- Last Updated: 05 December 2015 05 December 2015
Seiki Tajima of Osaka, Japan, launched the meeting with a study of activity monitoring and autonomic responses in sleep. Patients wore an activity monitor (similar to a pedometer, but worn on the wrist), which was able to discriminate periods of activity, rest, and sleep during a 24-hour period. Tajima was able to identify at least 5 types of abnormal sleep patterns in persons with CFS (PWCs), including a long-sleeping type, severe insomnia, hypersomnia, and sleep phase-shifting. Autonomic (that is, R-R spectrum) analysis revealed that poor sleep may be due to a lack of parasympathetic activity during attempted sleep periods.
Nicole Porter (DePaul University, Chicago) queried PWCs and healthy individuals about their experience of fatigue. She was then able to define at least 5 different fatigue states:
- Wired fatigue—feels over-stimulated but low energy
- Brain fog fatigue—mental or cognitive impairment is associated with fatigue
- Molasses fatigue—heaviness and immobilization, unable to prolong activity
- Flu-like fatigue—weakness with flu-like symptoms
- Post-exertional fatigue—a lack of energy following minor activity
Healthy individuals experienced only one type of fatigue (typically flu-like), while PWCs experienced fatigue in diverse ways.
Elizabeth Mahoney described a CDC-sponsored study of the effect of allostatic load. One's "allostatic load" is essentially your accumulated stressors. However, the CDC used objective measures (such as heart rate, blood pressure, C-reactive protein levels, waist-to-hip ratio, lipid levels, blood sugar, insulin levels, etc.) as a measure of "load." Based on this premise, women with a high allostatic load were 5 times more likely to develop CFS/ME compared to those with low allostatic loads. This did not hold true for men, however. Mahoney also pointed out that this study demonstrated a high prevalence of metabolic syndrome in PWCs. [Metabolic syndrome is characterized by central obesity, elevated cholesterol and triglycerides, elevated blood sugar; and the presence of metabolic syndrome frequently predicts later diabetes and cardiovascular disorders such as heart attack and stroke.]
Margaret Chicorella, both an exercise physiologist and an attorney from University of the Pacific, Stockton, CA, demonstrated how disability could be better defined using a two-part exercise test. When cardio-pulmonary exercise testing is repeated 24+ hours after the first test, oxygen consumption and the maximum achievable heart rate both decrease substantially. This is objective evidence of post-exertional malaise—a sine qua non of CFS/ME/FM—and could be very useful in disability determinations.
Paul Nestadt (Mt.Sinai School of Medicine, NYC) used Magnetic Resonance Spectroscopy (1H-MRS) to show that lactate is increased and N-acetyl-aspartate (NAA) is reduced in the brains of PWCs (persons with CFS/ME). Lactate levels correlated with the level of fatigue, and were not abnormal in persons with depression or anxiety. These findings are further evidence that CFS/ME is not psychiatric in origin, and that mitochondrial function and neuronal density (or metabolism) are reduced in PWCs.
Dubbo is small city in the northwest corner of New South Wales, Australia, and has been the site of several epidemiological studies concerning the clinical course of EBV mononucleosis (a DNA virus) and Q-fever (a rickettsial infection). Toni Whistler of the CDC described genetic findings in persons who developed PIFS, or Post-Infectious Fatigue Syndrome, which is very similar to CFS/ME. 30,000 genes were studied, and more than 40% of the pathways were found related to regulatory and metabolic pathways. Cell cycle regulation, gene regulation, and signaling were most commonly involved; and apoptotic, metabolic, and inflammatory (IL 10) pathways were prominent in the sickest patients. Whistler concluded that there is a subset of PIFS in which immune abnormalities play a significant role.