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Chemical Sensitivities and Sexual Abuse

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Multiple Chemical Sensitivities and Childhood Sexual Abuse

Mary Ellen Langston


Multiple chemical sensitivity (MCS) is a chronic disorder characterized by a diverse set of symptoms involving multiple systems. Patients respond to low-level exposure to a variety of substances without consistency of laboratory findings. The diagnosis of MCS is controversial in the fields of toxicology, immunology, allergy, psychology, and psychiatry. Definitions, differential diagnosis, and etiological theories have been debated without clear consensus. Symptoms overlap with those of other syndromes (e.g., chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome), and etiology is viewed as either physiological, psychological, or a combination of the two. Studies have demonstrated higher than normal levels of childhood sexual abuse in patients presenting with MCS. Stress-induced sensitization hypothesizes that a traumatic event sensitizes an individual to future symptoms unrelated and less intense than those experienced in the earlier traumatic event.

Multiple chemical sensitivity (MCS) has been considered by some theorists to be an indiscriminate diagnosis that lacks credibility. Those who acknowledge its diagnostic viability assign divergent causal mechanisms (e.g., immune system, neurological, psychological). In a review of theoretical and research literature, Labarge and McCaffrey (2000) assert that a substantial number of individuals with MCS have both physiological and psychological symptoms preexisting the MCS diagnosis, and these symptoms contribute to MCS presentation. Research evidence supports limbic system sensitization as a credible causation mechanism and views psychological variables as contributing to that process (Graveling, Pilkington, George, Butler, & Tannahill, 1999).  

Multiple Chemical Sensitivity 


            The most widely accepted definition of MCS is Cullen’s, who describes MCS as “an acquired disorder characterized by recurrent symptoms, referable to multiple organ systems, occurring in response to demonstrable exposure to many chemically unrelated compounds at doses far below those established in the general population to cause harmful effects” (Labarge & McCaffrey, 2000, p. 185). However, this definition implies specific chemical exposure and excludes patients without that awareness. A more useful definition states that MCS is a chronic multi-system disorder, usually polysymptomatic, caused by adverse reactions to environmental incitants, modified by individual susceptibility and specific adaptation” (Labarge & McCaffrey, p. 186). Graveling et al. (1999) define MCS as a set of symptoms that present in more than one system and are elicited by low levels of multiple, unrelated chemicals. Nethercott, Davidoff, Curbow, and Abbey (1993) suggest a set of five criteria for diagnosis of MCS including: (a) symptoms which are reproducible with exposure to the substance, (b) chronicity of the condition, (c) low exposure levels resulting in symptoms, (d) improvement of symptoms when substance is removed, and (e) includes responses to multiple, unrelated substances. McKeown-Eyssen (2001) state that seven case definitions have been proposed and that these include common features regarding onset, central nervous system involvement, multiple system involvement, chronicity, number of exposures, avoidance leading to symptom relief, multiple substance symptom provocation, addiction, and severity. In addition, Hartman (1995) states that a single test is not able to explain symptoms and determine diagnosis.

Differential Diagnosis and Symptoms

             MCS has been known by other names in the past, such as environmental illness, environmental sensitivity, chemical hypersensitivity, ecologic illness, and total allergy syndrome. Symptoms of other syndromes coincide, overlapping with somatoform disorders, toxicity, and posttraumatic stress disorder. It is difficult to achieve a clear case conceptualization to justify diagnosis (Hartman, 1995; McKeown-Eyssen, 2001; Nethercott et al., 1993). MCS is also referred to as toxicant-induced loss of tolerance (Caress & Steinemann, 2004). Hartman discusses symptom presentations that confound accurate diagnosis in sick building syndrome, mass psychogenic illness, workplace stress and in neurotoxic exposures (e.g., copper, arsenic, lead, manganese, mercury, selenium, zinc). The Interagency Workgroup on Multiple Chemical Sensitivity (1998) links syndromes to the discussion of MCS because of similarity of symptom presentation. These include Sick Building Syndrome, Porphyria, and conditions such as lupus, chronic fatigue, fibromyalgia, and multiple sclerosis. These related syndromes are also called functional somatic syndromes because characteristic symptoms identify their presence more than demonstrable physiological abnormality (Barsky & Borus, 1999).   

            Aaron and Buchwald (2001) reviewed the overlap among unexplained clinical conditions, noting the shared and discrepant symptoms of 12 functional somatic syndromes including chronic fatigue syndrome (CFS), fibromyalgia (FM), irritable bowel syndrome (IBS), MCS, temporomandibular disorder, headache, interstitial cystitis, and post-concussion syndrome. Many similarities exist in definition and symptom presentation. Kipen and Fiedler (1999) present syndromes presenting similar symptoms to MCS: CFS, FM, IBS, atypical connective tissue following breast implants, chronic hypoglycemia, non-specific building-related illness, and Gulf War Illness. Thirty percent of patients with MCS also meet criteria for FM. Patients with MCS, CFS, IBS, FM, and headache share more self-reported diagnoses. Patients with MCS report more physician-diagnosed IBS. Patients with CFS report more MCS symptoms. CFS patients present with comorbid MCS (41%) and FM (16%). (Kipen & Fiedler) also assert substantial overlap among symptoms, stating 30-50% of individuals with CFS, FM, and MCS qualify for either of the diagnoses.  

            Not only does MCS share symptoms with other functional somatic syndromes, but chemical sensitivity is a symptom common to those (e.g., classic neurotoxic syndromes, building-related illnesses, such as Legionnaire’s disease and Pontiac fever; sick building syndrome; mass psychogenic illness; FM, CF; Gulf War Syndrome) (Graveling et al., 1999). In discussing a review of the literature, Labarge and McCaffrey (2000) assert that individuals with MCS are probably a heterogeneous population with a variety of psychological disorders (e.g., somatization, depression, anxiety, dysthymia, PTSD, panic) whether single or combined. To assure appropriate differential diagnosis, they suggest neuropsychological evaluation. Symptoms and prevalence of MCS are highly variable. The most common symptoms include headaches, fatigue, confusion, joint pain, muscular pain, depression, shortness of breath, nausea, dizziness, problems with memory, and gastrointestinal and respiratory symptoms. Other symptoms are also reported such as anxiety and irritability, food craving, itching, and problems sleeping. MCS is more common in women and childhood abuse and trauma are highly represented in patients with this diagnosis. Prevalence appears to be approximately one percent of the population.

             Nethercott et al. (1993) describe symptoms as relating to more than one organ system and nonspecific (e.g., chronic fatigue, headache, upper respiratory complaints, lower respiratory complaints, muscular pain, skeletal pain, gastrointestinal dysfunction). Symptoms are also chronic or recurrent and include chemically unrelated substances such as food, medication, and allergens. Gibson (2005) states that symptoms affect respiratory, digestive, neurological, endocrine, urinary, cardiovascular, and immune systems. Friesen, Madray, and Murphy (2004) describe common MCS symptoms as (a) respiratory problems (e.g., difficulty breathing); (b) flu-like symptoms; (c) ear, eye, nose, throat problems; (c) gastrointestinal problems (e.g.., cramps, diarrhea); (d) neurological problems (e.g., burning, tingling, twitching); (e) cognitive difficulty (e.g., memory loss, confusion, headache, inability to concentrate); (f) mood dysregulation (e.g., irritability, depression); (g) cardiovascular difficulties (e.g., heart irregularity, chest pain); (h) muscle/skeletal problems (e.g., muscle spasms, pain, weakness); (i) tiredness; and (j) skin rashes (p. 10). However, symptoms present differently, including different response to substances, varying levels of disability, varying intensity of symptoms, and varying length of symptom presentation.

          Graveling et al. (1999) states that fifty percent of patients diagnosed with MCS report headache, weakness difficulty in concentrating, difficult remembering, low energy, congestion, sore throat, and joint pain. Thirty percent of MCS patients report abdominal pain, nausea, vision changes, sleep problems, muscle aches, rashes, and problems urinating. Other patients report symptoms from every symptom category

Known and Postulated Etiology

            Ross (2000) reports a review of 425 articles, stating that more than half suggest  physical causation, and less than a quarter state psychogenic basis for MCS. Etiology of MCS is not known, and much conjecture and debate exists around causation. Some assert that MCS is solely a reaction to chemical exposure. Others assert that MCS is not caused by chemicals, but rather is a misdiagnosis of another illness (i.e., psychological, physiological, or both).

             Pall (2005) hypothesizes a tenth paradigm of human disease featuring MCS and related illnesses. Elevated nitric oxide and peroxynitrite facilitate a vicious cycle that explains symptoms of MCS, CFS, FM, PTSD, and Gulf War syndrome. Elevations in these substances usually predict lifetime chronic illness.

            A balanced approach to causation asserts that MCS results from chemical exposure but is mediated by other factors (Labarge & McCaffrey, 2000). Three theories for the causation of MCS have been suggested, and these are (a) immunological, (b) neurological, and (c) psychological (The Interagency Workgroup on Multiple Chemical Sensitivity, 1998). Each of these theories represents the complex systemic nature of inter-relationships between an individual’s body, mind, and emotions, and responses in involved brain regions will result in neurochemical changes that affect the homeostasis of the system.

