Lourdes Salvador's Column
...Co-founder of MCS America discusses the latest Multiple Chemical Sensitivity issues.
Lourdes Salvador volunteers as a writer and social advocate for the recognition of multiple chemical sensitivity (MCS). She was a passionate advocate for the homeless and worked with her local governor to provide services to the homeless through a new approach she created to end homelessness. That passion soon turned to advocacy and activism for people with MCS and the medical professionals who serve them. She co-founded MCS Awareness in 2005 and went on to found MCS America in 2006. She serves as a partner for Environmental Education Week, a partner for the Collaborative on Health and the Environment (CHE), and a supporter for the American Cancer Society: Campaign for Smokefree Air.
Chronic Fatigue Syndrome Diagnosis and Treatment - Part 2
by Lourdes Salvador
The pathogenesis of CFS is uncertain and likely multi-factorial. Conditions that have been proposed to trigger the development of CFS include viral infection, immune disorders, hypothalamic-pituitary adrenal (HPA) axis dysfunction, and toxic exposure.
CFS is similar to many infections, including Epstein-Barr (EBV), human retroviruses, human herpesvirus 6, enteroviruses, rubella, Candida albicans, bornaviruses, and Mycoplasma. No one virus has been linked to every case of CFS; however, CFS may the result of post-viral infection from a variety of virus’.[1,10] Many studies have uncovered a flu-like sickness that precedes the onset of CFS. It is believed that a virus may trigger and lead to chronic activation of the immune system and altered cytokine production. 
“An alteration in cytokine profile, a decreased function of natural killer (NK) cells, presence of autoantibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported” in CFS.[11,12]
Various triggering events such as a traumatic injury or viral infection may lead to the chronic expression of cytokines and then to CFS. Serum chemokine and cytokine profiles have identified a distinct pathogen associated signature for the inflammatory serum chemokines, as well as the pro inflammatory cytokines. High levels of pro-inflammatory cytokines may explain fatigue and flu-like symptoms.
Studies have reported immune cell phenotype changes and NK cell dysfunction as common manifestations of CFS. Studies have shown that CFS patients are more likely to have a history of co-occurring allergies than are healthy controls, though not all CFS patients have allergies.[1
There may also be a disorder in the early activation of the immune system involving protein kinase C.
Hypothalamic-Pituitary Adrenal (HPA) Axis
Physical or emotional stress is frequently reported just prior to the onset of CFS. CFS patients produce lower levels of cortisol than do healthy controls which influences the immune system, behavior, and other body systems.  While the levels are lower, they are still within the normal range.
HPA axis is involved in the adaptive responses to stress. CFS patients report exacerbation of symptoms after physical and psychological stress. One study showed that CFS patients are capable of producing a sufficient cortisol response under some types of stress, but an overall subtle dysregulation of the HPA axis exists.
The HPA axis deregulation may exacerbate or perpetuate symptoms. Cortisol acts to suppress inflammation and cellular immune activation. Supplementary cortisol has been shown to temporarily alleviate fatigue.
Neurally Mediated Hypotension
Many patients with chronic fatigue syndrome (CFS) have neurally mediated hypotension when subjected to head-up tilt and disturbances of autonomic regulation of both blood pressure and pulse.[1,17]
A study performed by Michael Maes found that the functional symptoms of CFS have a genuine organic cause in the activation of peripheral and central inflammatory and oxidative and nitrosative stress pathways and gut-derived inflammation.
1. Centers for Disease Control and Prevention. Chronic Fatigue Syndrome. 2008, November 18. Retrieved January 21, 2009, from FirstGov -- The U.S. Government's Official Web Portal Department of Health and Human Services “Safer Healthier People” Centers for Disease Control and Prevention. Web site: http://www.cdc.gov/cfs/
2. Nisenbaum R, Jones JF, Unger ER, Reyes M, Reeves WC. A population based study of the clinical course of chronic fatigue syndrome. Health Qual Life Outcomes. 2003;1:49.
