By Gail Kansky

     For years, there were those who argued that abrupt onset CFIDS/ME and gradual onset CFIDS/ME resulted in different diseases.  Abrupt onset patients argued they were more severe while gradual onset insisted it just took more time for them to progress to severe.  And then there were those who argued that the cluster epidemics of CFIDS/ME were different than those who fell sick in sporadic and isolated onsets.  Science is pointing to the direction for both of these answers and they point to one main cause and one main illness with few differences. 

     The first research to answer the question of gradual vs. abrupt onset was the work on the ciguatera epitope that was published in 2003 in the Journal of Clinical Laboratory Analysis (Hokama et al.) where patients were tested for chronic phase lipids which indicated the high presence of a ciguatera-type toxin in their blood.  The patients were chosen, carefully, by two investigative physicians chosen by The National CFIDS Foundation, Derek Englander, M.D. and Edward Jordan, M.D.  They included patients from well-known cluster epidemics who had an abrupt onset as well as patients from other areas that had both gradual and abrupt onset.  Nearly 100% of the patients were found to be positive!  Some with a gradual onset had some strikingly high levels found of the endogenous lipid that was so similar to ciguatera but some with an abrupt onset also tested for the high levels.  In this major study, onset circumstances made no difference.

     The questions continued to be asked about those from clusters versus those from non-clusters.  The same year, 2003, a paper was published that showed the two, again, were identical diseases.  Under a block grant from the National Institutes of Health to the Roswell Park Cancer Institute, a study was funded and published called "Predictive Immunophenotypes:  Disease-Related Profile in Chronic Fatigue Syndrome" by Stewart et al.  Knowing that immune dysfunction plays a large part in CFIDS/ME, the researchers wanted to know why variable inconsistencies were found in past studies and if the event that triggered the illness led to separate or similar diseases. The Centers of Disease Control and Prevention put out a brochure that says, "Several investigators have reported lower numbers of natural killer cell activity or decreased naturals killer cell activity among CFS patients compared with healthy controls, but others have found no differences between between patients and controls." The researchers had a new tool at their disposal by 2003:  three-color flow cytometry.  To make the study particularly unique, they looked at patients from a large city and compared them to patients from a small cluster outbreak (Buffalo and Lyndonville, New York) to see if differences could be found in the number of cell types, the patterns of cell subsets and their absolute numbers and to compare the health status of both groups.

     To make sure that the healthy samples were really in a different category, they made sure none of them had been, even remotely, in contact with patients such as living with someone who had an undiagnosed illness.  The controls were also matched for age and sex.  Both patients and controls completed the Sickness Impact Profile (SIP) which is a reliable self-report  measure that shows the impact of an illness on a daily functioning.  As expected, the controls all tested well in the SIP and the patient groups both reported higher levels of health-related psychosocial dysfunction.  Those from the cluster epidemic tested higher than the Buffalo patients. 

    When the study reported on the T-cells along with NK (natural killer) cell subsets of CD8, "a somewhat different pattern emerged" yet the differences were not found between the cluster and non-cluster groups to account for the number of NK cells that lacked the CD8.  Instead, severity seemed to be the indicator as the numbers correlated with the SIP scores.  This NK cell decrease has been known to happen among cigarette smokers and the elderly but there has also been evidence of it in a number of autoimmune illnesses including multiple sclerosis, lupus, type 1 diabetes and rheumatoid arthritis.  While there were some cytotoxic T-cell subset differences found between the two groups, the outcome points to "a common etiological agent(s) yet to be identified."  Other past studies that showed inconsistencies in their results were not as carefully controlled. For example, in this study, even the blood draw of patients was carefully done at the same time of day.  The study only examined four cell phenotypes but it did suggest some factors of why some got sick while others did not.  The bottom line, however, was that patients from a cluster outbreak along with those who got sporadically sick from a large, metropolitan area, had the same disease.  From Lyndonville to Louisville and Buffalo to Boise, ME/CFIDS is the same disease.