Disaster Voyeurism

Posted on March 16, 2012 by Jennie Spotila

I believe in bearing witness. In many ways, that’s what Occupy CFS is about. Everyone suffers in this life, but bearing witness to another person’s suffering is a sacred act. To bear witness is to absorb the sufferer’s story, to accord that person her dignity, to connect her to the world, and to build the foundation for justice. Bearing witness honors our humanity.

But today, I face a dilemma: will my intention to bear witness be understood and received as I intend?

I am in New Orleans and struggling with how to bear witness to the suffering that resulted from Hurricane Katrina. I’ve read everything I can and seen every documentary about the hurricane, the breaking of the levees, and what happened after the flood. I could draw a map and show you where the levees broke. I could tell you how our government – at all levels – abandoned the people of New Orleans. I’ve learned a bit about the culture of New Orleans, and I can tell you why I think it must be saved.

There are bus tours of the Lower Ninth Ward so that tourists can see the neighborhoods. There is also at least one non-profit that can arrange personal tours of the devastated areas and the rebuilding. I feel drawn to this. I will enjoy my stay in New Orleans, but it feels wrong to enjoy the city and not honor what her people have endured. But it also feels wrong to ride through someone’s neighborhood like it was a zoo.

There is a heartbreaking scene in episode 3 of Treme where a few Mardi Gras Indians are singing to memorialize one of their members, recently found dead in the wreckage of his home. As the small group is singing, a tour van pulls up and the people inside start taking pictures. The bus driver asks “What’s this about?” and Albert responds, “What’s this about?” pointing to the van. The driver responds that, “People want to see what happened.” The mourners tell him to drive away, and after a moment the driver responds, “I’m sorry. You’re right, I’m sorry.”

I don’t want to be that person on the tour bus.

But I also don’t want to pretend that there is no need to bear witness. I don’t want to pretend that everything has been patched up, lives have been rebuilt, and I can stay in my nice hotel and relax while on vacation. That ostrich approach happens to me all the time. So many people in my life – doctors, friends, casual acquaintances – have assumed in one way or another that everything is ok. Yes, Jennie is sick and housebound. She can’t work or drive a car. But she looks great! Everything must be alright! And I do my part to contribute to that assumption. I try not to complain about the burden of this illness on my heart and my life. I say “I’m ok!” (with a certain tone that a few dear friends know means I am not really ok). I give meaning to my suffering through speaking out. I try to flow my life around CFS like a river flows around a boulder.

I believe that the failure of people to bear witness to the suffering caused by CFS perpetuates our history of inadequate research and medical care. When people truly see what CFS patients and their families endure, then they respond with action and support. I’ve seen that in my own life, and in CFS politics. Once you get it, you take action. It is also true that CFS has gotten more press attention in the last few years, and some of that coverage has come with an overtone of “look at them” finger-pointing instead of compassion. That “tour bus” approach doesn’t help us.

I share my story on my own terms, and I hope people will bear witness. Part of me feels like I should do the same for those who endured the hurricane, politely waiting for them to bring it up. The other part of me feels like I should show up and be present, so that they know I bear witness to whatever they wish to share (or not). I believe that our country abandoned this city to its fate before, during, and after the storm. Rebuilding is not over. Suffering is not over. Yes, money is coming in and rebuilding is happening. But the population of New Orleans almost seven years after the hurricane is 25% lower than pre-storm figures. This city has not finished recovering, and I assume the same is true of her people. That pattern should sound familiar to the CFS community. Our government has abandoned us to the storm of CFS, failing to invest the resources needed to help those affected and find a cure.

So here I am, in a hotel in New Orleans. How do I honor the people of this city? How do I bear witness without cheapening what they have endured and turning it into a sick tourist attraction?

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FITNET or Fairy Dust?

Posted on March 12, 2012 by Jennie Spotila

There has been much buzz in the CFS community over the latest CBT (cognitive behavioral therapy) study claiming astounding recovery rates in CFS. This time, the study is called FITNET, a test of internet-based CBT for adolescents with CFS in the Netherlands. I want to focus on two issues with the study: experiment design and results interpretation. For a detailed review of what the paper says, you might want check out the summary on Research 1st. There has also been a great deal of discussion in places like the Phoenix Rising forum, and I found a lot of helpful information there. Other advocates are much more knowledgeable about the issues related to CBT for CFS than I am, and I hope we will see critical examinations of the FITNET study from them as well.

FITNET compared two groups of adolescent CFS patients in the Netherlands. One group received “usual care,” consisting of face-to-face CBT, graded exercise therapy and/or other treatments. The other group received internet-based CBT for six months. School attendance, fatigue severity, and functioning were measured at study outset, 6 months and 12 months. The authors claim that 63% of the FITNET group recovered, compared to only 8% of the usual care group. (Table 3) But a close examination of the paper shows that the results are not so straightforward.

Experiment Design

Study design is arguably the most important part of any experiment. If the experiment design is flawed, then even perfect execution of that design will not give reliable results. In my reading of FITNET, I found many flaws in the design of the study.

First, FITNET was intended to test the effectiveness of internet-based CBT. But this is not as simple as putting some questionnaires on a secure website. Software design is a very complex field, and evidence is mounting that human beings process visual information on a computer in particular ways. Best practices in information design are emerging, but when the software in question is intended to deliver cognitive behavioral therapy, there are many layers of complexity to ensuring that the therapy is delivered effectively and as intended. The FITNET authors report in their study protocol that the textual content was revised by two children’s authors “on readability for adolescents.” That was a good step to take, but there is no indication that any other work was done on the design besides the “cooperation with adolescents with CFS who critically appraised text, lay-out and structure.” From an information design perspective, these steps are woefully inadequate. The paper provided a link to the FITNET module, but I could not access it to evaluate the language and presentation.

Second, there is almost no information reported about how completion of the FITNET modules was measured. Progress was monitored in terms of whether the modules were “completed.” But what about page views, time per page, and how module completion was measured? Were there essays or other assignments submitted to show the participant had understood and acted on each module? Or was there a questionnaire with check boxes that a participant could breeze through without really processing the information? Was any effort made to verify or confirm results/answers reported by participants? How was comprehension of the modules assessed? In face to face therapy, the therapist can use body language and facial expressions to help assess whether the patient “gets it.” How did this internet model ensure that participants were internalizing the lessons? In addition, the paper states that “parents followed a parallel program” but there is no data reported about what those modules consisted of, what advice the parents were given, and how their participation was monitored (if at all). Without any of this data, we cannot assess the quality of participation in FITNET.