            Various researchers hypothesize MCS as a (a) psychiatric disorder (i.e., PTSD); (b) sensitization; (c) clinical ecological construct; (d) consequence of CSA; (e) anxiety neurosis; (f) obsessive-paranoid personality presentation; (g) depression; (h) somatoform disorder; (i) somatic disorder with symptom of lowered threshold for irritants; (j) immune system hypersensitivity; (k) or neural damage caused by neurotoxicity (Nethercott et al., 1993). Hartman (1995) states that MCS is explained from the perspective of (a) immune regulation (i.e., autoimmune hypothesis); (b) biochemical imbalance, and (c) psychological disorders (e.g., PTSD, somatoform disorder).

            The MCS syndrome involves multiple symptom presentations including headache, dizziness, difficulty with concentration, and nausea. Subjects use avoidant behaviors, and the hypersensitivity sometimes results in disability. Many common chemicals (e.g., pesticides, solvents, perfumes, new carpet, automotive exhaust, and tobacco smoke) trigger symptoms. Subjects with chemical hypersensitivity are more likely to present with food allergies which are mediated by immunoglobulin-E and G (Bell, 2003). Almost all subjects with MCS present with central nervous system (CNS), respiratory, and gastrointestinal system dysfunction. They also report a higher rate of cardiovascular symptoms, endocrine abnormalities, and musculoskeletal symptoms. A higher number of patients with MCS report physical, sexual, and emotional abuse. Bell’s research demonstrates (a) associations between psychological distress and drug use; (b) correlations between chemical intolerance and the limbic system; (c) higher rates of anxiety and depression; (d) involvement of limbic and mesolimbic  systems; (e) associations between sensitization, cognitive symptoms, and mood symptoms; and (f)  changes in endorphin levels in chemically intolerant individuals. Other researchers view psychological symptoms as a central component of MCS but not the cause (The Interagency Workgroup on Multiple Chemical Sensitivity, 1998).

            Etiological mechanisms suggested for MCS include immune system dysfunction, limbic kindling, and psychological disorders. Clinical ecologists propose an explanation for MCS that includes principles of total load, spreading, switching, adaptation, and bipolarity. Total load includes all physical and psychological stress in the person’s life at the time. Spreading refers to the increasing effect of toxic chemicals on other body systems. Switching describes the chemical’s effect changing from one organ system to another. Adaptation or masking involves growing tolerance for a stressor so that repeated exposures result in reduced effect. Bipolarity refers to transitions from one symptom set to another when the individual is exposed to the chemical, as well as another set of symptoms when the stressor is withdrawn. All of these principles together describe the large variety of somatic, cognitive, and affective symptoms noted in individuals with MCS when exposed to low levels of chemicals (Labarge & McCaffrey, 2000, p. 189).

          The field of clinical immunology views MCS as related to an acquired sensitivity to an antigen or allergen that results in modification of the immune system. This occurs by either inhibiting or enhancing the immune reaction (i.e., immunosuppression or hypersensitivity).  Results of this immune system response involve changes in immunoglobins, complements, or lymphocytes. The mechanism of this change is proposed to be an excitation and irritation of olfactory and airway nerve fibers caused by chemical odor. This reaction stimulates neurogenic inflammation and provokes the immune response. 

          Time-dependent or neural sensitization is another mechanism that has been studied in relationship to CI and MCS (Bell, 2003). Sensitization involves progressive increases in response to repeated exposures to a stimulus in which even minute traces of a substance invokes reactivity. Chemicals, as well as stress, are known to initiate sensitization. Sensitization sometimes involves the mesolimbic system.

         Limbic kindling is an electrical stimulation in the primitive brain in which electrophysiological responses are triggered in response to low-level stimuli (Bell, 1993; Ross, 2000). It is a form of time-dependent sensitization and suggests that permanent increases in limbic neuron excitability are associated with repeated low chemical exposure and stimulation of the olfactory bulb, amygdala, piriform cortex, and hippocampus. The hypothesis involved in limbic kindling postulates that the limbic system is where immune, nervous, and endocrine systems interact, and these are involved with all other body systems. This model proposes that individuals with MCS may have limbic systems that are susceptible to kindling, and that progressive exposures over time result in increased physiological response to the chemical (i.e., sensitization) (Bell, 2003). Neurons are kindled (stimulated to fire) at low levels of stimulation by repeated exposure. It is hypothesized that individuals kindle their olfactory system in this way and become sensitized to common substances when exposed (Gibson, 2005). The mechanism of kindling, although not well-understood, can involve affective, sensory, autonomic, endocrine, immune, motor, and cognitive components depending on the limbic area kindled and the function regulated by that area (Bell, p. 5). 

            Olfactory limbic neural sensitization has been proposed as another model for the mechanism influencing MCS (Graveling et al., 1999). A history of cacosmia (i.e., altered sense of smell; feeling ill when exposed to certain chemical odors) in many MCS patients implicates the olfactory system in the development and maintenance of the systemic dysregulation. Stenn and Binkley (1998) discuss MCS as a phobic response to previously neutral olfactory stimuli. Panic symptoms are learned (conditioned) responses and generalized. This leads to anticipatory anxiety and phobic avoidance. 

          Porphyria is a chronic disturbance in the synthesis of heme, a substance which carries oxygen and is found primarily in the blood and bone marrow. Enzymes are required for the production of heme, and enzyme abnormalities result in several different disorders presenting symptoms similar to MCS. Exposure to substances such as drugs, chemicals, and alcohol and behaviors and internal processes such as emotional and physical stress, menstruation, or sun exposure, are known to trigger the symptoms of porphyria (National Digestive Diseases Information Clearinghouse, 2003). 

          Theories that view MCS as a psychological disorder propose that psychological symptoms are mediated by exposure to a chemical and stress the interactions among biological, psychological, and social variables. Psychological theories suggest that cognitive influences such as attentional focus and selective monitoring are also involved in the manifestation and interpretation of symptoms. Classical conditioning is purported to be involved in MCS. The initial exposure is the unconditioned stimulus; the physical reaction, the unconditioned response; stimuli such as chemical odor, the conditioned stimulus; and the conditioned response, the symptoms prominent in MCS. In the process of stimulus generalization, other substances, including perceptions of odors, become conditioned responses. A two-factor model of classical and operant conditioning explains avoidance of chemicals following the initial response and avoidance behavior negatively reinforced by fear and reduction of symptoms. Somatoform, depressive, posttraumatic stress, and panic disorders have been proposed as psychiatric explanations for MCS. However, opponents of this theory propose that psychiatric symptoms are secondary to physiological dysfunction. Diseases which are difficult to diagnose, such as Lyme disease, often involve multiple systems (i.e., the endocrine, metabolic, nervous, and immune systems), and symptoms manifest in multiple organs.

             Graveling et al. (1999) systematically reviewed several hundred references and evaluated evidence regarding MCS and its etiology. Physiological theories include (a) immunological deficits; (b) respiratory disorder or neurogenic inflammation; (c) toxicant induced loss of tolerance; (d) olfactory-limbic system, kindling, and sensitization models; and (e) porphyria. Psychological theories include conditioned responses and psychiatric disorders. The sensitization model involving the limbic system (both through kindling and non-kindling responses) demonstrates the most evidence. However, psychological factors predispose an individual to illness and influence its progression. Graveling et al. also discuss the potential role of c-fibers as a non-specific pathway involving c-fiber neurons and altered sensitivity to GABA as mediators in the development of MCS.

            In an overview of scientific literature, Fiedler and Kipen (1997) discuss studies addressing the etiology of MCS. In reviewing the literature regarding psychiatric disorders, they note that a significant percentage of patients with MCS do not meet criteria for psychiatric diagnosis. In reviewing neuropsychologic evaluation, neurophysiology, nasal pathology and olfaction, and immune system, they discuss methodologic issues that confound results.

             Aaron and Buchwald (2001) state that the most useful explanatory model for unexplained medical conditions (including MCS) would be a multifactorial model which includes environmental, cultural, biological, psychosocial, and genetic factors (p. 874). Friesen et al. (2004) state that MCS is clearly a result of a combination of mechanisms, including psychological, social, psychoneurological, and that these work in conjunction with individual risk factors and mechanisms. Some theories of physical causation are (a) limbic system mechanisms, (b) neurogenic inflammation, (c) neural sensitization, (d) neural sensitization in combination with nitric oxide/peroxynitrite, (e) biotransformation pathway overload, (f) sensitivity of olfactory threshold, (g) vascular problems, and (h) immune system dysregulation.  

Assessment Techniques

             Treatment of patients with MCS begins with a thorough medical, neuropsychological, and psychological assessment and measures of symptom severity (Labarge & McCaffrey, 2000). Caress and Steinemann (2004) utilized survey questionnaires in a prevalence study and did not attempt to assess true levels of MCS through neurophysiological testing. MCS involves interactions across systems (e.g., CNS and endocrine, metabolic, nervous, and immune systems) and affects neurochemical processes (i.e., hormones, neurotransmitters, and neuromodulators) throughout the brain and body. Physiological tests are used to evaluate and correlate symptom presentations, current and historical physical and psychological status, demographic data, and other variables.

             McKeown-Eyssen (2001) state that physical examination, diagnostic testing, exposure challenges with controlled conditions, and symptom provocation are important to accurate diagnosis. The most definitive assessments determine brain region involvement with MCS. The literature discusses use of (a) electroencephalograms (EEG), (b) single photon emission controlled tomography (SPECT), and (c) positron emission tomography (PET) (Fiedler & Kipen, 1997). Bell (2003) suggests PET scans and MRI studies to identify brain activity and analyze glucocorticoid levels in blood and cerebrospinal fluid. Bell also suggests acute double-blind laboratory testing of CNS reactivity to low levels of chemicals by EEG, SPECT, PET, neuropsychological tests, and studies of cacosmia (Bell, 1993).

