship between the perceived chemical exposure and the symptoms but are inconsistent with modern concepts of immunology. The concepts of total body load and chemical overload are made under the assumption that the immune system has a fixed capacity to handle a limited quantity of environmental antigen and that exceeding it provokes symptoms. Masked food sensitivity is a term used to explain the fact that sometimes a patient may react adversely to a food when it is eaten after several days of abstention, whereas frequent ingestion of the same food causes these symptoms to disappear. These concepts are sometimes referred to collectively as “adaptation-deadaptation,” but they have never been explained physiologically or even been documented as a valid observation. Spreading phenomenon is a concept that exposure to one environmental substance induces or predisposes to immune responses to other unrelated environmental substances and is used to explain periods of an increasing number of symptoms in the absence of environmental changes.
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Several nonimmunologic theories have been proposed. These include (1) deficiency of antioxidants induced by the generation of free radicals by environmental chemicals, drugs, and foods; (2) neurotoxicity caused by endogenous beta-endorphin “sensitization” induced by environmental stimuli, odor-induced “kindling” of olfactory-limbic neural pathways, immunologic-to-neurogenic inflammation “switching” mediated by neuropeptides; (3) end-organ dysesthesia involving the nasal mucosa, lung, the entire respiratory tree, or multiple organs; and (4) hereditary coproporphyria. None of these theories are supported by experimental or controlled clinical studies.
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