Third, FITNET did not seem to make adequate allowances for the fact that in some people, CFS tends to have a relapsing-remitting pattern. Data on school attendance and completion of three symptom inventories was collected at outset, 6 months and 12 months. The school attendance data was based on the two weeks previous to the measurement point. There is no data on school attendance and fatigue severity during the intervening months. This is a weakness in the study because if a participant was having a particularly good or bad two-week period, the data would capture that without capturing a more normal or average pattern over a longer period of time.

Fourth, and most importantly, the long list of variables between the FITNET and control groups makes it very difficult to discern what might account for the different results. The FITNET group had strong parental involvement. Their CBT was overseen by cognitive behavioral psychotherapists. FITNET participants did not receive graded exercise therapy or any other treatment for fatigue. The goal of FITNET was return to full-time school, and a back to school plan was discussed early in the process. Finally, the FITNET participants received their CBT at home on their own schedule, a huge energy saving measure.

In contrast, the control group received “usual care” which is not defined with much detail in the paper. Usual care consisted of one or more of the following: group or individual rehabilitation programs, face-to-face CBT, graded exercise therapy, “alternative treatment” or nothing at all. More than half of the usual care group was receiving more than one of those treatments, and 10% received none. There is no information available on how long those therapies were delivered, whether psychotherapists were involved, whether parents were involved, whether full-time school attendance was presented as a goal, or what other treatments may have been delivered.

In treatment studies, particularly psychological treatment studies, it is very difficult to control for all variables. But to me, this seems like a long and significant list of variables that were not controlled. This study has been portrayed as a test of internet-delivered CBT, and if the control group was receiving the same CBT face to face, then I think the results would tell us what benefit (if any) was derived from the internet delivery. FITNET doesn’t tell us this, and in fact, the authors acknowledged that in the study protocol published in 2011. We can’t determine the cause and effect for the FITNET results. Was it the flexibility of receiving internet therapy at home? Was it the support and involvement of parents? Was it the high number of contacts between therapist and participant? Or the focus on the goal of return to school? Or was it a result of the FITNET group not having to participate in GET? There is just no way to know.

We have to pay close attention to the design of CFS studies, especially studies testing psychological therapies. There are more of these studies in the pipeline, including the very expensive NIH-funded study by Dr. Fred Friedberg. Sloppy design will play out in the study results and, as we have seen with FITNET, the results are trumpeted far and wide.

Results Interpretation

In addition to the multiple differences between the FITNET and usual care groups, there are a number of other questions about how to interpret the reported results.

First, the study protocol published in 2011 promised collection of certain data that was not reported in the final paper. Specifically, the protocol stated that activity patterns would be assessed with an actometer in order to separate the FITNET group into relative active and passive groups. CBT modules would then be customized based on the pattern of the patient. None of this data was reported or referenced in the paper. Why? In addition, actometer data collected during treatment or at its conclusion would have been particularly helpful, but there is no indication that this data was collected. Were the FITNET participants able to become more active over the course of the study? The study focused on school attendance as the primary outcome – but anyone familiar with CFS knows that one activity can be emphasized to the detriment of others. Were the FITNET participants going to school but then bedridden the rest of the time? Was there any change in their socialization or physical activity? One study of graded exercise that originally reported increased activity by CFS patients later revised that conclusion based on further data analysis. They found that the patients did sustain more walking, but cut back on other activities, resulting in no increase in activity overall. We don’t know if this happened in FITNET or not, but I think it is fair to ask whether return to school actually represented any overall increase in physical capacity.

Second, I am confused by the study’s definition of “recovery.” The authors state that recovery was defined post hoc. This means that recovery was not defined in the study protocol, but only after all the data was collected. I do not know how typical this is in behavioral studies, but it seems to me to be a practice fraught with bias. Looking at your data clusters and then defining a subset as recovered seems to be the exact opposite of how it should be done. Recovery, defined by objective measures as in this paper, should be established in advance. And in a sense, the authors did this by setting return to school as the primary outcome of the study. But as I mentioned above, return to school does not actually equate to recovery. The participants could have been in school at the cost of other parts of their lives, and there is the further issue that attendance in school says nothing about performance in school. Can we define a previously A student as recovered if she attends school full time but gets Cs and Ds?

Another aspect of the recovery definition is troubling to me. Recovery is defined as having a fatigue severity score of less than 40, physical functioning score of 85% or more, and school absence of 10% or less in the past two weeks. But in order to be eligible for the study, patients were considered to have severe fatigue is they had a fatigue severity scale of 40 or more, physical functioning score of 85% or less, or a school attendance of 85% or less. This puts a single bright line down the fatigue severity and physical functioning scores: fatigue severity of 40 or more = severe fatigue, but less than 40 = recovered; a physical functioning score of 85% or less = severe fatigue, but 85% or more = recovery. I don’t think you have to be familiar with CFS to recognize that people are not severely fatigued or recovered with no gray area in between. The school attendance requirement does allow for a little wiggle room. Missing 1 day of school or less in the previous two weeks = recovered; missing 1.5 days or more in the previous two weeks = severe fatigue. No correction appears to have been made for missing school for other reasons, such as other illness or family obligations.

Fourth, the authors chose to use a standard deviation of 2 in analyzing their results. What is standard deviation? Basically, standard deviation represents how much variation exists from the average result. If you picture a typical bell curve, the middle of the curve is the average result. As you move away from the center in either direction, the results on the curve are more and more different from the average. The curve can be “sliced” into standard deviations using a mathematical formula. The lower the standard deviation, the less variability there is among individual results. A higher standard deviation means there is more variation among individual results. Defining recovery based on a standard deviation of 2 means that the outcomes for a “recovered” patient are more different from the average outcome than they would be if the standard deviation was 1. This made a huge difference in the results of this study, as can be seen in the appendix to the paper.

The results reported in the main paper were calculated with a standard deviation of 2. In order to be counted as recovered, participants needed to have school absence in the previous two weeks of 10% or less (1 day), fatigue score of less than 40, physical function score of 85% or greater, and report either “I have completely recovered” or “I feel much better but still experience some symptoms.” With these parameters, 63% of the FITNET group was recovered compared to 8% of the usual care group. (Online appendix Table 3a)

When the authors calculated the results with a standard deviation of 1, the numbers are very different. In order to be counted as recovered in this calculation, participants needed to have school absence in the previous two weeks of 6% or less (~ half a day), fatigue score of less than 35, physical function score of 90% or greater, and report “I have completely recovered.” With these stricter parameters, only 36% of the FITNET group was recovered compared to 5% of the usual care group (Online appendix Table 3b).