            Immune system involvement can be determined through White Blood Cell Counts and Differential Counts which measure leukocytes, neutrophils, lymphocyte, monocytes, eosinophils, and basophils. Each of these types of white blood cells is involved in either inflammatory disorders or allergic reactions which result in either elevation or decreased levels (Pagana & Pagana, 2002). Serum neopterin could be measured in determining levels of inflammation involved in MCS (Bell et al., 1998). Tests to determine immune system involvement in MCS include laboratory measurement of immune markers, including alterations in blood lymphocyte subsets, increases in circulating T-cells, levels of circulating hormones, and abnormal serum antibodies. Nasal biopsies measure cytokines and neuropeptides (The Interagency Workgroup on Multiple Chemical Sensitivity, 1998;, 2006). Fiber-optic rhinoscopy and nasal biopsies detect nasal inflammation (The Interagency Workgroup on Multiple Chemical Sensitivity). C-fibers and GABA could be assessed because of their potential role as mediators in the development of MCS (Graveling et al., 1999).   

             The relationship between the immune system and CI is assessed by measuring blood levels of serum neopterin, a metabolite occurring in polysymptomatic conditions that involve inflammation. Tests to determine immune system involvement in CI and MCS include laboratory measurement of immune markers, including alterations in blood lymphocyte subsets, increases in circulating T-cells, levels of circulating hormones, and abnormal serum antibodies (, 2006; The Interagency Workgroup on Multiple Chemical Sensitivity, 1998).

             White Blood Cell Counts and Differential Counts measure leukocytes, neutrophils, lymphocyte, monocytes, eosinophils, and basophils in the evaluation of immunosuppression. Each of these types of white blood cells is involved in either inflammatory disorders or allergic reactions which result in either elevation or decreased levels (Pagana & Pagana, 2002). Immunoglobins (e.g., IgE, IgG) are classic hallmarks for allergic reactions (Labarge & McCaffrey, 2000). Labarge & McCaffrey also report studies utilizing measures of EEG beta activity; EEG spectral frequencies below 15 hZ; EMG; MRI; PET; nerve conduction; ear, nose, and throat examination; chest and sinus X-ray; respiration rates and inhalation/exhalation nasal resistance; odor discrimination; phenylethyl alcohol threshold; intradermal or sublingual symptom provocation; tests of pulmonary function, levels of carbon dioxide, pulmonary oxygen, and oxygen saturation; and tests of peripheral temperature and skin resistance.

            Testing for the misattribution model includes lactate infusions, carbon dioxide exposures, and measurement of CO2 and cholecystokinin receptor allele 7. Testing for neurogenic inflammation is done with measurement of substance P, calcitonin, and neurokinin A (Bell, 2003). Smell identification tests evaluate the olfactory mechanism’s involvement in CI and MCS. Fiedler and Kipen (1997) report testing subject discrimination of PEA or pyridine, methyl ethyl ketone (MEK), or phenyl ethyl alcohol (PEA) to determine nasal pathology. Bell (2003) suggests (a) PET scans and MRI studies to identify brain activity; (b) blood and cerebrospinal fluid analysis to determine glucocorticoid levels; (c) acute double-blind laboratory testing of CNS reactivity to low levels of chemicals by EEG, SPECT, PET, neuropsychological tests, and studies of cacosmia (Bell, 1993).

            Fiedler and Kipen (1997) suggest neurophysiologic testing which includes electroencephalograms (EEG), single photon emission controlled tomography (SPECT), positron emission tomography (PET), and electromylogram (EMG) to evaluate MCS. The University of Pennsylvania Smell Identification Test has been used to identify difference between patients with MCS and normal subjects. Odor sensitivity is measured by observing detection thresholds for phenyl ethyl alcohol (PEA), methyl ethyl ketone (MEK), or pyridine (PYR). Immune function tests include assessing levels of autoantibodies (e.g., antismooth muscle, antiparietal cell, antimitochrondria); antichemical antibodies (e.g., formaldehyde); T-cell subsets; B-cell subsets; lymphocyte count; and interleukin cells. Genetic testing of MCS patients to determine levels of cholecystokinin receptor allele 7 examine the presence of panic disorder-associated chemicals (Bell, 2003). The intervening mechanism suggested by Pall (2005) indicates the importance of assessing increases in levels of nitric oxide and peroxynitrite, NMDA receptor activity (which increases nitric oxide and peroxynitrite), elevated Nf-kB activity, elevated cytokines, increased vanilloid sensitivity, ATP depletion, and mitochondrial dysfunction. 

Mechanisms of Action 

             Rowat (1998) discusses integrated defense systems (IDS) as communicators between various systems (i.e., nervous, immune, endocrine). This model illustrates the complexity and systemic interconnectedness of the body. The nine IDSs are: time-dependent sensitization (TDS), immune response to antigen (IRA), kindling, nonspecific immune response (NIR), acute-phase response (APR), stress response (SR), neurogenic switching (NS), tolerance (T), and traumatic dissociation (TD).

            Neuroimmune-endocrine interactions involve messengers traveling among IDSs. These include thymic peptides, adrenocorticotropic hormone (ACTH), tumor necrosis factor alpha (TNF), interleukins, β-endorphins, and interferons. These messengers overlap between the systems. Other significant interactions in the IDS are: (a) all IDSs have symptoms that affect more than one system; (b) many IDSs utilize the same neurotransmitters and/or interleukin-1, interferons, ACTH, endorphins, T cells, or substance P; (c) many are incited by the same chemicals; (d) many have similar tolerance, kindling, and traumatic dissociation processes; (e) many have a threshold mechanism (perhaps all); and (f) studies have demonstrated that conditioning occurs in the central nervous system, immune system, and endocrine system.

            Each IDS involves specific brain structures and chemicals. TDS includes neurotransmitters (e.g.., dopamine, norepinephrine, serotonin, GABA); hormones (e.g., ACTH, β-endorphin); immune system. IRA includes T-cells, B-cells, IgA, IgE, IgM, ACTH, substance P, endocrine hormones, and others. Kindling includes the cortex, olfactory bulb, amygdala, acetylcholinesterase, calcium-binding protein, GABA, and others. NIR includes natural killer T-cells, macrophage, TNF, IL-1 through IL-6, histamine, serum proteins, and others. APR includes macrophages, monocytes, mast cells, cytokines, prostaglandins, leukotrienes, glucocorticoids, C-reactive protein, and others. SR includes brain regions (e.g., hypothalamus, limbic system, pituitary gland, adrenal gland, ACTH, β-endorphins, glucocorticoids, catecholamines, and others. NS includes immune system T-cells, B-cells, cytokines, substance P, and others. Tolerance involves multiple mechanisms and organ systems (i.e., all of the nervous, immune, and endocrine systems). TD is an emergency defense system only used during the most severe trauma and involves all of the cerebral organization and affect regulation, causing permanent systemic changes. It may involve all of the brain, endocrine, and immune systems and such chemical messengers as cortisol, ACTH, norepinephrine, and neurotransmitters (e.g., GABA, serotonin). Mechanisms hypothesized by Rowat (1998) to be involved in MCS involve biomarkers and symptoms. IDS mechanisms are grouped as (a) MCS caused by damage to CNS; (b) MCS caused by chemical and stress overload; and (c) MCS caused by evolution and learning.

            The Interagency Workgroup on Multiple Chemical Sensitivity (1998) purports two categories to explain the mechanism involved in MCS: (a) psychological or (b) physiological with psychological components. The immune system, neurological mechanisms, and psychological mechanisms are implicated in the causative processes. One potential mechanism discussed by The Interagency Workgroup on Multiple Chemical Sensitivity is the chemical interaction caused by chemoreceptors on sensory nerves, releasing substance P, and causing neurogenic inflammation. Graveling et al. (1999) summarize theories into two categories, physiological and psychological and then subsume related research findings. Included under physiological theories are (a) immunological deficits; (b) respiratory disorder or neurogenic inflammation; (c) toxicant induced loss of tolerance; (d) olfactory-limbic system, kindling, and sensitization; and (e) porphyria (i.e., group of disorders caused by abnormalities in production of heme, a substance that carries oxygen in the blood and bone marrow).

            The immune system is viewed by researchers as involved in MCS but not a sole determinant. Rather, the immune system is seen as interacting with the neuroendocrine system. Immune response and inflammation are viewed as overlapping processes. Inflammation is viewed as occurring from several mechanisms; however, the primary mechanism is stated to be inflammation caused by irritation of upper airway epithelium (i.e., thin tissue lining organs and cavities) seen as primary. The hypothesis is that a single acute exposure to a chemical results in chronic intolerance to chemicals at low levels. (This is also known as a reactive upper-airways dysfunction syndrome.) Airway inflammation occurs when the chemoreceptors on sensory nerves interact with the chemical. This leads to the release of substance P and other inflammatory mediators such as cytokines and neuropeptides (The Interagency Workgroup on Multiple Chemical Sensitivity, 1998). 

