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PHOENIX RISING: A CFS/ME/FM Newsletter by Cort Johnson (Oct. 2006)

http://capwiz.com/cfids/issues/alert/?alertid=8548931&type=CU

 Exercise and CFS – Check out this excellent overview of post-exertional fatigue in CFS. It includes ways that many CFS patients can use to bolster their health. Done by Lucinda Batemen, a well-known CFS physician, on the International Association of Chronic Fatigue Syndrome website. We don’t get overviews like this often. http://www.aacfs.org/p/260.html

 Check Out the Latest CFSAC Meeting – the CFSAC is the committee that advises the Department of Health and Human Services on CFS. http://www.cfids.org/advocacy/cfsac-nov06.asp

 Agenda Set for the Big CFS Conference – check out who’s speaking at the big event! – the 2-year International CFS Conference in  Florida starting Jan 10^th. It looks like everyone’s going to be there. http://www.aacfs.org/p/224.html

 Eat Your Vegies – New study shows that eating veggies may help stem brain decline as we age – http://news.yahoo.com/s/ap/20061023/ap_on_he_me/diet_vegetables_aging

 Cheney DVD Available - A 2-disc DVD set of Dr. Cheney’s latest seminar "CFS: The Heart of the Matter" is available. The prices quoted below are in US dollars and include shipping. ($13 - $16 within the US; $13 - $18 to Canada; Australia and New Zealand yet to be determined; $16 - $18 all other countries.)

This seminar contains an overview of CFS, an in-depth look at the cardiovascular issues in CFS; a new model of the illness, and a full update on Dr. Cheney's latest study, including the treatment protocol. Dr. Cheney also addresses the following: sleep issues, blood volume, candida, Chlamydia, Lyme, MCS, FM, GWS, phenotypic and genotypic changes in DNA, hyperbaric oxygen, and the use of stem cells from umbilical cord blood. http://www.dfwcfids.org/videos/video200609cheney_about.shtml

New Research Study -  “Immunological and Genetic Analysis of Autoinflammatory Genes In Fibromyalgia” CenterWatch - In the Los Angeles area, biomedical researchers are embarking on a three-year investigation involving selected patients of Fibromyalgia specialist R. Paul St. Amand, MD – developer of the “Guaifenesin Protocol.”™ The research (listed as study # 80703 at CenterWatch.com) addresses the theory that FM may be triggered by trauma or chronic infection that causes changes in a “family of genes” now known to be associated with prolonged inflammation. The City of Hope site provides the following summary of the study (italics ours) at http://clinicaltrials.coh.org/study_display.aspx?pid=3715518 Or at http://www.immunesupport.com/library/showarticle.cfm/ID/7428

RESEARCH

 RESEARCH – Unless otherwise noted the research summaries are by Cort Johnson, a laymen and CFS patient. Submissions from others are gratefully accepted. Comments, suggestions, clarifications, etc, negative or positive, only add to the editors and others understanding of CFS. Please send them to Phoenixcfs@yahoo.com).

Rating The Months Research - D

A – several difference making papers on CFS pathophysiology / B – a difference making  paper on CFS pathophysiology plus several important ones / C -  several important papers on CFS pathophysiology / D – 1 or no important papers on CFS pathophysiology but several on other aspects of CFS / F – no important papers on CFS

THE PAPERS

 DEATH AND CFS

Studies have shown that there is a lot of disability in CFS - that people are really hurting. It doesn’t seem possible that so much pain and torment would not ‘catch up’ with one at some point. Researchers are finally beginning to address whether or not having CFS shortens one’s lifespan.

Jason, L., Corradi, K., Gress, S., Williams, S. and S. Torres-Harding. 2006. Causes of death among patients with Chronic Fatigue Syndrome. Health Care For Women International 27: 615-626.

The sample set for this study was the National CFIDS Foundation’s Memorial list. This list was composed of 166 people with CFS whose deaths were reported to the NCF by a relative or friend. Most did not appear to have died of CFS per se; they died of another disease such as heart disease or cancer, etc. The information on the list is quite variable – some of it is quite precise; much of it is very vague. We don’t know much about these people; where they lived, who diagnosed them with CFS, how long they’d had CFS, if they came down with CFS before or after they developed the disease that ultimately killed them, etc. It is a very vague data set and, speaking as a laymen, I was surprised to see it used as the basis of a scientific study, but Jason – a well published researcher – felt it might say something about CFS.

