People with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are often said to have an erratic activity pattern, where sudden bursts of activity are followed by prolonged bed rest. This ‘boom and bust’ pattern is thought to be the reason why ME/CFS patients experience frequent crashes and setbacks. Despite the popularity of this view, there is no evidence to support it.
An erratic activity pattern
In our previous blog post, we looked at the weak evidence supporting the deconditioning theory for ME/CFS. When researchers noted that a lot of patients are not deconditioned, they formulated another popular explanation for ME/CFS symptoms. The focus remained on the activity of patients but rather than being too low, the idea was that the activity pattern was too irregular. Patients were thought to overdo it when they have a bit more energy, then crash, causing fatigue and frustration.
These spikes of high activity followed by prolonged rest are often referred to as ‘boom and bust’, a term originally used to describe the cycles of economic expansion and recession. In ME/CFS patients, boom and bust means doing lots one day and then very little the next. The GETSET trial used the following description:
“on some days you may feel reasonably well and rush about doing a lot (the boom time). The next day you may feel tired and overcome by CFS/ ME symptoms, or even unable to function (the bust time). This pattern may be better known to you as relapsing, crashing or having a setback. By following this boom-bust pattern the body does not have a chance to recover.”
Another paper described it as “a presumably unhealthy symptom-producing behavior of unsustainable high activity levels followed by steep declines into inactivity.”
It remains unclear, however, how an irregular activity pattern would produce disabling symptoms. Some sources emphasize that boom and bust makes it difficult to establish a routine and that the body needs consistent, regular exercise to adapt to. In their book ‘Overcoming Chronic Fatigue in Young People’, Katerine Rimes and Trudie Chalder write that “this overactivity/underactivity pattern (sometimes called ‘boom and bust’) can become a cycle that’s hard to get out of. Through this process your body can end up getting weaker rather than stronger.” Others suggest that the crashes cause frustration and strengthen the idea that the patient is diseased. This is usually tied with the belief that ME/CFS patients are perfectionistic and have unrealistically high standards. One paper on activity levels argued, for example, that “patients with CFS are often perfectionists, and they may easily go in over drive to meet their own or others’ requirements.”
Rehabilitative approaches such as cognitive behavioral therapy (CBT) and graded exercise therapy (GET) aim to address the boom and bust cycle. Treatment often starts by letting patients recognize that they have this unhelpful activity pattern and that is necessary to develop a more structured and consistent routine, otherwise, progress is not possible.
Lack of evidence
For the past 25 years, this boom-and-bust hypothesis appeared in multiple papers, books, and information leaflets on ME/CFS. It was used in the biggest trials of behavioral interventions including PACE, FINE, GETSET, and MAGENTA. Yet despite the popularity of the theory, there appears to be no evidence for it.
Several studies used accelerometers – small, wearable devices that measure movement and activity – to examine the physical activity patterns of ME/CFS patients. None found evidence of a boom and bust cycle.
The biggest study was done by the Dutch research team of Sieberen Van der Werf and his colleagues. They registered the activity levels of 277 ME/CFS patients and 47 healthy controls over a period of 12 days. The authors looked at large day-to-day fluctuations, defined as changes of 33%, 50%, or 66% from the mean. However, at each of these thresholds, they could not find evidence for a boom and bust pattern. “Compared to healthy controls”, Van der Werf and colleagues write, “no indication was found that the CFS patients as a group were characterised by a high number of large day-to-day fluctuations in activity.” The researchers also tried excluding pervasively passive ME/CFS patients, thinking that their low activity levels diluted the activity patterns of the more active patients. This was not the case, however. Even after omitting passive patients from the analyses, no differences in day-to-day fluctuations were seen. The Dutch researchers did find that the height and duration of activity peaks were higher in the healthy controls than in people with ME/CFS.
A Belgian study tested 67 ME/CFS patients and 66 healthy controls for 6 days. The authors hypothesized that patients would present a more fluctuating activity pattern, with greater variations and a bad staggering of activities during the day. The latter was calculated by taking the peak hourly activity and dividing it by the average. For both measures, however, there was no significant difference between ME/CFS patients and controls. The authors concluded: “The present study was not able to confirm the hypothesis of a more fluctuating activity pattern in patients with CFS, nor during the day, nor during the registration period.”
The British research team of Julia Newton at Newcastle upon Tyne also did a large accelerometer study. 107 ME/CFS patients and an equal number of healthy controls were studied for 7 days. The authors focused on sedentary behavior and found “no differences in the transition from being sedentary to being active […] or in the duration of sedentary bout length.”