          Neurological mechanisms include the olfactory-limbic model and the neural sensitization model. Neural stimulation is hypothesized to be the mechanism for MCS and is defined as a progressive response to repeated chemical exposures so that low-level exposures initiate higher responses. Limbic kindling is a sub-category of sensitization in which abnormal electrical activity occurs in the brain as a result of the exposure. Time-dependent sensitization of neurochemical, immunological, endocrinological, and behavioral systems involve brain regions (i.e., limbic and mesolimbic brain systems) associated with an individual’s emotions and thought process. Ross (2000) discusses the process of time-dependent sensitization with limbic kindling, a process involving electrical stimulation in the primitive brain. This sensitization is promulgated to be a model for the mechanism of MCS.

          Bell (2003) discusses two mechanisms in MCS: sensitization and neurogenic inflammation. In sensitization, responses are heightened over time with repeated, intermittent exposures to substances. Drugs, chemicals, and stress can initiate sensitization, which involves the mesolimbic system (including the nucleus accumbens). Limbic kindling is a unique form of sensitization in which derealization occurs. Neurogenic inflammation is nonimmunological inflammation and is caused by release of mediators (e.g., neuropeptide, via substance P, calcitonin gene-related peptide, neurokinin A). Bell asserts that these two mechanisms account for a significant amount of the mechanism involved in MCS. Fernandez (1998) investigates the associations between effects of trauma and sensitization as an explanatory model for MCS. Sensitization is defined as “an unusual form of memory, enabling the organism to make an accelerated defense response to a previously experienced threat” (Fernandez, p. 12). The traumatic event is hypothesized to sensitize the individual to other stressors which may act as sensitizing events. In MCS the earlier trauma is thought to sensitize the person to less intense symptoms now presented (due to exposure to substance). 

          Psychological factors are viewed as causative in MCS, result from MCS, predispose an individual to MCS, and co-occur with MCS. Some researchers view MCS as a somatoform reaction or a panic disorder. The literature reports a prevalence of anxiety and/or depression but doesn’t report that these diagnoses preceding MCS. Classical conditioning has been hypothesized as the mechanism promoting MCS in which a conditioned stimulus paired with an unconditioned stimulus creates an unconditioned response with generalization occurring to other stimuli. It appears that psychological theories promote the view that psychiatric symptoms are secondary to a physiological disease process.

              Some researchers see porphyria, a disorder of heme metabolism resulting in GI and psychiatric symptoms, as a mechanism for MCS symptoms. The clinical ecology approach emphasizes specific language and descriptions to define processes viewed as inherent to MCS. These include total load, adaptation, maladaptation, deadaptation, bipolarity of response, spreading, switching, and individual susceptibility. These processes relate to the body’s attempt to deal with the substance, maintain homeostasis, and adapt to the stressor (The Interagency Workgroup on Multiple Chemical Sensitivity, 1998, p. 9-12).  

          Overexposure to toxic chemicals stresses organic systems, disrupting the body’s homeostatic balance. Stress pathways are activated, including organs and brain regions mediating stress (i.e., hypothalamus, amygdala, cortex, hippocampus, locus coeruleus, pituitary gland, adrenal glands, thyroid, thymus, and reproductive glands) and hormones, neurotransmitters, and neuromodulators (i.e., adrenal cortical hormones, epinephrine, glucocorticoid, corticotrophin-releasing hormone (CRH), serotonin, dopamine, norepinephrine). Epinephrine turns on the inflammatory, defensive, and immune systems, and cortisol initiates the anti-inflammatory response. These hormones also impact blood pressure, cholesterol, renal function, digestive and muscle function, and regulation of the heart rate. This series of chemicals is released in a progressive attempt to restabilize the system.

            In a study by Bell (1993), 643 undergraduate college students completed questionnaires which assessed scores for illness that resulted from specific chemical smells, frequency of symptoms, and psychological variables. Data showed that approximately 15% of the students reported feeling ill when smelling common chemicals. Depression and anxiety did not significantly correlate with scores for cacosmia. Time-dependent sensitization and kindling are described as the mechanisms for MCS.

            The effect of emotions on the immune system is well supported in research literature.   The role of cytokines is to regulate inflammation; however proinflammatory cytokines are associated with infection and disease. These cytokines, such as interferon-gamma and interleukin-12 motivate the inflammatory response. Negative emotions directly affect the immune system by causing dysregulation of the secretion of proinflammatory cytokines. However, an indirect effect occurs when prolonged infection results in continued cytokine production bringing even greater health risks to the individual. Research shows that stress results in a decrease in the production of lymphocytes (Pelletier, 2002). Glucocorticoids are released in response to stress and have an effect on the immune system by controlling the number of lymphocytes in the body. The role of glucocorticoids is immunosuppressive in that they suppress the immune system while the body is responding to the threatening situation (i.e., stress). Lymphocytes and neutrophils are the most prevalent type of leukocyte or white blood cell, and white blood cells play a critical role in fighting infection in the body and invasion by foreign bodies. Neutrophils function as phagocytes, killing bacterial organisms. The two types of lymphocytes, B cells and T cells, are involved in the production of antibodies and with the body’s cellular immune response. Caress and Steinemann (2004) state that research suggests MCS develops as a two-step process including initiation, when sensitivity begins, and triggering, when reactions occur after a later exposure to the substance.

Treatment Techniques

             Labarge and McCaffrey (2000) discuss treatment of MCS and state that the hallmark treatment is avoidance to chemicals causing reactions. Avoidance, however, is not an effective strategy because individuals may be reactive to a number of everyday substances and may develop additional chemical reactions through generalized sensitization. Intradermal or sublingual provocation of symptoms is, therefore, a treatment of choice for MCS. Psychological treatment for MCS utilizes cognitive and behavioral techniques (e.g., cognitive restructuring, exposure, response prevention, relaxation, stress inoculation, medication). Labarge and McCaffrey describe the three main treatment tasks as (a) changing behaviors, (b) changing cognitions, and (c) learning how to deal with stressors. Behavioral change involves decreasing behaviors that strengthen symptoms (e.g., avoiding exposure, perceptions of illness, repeated medical visits) and increase behaviors that increase adaptive abilities (e.g., resume work, enjoy leisure activities). Cognitive strategies aim to assist the patient in changing maladaptive thoughts, beliefs, and assumptions. Learning how to deal with stressors involves therapeutic techniques such as stress management training, biofeedback, and relaxation training. Wessely, Nimnuan, and Sharpe (1999) suggest that all functional syndromes respond to the same therapies: (a) engage with the patient and provide education for the physiological nature of the illness and symptoms; (b) offer antidepressant medication; and (c) provide psychological therapy (e.g., cognitive behavioral therapy). Bell (2003) suggests an eight-week intervention that includes (a) self-help program; (b) acupuncture; (c) psychosomatic support therapy group; (d) other patient-centered interventions (e.g., journaling, guided imagery, biofeedback); and (e) inhibitors of substance P and blockers of other neurogenic inflammatory mediators. Girdler et al. (2003) studied the efficacy of 101 treatments used by 917 persons with MCS. Treatments included environmental medicine techniques, nutritional supplements, detoxification techniques, body therapies, Eastern psychology techniques, medication, creating a chemical-free environment, chemical avoidance, and prayer. Stenn and Binkley (1998) report use of cognitive behavioral therapy (i.e., psychological desensitization including relaxation training and visualization) and medication (i.e., selective serotonin reuptake inhibitor) to assist the client in managing panic symptoms. Friesen et al. (2004) discuss treatment options when symptoms are mild, including avoidance of triggers and lifestyle changes. They state that as symptom severity increases, treatment plans may require medical supervision. Suggestions for treatment include (a) lifestyle modification (e.g., avoidance of triggers, changes in environment); (b) accommodation in workplace; (c) nutritional supplements; (d) adequate sleep pattern; (e) healthy, organic diet; (f) restricted diet; (g) exercise; (h) psychotherapy; (i) supportive care; (j) desensitization; and (k) sauna detoxification (p. 14). Pall (2005) suggests the use of antioxidants (e.g., magnesium supplements, dextromethorphan, vitamin B12) as peroxynitrite scavengers that lower NF-kB activity; L-carnitine, complex nutritional supplements, or coenzyme Q10 supplements..   Research Limitations and Recommendations

           MCS research is inconclusive due to sample sizes, inexact selection criteria, bias, lack of control groups, and self-report. Although correlations can be ascertained, determination of causation is not possible. Immunological studies involving test levels of immunoglobulins, lymphocyte, B-cell, and T-cells reflect no consistent pattern of results. Exposure tests have produced no reliable patterns of response. Neuropsychological studies which test visuomotor skills, concentration, and memory also do not produce consistent data. Studies testing for psychological disorders (e.g., somatoform, posttraumatic stress, panic, phobia, anxiety, and depression) are confounded by psychiatric histories predating the MCS and the impossibility of dissecting physiological cause and effect. Due to the lack of consistent research findings, the author proposes research to determine what psychological disorders support the range of MCS symptoms.

           Graveling et al. (1999) assert that significant problems exist in the current analysis of MCS as a disorder. No valid prevalence statistics exist that correspond to the extent of MCS in the general population. Symptom patterns are inconsistent. Also, both doctors and patients use MCS as an “umbrella term” (Graveling et al., p. 75) with varying symptom compilations subsumed in the label. Both qualitative and quantitative data is limited and methods are questionable due to (a) poor exposure information, (b) self-report, and (c) subjective testing protocols. Research suggestions include evaluation of the sensitization process as a causal mechanism and more studies of the limbic system.