These researchers found three major causes of death: heart disease, cancer and suicide, each of which accounted for about 20% of the deaths on the list. They found that these people died at a dramatically earlier age than would be expected; 25 years earlier on average for the cancer and heart disease patients, and 9 years earlier for people who died of suicide. Since the average age of death from CFS was in the forties – about the age of the average CFS patient according to the CDC - this could suggest that CFS rapidly works to predispose people to serious disease and death. The authors pointed out how some of the abnormalities seen in CFS might contribute to the health problems that ultimately killed these patients.

These were very startling figures and very startling figures always raise a red flag suggesting that methodological or sampling problems may be present. Could CFS patients really be dying so young?  We know that some certainly do (click here) but is everyone with CFS at risk from an early death?  The authors noted that neither CFS physicians nor researchers, some of whom now have 20 years experience with CFS, have reported increased mortality rates in their patients. Nor did the neurasthenic (aka CFS) physicians of 100 years ago report early deaths due to CFS.

After listing a number of provisos regarding the vague nature of the sample set, the authors closed the paper by stating “Clearly it is not possible to generalize the data from this memorial list to the overall population of patients with CFS”.  This study, then, did not tell us about CFS patients in general. Instead it suggested that this unusual mortality picture is a subject that should get some attention. Fortuitously we did have a mortality study come out right after this – and this one did have a strong statistical foundation.

Smith, W., Noonan, C. and D. Buchwald. 2006. Mortality in a cohort of chronically fatigued patients. Psychological Medicine 36: 1301-1306.

These researchers followed a group of 1201 CFS and CFS-like patients for an average of 9 years. At the end of that period they assessed how many had died and what they had died of. They found that three percent, or 38, had died: 9 of cancer, 9 by suicide, 3 of heart disease, etc. Neither the number of deaths nor the type of death was significantly different than would be expected in the general US population; this study, then, found that CFS does not predispose one to any of the major diseases that cause mortality or to an early death.

One subgroup did die earlier than expected; fatigued people who did not meet the criteria for CFS but were depressed had increased mortality rates – from suicide.

While this good news it does seem counterintuitive. How could a disease that causes so much distress not ultimately effect mortality? The authors noted that since people with CFS by definition do not have most major medical conditions that we know are associated with death that they might in fact be expected to have normal or even lower than normal mortality rates.

This appears to make sense.  Modern medicine is probably very good at assessing the presence of the major diseases that cause death. The standard blood work we are all familiar with is designed to pick up evidence of commonly occurring serious problems – tests that CFS patients usually pass with flying colors. Their ability to do so is one indication that they may have a disease that while associated with a lot of misery it is not necessarily with increased mortality.

Just because you have CFS doesn’t mean, however, that you can’t have another major disease as well. A recent CDC study found that 17% of CFS patients diagnosed between 1997 and 2000 had developed exclusionary factors (i.e. major depression, heart problems, etc., that would have kept them from participating in a research study in 2003. That shows that CFS patients do – as does every group – develop major health problems as they age. This present study indicates, however, that CFS patients don’t appear to develop more of them than would be expected.

There is one disorder that is relatively commonly found in CFS that is usually associated with increased rate of death - mood disorder. Although increased rates of mood disorder are strongly associated with early death due to suicide, the suicide rate, oddly enough, was not increased among the CFS patients. The authors declined to speculate why this should be so but could it suggest that mood disorder is over diagnosed in CFS? It was interesting that while the lifetime rate of major depression in these CFS patients was quite high (55%) the percent of CFS patients currently with depression was not very high (14%). Could the high rate of lifetime depression diagnosis in CFS be due to the tendency of physicians to use the ‘depression card’ in patients whose illness they cannot explain?

A Laymen’s Speculations – But what about all the abnormal findings in CFS, the RNase L fragmentation rates, the low NK cell functioning, the T-cell activation? What about the low brain blood flows, the reduced brain volumes, the viral infections, etc.?  How to account for these? We don’t really know what long term effects many of these have – it may be that they don’t cause mortality. Several of the viruses proposed to act in CFS, for instance, are opportunistic pathogens that may be more adept at causing misery than mortality.

