CFS Personal Story

CHRONIC FATIGUE SYNDROME: A PERSONAL ACCOUNT

Chronic fatigue syndrome has played a big role in my life. I first started to see patients with the illness as far back as 1987, when I went to work as a junior psychiatrist at the National Hospital for Neurology, usually known as “Queen Square” . It is breaking no professional secrets to say that the patients weren’t very popular with the neurologists who ran the place, some of whom seemed almost to be irritated by the fact that although many of the sufferers had neurological sounding symptoms, on investigation the same neurologists couldn’t find any abnormalities to account for this. Some thought that the problem was at best depression, and even occasionally that patients might be making it up, a view that was sadly confirmed for the sufferers when their next port of call was myself.

Anyway, I didn’t then, and never have, thought that the patients I saw then, and the ones I still see to this day, are “swinging the lead”, as some put it. Instead, I became fascinated with the condition, and, even though I was pretty low down in the Queen Square pecking order, decided to start doing some research. It was the start of my academic career and for the next ten years or so it was the main, but not the only thing, that I was doing.

Sometimes when one looks back, one gets a sense of “why on earth did I do that?”. But not in this case. Yes, one would do some things a little differently. And yes, my writing style has improved over twenty years. But overall, I think that we (and like all medical research, it most definitely was a “we”) achieved quite a lot for the benefit of medicine and patients.

Back then, and I am talking about the late 1980s, the illness itself wasn’t really much known. The first media articles in this country had only appeared in 1982 I think. There were hardly any scientific papers – some of them were pretty old by then, and a new generation of research was only just kicking off. The media tended to call it “Yuppie ‘flu”, back then, an unhelpful stereotype. But perhaps the single most depressing thing was what happened to sufferers in the way of treatment, since the answer was very little. There were, and probably always will be, those who pushed various unproven and untested therapies, often from plush clinics in Harley Street, but for your average patient, the single most common piece of advice given was to rest, and wait either for the illness to go away of its own accord (and we soon showed that didn’t happen very often) or for doctors to come up with a magic bullet. It was very nihilistic, and pretty demoralising and depressing if you were unlucky enough to be a sufferer.

So what contribution did I and my colleagues make?

We set up the first proper epidemiological studies in this country.
As part of that, we were able to show that the label “Yuppie Flu” was a misnomer. In fact the illness was commoner in those lower down the socio economic ladder, not higher. Most of those in lower socio economic levels didn’t use words like ME or CFS to describe their condition, and many of them were not being seen in hospital clinics, which is why the “yuppie flu” label had been used, but it was wrong.
At the start I did think that this might be a form of what we called atypical depression, and early work suggested that there were definitive overlaps with depression. But we showed that about half of those with CFS at the Square weren’t depressed anyway. And then once I moved down to King’s, we did a series of neuro endocrine studies, in which one of the first findings was that there was a different neuro endocrine profile in CFS to that in classic depression. The same neurotransmitter systems seemed to be involved, but in a different way.
That led to a long series of neuro endocrine studies, largely led by my then lecturer, and now Professor, Tony Cleare. The work showed that the hypothalamic pituitary axis functioned differently in CFS to how it does in well people – with a particular pattern of low diurnal cortisol. This finding is now I think the single most replicated biological abnormality in CFS
That in turn led to one of our first randomised controlled trials – of low dose hydrocortisone. It worked, confirming that low cortisol was playing a role, but sadly its not a treatment that one can use over the medium or long term.
We looked at how infection is related to CFS – an obvious thing to do since so many patients told us that their condition had started with a virus, and one of the other labels for the illness at the time was postviral fatigue syndrome. We did a big study in primary care, in which we followed up over a thousand people who presented to their GP with an infection, and then the next person in the surgery who didn’t. This study failed to show that common viruses such as influenza were triggering CFS. But at the same time, looking at more severe infections, we showed that viral meningitis definitely did. Meanwhile our colleague Peter White at Barts produced the definitive study that linked the Epstein Barr virus, the virus that causes glandular fever, to CFS. We went on to replicate that, and look at what predicted early symptoms versus late symptoms after confirmed EBV.
Back then, another big theory around was that CFS was due to hyperventilation. We linked up with our chest physicians, and showed that it wasn’t.
Sufferers didn’t just have physical fatigue and fatigability, they had mental fatigue and fatigability as well. So we did a neuropsychological study, using something called the CANTAB battery of neuropsychological testing, and showed that although most cognitive function was normal, patients did have problems with selective attention. CFS wasn’t dementia (as some were saying) but there was a higher level cognitive impairment.
We teamed up with our local immunologists. We found evidence of an increase in a particular subset of cytokine producing immune cells, confirming a mild immune activation, although we were not sure of the cause. It is possible still that this is a reflection of either sleep deprivation or the low levels of circulating cortisol hormone that we had earlier demonstrated. Its a pity that this still isn’t really sorted. At the same time we showed that immune dysfunction didn’t relate to clinical outcomes.
Which takes us to prognosis – in a much cited paper we showed that the prognosis of patients attending specialist clinics was rather poor, especially if they weren’t treated (as they usually weren’t) but we also found evidence that the situation was more optimistic for the less severe cases seen in primary care, and also children.
We did a lot of biological studies – you can see from the paper list on the website. We published on vitamin levels, the autonomic nervous system, HLA antigens and other genetics papers, growth hormone, why you need to test for celiac disease, anti nuclear antibodies, neuro imaging, DHEA and others. No, we didn’t find the elusive biomarker, but it was not for want of trying.
And we did psychological studies as well. We published papers showing differences between CFS and depression, but also in a long series of work spanning many years established that previous depression increases your risk of developing CFS later in life, or after you are exposed to an infection, something confirmed in several studies now. We looked at personality – linked to the “yuppie flu” stereotype was a perception that sufferers tended to be perfectionistic, hard driving people. We found that once you controlled for the effect of chronic illness, there was no such thing as a “CFS prone personality”. We also showed that our patients were not anti psychiatry, which was in contrast to some of those who were writing about this on the internet.
Whilst at Queen Square I had met up with Trudie Chalder, then working as a behavioural nurse therapist on the same ward. It was the start of a 20 year collaboration that is still going strong. We talked a lot about CFS, and why everyone seemed to think that nothing could be done. So in 1989 we wrote a paper advancing a theory, which was that cognitive and behavioural factors might help explain not why patients got ill in the first place, but why they weren’t getting better. And from that we developed a specific intervention for CFS, adapting something known as cognitive behaviour therapy, which was already achieving considerable success in the pain world. So we first of all simply tried treating 50 patients at Queen Square, with good results (1991), and perhaps most interestingly, with improvements that could still be detected some years later.
Then in 1991 I got a consultant/senior lecturer post at King’s College Hospital. I set up what was one of the first NHS only services exclusively devoted to CFS patients – still going strong today, with Trudie, now Professor Chalder, in charge. We got a grant to do what was needed, which was an randomised controlled trial (RCT) of CBT, comparing it with the same number of sessions of relaxation therapy. CBT performed well. At the same time Mike Sharpe at Oxford, now Professor Sharpe, had independently developed a cognitively behavioural approach to treatment and carried out a trial that had similarly positive results. We both published our results in 1997.
A lot of work followed that. During that decade we showed that you could even get good results in the most severely disabled patients (either in wheel chairs or bed bound) using the same principles, although it was never possible to do an RCT. Trudie opened a clinic for families with children with CFS, and developed a new way of delivering family oriented CBT, which has been the most successful intervention of all. We tried new ways of outreach, such as telephone CBT, and even now Trudie is leading on a study delivering home based treatment to adolescents who are too sick to even get to the clinic.

