Tag Archives: research

HEDGE study day

A fortnight ago I went up to Edinburgh to take part in the HEDGE study, which is recruiting 1000 patients from America, Britain and Europe in order to try to establish the gene(s) responsible for Hypermobile Ehlers-Danlos Syndrome.

By the time I received my invitation there were only early morning slots available, so I chose the latest one which was for 10am.  It takes about 1hour 40 mins to get from where I live in the north of England to Edinburgh, so I caught the 8am train.  This meant I was up at 5.30am (it takes a good while for my joints to ‘thaw out’ in the mornings so I need time for this to happen), had breakfast and got dressed, put a packed lunch up, got myself and the dog in the car, walked the dog in the dark, dropped him off at my parents’ house then recruited my 80 year old, disabled Dad to take me to the station in his car to avoid astronomical parking charges.  By the time 8am, and the train, arrived I was buggered and the day hadn’t even started yet!

Although marginally better at travelling on trains than in cars, I still find it an ordeal.  My nervous system is high as a kite at the best of times, so when the train pulls out of the station it shouts at me in a very loud voice “what the FUCK is happening?!” as it tries to cope with the swaying and vibrations.  My entire body buzzes like I’m being electrocuted and my brain feels like it’s swishing about in my skull, the effect of which is to make me as dizzy as a kid on a roundabout and twice as disorientated.  It didn’t help that I was facing the early morning sun which flashed as it disappeared behind every tree on the banking and inevitably led my light-sensitive brain to develop a migraine before we’d even reached Carlisle.

The testing was being carried out at the Royal College of Physicians, which is luckily only a 5 minute walk from the station.  I arrived at 9.50am and only had a short wait before I was called in to see an American lady who took me through the consent forms etc.

I was then shown in to see an American physician.  She introduced herself but I was so spaced out I have no clue now who she said she was, but she was lovely and immediately put me at my ease.  She explained all participants in the study had to conform to the 2017 definition of hEDS so that the study was based on identical symptoms, which is of course completely understandable.

We then went briefly through my medical history and I was quickly examined.  The appointment went belly-up at this point.  When I was diagnosed back in 2010, my Consultant explained that I did not fulfil the Beighton Score criteria.  I’ve never been able to put my thumb to my wrist, for example.  However my wrists are clearly hypermobile, they just bend in the opposite direction from that listed on Beighton, therefore my Consultant still scored me.

Beighton score wrist & thumb hypermobility

My hypermobile wrist not on the Beighton Score

Photo of hypermobile thumb

My hypermobile thumb not on the Beighton score

The HEDGE Physician explained that, in a clinical setting, she would still give me 2 points for the hypermobility of both wrists however the study has to stick rigidly to the Beighton Score and because of that I was awarded 0.  Here begins my first gripe with the current diagnostic criteria.  It is absurd to award me zero points when I’m clearly hypermobile.  Why on earth the Beighton Score wasn’t updated when the diagnostic criteria were re-designed in 2017 still baffles me and even the Physician agreed it needs to be re-examined.

On to my fingers.  I am now 52 years old and Menopausal.  While I am still more flexible than the general population most adults, as they age, stiffen up and hypermobile people are no exception.  On top of the normal stiffening of age we also have decades of trauma to contend with, which causes chronic pain.  My hands are now really quite sore, to the point where I can’t take the tops off jars or cut up dense food.  I was asked could I bend my pinky fingers back by 90 degrees, as per the Beighton Score.  “I used to be able to” I say, “but these days they’re just too sore and stiff”.  Another zero is added to my tally 😦

Beighton Score: 1 point each pinky finger

Photo of hypermobile finger

My hypermobile pinky finger

And so on to my back, which has been painful since I was 11 years old and is currently absolutely killing me and my hips which are even worse.  I was asked if I could place my hands flat on the floor with straight legs, my answer to which was also that I used to be able to but these days it’s a definite no no.  I accumulate another zero, despite the fact I could do the splits until I was well into my thirties.

In the end I scored a borderline 4/9 on the Beighton Score (my original diagnostic score was 8/9) and this is where I got miffed, though I didn’t say anything – it’s not the physician’s fault!  Ever since I was diagnosed with hEDS I’ve realized that the emphasis is on children and young adults  (and by young adults I mean under the under 40s).  No-one wants to know about older adults and definitely not about the elderly or what happens after the menopause.  We’re written off.  The attitude seems to be that the damage has been done by the time you’re 40, so what’s the point in studying us oldies?  What does anyone hope to gain?  An understanding of how age affects us, I would have thought, and ways in which not only our symptoms can be effectively treated but how our issues could be avoided by the younger generation!  It makes my blood boil if I’m honest.