A smaller Dutch study had data on 35 ME/CFS patients and 35 controls for a period of 3 to 7 days. Here, the results were mixed. The activity pattern of patients did not show more variation during the day compared to controls although there was a difference during the afternoon. Patients were equally active as the controls during the morning ,but less active during the afternoon and evening.
A tiny study of 8 ME/CFS patients by the research team of Leonard Jason in Chicago, found that patients had “less regular activity–rest cycles” than controls. The average hourly profile of activities, however, confirmed that healthy controls have higher activity peaks than ME/CFS patients.
This was also found in another Dutch paper that studied 38 ME/CFS patients for 5 days. Although patients had similar average activity levels as controls, they had lower peaks and spent less time in high-level activities.
Lastly, the MAGENTA trial had baseline data on 138 children and adolescents with ME/CFS who wore accelerometers for 3-7 days. The authors conclude that a “fluctuating active’ or ‘boom-bust’ physical activity pattern” […] did not emerge from the present analyses.”
In conclusion, several large studies looked at the variation in activity patterns but found no consistent difference between ME/CFS patients and controls. These studies, however, have limitations. The number of days tested might have been too short to measure a boom and bust cycle. The Hawthorn effect, where participants modify their behavior because they know they are being watched, might have also affected the results. In the study by Van der Werf, however, patients were studied for 12 days, and the sample size was large enough to detect patterns in subgroups of patients.
EDIT: On Twitter some argued that the boom and bust cycle may be present in ME/CFS patients but only at the very beginning of their illness when they do not yet fully comprehend what is going on.
The confusion with post-exertional malaise
Where does the boom and bust theory come from if it does not appear in the data? It seems to arise from patient reports that mention frequent crashes following activity. Several psychiatrists highlighted this in their descriptions of ME/CFS and they needed an explanation for this phenomenon. These psychiatrists adhered to the cognitive-behavioral model of ME/CFS which assumes that symptoms are not perpetuated by a somatic disease process but by unhelpful thoughts and behaviors. Therefore, if patients report an unusual number of crashes or symptom flares following physical activity, the model suggests that this must be due to behavioral factors such as perfectionism or an irregular activity pattern.
There is an easier explanation, however, that is more in line with the accelerometer data. This view assumes that crashes and symptom flares are caused by the illness ME/CFS even when patients have the same activity pattern as healthy controls. The terms used in the literature for this phenomenon are post-exertional symptom exacerbation or post-exertional malaise. This is considered the hallmark feature of ME/CFS in the NICE guideline and diagnostic criteria such as the one formulated by the National Institute of Medicine.
Some researchers appear to have picked up on the language of post-exertional malaise, but rather than thinking that the illness causes this phenomenon, they assumed that the patients’ behavior was responsible for it.
Patient blaming
One could argue that this is not a big issue because learning patients how to avoid crashes and stabilizing their activity levels is useful, even if based on a false premise. But there is something more problematic at the heart of the boom and bust theory. It blames patients for the symptoms they experience. Here’s how an articulate member of the Science for ME forum described the boom and bust theory:
“The idea succeeds in somehow labelling any level of activity that a patient engages in as pathological. The patient cannot win. When the patient rests, they are being dysfunctional, and when they are active they are also being dysfunctional. In other words, whatever the patient is doing, its either too little or too much – else we woudn’t be sick, or so the reasoning goes.”
Another problem is that the theory can set unrealistic standards. Normal activity patterns are often erratic. There is a limit to how much you can plan and structure activities. As one ME/CFS patient noted:
“It is simply not possible to do the same amount each day. It is also perfectly reasonable to budget energy quotas so that a somewhat more energetic day (eg my daughter’s recent wedding) is intentionally sandwiched between other less active days.”
The boom and bust theory risks blaming patients if they have an activity peak that causes a crash. There are many cases where this is unavoidable such as medical visits or to maintain social contact. Post-exertional malaise is part of living with ME/CFS, no matter how hard one paces.
A PEM signature
If post-exertional malaise is a characteristic of ME/CFS, then there might be something unusual in the activity pattern of ME/CFS patients. It would, however, be a more subtle abnormality than large day-to-day fluctuations or a boom and bust cycle.
To know what to look for, it is important to zoom in on what post-exertional malaise (PEM) entails. Although definitions vary, current evidence suggests it is not so much one symptom but a temporal pattern in the intensity of ME/CFS symptoms. Studies found that PEM is triggered by many types of exertion (not just exercise) and that it often has a delayed onset. Patients have also reported a cumulative effect where overexertion builds up slowly over time.