The heart problems seem to be in a different class. Dr. Cheney has reported high rates of heart failure in CFS and heart failure is a progressive, serious disease that almost always ends in early death. Yet even here CFS seems different. Dr. Cheney has stated he has never in his 20 years of treating CFS seen a case of heart attack. He believes CFS patients are locked into a low energy state that is protective in nature and that precludes their heart problems from progressing. Despite the plethora of findings indicating problems in CFS it appears possible that they are not the kind of problems that kill people – they just debilitate them.

Paper of the Month

 EXERCISE IN CFS AND FIBROMYALGIA

Cook, D., Nagelkirk, P., Poluri, A., Mores, J. and B. Natelson. 2006. The influence of aerobic fitness and fibromyalgia on cardiorespiratory and perceptual response to exercise in patients in chronic fatigue syndrome. Arthritis and Rheumatixm 54, 3351-3362.

Dr. Natelson, the former head of the NIH-sponsored New Jersey CFS research center, has been looking at how CFS patients respond to exercise for several years now. Although thus far he has mostly failed to find consistent evidence of cardiorespiratory or metabolic dysfunction during exercise, other researchers have found cardiorespiratory abnormalities (low heart rate, low ventilation and low end-tidal CO2) that they felt could explain some of the problems in CFS. As in other areas the results of the CFS cardiorespiratory studies have been inconsistent.

Low heart rates would indicate an inability to supply the muscle with sufficient amounts of blood during exercise. Since ventilation measures the rate of gas exchange in the lungs, reduced ventilation would impair oxygen delivery to the tissues. Low levels of CO2, a metabolic waste product, might signal reduced metabolic activity or result from hyperventilation or overbreathing.

In this study Dr. Natelson also takes a look at whether having both CFS and fibromyalgia (FM) makes it more difficult to exercise. He believes that the presence of a CFS/FM subset could contribute to the inconsistencies thus far seen in the CFS cardiorespiratory studies. Since from 40-60% of people with CFS are estimated to have FM as well, this could be an important subset.

Dr. Natelson believes an inability to control for fitness has been a critical shortcoming in most CFS exercise studies. It is possible that it is inactivity caused by CFS rather than an integral factor of CFS itself that is causing the cardiovascular abnormalities (low heart rate, low end-tidal CO2) seen in some studies. The only way to determine how important a role inactivity (or deconditioning) plays in causing these abnormalities is to compare equally inactive CFS and healthy control patients. The problem has been that CFS patients are often so inactive that it has been impossible to find a sedentary control population with equally low levels of activity.

Dr. Natelson did use very sedentary group for his healthy controls but the CFS patients were still much less active than them. Therefore he used a measure called peak oxygen consumption (VO2 max) as a marker of fitness and expressed all the other variables relative to it. He reasoned that CFS patients with low peak oxygen consumption would be expected to have very low maximal heart rates, low ventilation, low end-tidal CO2, etc. If this is true, it would suggest that the cardiorespiratory problems sometimes seen in CFS are not due to CFS per se but are a by-product of the inactivity caused by CFS.

A Sports Medicine website gave the following explanation of VO2 and Fitness; "Fitness can be measured by the volume of oxygen you can consume while exercising at your maximum capacity. VO2 max is the maximum amount of oxygen in milliliters, one can use in one minute per kilogram of body weight. Those who are fit have higher VO2 max values and can exercise more intensely than those who are not as well conditioned.

The physical limitations that restrict the rate at which energy can be released aerobically are dependent upon: (1) the chemical ability of the muscular cellular tissue system to use oxygen in breaking down fuels, and (2) the combined ability of cardiovascular and pulmonary systems to transport the oxygen to the muscular tissue system". Although the test results are not always consistent Dr. Natelson believes the first is fine in CFS;  he is measuring the second factor in this  study. 

Since some researchers believe that the inactivity found in CFS is caused by CFS patients perceiving exercise to be more difficult than it actually is, these researchers also measured sense of effort and expressed it relative to peak oxygen consumption.