Examining this data, it is very hard for me to understand why the authors chose to report the more dramatic results from Table 3a – except for the fact that the results were so dramatic. The recovery rate of 63% sounds so impressive, and supports the authors’ conclusion that “Cognitive behavioral therapy for adolescents with chronic fatigue syndrome can now be broadly made available as FITNET.”  Any treatment that can cure 2/3 of CFS patients should be widely adopted, right? The 36% recovery rate under the tighter definition just doesn’t sound as impressive a marketing statement. But that tighter definition is much more reasonable. It allows for a small gray area between the measurements that indicate severe fatigue vs. recovery, as I discussed above. It also applies common sense in requiring the participant to say “I have completely recovered” in order to count as recovery.

What has been lost in the discussion of FITNET is that the 36% recovery for FITNET users vs. only 5% for usual care is a significant result. The real question is WHY? Why did FITNET users do so much better than usual care? Now we’ve come full circle to my point about all the variables between the FITNET and control groups. There are many possible explanations, including parental involvement, focus on return to school, therapy delivery at home, and the use of graded exercise therapy. The FITNET group did not have GET, but 49% of the usual care group did. Because of the study design, and the failure to control for all these variables, we cannot accurately identify why the FITNET group responded so well. Because we cannot accurately identify why the FITNET group responded so well, we cannot draw any reliable conclusions about internet delivery of CBT and the likelihood of its success.

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Easy (Chick)Peasey

Posted on March 8, 2012 by Jennie Spotila

Once upon a time, there lived a young woman who was a foodie. She loved spending hours over a meal at the dearly departed Striped Bass. She also loved executing multi-course meals that used every pot and pan in the house. Then she got sick, and while she is still a foodie, the young woman had to give up meals that used every pot and pan in the house. She had to switch to one pot meals, and this is one of those.

Adaptable Chick Pea Stew (inspired Yarn Harlot’s Emergency Soup)

half an onion, diced
2 cloves garlic, minced
5 carrots, sliced
5 potatoes, peeled and diced
2 15oz. cans chickpeas, rinsed
4 cups chicken broth
1 tsp. curry powder
salt & pepper to taste
1 cup frozen peas

  1. Heat oil and/or butter in a heavy pot over medium heat. Add onion and garlic and saute until translucent.
  2. Add carrots and saute about 5 minutes, stirring occasionally.
  3. Add potatoes and saute about 3 minutes, stirring occasionally.
  4. Add chicken stock to desired brothiness. Stir in curry powder, salt and pepper.
  5. Cover and simmer at least 30 minutes, longer is better.
  6. Use immersion blender (best $25 I ever spent) to puree a small portion of the soup to help thicken it.
  7. Add frozen peas.
  8. Five minutes before serving, add a splash of heavy cream if desired.
  9. Serve warm with biscuits, cornbread, baguette, or just on its own.

The best part about this recipe is how versatile it is. Change it up to fit your mood, supplies on hand, or food sensitivities.

  • Want a more French country style? Substitute leeks for the onion, and thyme for the curry powder.
  • Reduce the amount of stock for a more stew like consistency.
  • Vegetarian? Use vegetable broth instead of chicken stock.
  • Different vegetables? This would be great with sweet potatoes, squash, mild greens, bell peppers, green beans, fresh or canned tomatoes, or different beans – pinto, cannellini, or even lentils.
  • No dairy? Just leave out the cream.
  • Meat flavor? Use beef stock or saute sausage in pan before adding onions, etc. Actually, sausage, cannellini beans, and kale or escarole would be a rather traditional Italian soup.

I love this recipe because I can make it in the afternoon while my energy is still holding out. Everything can be chopped ahead of time (except potatoes), and I can take breaks after each step (just turn down the heat). Once assembled, it can simmer unattended for awhile (but don’t forget about it completely!) and tastes better the next day. My husband, who is a meat and potatoes kind of guy, LOVES this easy, hearty dinner.

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App for That

Posted on March 6, 2012 by Jennie Spotila

Dr. Esther Crawley recently announced the availability of a new iPhone app for CFS patients: ActiveME. The app is designed to help patients monitor their activity levels with the goal of identifying “boom and bust” energy cycles. I decided to take it for a test drive.

The app has a very easy to use interface. When you open the app, you see a chart for that day with a box for each hour of the day. Clicking an hour box brings up a slider screen where you set the level(s) of activity you sustained in that hour. Multiple hours can be set at once, saving the tedium of entering many hours of the same activity level. You can also enter notes when setting activity levels, such as what type of activity you were doing during that hour.

At the end of the day, you have a chart that shows your activity intensity throughout that day. You can email daily or weekly reports to your own email address or someone else’s (although that is not recommended for security reasons). However, the reports only provide a simple line graph of the high energy activity you have entered. Your data on sleep, deep rest and low energy time is not shown in the graph report.

Security for your data is basic. You can set a password to protect the data, and all your data stays on your phone. It is not synced to a server or iCloud. While this is good for security, it does mean that if you lose your phone you will also lose your data. There are no backups.

One difficulty I have with this app is the definition of activity levels, which are just not sensitive enough in my opinion. Low energy activity is defined as “television that you are not engaged in (not concentrating on); listening to music; watching animals outside; doodling; hobbies that do not require concentration; such as easy routine cooking jobs.” This is just not clear enough. What is “concentration”? I knit a great deal, and at multiple levels of difficulty. But all knitting takes some degree of concentration in terms of paying attention to what you are doing. This is true of all the sedentary hobbies I can think of. And “easy routine cooking jobs” may not require a great deal of concentration, but do require standing. Is it still low energy?

The definition of high energy activity is even more troublesome. The app defines three types of high energy activity:

1. Physical activity: walking; cycling; sports; dancing, etc. If you are severely affected this will include activities such as toileting and showering. 2. Thinking activity: this includes any activity that requires concentration e.g. work; school work; reading a book; any computer time; talking with friends; visiting doctors; watching TV that you are concentrating on or engaged in. 3. Emotional activity. This includes time when you are anxious or worrying. Some people use this for time when they are excited or nervous.

There are so many problems with this definition. What if you are anxious but lying down listening to music? Is that high energy or low energy? Why is concentrating on TV categorized the same as walking? In my experience, there is a huge difference in the energy cost of those two activities. The same is true for talking with friends, reading a book, or even writing this blog post. All of those activities are lower energy for me than walking, as well as different energy intensities from each other. Obviously, the user can define the low and high energy classification however he or she wants. Activity tolerance varies so much from person to person, customizing the definitions seems essential to me. But having only two categories – low vs. high – is pretty simplistic.

My big disappointment with the app is that there is no way, other than entering notes, to track symptom levels. The app is supposed to help the user identify “boom and bust” cycles. But all it really tracks is how often you engage in “high energy” activities. The true value in tracking one’s activity is tying it to symptoms. For example, I might see that using the computer for more than an hour causes increased symptoms, and that might motivate me to set a computer time limit. I might also see that I can do easy cooking for 30 minutes without symptoms, longer than I might have predicted on my own. But without tracking both activity and symptoms, it will be very challenging for me to derive meaningful data from activity tracking alone. It is seeing the relationship between activity and symptoms that will really help a person identify a boom/bust cycle.