The 2nd section of the 2017 diagnostic criteria deals with issues other than hypermobility.  I was asked do I have Piezogenic foot papules, to which I could answer a definite “yes”.  Only the physician said there weren’t enough of them – how many does one need?!  I can see 5 on the inside of one heel alone!  I scored zero, though I’m not sure why.

Photo of piezogenic papules

Piezogenic foot papules

I was then asked if I had any atrophic scars, the answer to which is also a resounding “yes” as I had spinal surgery as a teenager.

Widened, atrophic, cigarette paper scar

“Is that the only scar you have?” I was asked.  No, but it’s the only major scar I have.  I do have one on my forehead from when I fell as a 3 year old and banged my head on the kitchen chair, but as it’s 50 years old it’s quite faded now.  Again, I scored a big fat zero as you need two scars to qualify, even if your one humongous scar is clearly atrophic.  FFS it’s ridiculous.

The next question related to stretch marks, of which I have none.  I’ve never been pregnant, you understand, or overweight – the two main reasons why anyone would have stretch marks (my Mum’s stomach and bum are covered in them from her pregnancies).  Again I scored zero.  Not only is the 2017 diagnostic criteria discriminatory towards older people, it’s also discriminatory towards child-less people too!

“And have you ever had a prolapse?” the anwer to which was also no, thank God.  Y’see, prolapses are usually events which happen after child-birth, or in women over the age of 65, neither of which apply to me (although they can also be caused by long term constipation).  More discrimination of middle-aged, child-less women, not to mention men.  I would honestly love to know the proportion of average weight, child-less patients who fulfil the stetch-mark and prolapse criteria.  In order for criteria to be diagnostic they surely have to apply to the majority of patients and I’d kill to know the statistics in child-less women, and of course men, because I’d bet my house on these two symptoms applying to very few.

I knew I would fail the 3rd section of the criteria, which insists on a closely-related family member also having an EDS diagnosis.  Now this really is discriminatory.  What if you’re adopted?  Or your parents died young?  Or you’re a refugee or immigrant whose parents are still abroad?  Or, like me, you’re simply not in touch with one side of your DNA family?  I do still have my Mum, who has all the signed of both hEDS and MCAS, but she’s 79 years old and in very poor health and has absolutely no intention of trying to get diagnosed with hEDS (which is hard enough for young people and, as discussed above, almost impossible for the elderly).  Needless to say I failed the 3rd section in spectacular fashion.

I have some issues with the 2017 criteria, in case you hadn’t guessed 😉

The upshot of the appointment was that I didn’t qualify for the study.  All that effort, not to mention losing £50 in train fares (no expenses were provided) and having to wander Edinburgh for nearly 2 hours in the rain, dizzy, in pain and disorientated, waiting for my train home.

I wish the study every success.  We clearly need to know the gene(s) responsible for our disease.  However, I wonder how many hEDS patients are being excluded when they clearly have hEDS and how representative the actual results will be?


In 2017 the diagnostic criteria for Ehlers-Danlos Syndrome changed and there are now 13 defined types.  By far the most common is Hypermobile EDS (hEDS) yet this is the only form for which no gene has been identified, so The Ehlers-Danlos Society have decided to enroll 1000 patients who fulfil the 2017 criteria for hEDS in a genetic study to try and find the gene(s) responsible.  This would be a huge breakthrough not only in our understanding of hEDS but also as an aid to diagnosis.

As far as I’m aware, the study is using patients from both the USA, Europe and the UK and I am delighted to say I have been accepted as a participant 🙂  I will be travelling up to Edinburgh at the start of November for my blood draw.  It’s a 3½ hour return journey for me and there are no travel expenses, however I feel it’s too important an opportunity to miss so despite the huge effort involved I am very much looking forward to taking part.

For more information on the HEDGE study, including how to be included in the EDS global registry which is a pre-requisite to taking part in HEDGE, click here.

So what CAN I eat?

Following on from yesterday’s post on new research into the histamine content of non-fermented fruit, nuts & vegetables I thought I’d break down the information contained in the paper for us mere mortals to understand.

Histamine Intolerance (HIT) is thought to be caused by low levels of two enzymes: HNMT and DAO.  DAO is an enzyme in the gut which breaks down and converts the histamine we eat in our food, and if levels are low this process isn’t effective and results in high levels of histamine in our bodies (at least, that’s the layman’s version!).  In order to keep symptoms at bay, HIT patients need to stick to a low histamine diet, which makes perfect sense and has worked miracles for me personally.