          Fiedler and Kipen (1997) discuss methodologic issues involving cross-sectional study designs, subject selection, control selection, laboratory blinding, and techniques utilized. They suggest controlled studies which utilize neurophysiologic testing, including electroencephalograms (EEG), single photon emission controlled tomography (SPECT), positron emission tomography (PET), and electromylogram (EMG) to evaluate MCS.

           Aaron and Buchwald (2001) state that study limitations include inadequate sample sizes which prevent statistical evaluation of relationships. Other methodologic problems include: (a) recruitment procedures, (b) subjective diagnosis, (c) self-report, and (d) referral process.

Child Sexual Abuse

Consequences of CSA

           Child sexual abuse is reported to affect up to 20% of children and adolescents (Paolucci, Genuis, & Violato, 2001). Stop It Now! (2005), an online campaign to prevent sexual abuse,   states that 500,000 children are sexually abused each year. Physiological, neurochemical, and psychological sequela impede healthy childhood development and healthy adult lives for CSA victims. Empirical evidence indicates that sexually abused children experience a wide range of negative consequences including emotional consequences (e.g., guilt, anger, depression, anxiety, helplessness, isolation, inability to trust, loss of self-esteem); behavioral problems (e.g., emotional and behavioral dysregulation, somatic complaints, sleep difficulties and nightmares); and self-destructive behaviors (e.g.,  eating disorders, self-mutilation, suicide attempts, chemical dependency). Previous sexual abuse affects the ability to establish relationships with others and, in many, will affect the future sexual activity of the victim. Other consequences include attachment problems, inability to trust,  academic difficulties,  juvenile delinquency, adult criminal behavior, and a range of other effects and diagnoses (e.g., anxiety disorders, depression disorders, posttraumatic stress disorder, dissociation, conduct disorder, aggression, inappropriate sexual behavior) (Courtois, 2000; Creed et al., 2005; Finkelhor & Browne, 1985; Haugaard & Reppucci, 1988; Heim, Ehlert, Hanker, & Hellhammer, 1998; Herman, 1992; Leserman, 2005; Paolucci et al., 2001; Phillips & Daniluk, 2004; Santrock, 2006; Weiss, Longhurst, & Mazure, 1999).

          Finkelhor and Browne (1985) created a paradigm which delineates four trauma-causing factors of CSA as: traumatic sexualization, betrayal, powerlessness, and stigmatization and postulate that the child’s entire world view is affected by these four aspects. These factors combine to total a huge array of potential symptoms: confusion about sexuality, the child’s feeling of being manipulated by an adult, depression, dependency, mistrust, hostility, vulnerability, anxiety, fear, self-blame, guilt, low self-esteem, nightmares, phobias, somatic complaints, lack of emotionality, learning problems, employment problems, running away from home, aggression, and mimicking the behavior and becoming an abuser. Paolucci et al. theorize that the impact of CSA adheres to a “multifaceted model of traumatization” because consequences are complex and multifaceted (p. 19). 

Adult Somatic Complaints 

               CSA results in long-term medical consequences and adult somatic complaints. Physical illness and disease are predicted based on the brain and chemical physical consequences of childhood trauma. However, hypotheses of ongoing somatic complaints promote theory based on the child’s response to physical violation. When children are intruded on physically, as is the case with abuse, they are vulnerable to later increased concerns about bodily functioning. Some disorders are up to four times more likely to occur in subjects with sexual  abuse histories than in control groups, and the severity of abuse correlates with the severity of somatic complaints (Abraham, Anderson, & Lee, 1997; Creed et al., 2005;  Farley & Keaney, 1997;  Morrison, 1989; Salmon & Calderbank, 1996; Salmon, Al-Marzooqi, Baker, & Reilly, 2003; Sansone, Gaither, & Sansone, 2001; Waldinger, Schulz, Barsky, & Ahern, 2006). Salmon, Skaife, and Rhodes (2002) suggest a causal chain that links CSA, dissociation, and somatization. Early CSA is associated with lifetime rates of somatization disorder (Walker, Carey, Mohr, Stein, & Seedat, 2004). 

               Common somatic complaints. Somatic complaints common to individuals with histories of child sexual abuse include gastrointestinal symptoms (Creed et al., 2005; Leserman, 2005; Reilly, Baker, Rhodes, & Salmon, 1999); headache (Leserman, 2005; Romans, Belaise, Martin, Morris, & Raffi, 2002); and pelvic pain (Ehlert, Heim, & Hellhammer, 1999; Heim et al., 1998). In reviewing the literature, Leserman (2005) found sexual abuse history to be related to headache, gastrointestinal, gynecologic, and panic-related symptoms. Other studies evaluated the relationship between child sexual abuse and physical symptoms associated with: (a) Sphincter of Oddi dysfunction (Abraham et al., 1997; Koszycki, Torres, Swain, & Bradwejn, 2005); (b) premenstrual dysphoric disorder (Girdler et al., 2003); (c) psychogenic non-epileptic seizures (Bailles et al., 2004; Reilly et al., 1999; Salmon et al., 2003); (d) upper abdominal and chest pain (Biggs, Aziz, Tomenson, & Creed, 2003); and (e) gynecologic disorders (Leserman, 2005). In a New Zealand study of medical disorders in women who have experienced child sexual abuse, seven medical conditions were significantly increased in subjects with child sexual abuse histories: chronic fatigue, bladder problems, headache including migraine, asthma, diabetes, and heart problems (Romans et al., 2002). Some theorists attribute these physical symptoms to somatoform disorders.  

            Somatoform Disorders. Somatoform disorders are characterized by the presence of physical symptoms that cause distress but have no diagnosable medical condition to account for the symptoms. CSA is often linked to somatic complaints in studies which investigate somatization disorders, conversion disorders, somatoform pain disorders, and hypochondriasis. A somatization disorder is a chronic condition marked by many physical complaints that persist for years and result in significant impairment. The severity of symptoms can interfere with work and social responsibilities and is usually exacerbated by stress. Research shows that somatization disorders are closely associated to trauma, childhood abuse, and level of family-of-origin functioning (Brown, Schrag, & Trimble, 2005). A conversion disorder usually follows a stressful situation and involves loss of bodily function. In patients studied by Sar, Akyuz, Kundakci, Kizltan, and Dogan (2004), they found that those with conversion disorder manifested symptoms of paralysis, paresthesia, and inability to speak. Over 80% of these patients scored high on dissociation with significant correlations to childhood trauma. Patients with somatoform pain disorders exhibit chronic pain that limits functioning, and the pain is rooted in psychological factors. In patients with chronic pain, the trauma of childhood sexual abuse is hypothesized as the root factor marking the continuance of irresolvable physical complaints. Pelvic pain, chest pain, pain from irritable bowel pain, and generalized pain have been studied, and factors of dissociation, somatization, and childhood trauma have marked correlations (Biggs et al., 2003;   Ehlert et al., 1999; Heim et al., 1998; Zlot, Herrmann, Hofer-Mayer, Adler, & Adler, 2000). Hypochondriasis is viewed as the patient’s belief that symptoms, whether real or imagined, are signs of serious illness. Salmon and Calderbank (1996) studied the relationships between childhood abuse, somatization, and hypochondriasis and found abuse history to be a significant risk factor for adult illness. Noyes et al. (2003) found significant correlation between insecure attachment and hypochondriacal symptoms.

Concurrent Factors in Women with Childhood Sexual Abuse History

               Posttraumatic stress disorder. It is well known that individuals who have experienced

childhood sexual abuse are at increased risk for posttraumatic stress disorder (Bowman, 1993;   Diseth, 2005; Hetzel & McCanne, 2005; Johnson, Pike, & Chard, 2001; Pintor & Bailles, 2005;  Silberg, 2000) and PTSD influences physical adult health (Bailles et al., 2004; Heim et al., 1998). The National Comorbidity Survey (NCS) studied 5,877 subjects, and data revealed that subjects in the PTSD group had a higher frequency of negative health outcomes (Lauterbach, Vora, & Rakow, 2005). Research has shown that the ability of individuals to cope effectively with distress is closely associated to PTSD symptoms, dissociation, and somatization  (Farley & Keaney, 1997).

               Research shows that one-half of all diagnosed PTSD involves women who have been sexually assaulted, a significant proportion having occurred during childhood. PTSD’s maladaptive characteristics include reexperiencing the trauma, avoidance, and increased arousal (i.e., sleep difficulty, irritability, anger, hypervigilance, startle response) and significant negative effects on daily functioning (Brunello et al., 2001). PTSD results in hypothalamic-pituitary-adrenal (HPA) axis alterations, alterations in neuroanatomical structures and neural pathways, reductions in hippocampal volume, dysfunctions in noradrenergic and dopaminergic functioning, elevated glucocorticoid levels, and changes in benzodiazepine and opiate receptors (Heim et al., 1998; O'Donnell, Hegadoren, & Coupland, 2004; Horner & Hamner, 2002).        

