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Early life stress, negative paternal relationships, and chemical intolerance in middle-aged women: support for a neural sensitization model.

  [ 24 votes ]   [ Discuss This Article ]
By Bell IR, Baldwin CM, Russek LG, Schwartz GE, Hardin E. • • November 1, 1999

This study (n total = 35) compared early life stress ratings, parental relationships, and health status, notably orthostatic blood pressures, of middle-aged women with low-level chemical intolerance (CI group) and depression, depressives without CI (DEP group), and normals. Environmental chemical intolerance is a symptom of several controversial conditions in which women are over represented, that is, sick building syndrome, multiple chemical sensitivity, chronic fatigue syndrome, and fibromyalgia. Previous investigator shave postulated that people with CI have variants of somatization disorder, depression, posttraumatic stress disorder (PTSD) initiated by childhood abuse or a toxic exposure event. One neurobehavioral model for CI, somatization disorder, recurrent depression, and PTSD is neural sensitization, that is, the progressive amplification of host responses (e.g., behavioral, neurochemical) to repeated intermittent stimuli (e.g., drugs, chemicals, endogenous mediators, stressors).

Females are more vulnerable to sensitization than are males. Limbic and meso-limbic pathways mediate central nervous system sensitization. Although both CI and DEP groups had high levels of life stress and past abuse, the CI group had the most distant and weak paternal relationships and highest limbic somatic dysfunction subscale scores. Only the CI group showed sensitization of sitting blood pressures over sessions. Together with prior evidence, these dataare consistent with a neural sensitization model for CI in certain women.

The findings may have implications for poorer long-term medical as well as neuropsychiatric health outcomes of a subset of women with CI. Subsequent research should test this model in specific clinical diagnostic groups with CI.

J Womens Health 1998 Nov;7(9):1135-47.
Department of Psychiatry, University of Arizona, Tucson, USA.

PMID: 9861591, UI: 99078584

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