I’ve been tracking my activity, symptoms and medications for years using a paper chart adapted from Bruce Campbell’s program. While I love the idea of being able to track my activity on the iPhone, ActiveME just doesn’t provide the level of detail and data that would be helpful to me. At $1.99, it’s not too much of an investment to try it out – if you have an iPhone. No word on versions for other mobile platforms.   Update: In an email, Louise Wilson said that the iPhone platform was chosen as the most widely available. If the app generates any income, then developing an Android version and incorporating user suggestions will be considered.

Overall, I think ActiveME is a good first attempt at an app to help with pacing. But I think it will be of little use to those who want to track their symptoms and post-exertional malaise in response to activity.

 

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The Holy Grail

Posted on March 1, 2012 by Jennie Spotila

Many CFS patients are holding their breath awaiting the results of the multiple lab XMRV study, nicknamed the Lipkin study after its coordinator Dr. Ian Lipkin of the Center for Infection and Immunity. I am not one of them.  I don’t usually judge a study before the results are in, but this research has been a roller coaster ride since it was first announced. I’ve collected all the public statements I could find about the study, mostly because I couldn’t find such a chronology anywhere else. I think it’s instructive to view these comments along with the evolving XMRV science in order to understand where the study is now, and what reasonable expectations we might have for its results.

In October 2009, researchers from the Whittemore Peterson Institute and collaborators published a paper in Science reporting their detection of a retrovirus, XMRV, in 67% of CFS patient samples and 3.7% of healthy control samples. To say this paper (Lombardi et al.) unleashed a firestorm would be an understatement. I won’t review all the circumstances here, but this article is a place to start for background.

Right Thing, Right Time

Almost one year later, in September 2010, the National Institutes of Health hosted its First International Workshop on XMRV.  No research group had replicated the XMRV findings during that year, including the Centers for Disease Control. However, an FDA study found MLV (mouse leukemia virus) sequences in a small CFS cohort (Lo et al.). The conflicting results between CDC and FDA had caused its own drama created earlier in the summer.

Dr. Francis Collins (Director of NIH) announced at the XMRV workshop that he had asked Dr. Anthony Fauci (Director of the National Institute of Allergy and Infectious Diseases) to coordinate a multi-lab study to sort out the mess. Dr. Fauci, in turn, appointed Dr. Ian Lipkin of Columbia University to run the study. Initial reports stated that the study would involve fresh blood samples from 100 CFS patients and 100 healthy controls drawn from multiple locations in the United States. Dr. Lipkin’s lab would receive the samples, blind and split them, and then labs at the CDC, FDA and the Whittemore Peterson Institute would test the samples for the presence of XMRV using their own assays.

I believe that Dr. Collins did the right thing in September 2010. In the CFS world, XMRV was a highly charged topic. The online equivalent of bar fights seemed to break out almost daily. The scientists on both sides of the issue were not behaving much better. Early news of the Lo et al. paper had created an expectation that it would replicate Lombardi et al., and so the controversy was only fueled by its publication in August reporting not XMRV, but MLV instead. For NIH to step in with some money for a blinded study with well-characterized samples was exactly what was needed. The study was widely viewed as most likely to provide the definitive answer on whether XMRV was or was not associated with CFS.  Personally, I felt everyone could take a deep breath and wait for the results, which were initially expected in mid-2011.

It All Falls Apart

But it wasn’t long before the XMRV theory took on the appearance of a teetering house of cards. At every step, Dr. Lipkin responded to questions about whether the study should continue and why it was necessary.

In December 2010, a paper by Hue et al. (pdf) used phylogenetic analysis to show that XMRV had acquired sequence diversity in a human cell line but not in human samples, a finding strongly suggestive of contamination in Lombardi et al. The study authors pronounced their findings as the end of XMRV as a human pathogen, but others were not so convinced. Dr. Vincent Racaniello of Columbia University even went so far as to retract his initial statements about the studies and stated that research should continue. Dr. Lipkin told Nature (as reprinted by the CFIDS Association):

These papers emphasize the pitfalls of molecular assays and raise concerns. Nonetheless, it is premature to rule out XMRV or related viruses as factors in prostate cancer or CFS. Links have also been made based on serology and the presence of viral proteins as well as of viral sequences. Thus, we still need appropriately powered, rigorous blinded studies of well characterized patients and controls. One such study is underway under the auspices of the National Institutes of Health.

In March 2011, data was presented at the Conference on Retroviruses and Opportunistic Infections that XMRV was actually the result of a recombination event that happened during the serial passage of a human tumor cell line through mice. Dr. Robert Silverman, a co-author on the October 2009 Science paper, told the Chicago Tribune that he was concerned about contamination in his lab. Also in March, more details emerged about the Lipkin study, now reported to involve 150 patients and 150 controls at a total cost of $1.3 million.

The NIH held a State of the Knowledge Workshop on CFS in April 2011, and included a session on XMRV chaired by Dr. Harvey Alter (a co-author on Lo et al.). Dr. Alter stated his opinion that the Lipkin study would be definitive on the issue. Dr. Judy Mikovits, in addressing the urgent needs of patients for treatment, said that patients couldn’t wait until “when the Lipkin study’s done two years from now.”   She made reference to the study design requiring her to test “1300” samples and that each one takes “2 months.”

In May 2011, XMRV researcher Dr. Ila Singh reported no XMRV in CFS patients. The paper included 14 CFS patients identified by the Whittemore Peterson Institute as repeatedly testing positive for XMRV, but Singh found none. Dr. Racaniello published the following statement from Dr. Lipkin:

We have a plethora of explanations for how CFS/XMRV/MLV studies could go awry. However, we don’t have evidence that they have. Absent an appropriately powered study representing blinded analyses by Mikovitz and Lo/Alter of samples from well characterized subjects using their reagents, protocols and people, all we have is more confusion.
I remain agnostic. We won’t have answers until the end of 2011.

So between September 2010 and May 2011, the study had expanded from 200 total samples to 300, with a reported cost of $1.3 million. Results had been promised in mid-2011, but now were pushed back to the end of the year. During these eight months, data suggesting XMRV was a contaminant continued to pile up and still no group had confirmed the Lombardi or the Lo papers.

Later in May 2011, Science published the recombination data presented at CROI in March along with a study by Dr. Jay Levy reporting that 61 CFS patients tested negative for XMRV, including 43 who had previously tested positive by WPI. Science published an Editorial Expression of Concern (pdf) along with these papers, saying that the validity of the original study “is now seriously in question.” Apparently, Science had asked the study authors to voluntarily retract the paper, but they refused. Despite all this, NIH continued with its plans for the Lipkin study. Lipkin told the Washington Post that the study would continue.  He was also quoted by the Wall Street Journal as saying: “We need to see whether [the Whittemore Peterson institute] can replicate their own work with blinded samples. I think they should have the opportunity to do that.”