         Dissociation. A close relationship between dissociation and somatic complaints can be hypothesized within the context of the utility of dissociation as a coping mechanism. Often used by children experiencing sexual abuse, dissociation is effective as a means of removing them psychologically from the source of pain and can become a persistent coping mechanism (Briere, Scott, & Weathers, 2005; Diseth, 2005; Farley & Keaney, 1997; Johnson et al., 2001; Panzer & Viljoen, 2004; Pappas, 2002; Pintor & Bailles, 2005). Dissociation involves disruption in normal external information processing in order to sustain an absorbed inner attention, suggesting a divided consciousness or a mind-body split (Pappas, 2002). With dissociation the survivor has been able to escape the pain, both in the moment of abuse (i.e., peritraumatic dissociation) and ongoing, but, because the dissociated state prevents awareness, it contributes to secondary problems such as somatization in the adult life. 

         Farley and Keaney (1997) found that dissociation and chronic physical symptoms were positively correlated in subjects with a history of sexual abuse and that the more severe the abuse, the greater the number of physical symptoms reported. Brosschot and Aarsse (2001) report significant links between somatization, dissociation, and restricted emotional response. (Waller et al., 2000) examined the link between childhood trauma, somatoform disorders, and dissociation and suggest that somatoform dissociation is an adaptive psychophysiologic response to trauma. In their study of psychophysiological stress response, Kanbara et al. (2004) found a significant positive relationship between dissociation and somatic disorders. Bowman (1993) views pseudoseizures as originating from dissociation related to memories of abuse and triggered by current life stress.

        The literature contains a preponderance of research validating the presence of concurrent dissociation with childhood sexual abuse, somatization, and other mental health disorders, including posttraumatic stress disorder (PTSD) (Bailles et al., 2004; Brown et al., 2005; Farley & Keaney, 1997). Dissociation and the report of chronic physical symptoms are positively correlated in subjects who have a sexual abuse history. The number of times, period of time the abuse occurred, and severity of sexual abuse are additional factors influencing the number, severity, and intractability of physical symptoms. Miliora (1998) discusses the connection between dissociation resulting from sexual trauma and its use in the process of somatization. Abuse, dissociation, and somatization have been linked as a causal chain in many physical symptom presentations (Pribor, Yutzy, Dean, & Wetzel, 1993; Romans et al., 2002;  Salmon et al., 2003; Sar et al., 2004). Pribor et al. (1993) found that two-thirds of patients with dissociative disorders also met criteria for somatization disorder.

        Ineffective coping strategies. Closely related to the discussion of dissociation are ineffective coping strategies utilized with women with histories of sexual abuse. Longstreth, Mason, Schreiber, and Tsao-Wei (1998) studied the effects of group psychotherapy in women molested in childhood and found psychological functioning, coping techniques, and somatization significantly improved. Farley and Keaney (1997) found that women presenting with PTSD, dissociation, and somatization used pathologic coping strategies. Romans et al. (2002) found immature coping strategies and dissociation to be important factors in certain somatic complaints. Diseth (2005) associated dysfunctional stress response and emotion-based functioning with childhood abuse, dissociation, PTSD, and somatization disorders.

               Attachment. Childhood trauma is associated with insecure attachment to caregivers in childhood and high levels of somatization. A biopsychological explanation for attachment disorders is explained by the increased cortisol present during stress. Serum cortisol increases glucose and impedes the function of the hippocampus, resulting in hippocampal damage and causing impaired social skills, impulsivity, and aggression (Weber & Reynolds, 2004). The development of insecure attachment to caregivers leaves the child vulnerable to somatization in adulthood. A possible explanation for this correlation may be that the abused child develops a self-image as unworthy of support, a conceptualization of adult caregivers as unreliable or dangerous, a fearful attachment style, characteristics of neediness, minimization of negative emotions, a compensatory focus on physical sensations, and a care-seeking style for perceived physical symptoms (Waldinger et al., 2006). It has been hypothesized that illness during childhood results in positive attention and temporary escape from neglect or abuse and becomes an effective coping strategy for the child because it results in relief and comfort. This learned strategy may shape the way the child relates to others and may influence adult response to medical providers (Noyes et al., 2003; Waldinger et al., 2006). Access to medical professionals has been hypothesized as continued learned childhood patterns of ineffective attachment.                 

               Anxiety and depression. Other common symptoms of childhood sexual abuse are anxiety and depression. In a community study involving 62,651 participants, the relationships between somatic complaints, anxiety, and depression were examined. Approximately one-third of somatic complaints treated were without organic explanation, and anxiety and depression are usually present in these cases. In this study, Haug, Mykletun, and Dahl (2004) found a strong         association between anxiety, depression, and functional somatic symptoms. Other studies have established significant correlations between abuse, somatic disorders, and mood disorders (Sar et al., 2004; Zlot et al., 2000). Thieme, Turk, and Flor (2004) found three to four times the general prevalence of depression and anxiety in patients with fibromyalgia and correlated mood disorders with somatic complaints, PTSD, and sexual abuse.

Neurobiology and Child Sexual Abuse

          Childhood sexual abuse results in significant damage to the brain including degeneration of neurons, neurochemical abnormalities, neuroendocrine disturbances, alterations to brain structure, and release of high levels of glucocorticoids harming the hippocampal formation (Weber & Reynolds, 2004). Repeated stress results in maladaptive stress responses,   homeostatic failure, and limbic system hyperarousal. Dissociation results in impaired development of neural networks, primitive parasympathetic regulation by the dorsal motor nucleus, and lack of integration of bodily sensations (Panzer & Viljoen, 2004). Neurobiological findings link childhood trauma, dissociation, PTSD, and somatization. In reviewing the literature, Diseth (2005) found evidence of permanent trauma-related neurochemical and functional changes in the brain. These findings clarified the cerebral mechanisms involved in trauma and dissociation and the subcortical processes linking these to PTSD and somatoform disorders. Studies show that PTSD results in both neuroendocrine and neurochemical alterations. Changes include decreased levels of cortisol, increased responsiveness of glucocorticoid receptors, and high glucocorticoid levels; increased sensitivity of HPA negative feedback inhibition; increased excretion of noradrenalin, adrenalin, and dopamine; increased noradrenaline following stress; abnormal catecholamine activity; abnormal arousal mechanisms in the sympathetic nervous system; abnormal hemispheric laterality; altered dopaminergic functioning; elevated cortisol; reduced immunosuppression; increased release of aminopeptide; increased release of ACTH; alterations in serotonergic metabolism; reduced volume in the hippocampal region; hyperresponsivity in the amygdala; and altered function in the limbic region (Brunello et al., 2001; Horner & Hamner, 2002; O'Donnell et al., 2004; Pappas, 2002; Weber & Reynolds, 2004). It appears that lack of cortisol as a protective factor contributes to the development of bodily disorders in women who have been traumatized (Heim et al., 1998). Bremner et al. (1999) found that women with CSA and PTSD show brain alterations which include (a) increased activation in posterior cingulate, anterolateral prefrontal cortex, and motor cortex; (b) deactivation in subcallosal gyrus region of anterior cingulate, (c) failure to activate anterior cingulate, and (d) deactivation in the right hippocampus, fusiform/inferior temporal gyrus, supramarginal gyrus, and visual association cortex (p. 1790). Women with CSA with and without PTSD show activation in the cerebellum, temporal pole, left inferior frontal gyrus, and thalamus while listening to scripts of CSA. PET studies show that the medial prefrontal cortex is involved in stress and emotion. This dysfunction in women with CSA is associated with the glucocorticoid and sympathetic stress response. Hippocampal volume is also smaller and declarative memory function impaired in subjects with CSA and PTSD. Decreases of yohimbine appear to be related to the decreased hippocampal metabolism. .   

               The literature elaborates on the dynamic relationship between trauma and the brain and explains the neurochemical and neuroendocrine components linking trauma, dissociation, and somatization (Saxe et al., 1994). Patients presenting with somatization disorders and childhood abuse histories exhibit significant lower resting norepinephrine (NE) level, greater NE reactivity to mental stress, and greater adrenoceptor responsivity (Girdler et al., 2003). This study suggests that even one traumatic abuse incident results in adequate stress to effect ongoing alterations in sympathetic and HPA axis responsivity to stress. Individuals with CSA, PTSD, and somatization disorder demonstrate HPA axis alterations (Heim et al., 1998).    

Intersecting MCS and CSA

         Individuals with MCS report significantly higher rates of physical and sexual abuse (Bell, 2003; Fiedler & Kipen, 1997). Studies find that patients with MCS present with somatization disorder, depression, and PTSD initiated by CSA (Bell, Baldwin, Russek, Schwartz, & Hardin, 1998). Fernandez, Bell, and Schwartz (1999) studied the sensitization model, hypothesizing that previous trauma (i.e., CSA) sensitizes limbic pathways. Graveling et al. (1999) assert that a very high incidence of CSA is discovered during treatment of MCS, and that results of one study showed 60% of patients with CSA. Righter and Sansone (1999) state that early developmental abuse (e.g., sexual, physical, witnessing domestic violence) is the most predictive factor for adult somatic complaints. Bell (2003) reports that individuals with MCS present with increased rates of CSA. Fernandez (1998) investigated associations involved in sensitization with trauma (e.g., CSA) as a necessary condition to sensitize limbic/mesolimbic pathways. EEG measures demonstrated abnormal limbic activity upon chemical exposure, supporting the hypothesis of stress-induced sensitization to future stress. Nethercott et al. (1993) state that research studies identify multiple etiological possibilities, one of which is that it is a consequence of CSA. Stenn and Binkley (1998) discuss the importance of prior psychological trauma in MCS. CSA is sometimes forgotten, repressed, or denied, but it facilitates a chronic hyperarousal state, thus decreasing the threshold for sensitivity reactions. It is hypothesized that an originally neutral stimulus is paired with traumatic stimuli, and hyperarousal occurs through an olfactory triggering process. The individual then develops a learned response, misattributing meaning to the event, and not recognizing the link to prior psychological events. The process is then promoted by anticipatory anxiety of future reactions, leading to phobic avoidance. Thorson (1999) discuss a study comparing subjects with and without CSA, and evaluating associations between sexual and physical abuse, somatization, and symptom presentations characteristic of IBS and non-epileptic seizures. Adults presenting with functional neurological syndromes and abdominal symptoms have greater percentage of CSA than controls. Wessely et al. (1999) state that CSA is more common in women with functional syndromes than in controls. Brown (2004) states that CSA and other physical and emotional abuse are correlated with unexplained illness. Rowat (1998) discusses the involvement of dissociation (a) as a defense system; (b) its involvement in the etiology of PTSD and other psychological disorders (i.e., borderline personality disorder, dissociative personality disorder); and (c) the shared factor of CSA. Research has shown that CSA produces permanent biological changes and is linked to adult psychiatric dysfunctions.