One small study, for example, found that ME/CFS patients could increase their physical activity for several days, as instructed. The researchers initially thought that this meant that graded exercise was feasible. After 4-10 days, however, the activity of ME/CFS patients started to drop suggesting they exceeded their limit. While controls were able to maintain increased exercise levels for 4 weeks, ME/CFS patients could not. Similarly, another study followed ME/CFS patients 7 days before and 7 days after a cardiopulmonary exercise test. Activity levels of ME/CFS patients were initially unchanged and only started to drop 5 days after the test.
According to Professor Emeritus Jonathan Edwards, such temporal patterns and delayed effects of PEM might leave a unique mark in the accelerometer data of ME/CFS patients that is not present in people without PEM. To detect it, we will need enormous sample sizes*, machine learning, and labeling by patients to indicate when they are in PEM and or not. Given the low cost of actimeters and the popularity of tracking apps such as Visible, this should be a feasible project.
A recent study had access to accelerometer data from more than 100.000 people and found that people with Parkinson’s disease already have lower activity levels, even before they are diagnosed. An Alzheimer’s study found that people with detectable amounts of the protein beta-amyloid had different activity patterns than people without this protein. It should be possible to set up a major accelerometer study for ME/CFS patients as well, for example using the Solve Together platform. What we might find is not so much a boom and bust cycle but an objective signal of ME/CFS pathology.
Notes
*Several studies have analyzed fractal patterns and complexity in the activity of ME/CFS patients but with sample sizes that are far too small. Examples are Ohashi et al. 2004, Burton et al. 2009, and Rabaey et al. 2024.
I am not an idiot. I have a PhD in Nuclear Engineering (plasma physics). If there had been a way to gradually increase my energy expenditure by being careful not to exceed limits (mine are so very low), after almost 35 years with this monster I would be running marathons and climbing mountains.
Just as you CAN’T do those things with a broken bone in your leg, you CAN’T do them with a broken metabolism (or whatever it turns out to be).
CAN’T, not won’t, not didn’t work hard enough at it, not pushed herself too hard – CAN’T.
I’m not an idiot. I’m doing the best I can, and am extremely careful – and it’s no more than maybe 5% of what I had before, when I worked research plasma physics – and that’s on a rare very good day.
THIS IS A PHYSICAL ILLNESS. You can’t exercise and diet yourself out of AIDS, cancer, blindness, or a host of other physical conditions or diseases, and I’m getting really tired of the total idiot ‘researchers’ who insist you can, and are just not trying hard enough.
I’ve done the very best possible with what I have left. I’m writing a mainstream trilogy. It has taken me TWENTY-FOUR years to get the first two volumes out. There is nothing I can do to BE better except use what I have left as carefully as possible, and wait for the research to MAYBE give me a bit of life back.
It also doesn’t make sense to measure fluctuating activity levels in a group and try to pin it as some hallmark of disease when those diagnosed have probably already learned to some degree, often subconsciously, how to pace to manage their energy. Especially when you consider the typical long wait for diagnosis. Of course if your body punishes you for energy fluctuations, you are going to come up with ways to balance that to adapt to live your life. The real time to capture would be early in the disease when people aren’t sure what they have or what is going on so haven’t modified baseline behaviour.
Also any chronic illness is about loss and change — patients are comparing their activity to what they could achieve before illness, but researchers can only ever capture that anecdotally. It’s the abilities you lose that make the illness disabling.
The long tail on PEM rings very true for me as someone moderately affected. For example, I used to be able to run a three day conference, was fine for a day or two after… Then a huge crash where I could barely even walk for a week.
Thanks for sharing your perspective Alicia. Just discovered your blog and writing, will have a look!
Love to have you come – the blog and my writing are my F* You to the disease, without being able to CHANGE it in the slightest.
There are two blogs, liebjabberings.wordpress dot com – for my personal and writing blog, prideschildren dot com for the trilogy’s books (still working on the third). ME/CFS makes me very slow, but it is the project of the heart, and I like to think, a darn good story.
Note: I’m a patient with a different complex chronic illness. That illness can’t possibly occur if the basic theory underlying medical practice and research is correct and complete, and it only took 2 weeks to figure that out back 28 years ago when my family and I were first affected. After my now adult daughter spiraled into disability after some mild virus 4 years ago, I started looking into Long Covid, and after a set of seemingly independent voices who had been denying and trivializing ME/”CFS” for years or decades pivoted in unison to deny and trivialize Long Covid in mid 2022, besides being apoplectic I started trying to understand ME / “CFS” as well.
The behavior of physicians doing mental gymnastics to preserve the basic theory they were taught in med school, rather than realizing there is a large gap in that theory through which about two dozen complex chronic conditions — including ME — have fallen over the last 140 years since medicine debated and psychologized the original “neurasthenia” is understandable. Lots of people don’t deal with cognitive dissonance well.
