We all feel a little bit run down now and again. Lack of sleep, too much work, keeping the children entertained, getting over illness, etc. But what happens when that run down feeling turns into something altogether more chronic and long-lasting? What happens when an active person who perhaps runs/jogs/walks miles every week suddenly can't even climb a flight of stairs without stopping half-way or maybe even not being able to get to the top at all? Welcome to Chronic Fatigue Syndrome (CFS) and/or Myalgic Encephalomyelitis (ME).
I would also like to acknowledge related conditions such as fibromyalgia (FM) and Multiple Chemical Sensitivity (MCS) but in order not to confuse either myself or the issue won't go any further into the terminology on this occasions. A caveat also before I continue: I am in no way suggesting that I am an expert on CFS/ME. Indeed I don't claim to be an expert on anything in particular (aside from a bit of Star Wars trivia) so please bear this, and my previous posting caveat about not giving medical advice in mind before reading on. Onwards. There are quite a few accounts of Chronic Fatigue Syndrome (CFS) and/or Myalgic Encephalomyelitis (ME) on the web and I would encourage readers to have a look. Some of them are pretty harrowing in terms of how sudden symptoms can appear and the far-reaching consequences they have on a person's health and their life in general. I would perhaps also draw readers attention to this site also which carries some fairly comprehensive information on the various research into CFS/ME.
The stats: prevalence of CFS at some point in life has been estimated at anything between 0.1% and around 2% of the population depending on where you look, what age-group you look at and what diagnostic criteria you use. Gender-wise, females are about 6 times more likely to be diagnosed. And there are also some interesting co-morbidities potentially attached to a diagnosis.
Why am I talking about CFS/ME on this blog?
Well, for many years there have been some suggestions that CFS/ME might share some interesting connections with autism, even if not in presented symptoms. The more generalised links first. In many ways like some cases of autism, CFS/ME is also a hidden condition. Outside of those people who are bed-bound, a person with CFS/ME exhibits no outward 'differences' which immediately label that person as having CFS/ME. One might even argue that CFS/ME is also a spectral condition - or at least a condition based on observable phenotypes, based on active and remissive periods of symptoms and determinations of what 'abilities' or 'functions' a person has as a consequence of their symptoms severity. Phenotypes have also been tentatively suggested via gene expression (thanks to Maff at the Environmental Illness Resource for this information). Likewise, when it comes to the big question "what causes CFS/ME" we are in the same territory as "what causes autism". A big, fat, juicy question mark or more precisely lots of different question marks over lots of different factors. Some general similarities at least.
There are also some grassroots suggestions that autism and CFS/ME might also share some commonality as co-morbidities also or at least as part of a familial element. Although not the focus on this post, some of the various studies conducted on CFS/ME and Xenotropic Murine Leukemia Virus-Related Virus (XMRV) demonstrate a familial connection between CFS/ME and autism as witnessed by the way that children were recruited for this study. At the moment I have not seen any formal data on the co-morbidity of autism and CFS/ME together so I cannot provide such information. What I will reiterate from previous posts is that, at the moment, a diagnosis of autism does not seem to confer any protection against the risk of developing other conditions potentially to include CFS/ME.
A few weeks back I posted this entry on an article describing some possible connections between some cases of CFS/ME and gluten sensitivity. Regular readers might know of my interest in all things gluten, particularly related to autism. Delving into the research on CFS/ME, there are a few other overlapping areas which also caught my eye. Leaky gut and gut bacterial issues? Yes, those has been mentioned in connection to CFS/ME. Gastrointestinal inflammation? Yep that too. Immune function markers such as cytokines? Yes, and possibly as biomarkers for specific phenotypes. Even those humble neuropeptides and blood-brain barrier permeability might have a role in at least some cases of CFS/ME. There are other areas too numerous to mention in detail.
Intervention-wise, outside of dietary intervention, there are also a few familiar names being used, whether to affect core or peripheral symptoms. Melatonin is one of the main ones, but there are also some initial suggestions that things like probiotics might also help with ancillary symptoms and naltrexone has been mentioned in the lay-literature. I would at this point also say that I am by no means offering any opinion on the safety or effectiveness of these strategies for CFS/ME or anything else nor on the more 'physical and psychological' therapies put forward for treating CFS/ME.
OK I am not going to get carried away here. It is easy for me to 'cherry-pick' studies to prove my argument (there is generally no peer review on blog entries) and I might add that there are studies which go contrary to those I have highlighted (such as this one). Also, as with autism, many of these findings require quite a lot more replication and information on whether they are 'correlation', 'causation' or 'epiphenonemal'; whether also we talking about core or peripheral symptoms presentation.
The possibility of some shared genetics, biochemistry, etc between CFS/ME and autism exists in probably the same way that it exists in lots of different conditions. I perhaps would however be interested to see if anyone takes up the research gauntlet and takes the first step to see for example, just how prevalent CFS/ME is in autism (allowing for the possible communication and intellectual disability issues) and take things from there. If there is a possible connection, maybe we could start talking about a more generalised model of aetiology and pathology. If not, nothing lost.