Organizations like the CFIDS Association and CFS patients alike stated their intentions to await the Lipkin results. In early September, the CFIDS Association reported that the results of the Lipkin study were now delayed to the beginning of 2012.  The cause of all the delay was not discussed publicly to my knowledge, but the study was now running more than 6 months behind schedule. This is not unusual in science, but this study was designed to put an end to the controversy. The results were desperately needed, at least by the patient community. Every time someone expressed doubts about the XMRV theory, a chorus of voices was raised in support of waiting for the Lipkin results. The study would be the gold standard, and it was unfair to draw conclusions before it was finished.

Science published two more papers in September 2011 that really seemed to be the death knell of XMRV in CFS. The Blood Working Group, formed to investigate whether XMRV posed a threat to the blood supply, published results of testing by nine separate labs of 15 patient samples reported to be XMRV or MLV positive in previous studies. Bottom line – only WPI and Dr. Frank Ruscetti’s lab at NCI detected any positives, and their results did not agree. In addition, Dr. Silverman officially retracted his data from the Lombardi paper. Behind the scenes shenanigans around the retraction were summarized by Retraction Watch.

Much drama ensued in the following months, including allegations that Dr. Judy Mikovits (no longer with WPI) wanted to stop the Lipkin study. With the end of the Blood Working Group, some patients began to move on from the XMRV hypothesis. Others focused on the Lipkin study as the last possible hope to confirm the theory. And others seemed to become entrenched in the belief that the Lipkin study would prove nothing, and therefore should be stopped because its results would do more harm than good.

Just before Christmas 2011, Science retracted the Lombardi paper in full followed by the full retraction of the Lo study by its authors on December 27th. Despite the retractions, Dr. Lipkin told the New York Times that the retraction was premature “while we sort out what’s real and not real.” Dr. Mikovits was quoted in the same article as saying that the Lipkin study would be the definitive answer.  In contrast, Bruce Alberts (the editor of Science) told the Washington Post that there was no reason for the Lipkin study to continue. (the Post reports the cost of the study as $2.3 million but I have not seen that figure elsewhere)  Dr. Racaniello described the study as “less compelling” and unlikely to clarify things. Finally, on December 28th, Dr. Lipkin posted a statement on his website saying that the study would continue. He further stated that results were expected in early 2012, with 123/150 CFS samples and 88/150 control samples already distributed for analysis.

Where Are They Now?

It is now March 2012, eighteen months after this study was announced by Dr. Collins. Why are we still waiting for results? The study criteria were settled in November 2010. But more than a year later, not all the samples had been collected. There have undoubtedly been complications, including Dr. Mikovits’ departure from WPI, and we know that patient recruitment can take time. But does it take more than a year to collect 300 samples? I asked Dr. Lipkin by email on February 28th when study results could be expected and he said “This depends on when the labs complete their work.” This seems to indicate that the labs are not finished. Even when the three labs have completed their testing, the results have to be unblinded by Dr. Lipkin and then analyzed. My conjecture is that we will be waiting at least several more months for the results of this study.

There has also been some confusion over whether the samples collected for this study will be used for any other research. In his December 28, 2011 statement, Dr. Lipkin stated:

please be assured that more than 85% of the funding associated with this initiative is invested in patient recruitment and characterization and sample collection, archiving, and distribution. Thus, irrespective of study outcome there will be unprecedented opportunity to explore hypotheses other than that disease is due to XMRV or MLV infection.

The CFIDS Association reported in January 2012 that the samples from the Lipkin study would be evaluated for other pathogens by Lipkin’s team and that this work would be funded by CFI.  However, in a comment on that post, Dr. Nancy Klimas stated “In the end there are no samples left at Columbia for future studies.” According to Dr. Klimas, the CFI-funded study collected separate samples from the same patients, to be used in the separate CFI study. I asked Dr. Lipkin for clarification about the use of the XMRV/MLV study samples and he said, “The samples will be banked for future work. I don’t have funding for this work. Any help toward securing it would be deeply appreciated.” This seems to conflict with what Dr. Klimas posted on the CFIDS Association blog.

Why is this important? The XMRV/MLV study is quite expensive by CFS research standards: $1 million in NIH funding is supporting the research. Is that money supporting the collection of well-characterized samples that can be used for other purposes? That would be wonderful. Is CFI going to tack its pathogen discovery effort on to this federally funded work? The IRB approvals and patient consent forms for collecting the samples would have to be clear on what was being done with them. I’m not sure why there are contradicting versions of what the samples will be used for, since that should have been settled months ago.

There is also the issue of where Dr. Mikovits will do the work planned in this study. Dr. Lipkin’s December 2011 statement said that he believed Dr. Mikovits, not WPI, should participate in the study, and that a way had been found to fully engage her. According to Caroline T. Anderson’s blog, Dr. Lipkin worked with Drs. Mikovits and Ruscetti to find a lab where they could do the work. He told Nature that:

“[The WPI is] no longer involved because the whole point was to have Mikovits try to reproduce her work, and having someone else at the institute do so wouldn’t address the questions,” Lipkin says. “It’s critical that she do the work. She doesn’t have a lab at present, so it’s going to be done at NCI.”

When I asked him to confirm this arrangement, Dr. Lipkin referred me to Drs. Mikovits and Ruscetti. I contacted both by email, and Dr. Mikovits responded that she is unable to answer any questions at the present time due to her legal situation. This is quite understandable. I have not received a response from Dr. Ruscetti.

Don’t Hold Your Breath

Even if all these questions about timing, samples and location are sorted out, I don’t think the patient community should be holding its breath in anticipation of the results. I have no problem with the study design itself. A blinded, multi-site study looking for XMRV/MLV in well-characterized CFS patients was exactly the study we needed in 2010. And if the study could have been completed on schedule by early 2011, it would likely have been a contribution to the discourse about XMRV and CFS. But now? Now the study as designed is completely unnecessary.

First there is the cognitive dissonance caused by NIH’s conflicting positions on the study. On the one hand, NIH is investing approximately $1 million in this study. For CFS, that is a significant investment of resources. But on the other hand, NIH says on its own website that:

The body of evidence now indicates that XMRV does not play a role in ME/CFS.  . . . . Although it appears that XMRV is a contaminant and not associated with human disease, NIH continues to fund studies to determine whether results of this study can be replicated and the lack of association between XMRV and ME/CFS confirmed.

Why continue to spend money on looking for evidence of something that the funding institution has stated is a contaminant?