I want to plant a thought with you. I’ve been planting it with thoughtful people since reaching a conjecture about the nature of PEM PESE PENE back in February 2024, and writing it in narrative form for the NIH NINDS ME/”CFS” crowdsourcing effort at that time. Remember, I’m a retired computer designer and thus when presented with a vague, semi repeatable syndrome which defies controlled experiment, immediately look at the power distribution, particularly power distribution at time intervals during which light can only go a few inches, to the transiently malfunctioning part. That means I’m trained, and experienced, thinking from a point of view utterly foreign (and inconceivable) to anyone trained in medicine or biology.
Here’s the thought: there’s a protein called myoglobin. It is expressed in muscle cells. One end of the myoglobin is folded in an almost spherical shape (the “globin” end) and is extraordinarily good at pulling oxygen off passing hemoglobin. The globin also stores a single oxygen molecule. There are things science and medicine know about myoglobin (a disorder of athletes overtraining which results in muscle cell walls rupturing and myoglobin being spilled to the blood, where it harms kidneys and discolors blood) (whales have far more myoglobin than people, and elite breath holding divers express more myoglobin than ordinary people). But science and medicine don’t seem to have a clue how myoglobin somehow helps oxygen get into a cell. So I’m going to make an assumption, and say myoglobin folds itself into one of those selective tunnels which goes through a cell wall; at rest each protein holds one oxygen molecule ready for the cell to use; the max rate at which oxygen can enter a muscle cell is proportional to the number of myoglobin tunnels (probably between the cell and the adjacent capillary) expressed.
Neuroglobin does the same things for certain neurons.
So here’s my conjecture: (assume this is wrong, but when science finally figures out PEM PESE PENE it will be something like this):
Exertion leads the cells to use oxygen stored in their myoglobin/neuroglobin
There is a molecule loose in the bloodstream which happens to geometrically fit the “globin” oxygen storage site, but can only land there when the oxygen site is empty
That molecule acts as a hapten
The immune system then (at its leisure) destroys the combination of the globin (sticking up out of the cell like a dandelion) and that loose molecule
This results in a decrease of the number of tunnels which bring oxygen into that cell (times nearly every cell in the body), which reduces the peak rate at which oxygen can enter the cell, and the sustained rate at which an (aerobic) performance athlete can use energy in that cell (a muscle cell stores glycogen, the limit is getting oxygen into the cell)
The body will keep trying to make more myoglobin / neuroglobin and get more tunnels through the cell wall, but a new tunnel has no oxygen, so it’s playing a probability game of whether an oxygen lands on it first, or that loose molecule does
If the body loses 10% of its peak oxygen capacity, the performance athlete will notice; no one else will
If a person with ME (PEM PESE PENE) loses, say, 80% of their peak oxygen capability, they will notice a rate of consuming energy beyond which a temporary or permanent “crash” occurs. Medicine doesn’t believe in that ceiling and has no way to measure it. My conjecture is this ceiling occurs when the remaining myoglobin / neuroglobin has so little capacity that when exertion occurs the oxygen binding site stays empty for an extended period of time (the cell grabs whatever oxygen lands on one immediately). This makes the surviving tunnels vulnerable to that loose molecule landing, and the immune system destroying further tunnels.
If all of the myoglobin and/or neuroglobin is destroyed, the cells stay alive by diffused oxygen, but every bit of energy use is by anaerobic metabolism. That is the patient who is bedbound unmoving in a dark silent room.
Buried in the conjecture I just proposed is medical blasphemy, because if it’s true there are three beliefs medicine teaches as absolute to every new doctor, which turn out to be approximations which do not hold in the bodies of the % of the population with complex chronic illness. It would be career ending for a researcher, much less a clinician, to discuss, much less attempt to publish, work even adjacent to this conjecture. Just ask Semmelweis.
This is terrible journalism! You’ve literally misquoted the 2020 Dutch Sieberen Van der Werf study. It’s not what was said; and it’s misinterpreted as well. As interesting as is, methodologically it’s also tricky. That’s not a criticism to the authors – its just measuring activity level changes on a group of people that don’t move much over time is methodologically tricky to anyone and why doing this research is challenging, which they also acknowledge.
It’s great that you agree towards the end that ulimately future studies are likely to show more nuanced and objective temporal patterns.
We used a direct quote from the 2000 Van der Werf study, so not sure what you mean. We appreciate critical feedback and are happy to correct the blog if there are errors or misunderstandings. But we do not appreciate statements such as ‘This is terrible journalism!’ or ‘It’s not what was said; and it’s misinterpreted as well’ without providing any clarification of what you mean.