Aaron, L. A., & Buchwald, D. (2001). A review of the evidence for overlap among unexplained clinical conditions.
Annals of Internal Medicine, 134
(9), 868-880.

Abraham, H. D., Anderson, C., & Lee, D. (1997). Somatization disorder in Spincter of Oddi dysfunction.
Psychosomatic Medicine, 59
(5), 553-557.

Bailles, E., Pintor, L., Fernandez-Egea, E., Torres, S., Matrai, S., de Pablo, J., et al. (2004). Psychiatric 
disorders, trauma, and MMPI profile in a Spanish sample of nonepileptic seizure patients. General Hospital 
Psychiatry, 26
(4), 310-315.

Barsky, A. J., & Borus, J. F. (1999). Functional somatic syndromes. Annals of Internal Medicine, 
(1), 910-921.

Bell, I. R. (1993). Self-reported illness from chemical odors in young adults without clinical syndromes
or occupational exposures. Archives of Environmental Health, 1, 1-8. Retrieved August 18, 2006, from

Bell, I. R. (2003). Multiple chemical sensitivities. Psychiatric Times, 20(1), 1-7. Retrieved August 18, 2006, 

Bell, I. R., Baldwin, C. M., Russek, L. G., Schwartz, G. E., & Hardin, E. E. (1998). Early life stress, 
negative paternal relationships, and chemical intolerance in middle-aged women: Support for a neural 
sensitization model. Women's Health, 7(9), 1135-1147. Retrieved August 16, 2006, from PubMed

Bell, I. R., Patarca, R., Baldwin, C. M., Klimas, N. G., Schwartz, G. E. R., & Hardin, E. E. (1998). 
Serum neopterin and somatization in women with chemical intolerance, depressives, and normals.
Neuropsychobiology, 38
(1), 13-18.

Biggs, A., Aziz, Q., Tomenson, B., & Creed, F. (2003). Do childhood adversity and recent social 
stress predict health care use in patients presenting with upper abdominal or chest pain?
Psychosomatic Medicine, 65
, 1020-1028.

Bowman, E. S. (1993). Etiology and clinical course of pseudoseizures: Relationship of trauma, 
depression, and dissociation. Psychosomatics: Journal of Consultation Liaison Psychiatry, 34(4), 333-342.

Bremner, J. D., Narayan, M., Staib, L. H., Southwick, S. M., McGlashan, T., & Charney, D. S. (1999). 
Neural correlates of memories of childhood sexual abuse in women with and without posttraumatic stress 
disorder. The American Journal of Psychiatry, 156(11), 1787-1795.

Briere, J., Scott, C., & Weathers, F. (2005). Peritraumatic and persistent dissociation in the presumed 
etiology of PTSD. American Journal of Psychiatry, 162, 2295-2301. Retrieved September 22, 2006

Brosschot, J. F., & Aarsse, H. R. (2001). Restricted emotional processing and somatic attribution 
in fibromyalgia. International Journal of Psychiatry in Medicine, 31(2), 127-146.

Brown, R. J. (2004). Psychological mechanisms of medically unexplained symptoms. Psychological 
Bulletin American Psychological Association, 130
(5), 793-812. Retrieved April 10, 2006, from

Brown, R. J., Schrag, A., & Trimble, M. R. (2005). Dissociation, childhood interpersonal trauma, and family functioning in patients with somatization disorder. The American Journal of Psychiatry, 162(5), 899-905.

Brunello, N., Davidson, J. R. T., Deahl, M., Kessler, R. C., Mendlewicz, J., Racagni, G., et al. (2001). Posttraumatic stress disorder: Diagnosis and epidemiology, comorbidity, and social consequences, biology, and treatment. Neuropsychobiology, 43, 150-162.

Caress, S. M., & Steinemann, A. C. (2004). Prevalence of multiple chemical sensitivities: A population-based study in the southeastern United States. American Journal of Public Health, 94(5), 746-747.

Courtois, C. A. (2000). The sexual after-effects of incest/child sexual abuse. SIECUS Report, 29(1), 11-16.

Creed, F., Guthrie, E., Ratcliffe, J., Fernandes, L., Rigby, C., Tomenson, B., et al. (2005). Reported sexual abuse predicts impaired functioning but a good response to psychological treatments in patients with severe irritable bowel syndrome. Psychosomatic Medicine, 67(3), 490-499.

Diseth, T. H. (2005). Dissociation in children and adolescents as reaction to trauma: An overview of conceptual issues and neurobiological factors. Nordic Journal of Psychiatry, 59(2), 79-91.

Ehlert, U., Heim, C., & Hellhammer, D. H. (1999). Chronic pelvic pain as a somatoform disorder. Psychotherapy and Psychosomatics, 68(2), 87-94.

Farley, M., & Keaney, J. C. (1997). Physical symptoms, somatization, and dissociation in women survivors of childhood sexual assault. Women & Health, 25(3), 33-45.

Fernandez, M. (1998). EEG measures of subjects with idiopathic chemical sensitivity: A test of the sensitization model. Dissertation Abstracts International, 59(04), 1904.

Fernandez, M., Bell, I. R., & Schwartz, G. E. (1999). EEG sensitization during chemical exposure in women with and without chemical sensitivity of unknown etiology. Toxicology of Individual Health, 15(3-4), 305-312. Retrieved August 16, 2006, from PubMed

Fiedler, N., & Kipen, H. (1997). Chemical sensitivity: The scientific literature. Environmental Health Perspectives, 105(2), 409-415.

Finkelhor, D., & Browne, A. (1985). The traumatic impact of child sexual abuse. American Journal of Orthopsychiatry, 55, 530-541.

Friesen, M. K., Madray, S. A., & Murphy, D. (2004). Multiple Chemical Sensitivity (MCS): An Overview. Retrieved September 22, 2006, from

Gibson, P. R. (2005). Understanding & Accommodating People With Multiple Chemical Sensitivity in Independent Living. Retrieved August 18, 2006, from inet

Girdler, S. S., Sherwood, A., Hinderliter, A. L., Leserman, J., Costello, N. L., Straneva, P. A., et al. (2003). Biological correlates of abuse in women with premenstrual dysphoric disorder and healthy controls. Psychosomatic Medicine, 65(5), 849-856.

Graveling, R. A., Pilkington, A., George, J. P. K., Butler, M. P., & Tannahill, S. N. (1999). A review of multiple chemical sensitivity. Occupational Environmental Medicine, 56(1), 73-85.

Hartman, D. (1995). Neuropsychological Toxicology: Identification and Assessment of Human Neurotoxic Syndromes (2nd). New York: Plenum Press.

Haug, T. T., Mykletun, A., & Dahl, A. A. (2004). The association between anxiety, depression, and somatic symptoms in a large population: The Hunt-II study. Psychosomatic Medicine, 66(6), 845-851.

Haugaard, J. J., & Reppucci, N. D. (1988). The sexual abuse of children. San Francisco: Jossey-Bass.

Heim, C., Ehlert, U., Hanker, J. P., & Hellhammer, D. H. (1998). Abuse-related posttraumatic stress disorder and alterations of the hypothalamic-pituitary-adrenal axis in women with chronic pelvic pain. Psychosomatic Medicine, 60(3), 309-318.

Herman, J. L. (1992). Trauma and recovery. New York: Basic Books.

Hetzel, M. D., & McCanne, T. R. (2005). The roles of peritraumatic dissociation, child physical abuse, and child sexual abuse in the development of posttraumatic stress disorder and adult victimization. Child Abuse & Neglect, 29(8), 915-930. Retrieved March 2, 2006, from Proquest

Horner, M. D., & Hamner, M. B. (2002). Neurocognitive functioning in posttraumatic stress disorder. Neuropsychology Review, 12(1), 15-30.

Johnson, D. M., Pike, J. L., & Chard, K. M. (2001). Factors predicting PTSD, depression, and dissociative severity in female treatment-seeking childhood sexual abuse survivors. Child Abuse & Neglect, 25(1), 179-198. Retrieved March 2, 2006, from Proquest

Kanbara, K., Mitani, Y., Fukunaga, M., Ishino, S., Takebayashi, N., & Yoshihide, N. (2004). Paradoxical results of psychophysiological stress profile in functional somatic syndrome: Correlation between subjective tension score and objective stress response. Applied Psychophysiology and Biofeedback, 29(4), 255-268.