Meanwhile, my own career was changing. In the mid 1990s I became interested in what was then called Gulf War Syndrome, because first of all the symptoms that some of those who had served in the 1991 Gulf War sounded remarkably similar to those that I was already extremely familiar with in the CFS clinic, but who were in other ways rather different to the Gulf veterans. Secondly, I had by that time completed my Master’s and Doctorate in epidemiology, the study of disease in populations. If ever there was a problem that needed an epidemiological approach, this was it.

And so I set up the first large scale cohort study looking at a random sample of gulf veterans compared to British military personnel who had served elsewhere. The work took off, and was both challenging and exciting. It was the beginning of what turned out to be a long term engagement with our Armed Forces. I established something that we called the Gulf War Syndrome Research Unit, which later turned into the King’s Centre for Military Health Research.

And it was the right time for me to disengage from CFS. Right from the start, myself and all my colleagues had from the start been targeted by a small group of activists, who mission was, and still is, to impede our work in as much as they are able. Thankfully as the above demonstrates, and perhaps even more the continuing success of the research programme without me at the helm, they haven’t succeeded and won’t. But as the principle target of the aggression, it wasn’t very pleasant personally. I gradually realised that it was going to be increasingly difficult for me to continue to make a positive contribution in this atmosphere, and it was a good time to move on. Plus I was really loving the work with the military.

And so I did. Of course you can’t just switch off a research programme overnight. Existing grants need to be supervised – I had just taken on a new ph d student who turned out to be a real star, and together we were publishing papers from his thesis up to a couple of years ago. We even finally published last year a paper based on data that we had collected during the longitudinal study of the outcome of viral infections that began in 1991. But the research and clinical unit was handed over to the more than capable hands of Professor Chalder and her team, and I am pleased to say goes from strength to strength. My main research interest has been for many years the health of the UK Armed Forces, as you can tell if you look at my publication record. And I am afraid that I have also become a university bureaucrat – I became Head of Department, then Vice Dean, where I have responsibility for the whole of academic psychiatry here at King’s and the Maudsley (an awesome legacy to follow) and the largest medical postgraduate training scheme in the world.

CONCLUSION
I remain proud of the work myself and colleagues did in the early days of CFS, and delighted that my colleagues are continuing to research the illness in a broad multi disciplinary way, and refine or develop new treatments. There is still so much to do, and so much to learn. Speaking for myself, and as I said recently in a journal piece (pdf nature neurosciences 2011), I do not think that CFS will be solved in a “eureka” single moment, but that progress will come, as it does in most of science, from a series of slow incremental steps. I would hazard a guess that the most fruitful area of research will come from a combination of neurosciences and psychology, and will be focussed around the sense of physical effort and effortful cognition, but we shall see. As it is, I don’t regret being involved in CFS research, and I think that with all my colleagues we made a very positive contribution to improving patient care. I still see CFS patients to this day, and that keeps me in touch and remains very satisfying.
But there has been a downside I and others have indeed gone public recently documenting some of the intimidation and threats that we have all received over a long period of time from a very small number of activists. But because I do still stay in contact with sufferers in the clinic, I know for sure that these extremists are a tiny minority, and do not speak for real patients in any shape or form, indeed they do them a major disservice. Likewise, I do not blame those who repeat some of the things that they have read about me, and can understand why they might get angry or upset. Most people do not have the time or the access to check each and every quotation for accuracy or context. I feel however differently towards those who originally extracted or altered the quotes, and persist in doing so over the years despite knowing that these are wrong.

So next time you come across something that purports to be an unfavourable or unflattering quote from myself or one of my colleagues, make sure you check it out first with the actual article. By all means then feel free to disagree – that’s fine. Because in the end science proceeds by debate, discussion and disagreement. What it doesn’t do is proceed by distortion.

MYTHS