Study Findings - This study found that heart rate, ventilation and end-tidal CO2 often were reduced in the CFS/FM groups (but not the CFS-only group) compared to controls but that, when fitness was taken into account, these differences did in fact disappear. This suggests that Dr. Natelson was correct on both accounts; the cardiorespiratory abnormalities (low heart rate, ventilation, end-tidal CO2) are only found in CFS patients who also have FM, and that they are a by-product of the inactivity caused by CFS/FM not the cause of it. This suggests that if these CFS/FMS patients could exercise more these anomalies should disappear.  

But what about the exercise problems CFS patients have? What about the post-exertional fatigue that is so prominent?  All that this study suggests is that these problems do not lie in the cardio-respiratory system or in a metabolic problem in the muscles; i.e. they are not caused by an inability of the heart to pump fast enough or the lungs to fill with enough oxygen, etc. to keep up with the demands of exercise.

Or does it? One CFS patient has pointed out that his VO2 max levels were reduced even while he was still able to and still did regularly exercise. While reduced VO2 max could result from low activity levels it is possible, then, that reduced VO2 max levels precede the low activity levels found in CFS. This certainly makes sense for CFS patients who find their ability to exercise recede more and more as they struggle with this disease. One study found that low V02 max levels were correlated with rates of RNase L fragmentation, others that exercise is associated with immune abnormalities and mitochondrial problems. This suggests that too much exercise in CFS could impair not improve VO2 max - again not a surprising for exercise impaired CFS patients. CFS patients always walk a fine line with  exercise; some is undoubtedly good for those  who can do it and too much is very bad. 

So what is causing the post-exertional fatigue in CFS? Nobody really knows but the IACFS recently posted an excellent overview of post-exertional fatigue and ways to ameliorate it on their website http://www.aacfs.org/p/260.html.   

This study found much the same pattern with regards to ‘perceived effort’. The CFS group perceived the exercise period to be much more difficult than did the sedentary but still healthy controls but when their fitness levels were taken into account this effect disappeared as well; this means that the CFS patients perceived exercise to be more effortful because given their low fitness levels it was, in fact, more difficult for them to exercise than for the controls. This suggests that CFS is not a disease of altered perception or interception as some researchers believe.

This study did find two abnormalities. Even when fitness was taken into account the CFS patients with fibromyalgia still perceived the exercise to be more effortful; for them something other than low fitness was causing their difficulty with exercise. A potential reason for this was illuminated by the fact that this group also reported increased muscle pain at rest and during exercise. This suggests that the muscles in CFS/FM patients are painful and that this pain increases during exercise. This is an unusual finding – exercise usually decreases not increases ones sensitivity to pain.

Increased pain during exercise could be due to metabolic problems in the muscles but this group of researchers has found no evidence of that and they discarded that idea. Instead they believe that the pain inhibition process in the brain has somehow been short-circuited, and they posit, interestingly, this process is responsible for the post-exertional fatigue seen in CFS. (The brain has both pain inhibition and pain activation circuits.) Some studies have show that post-exertional fatigue is present in about 70% of CFS patients. Is this CFS/FMS subset?

A Laymen’s Speculation – What about the other cardiovascular abnormalities? Could deconditioning contribute to some of  the problems Dr. Cheney is reporting? One of Dr. Cheney’s innovations was to conduct his heart tests in the upright position when the cardiovascular system is under more stress.  It is in this position that the cardiovascular problems in both his (and Dr. Lerner’) CFS patients really showed up. Unfortunately we may never know. The cardiovascular studies that so sparked Dr. Cheney’s interest emanated from Dr. Natelson’s research center and he certainly would have looked at this.  Since his Research Center was closed in 2002, however, the NIH has not funded any cardiovascular studies.

Summary – The disappearance of any cardiorespiratory abnormalities in CFS/FM patients when fitness was taken into account suggests that they were caused by deconditioning. A similar finding with regard to perception of effort suggests that CFS/FM patients are not exaggerating how effortful exercise is for them. Increased effort levels in these patients are probably linked to their more painful muscles, a problem probably caused by increased activity levels in the pain centers in the brain. The cause of the post-exertional fatigue in CFS was not elucidated.