Second, there are the contradictory positions taken by some participants in the study. In retracting their paper, Lo et al. said “it is our current view that the association of murine gamma retroviruses with CFS has not withstood the test of time or of independent verification and that this association is now tenuous.” Lo et al. were unable to replicate their own findings on their own samples. They have retracted their data. How does it make sense to participate in the Lipkin study to test more samples looking for retroviruses that they do not believe are associated with CFS?

Third, there are the retractions. This is the deal breaker for me. Both Lombardi and Lo have been completely retracted. In other words, that data is gone. Retraction is not like divorce, where the parties agree the marriage is over. Retraction is annulment, where the marriage is considered to have never happened at all. It’s like rewinding the clock to September 2009 before Lombardi was published. There is no published evidence linking XMRV or MLVs to CFS. None. The Lipkin study was designed to clear up the conflicting data between Lombardi and Lo on one side and everyone else on the other. But now, there is only one side. There are dozens of papers that show no association between XMRV and CFS. Three papers published in Science retested some Lombardi and/or Lo samples and found them negative. And the original papers are gone – whoosh – evaporated. There is no data to support the hypothesis. There is no conflict in the published data now. There is nothing to verify.

If NIH wants to fund some sort of million dollar pathogen study in well-characterized CFS samples, I am fully in support. But shouldn’t such a study go through the usual peer review process? The Lipkin funding did not. It was a special allocation because of the controversy in the field. The NIH typically spends $6 million per year on CFS research. This study represents an allocation of almost 17% of the annual budget to a study that did not go through peer review, and that is trying to verify a hypothesis that has no supporting data. I don’t think this is the right precedent to set in CFS research.

Dr. Lipkin said in December that “85% of the funding associated with this initiative is invested in patient recruitment and characterization and sample collection, archiving, and distribution.” Great, but don’t waste that money! $850,000 worth of patient recruitment and sample collection is a treasure trove in CFS research. Correctly identifying and recruiting CFS cohorts is very expensive, and a barrier to many researchers. Why not save all the samples for a study to test a valid hypothesis? Why not create an NIH repository of CFS samples? Using up the samples on XMRV tests is almost like pouring the plasma down the drain. It won’t tell us anything. The Blood Working Group study already established that no lab (including NCI and WPI) had assays that could reliably detect XMRV/MLV in blood.

In his email to me, Dr. Lipkin said “we are doing our best under difficult circumstances to bring the best science to CFS.” Of that I have no doubt. Throughout his entire involvement in the study, Dr. Lipkin has been consistent in his statements. He expanded the size of the study, recruited the best CFS clinicians to identify patients, and secured consensus on how CFS would be defined in the study. He has a tremendous track record in controversial pathogen investigations. I am not questioning the caliber of his science.

I question whether the study is the best use of one million extremely scarce and desperately needed CFS research dollars. I question whether the study results will be accepted by all the parties. Mixed results will leave a tiny toehold for the XMRV believers to insist on their theory, and even fully negative results will still not satisfy those who have adopted the HGRV theory. Positive results would cause quite a quandary, given the conviction among most researchers that XMRV is not a human pathogen. I question whether we can learn anything of value from the study at this point in the scientific process. This study is not the holy grail that some have made it out to be, if for no other reason than that the results are unlikely to change anyone’s mind or provide any new answers.

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I Think I Can

Posted on February 27, 2012 by Jennie Spotila

Today I am feeling like the Little Engine That Almost Can. I’ve been drafting a post about the Lipkin XMRV study, and my own views on whether it should be completed. After much work, and several thousand words, I’m out of steam. My goal is to post on the blog twice a week, but it will be just one massive post this week (I hope). So in the next couple days, expect a large post chronicling the story of this study and whether patients should expect the results to help advance CFS research.

I think I can I think I can I think I can . . . . .

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Virtually Reality

Posted on February 23, 2012 by Jennie Spotila

Today, the CFIDS Association announces its latest research grants and projects. I know many of us want to dive into the details of the grants, but I want to first take a look at the big picture. The Association describes its research program as an “institute without walls” and all the pieces of the program are designed to work together. With a $2 million investment in 2012 and 2013, this program is one of the most diverse and complex in the field.

Before 2008, the focus of the Association’s research program was funding studies initiated by principal investigators. But after the Association re-focused its strategy to put research first, and with the hiring of Dr. Suzanne Vernon as Scientific Director, the research program became multi-prong. In addition to providing direct funding to researchers, the Association created the SolveCFS BioBank  – the first national bank of CFS biological samples and clinical data that any researcher could apply to use. The 2009 grantees were linked, both via computer network and in person, to increase the sharing of information and ideas. Dr. Vernon has presented at dozens of meetings all around the world, and provided expertise to other researchers and institutions. And last year, the Association recruited a Scientific Advisory Board of experts both inside and outside the field.

Positioned at the hub of the wheel, the Association will direct all aspects of the program announced today: maintaining and expanding the SolveCFS BioBank; funding and administering the five new research grants; investigator meetings; Scientific Advisory Board meetings; work with LogosOmix (see below) to create a biomarker hit list; coordination and management of the research program to drive outcomes and results; and, travel to meetings and to build collaborations with other organizations and institutions.

There are five new grants investigating pain, immune/HPA axis dysfunction, neurocognitive impairment, post-exertional relapse, and drug repurposing. Grants have been and remain a key piece of the program. The Association also announced two new BioBank studies today:

  • Dr. Leonard Jason (DePaul University), who has done great work on the case definitions used in CFS, will use clinical information from SolveCFS BioBank participants to examine the multiple case definitions that clutter the landscape. Dr. Jason has previously demonstrated the danger that the CDC’s 2005 empirical definition of CFS may include many patients with primary depression. The SolveCFS BioBank has very detailed data on participants’ symptoms, and comparing that data to the case definitions may reveal the utility of one definition over another.
  • Dr. Eric Delwart (Blood Systems Research Institute and University of California, San Francisco) will use metagenomics to search BioBank samples for infectious agents. (Listen to a June 2010 interview with Dr. Delwart on This Week in Virology Episode 86) Metagenomics  is an approach to deep sequencing in which all the DNA in a sample is sequenced, including microbes that cannot be cultured. Bioinformatics is then used to sort out the sequences, identifying known and unknown microorganisms in the sample. This approach is similar to that used by Dr. Ian Lipkin at the Center for Infection and Immunity.