Kipen, H. M., & Fiedler, N. (1999). Invited commentary: Sensitivities to chemicals - Context and implications. American Journal of Epidemiology, 150(1), 13-16.

Koszycki, D., Torres, S., Swain, J. E., & Bradwejn, J. (2005). Central cholecystokinin activity in irritable bowel syndrome, panic disorder, and healthy controls. Psychosomatic Medicine, 67(4), 590-595.

Labarge, A. S., & McCaffrey, R. J. (2000). Multiple chemical sensitivity: A review of the theoretical and research literature. Neuropsychology Review, 10(4), 183-211.

Lauterbach, D., Vora, R., & Rakow, M. (2005). The relationship between posttraumatic stress disorder and self-reported health problems. Psychosomatic Medicine, 67(6), 939-947.

Leserman, J. (2005). Sexual abuse history: Prevalence, health effects, mediators, and psychological treatment. Psychosomatic Medicine, 67(6), 906-915.

Longstreth, G. F., Mason, C., Schreiber, I. G., & Tsao-Wei, D. (1998). Group psychotherapy for women molested in childhood: Psychological and somatic symptoms and medical visits. International Journal of Group Psychotherapy, 48(4), 533-541.

McKeown-Eyssen, G. E. (2001). Multiple chemical sensitivity: Discriminant validity of case definitions. Archives of Environmental Health, 56(5), 406-412. (2006). Multiple Food and Chemical Insensitivities. Retrieved August 8, 2006, from

Miliora, M. T. (1998). Trauma, dissociation, and somatization: A self-psychological perspective. Journal of the American Academy of Psychoanalysis & Dynamic Psychiatry, 26(2), 273-293. Retrieved February 14, 2006, from Proquest

Morrison, J. (1989). Childhood sexual histories of women with somatization disorder. The American Journal of Psychiatry, 146(2), 239-241.

National Digestive Diseases Information Clearinghouse. (2003). Porphyria. Retrieved August 18, 2006, from

Nethercott, J. R., Davidoff, L. L., Curbow, B., & Abbey, H. (1993). Multiple chemical sensitivities syndrome: Toward a working case definition. Archives of Environmental Health, 48(1), 19-26.

Noyes, R., Stuart, S. P., Langbehn, D. R., Happel, R. L., Longley, S. L., Muller, B. A., et al. (2003). Test of an interpersonal model of hypochondriasis. Psychosomatic Medicine, 652(2), 292-300.

O'Donnell, T., Hegadoren, K. M., & Coupland, N. C. (2004). Noradrenergic mechanism in the pathophysiology of post-traumatic stress disorder. Neuropsychobiology, 50(4), 273-283.

Pagana, K. D., & Pagana, T. J. (2002). Mosby's manual of diagnostic and laboratory tests. St. Louis, MO: Mosby.

Pall, M. L. (2005). Multiple chemical sensitivity: Towards the end of controversy. Retrieved September 18, 2006, from LookSmart

Panzer, A., & Viljoen, M. (2004). Dissociation: A developmental psychoneurobiological perspective. South African Psychiatry Review, 7(3), 11-17. Retrieved March 2, 2006, from African Journals Online

Paolucci, E. O., Genuis, M. L., & Violato, C. (2001). A meta-analysis of the published research on the effects of child sexual abuse. The Journal of Psychology, 135(1), 17-36.

Pappas, J. D. (2002). Dissociative consciousness: The mind-body split in childhood abuse trauma. Dissertation Abstracts International, 40(04), 1079.

Pelletier, K. R. (2002). Mind as healer, mind as slayer: MindBody medicine comes of age. Advances, 18(1), 4-15.

Phillips, A., & Daniluk, J. C. (2004). Beyond "survivor": How childhood sexual abuse informs the identity of adult women at the end of the therapeutic process. Journal of Counseling and Development, 82(2), 177-184.

Pintor, L., & Bailles, E. (2005). Patients with psychogenic non-epileptic seizures: What happens to them? In T. A. Corales (Ed.), Focus on Posttraumatic Stress Disorder Research (pp. 225-244). Hauppauge, NY: Nova Science.

Pribor, E. F., Yutzy, S. H., Dean, J. T., & Wetzel, R. D. (1993). Briquet's syndrome, dissociation, and abuse. The American Journal of Psychiatry, 150(10), 1507-1511.

Reilly, J., Baker, A., Rhodes, J., & Salmon, P. (1999). The association of sexual and physical abuse with somatization: Characteristics of patients presenting with irritable bowel syndrome and non-epileptic attack disorder. Psychological Medicine, 29(2), 399-406.

Righter, E. L., & Sansone, R. A. (1999). Managing somatic preoccupation. American Family Physician, 59(11), 1-11. Retrieved September 18, 2006, from

Romans, S., Belaise, C., Martin, J., Morris, E., & Raffi, A. (2002). Childhood abuse and later medical disorders in women. Psychotherapy and Psychosomatics, 71(3), 141-150.

Ross, G. H. (2000). Response to errors prevalent in the understanding of environmental illness. Retrieved August 18, 2006, from

Rowat, S. C. (1998). Integrated defense system overlaps as a disease model: With examples for multiple chemical sensitivity. Environmental Health Perspectives, 106(1), 1-48. Retrieved September 18, 2006, from

Salmon, P., & Calderbank, S. (1996). The relationship of childhood physical and sexual abuse to adult illness behavior. Journal of Psychosomatic Research, 40(3), 329-336.

Salmon, P., Al-Marzooqi, S. M., Baker, G., & Reilly, J. (2003). Childhood family dysfunction and associated abuse in patients with nonepileptic seizures: Towards a causal model. Psychosomatic Medicine, 65(4), 695-700.

Salmon, P., Skaife, K., & Rhodes, J. (2002). Abuse, dissociation, and somatization in irritable bowel syndrome: Towards an explanatory model. Journal of Behavioral Medicine, 26(1), 1-18.

Sansone, R. A., Gaither, G. A., & Sansone, L. A. (2001). Childhood trauma and adult somatic preoccupation by body area among women in an internal medicine setting: A pilot study. International Journal of Psychiatry in Medicine, 31(2), 147-154.

Santrock, J. W. (2006). Life-Span Development (10th ed.). New York: McGraw-Hill.

Sar, V., Akyuz, G., Kundakci, T., Kizltan, E., & Dogan, O. (2004). Childhood trauma, dissociation, and psychiatric comorbidity in patients with conversion disorder. The American Journal of Psychiatry, 161(12), 2271-2276.

Saxe, G. N., Chinman, G., Berkowitz, R., Hall, K., Lieberg, G., Schwartz, J., et al. (1994). Somatization in patients with dissociative disorders. The American Journal of Psychiatry, 151(9), 1329-1334.

Silberg, J. L. (2000). Fifteen years of dissociation in maltreated children: Where do we go from here? Child Maltreatment, 5(2), 119-136. Retrieved March 2, 2006, from Proquest

Stenn, P., & Binkley, K. (1998). Successful outcome in a patient with chemical sensitivity. Psychosomatics, 39(6), 547-550.

Stop It Now! (June 6, 2005). Retrieved December 4, 2005, from http://www.stopitnow/csafacts.html:

The Interagency Workgroup on Multiple Chemical Sensitivity. (1998). Theories of causation and mechanisms. In A Report on Multiple Chemical Sensitivity (MCS) (chap. III). Retrieved August 18, 2006, from

Thieme, K., Turk, D. C., & Flor, H. (2004). Comorbid depression and anxiety in fibromyalgia syndrome: Relationship to somatic and psychosocial variables. Psychosomatic Medicine, 66(1), 837-844.

Thorson, M. (1999). Somatization caused by sexual abuse. Psychological Medicine, 29(2), 399-406.

Waldinger, R. J., Schulz, M. S., Barsky, A. J., & Ahern, D. K. (2006). Mapping the road from childhood trauma to adult somatization: The role of attachment. Psychosomatic Medicine, 68(1), 129-135.

Walker, J. L., Carey, P. D., Mohr, N., Stein, D. J., & Seedat, S. (2004). Gender differences in the prevalence of childhood sexual abuse and in the development of pediatric PTSD. Archives of Women's Mental Health, 7, 111-121.

Waller, G., Hamilton, K., Elliott, P., Lewendon, J., Stopa, L., Waters, A., et al. (2000). Somatoform dissociation, psychological dissociation, and specific forms of trauma. Journal of Trauma and Dissociation, 1(4), 81-98.

Weber, D. A., & Reynolds, C. R. (2004). Clinical perspectives on neurobiological effects of psychological trauma. Neuropsychology Review, 14(2), 115-129.

Weiss, E. L., Longhurst, J. G., & Mazure, C. M. (1999). Childhood sexual abuse as a risk factor for depression in women: Psychosocial and neurobiological correlates. The American Journal of Psychiatry, 156(6), 816-828.

Wessely, S., Nimnuan, C., & Sharpe, M. (1999). Functional somatic syndromes: One or many? The Lancet, 354(1), 1-6. Retrieved September 18, 2006, from

Zlot, S. I., Herrmann, M., Hofer-Mayer, T., Adler, M., & Adler, R. H. (2000). Childhood experiences and adult behavior in a group of women with pain accounted for by psychological factors and a group recovered from major depression. International Journal of Psychiatry in Medicine, 30(3), 261-275.