3. Buchwald D, Pearlman T, Umali J, Schmaling K, Katon W. Functional status in patients with chronic fatigue syndrome. Am J Med. 1996;101:364-370.
4. Christodoulou C, DeLuca J, Lange G, et al. Relation between neuropsychological impairment and functional disability in patients with chronic fatigue syndrome. J Neurol Neurosurg Psychiatr. 1998;64:431-434.
5. Reeves WC, Jones JF, Maloney E, et al. Prevalence of chronic fatigue syndrome in metropolitan, urban, and rural Georgia. Popul Health Metr. 2007;5:5.
6. Reyes M, Nisenbaum R, Hoaglin DC, et al. Prevalence and incidence of chronic fatigue syndrome in Wichita, Kansas. Arch Intern Med. 2003;163:1530-1536.
7. Jones JF, Nisenbaum R, Solomon L, Reyes M, Reeves WC. Chronic fatigue syndrome and other fatiguing illnesses in adolescents: a population based study. J Adolesc Health. 2004;35:34-40.
8. Myhill S, Booth NE, McLauren-Howard, J. Chronic Fatigue Syndrome and Mitochondrial Dysfunction. Int J Clin Exp Med (2009) 2, 1-16.
9. Lombardi VC, Redelman D, White DC, Fremont M, DeMerirleir K, Peterson D, and Mikovits JA. Serum cytokine and chemokine profiles of individuals with myalgic encephalomyelitis (ME) reveal distinct pathogen associated signatures. September 2008:43(3):245.
10. Sairenji T, Nagata K. Viral infections in chronic fatigue syndrome] Nippon Rinsho. 2007 Jun;65(6):991-6.
11. Lorusso L, Mikhaylova SV, Capelli E, Ferrari D, Ngonga GK, Ricevuti G. Immunological aspects of chronic fatigue syndrome. Autoimmun Rev. 2009 Feb;8(4):287-91. Epub 2008 Sep 16.
12. Barker E, Fujimura SF, Fadem MB, Landay AL, Levy JA. Immunologic abnormalities associated with chronic fatigue syndrome. Clin Infect Dis. 1994 Jan;18 Suppl 1:S136-41.
13. Mihaylova I, DeRuyter M, Rummens JL, Bosmans E, Maes M. Decreased expression of CD69 in chronic fatigue syndrome in relation to inflammatory markers: evidence for a severe disorder in the early activation of T lymphocytes and natural killer cells. Neuro Endocrinol Lett. 2007 Aug;28(4):477-83.
14. Van Den Eede F, Moorkens G, Van Houdenhove B, Cosyns P, Claes SJ. Hypothalamic-pituitary-adrenal axis function in chronic fatigue syndrome. Neuropsychobiology. 2007;55(2):112-20. Epub 2007 Jun 27.
15. Cleare AJ. The HPA axis and the genesis of chronic fatigue syndrome. Trends Endocrinol Metab. 2004 Mar;15(2):55-9.
16. Gaab J, Hüster D, Peisen R, Engert V, Heitz V, Schad T, Schürmeyer TH, Ehlert U. Hypothalamic-pituitary-adrenal axis reactivity in chronic fatigue syndrome and health under psychological, physiological, and pharmacological stimulation. Psychosom Med. 2002 Nov-Dec;64(6):951-62.
17. Davis SD, Kator SF, Wonnett JA, Pappas BL, Sall JL. Neurally mediated hypotension in fatigued Gulf War veterans: a preliminary report. Am J Med Sci. 2000 Feb;319(2):89-95.
18. Maes M. Inflammatory and oxidative and nitrosative stress pathways underpinning chronic fatigue, somatization and psychosomatic symptoms. Curr Opin Psychiatry. 2009 Jan;22(1):75-83.
For more articles on this topic, see: MCSA News.
Copyrighted 2009 Lourdes Salvador & MCS America