CFS patients know the importance of finding biomarkers for this illness. How many of us have longed for a simple clinical test that would definitively say that we do (or do not) have CFS? In 2009, the Association funded a project to mine the published literature and develop a relational database to identify possible etiologies for CFS.  Now LogosOmix, a startup venture, will partner with the Association to develop a hit list of possible targets for clinical biomarkers. The Association plans to shop that hit list to biotech firms and researchers to facilitate development of the markers for clinical use. Details on LogosOmix are scarce, but Association CEO Kim McCleary told me, “LogosOmix is a very exciting project that is a product of the grant made in 2009-2010 to Dr. Bud Mishra at New York University. This project will give us a ‘big data’ tool to help guide the next generation of CFS studies and may have applications beyond the CFS as well. We are still working through various details and will have more information to share in the coming weeks.” When more details become public, I will write about them here on Occupy CFS.

Taken together, these projects address the top issues in CFS research: case definition, pathogen discovery, clinical biomarkers, and treatment development. The CFIDS Association is outsourcing these components to researchers, but is facilitating and coordinating their work. This approach has already proven itself in the outcomes of the Association’s 2009 grants, which resulted in a 7 to 1 return on the Association’s investment.

One more part of today’s announcement deserves mention. Author Laura Hillenbrand  has made a gift of $250,000 to the CFIDS Association in support of the research program. I have admired Laura Hillenbrand for years, and I am truly inspired by what she has achieved while living with severe CFS. Her generous support of CFS research could have an impact beyond the research itself. CFS advocates have wanted a celebrity spokesperson to help legitimize and publicize this illness. While Laura is not offering herself as that spokesperson (and I completely respect that choice), her support of CFS research may help legitimize CFS research in the eyes of the public.

At last year’s NIH State of the Knowledge Workshop,  Dr. Suzanne Vernon pointed out that a major opportunity in CFS research was to make it “silo transparent.” The traditional way of doing research doesn’t work in CFS. Researchers have stuck to their own specialties, and it has been difficult to attract new researchers to the field. One of the major contributors to the advances in treating childhood cancers was that researchers got together and worked through problems together, creating a level of coordination and cross-pollination that would not have existed otherwise. The Association is poised to facilitate the same kind of progress in CFS. This research portfolio resembles, in many ways, a virtual center of excellence. It does not include a clinical care component, something that patients want and need. But rather than wait years to build a physical institution that can provide clinical care, the Association is deploying resources to move research forward and pursue improved diagnostics and treatments now. Hopefully, the answers found through this effort will be deployed in treating CFS patients in all clinical settings, not just one center.

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Diverse and Coordinated

Posted on February 23, 2012 by Jennie Spotila

Today, the CFIDS Association announced five new research grants as part of its “institute without walls” CFS research program.* The Association has funded more CFS research than any other non-profit to date, and expectations are high following on the success of the last round of grants.  As in the past, these grants cover diverse aspects of CFS but have a certain synergy in combination. (For information on other aspects of the research program, see Virtually Reality)

  • Body systems covered: immune, HPA axis, central nervous system processing, mechanisms of post-exertional malaise
  • Expected outcomes: drug repurposing, biomarker discovery and validation, new treatment directions
  • Methods: exercise testing, brain imaging, gene expression, epigenetic changes, brain blood flow measurements, body position, proprietary drug repurposing platform
  • Principal investigators new to CFS: Spyros Deftereos (Biovista), Patrick McGowan (University of Toronto, Scarborough)

Peter Rowe  (Johns Hopkins Children’s Center) will use a simple test to establish whether central sensitization of the nervous system plays a role in CFS. Central sensitization of the central nervous system results in an amplified response to a stimulus, causing pain and other symptoms. Dr. Rowe has observed that simple position changes, such as a passive leg raise, can bring on symptoms of CFS in patients. This new study will investigate the observation by applying either a real or sham neuromuscular strain to both CFS patients and controls. If only the CFS patients respond to the real strain with increased symptoms, then central sensitization may be involved in CFS. Dr. Rowe’s clinical practice focuses on children and young adults with CFS, but it is unclear from the published materials whether the study population will also be younger patients. Expected outcome: Passive neuromuscular strain could be a cheap and easy clinical biomarker for CFS. It is also possible that manual physical therapy addressing neuromuscular mobility could be used as a treatment to lessen the effects of central sensitization.

Spyros Deftereos (Biovista) will use the company’s proprietary drug repurposing platform to identify new treatments for CFS. Drug repurposing, called “eHarmony for medicine,”  looks for FDA-approved drugs that might be repurposed in new ways. For example, Rituximab is currently approved for use in non-Hodgkin’s lymphoma and several other diseases, but shows promise for CFS patients.  One huge advantage of this approach is that since the drugs are already approved, the decade-plus required to create a new drug is circumvented. Drug candidates could proceed directly to animal model or early clinical trial research. Biovista will screen all FDA-approved drugs to identify treatments for cognitive impairment and unrefreshing sleep in CFS, as well as other CFS symptoms. Drugs identified will then be examined to see if combination therapy might be more effective than using one drug alone. One thing that is not clear from the published materials is why cognitive impairment and unrefreshing sleep were selected as the focus for the study. Expected outcome: A list of approved drugs that warrant further study for treating cognitive impairment and unrefreshing sleep in CFS.

Dane Cook (University of Wisconsin-Madison) will partner with Dr. Gordon Broderick and Drs. Kathy and Alan Light to link and validate information from earlier studies. Dr. Cook has conducted studies on brain imaging and post-exertional malaise in CFS. Dr. Broderick used his 2009 grant from the CFIDS Association to identify gene expression measures in a post-infectious mononucleosis cohort of CFS patients. Drs. Alan and Kathy Light used their 2009 Association grant to identify post-exercise gene expression changes in CFS, as distinguished from several control groups. All of these researchers presented results of their studies at the 2011 NIH State of the Knowledge Workshop. In this new grant, the investigators will examine functional brain imaging and analysis of blood markers after an exercise challenge. Systems analysis will map the links between reported symptoms, brain function, and gene expression of sensory, adrenergic and immune functions. Cook, Broderick and the Lights will attempt to link their findings in order to better understand post-exertional malaise. A potential weakness here is that it appears only a single exercise challenge will be used rather than the test-retest protocol used by the Pacific Fatigue Lab, but that may or may not impact the results of the study.  Expected outcome: Cross-validation of novel blood and brain biomarkers in CFS which may identify contributing factors to post-exertional malaise.

Marvin Medow (Center for Hypotension, New York Medical College) was funded by the Association in 2009 to investigate the role of orthostatic intolerance in the cognitive dysfunction experienced by CFS patients. His research showed that CFS patients with postural tachycardia syndrome had decreased brain blood flow and greater cognitive impairment than healthy controls during an orthostatic challenge. This new grant will allow him to expand that earlier research, and test three interventions that increase blood flow (inhaled supplemental CO2 and two intravenous drugs). Those treatment interventions may help alleviate the cognitive impairment seen during the orthostatic challenge. Results will likely only be applicable to CFS patients who have POTS. Expected outcome: Identification of potential treatments to improve cognitive impairment that is aggravated by orthostatic intolerance.

