Early Life Stress, Negative Paternal Relationships, and Chemical Intolerance in Middle-Aged Women: Support for a Neural Sensitization Model

Abstract

This study (ntotal = 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 overrepresented, that is, sick building syndrome, multiple chemical sensitivity, chronic fatigue syndrome, and fibromyalgia. Previous investigators have 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 mesolimbic 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 data are 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.

Annoyance and performance during the experimental chemical challenge of subjects with multiple chemical sensitivity

“…It is unclear whether this finding indicates the presence of a subtle brain dysfunction in multiple chemical sensitivity. A vulnerability to conditioning and sensitization due to a deviation in the functioning of the limbic system has been suggested (28). Such vulnerability could be explained in different ways.…”

Deranged Dimensionality of Vestibular Re-Weighting in Multiple Chemical Sensitivity

“…For instance, many studies have tried to find an unifying pathophysiology for all IEIs, focusing on CNS reactions to environmental stimuli, with activation changes of the brain areas related to sensory processing and emotional responses [1,[5][6][7][8][9][10][11][12][13][14][15]41,42]. Since environmental noise has been recognised as an important health quality stressor [43], relevant literature up to now has focused mainly on auditory symptoms [21,22] without highlighting possible vestibular and postural consequences.…”

“…Possible explanations for the rearranged model along vestibular processing and symptoms cohort referred to by MCS patients could be considered to reside within pathophysiological cascades, such as those involving limbic structures in the natural history of MCS [1,[4][5][6][7][8][9][10][11][12][13][14][15]. According to these notions, repeated exposure to MCS inducing agents were found to provide in MCS subjects both time-dependent sensitization and kindling, especially within hippocampal and limbic areas [65].…”

“…According to these theories, several studies in the last few years have shown cerebral blood flow distribution abnormalities in patients with MCS, especially while processing odorous substances [10][11][12]. In particular, MCS sufferers have been seen to react peculiarly to sensory stimuli, with activation of brain areas connected with motivational, emotional and non-conscious processing of information, such as the amygdala and the hippocampus, encompassed in the limbic system [10][11][12][13][14], whose pathways are known to mediate CNS sensitization and their dysregulation contributes to abnormalities of behaviour and mood, endocrine, autonomic and immune function [15].…”

“…Thus, due to (i) the overlapping psychogenic and organic burdens that, below the level of consciousness, are shared not only in MCS development but also in the vestibular disorders [1,[10][11][12][13][15][16][17]20]; (ii) the number of previous studies describing central processing impairment related to inner ear inflow in this syndrome [21,22]; and (iii) the lack of literature on clinical evidence of the presentation of dizziness [2,3], the purpose of the present exploratory study was to highlight the possible MCS hidden clinical/subclinical aspects of vestibular impairment by inferential and principal component (PC) analysis applied on the contribution of recently implemented otoneurological testings. This, with the aim of disclosing possible implementations in diagnosing and monitoring undiscovered aspects underpinning the natural history of MCS, will possibly assist in suggesting future treatment choices in a clinical setting.…”