Patrick McGowan  (University of Toronto, Scarborough) will use SolveCFS BioBank samples to look for epigenetic changes related to the immune and HPA axis systems in CFS patients. Epigenetics is the study of changes in gene expression that are not the result of changes to the DNA sequence itself. Epigenetic changes, frequently the result of environmental factors such as nutrition or infections, cause genes to “behave” differently by activating or silencing their expression or by modifying the way a gene is transcribed. This study will observe the response of immune cells from CFS patients and healthy controls to a synthetic stress hormone, and then survey the genome looking for epigenetic changes in the immune cells. One potential weakness of the study is that it uses banked samples, rather than fresh samples with changes induced by a stressor like exercise testing. It would be wonderful to correlate an epigenetic survey with the gene expression changes detected in the Lights’ ion channel study. Still, this is one of the first systematic epigenetic studies in CFS. Expected outcome: Identifying epigenetic changes in CFS immune cells could identify biomarkers and treatment targets.

*Clarification – I served on the CFIDS Association Board of Directors from 2006 through 2011, but I did not participate in any stage of the review of grant applications submitted in response to the 2011 RFA.

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Speak Up About ME

Posted on February 21, 2012 by Jennie Spotila

I have devoted substantial energy in the last several years to following the work of, and preparing testimony to, the CFS Advisory Committee to the Department of Health and Human Services. The committee exists to advise the Department on CFS research and issues affecting the lives of people with CFS.

Speak Up About ME organizes the participation of young people with CFS in the twice annal meetings of the Committee. Speak Up also coordinates meetings on Capitol Hill to bring the stories of these kids to Congressional representatives and their staff, and collects and delivers testimony by kids who are too ill to attend.  I have been both moved and impressed by what these children and their families have said at CFSAC meetings. They speak honestly about how CFS is affecting their lives now and their hopes for the future.

Denise Lopez-Majano, a leader in Speak Up, has asked me to help spread the word about Speak Up plans for the spring 2012 CFSAC meeting. The date for this meeting has not been set, but Denise is asking young people with ME/CFS and their families to consider participating in whatever way they can. For more information, please contact Speak Up at SpeakUpAboutME@gmail.com.

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Not Just Us

Posted on February 15, 2012 by Jennie Spotila

The Senate Health, Education, Labor & Pension Committee hearing on Pain in America (read a summary here  or watch the hearing here) made me realize something: it is not just the CFS community that has to struggle against psychogenic arguments and labeling.

Most people in the CFS world are familiar with the theories and pronouncements of Dr. Simon Wessely  and others who believe that CFS has a mental/emotional cause. I won’t derail this post to go over that well-traveled ground. But I was unpleasantly surprised to hear some of the same language and arguments at the hearing on chronic pain.

The first four witnesses (Dr. Lawrence Tabak, NIH; Dr. Philip Pizzo, Stanford; Dr. William Maixner, UNC; and Christin Veasley, National Vulvodynia Association) were truly excellent, and they made many of the same arguments for increased funding of pain research that we routinely make for increased funding of CFS research. But then Dr. John Sarno of NYU delivered his comments, focused on a pain syndrome he calls Tension Myoneural (or myositis) Syndrome. According to Sarno (who coined the term), TMS is physical pain, particularly back pain, produced by unconscious and suppressed rage or other negative emotional states. Sarno stated in his testimony that the physical pain is real and results from physiological changes induced by those emotional states.

Dr. Pizzo was masterful in his responses to Dr. Sarno’s comments, pointing out that we need to be “very sensitive to the words we use.” He contrasted the way cancer pain is perceived and treated, where providers and family rally around the patient, with how pain syndromes like fibromyalgia are perceived and treated. Both he and Dr. Maixner spoke eloquently about the role of situational factors in chronic pain, including lack of access to care, injury from heavy physical labor, and stress-activated genetic pathways. In response to a question from Senator Bernard Sanders (I)(VT), Dr. Maixner described socioeconomic status as a “surrogate marker” for chronic pain, as the incidence of chronic pain is higher among people of lower socioeconomic status. Dr. Sarno, on the other hand, stated: “Poor people are poor and they’re angry. They’re furious. Fury evokes physical symptomatology as a defense against the rage.” Yes, that is a direct quote, as best as I could transcribe it.

It turns out that the reason Dr. Sarno was invited to testify at the hearing was because Senator Tom Harkin (D-IA), chairman of the committee, invited him. Why? Because, as Senator Harkin shared during the hearing, he used Sarno’s techniques (described in Sarno’s four books) to “cure” himself of disabling back pain. Furthermore, a female relative of Senator Harkin’s “cured” herself of fibromyalgia using the same techniques. Senator Harkin expressed disappointment several times that the Institute of Medicine’s report, Relieving Pain in America,  did not address the psychological origins of pain and the possibilities of treating pain with psychological techniques. To be fair, Harkin stated his strong support for increased funding for pain research, but wants research to “look at everything,” including psychogenic explanations for pain.

Dr. Pizzo thanked Senator Harkin for sharing his story, but cautioned that we cannot lose sight of the patients who have tried and not benefited from currently available treatments. Christin Veasley was impressive throughout the hearing, but I especially loved the way she responded to Senator Harkin on this point. She stated that she has tried all the mind-body techniques to manage her own chronic pain, including yoga, biofeedback, stress reduction and more. But none of those treatments have cured her pain. She acknowledged to Senator Harkin that “Your experience is real, as mine is real.” Ms. Veasley pointed out that we can’t expect to understand or tease apart the multiple contributing factors in pain if we don’t research it, and no answers will be found until there is adequate research.

Perhaps I should be grateful that Dr. Sarno was the only witness peddling a psychogenic cause for chronic pain and, indirectly, peddling his “cure.” Perhaps I should not have been surprised that Dr. Sarno and Senator Harkin so vigorously embraced this simplistic explanation for pain. But truthfully, I was appalled, just as I am every time I hear the claim that there is a psychogenic explanation for my own illness. Emotions certainly play a role in coping with chronic pain and CFS, but that does not make emotions the cause of either condition.

Dr. Sarno claims that once patients understand that their pain is a surrogate for their suppressed rage, the “need” for the pain disappears and they are cured. It’s true that I am angry, Dr. Sarno. I’m angry that doctors like you are so dismissive of my experience. I’m angry that inadequate levels of research funding mean I will have to endure advice like yours, in addition to my physical pain, until the real answers to CFS and chronic pain are understood. And despite the fact I have just recognized and acknowledged my anger, I am still in pain and reliant on the inadequate treatments I described in my written testimony to the committee.

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