However, there is very little information on the actual histamine content of foods and the researchers found that many foods excluded from low histamine diets actually have been shown to be low in histamine and therefore are safe to eat which is fabulous news!

What constitutes a high level of food histamine is currently guesswork – we don’t know what ‘high’ is, and safe levels of histamine in food probably differs from patient to patient depending on how well their DAO and HNMT are functioning.  I’m making the assumption that ‘high’ is anything over 20mg/kg but this is a purely made-up number in the absence of any guidelines.  Based on this, then,  the only non-fermented plant foods tested in this research paper and found to be high in histamine are:

  • Eggplant (aubergine)
  • Spinach
  • Avocado is borderline at just over 20mg
  • Fresh tomato & tomato ketchup is borderline at just over 20mg & chopped tomato is fine!

So as you can see, there are less than a handful of non-fermented plant foods which are high in histamine (though of course fermented plant foods like sauerkraut aren’t included and are known to be high in histamine).  I don’t know about you but this tiny list is a massive shock!  To think I’ve been missing out on loads of foods for no good reason for the past five years is heartbreaking.

This isn’t the full picture however.  The research paper suggests that it isn’t just histamine which may be causing a problem for HIT patients.  Other biogenic amines, such as putrescine, compete for DAO and the reason that patients report issues with foods low in histamine may be that they’re high in other amines.  We have no evidence this is true though – bare in mind it’s just a theory and might be totally wrong.

The biogenic amine putrescine is found in nearly all foods to some degree, so again we have no idea what a high level is, so I’m using 20mg/kg as my figure but it’s not based on anything.  The following is a list of ‘high’ putrescine foods – if you react to any of these, none of which are high in histamine, it might be you have an issue with putrescine instead:

  • Green pepper
  • Sweetcorn
  • Tomato, fresh, concentrate & ketchup
  • Peas (fresh & frozen)
  • Soybeans, dried & sprouted (but not soya milk or tofu!)
  • Banana
  • Grapefruit, fresh (juice is borderline)
  • Mandarin
  • Orange
  • Passion fruit
  • Pear is borderline
  • Papaya is borderline
  • Pistachios
  • Wheatgerm (but not bread or other wheat based products)
  • Green beans
  • Purple beans
  • Broccoli was borderline in 1 study but fine in the others
  • Courgette was borderline
  • Cucumber was borderline in 1 study but fine in the others

I regularly eat several of the foods on this list, including bananas, passion fruit, pear, broccoli, courgette, green peppers, sweetcorn and peas and have no problems with them whatsoever.  However, you may have a totally different experience.

Tyramine, another amine, was found in some of the foods tested, though in very low levels.   So using pure guesswork and nothing else I’ve based my ‘high’ figure on foods which contain a level of tyramine of 5m/kg – it’s not based on anything though and could be way off the mark.  Foods with a ‘high’ level of tyramine include:

  • Fresh tomato
  • Avocado
  • Plum
  • Green beans are borderline

Bare in mind that tomatoes and avocado contain relatively high levels of histamine, so you may react to those due to their histamine content, but if you have a problem with plums or green beans it might be due to their tyramine content.

Cadaverine was found in some of the foods tested, though like Tyramine in very low levels.   So using pure guesswork and nothing else I’ve based my ‘high’ figure on foods which contain a level of cadaverine of 5m/kg.  These include:

  • Spinach
  • Soy milk was high in 1 study but fine in the other
  • Tofu
  • Pistachios
  • Green peppers were borderline
  • Banana was high in 1 study but undetectable in the others
  • Grape was borderline
  • Almonds were borderline
  • Sunflower seeds were high in 1 study but undetctable in the other

The biggest question people new to low histamine diets asks is, “now I know what I can’t eat, but no-one tells me what I can eat!” and this new paper helps with this.  There is a long list of plant based foods which are low in all amines including:

  • Lettuce
  • Onion
  • Red pepper
  • Potato
  • Apple, fresh & juice
  • Grape
  • Cherry
  • Guava
  • Kiwi
  • Lemon
  • Mango
  • Peach
  • Pineapple (fresh & juice)
  • Strawberry
  • Hazelnuts
  • Barley
  • White bread
  • Wholemeal bread
  • Corn-based cereal
  • Oats
  • Pasta
  • Rice
  • Asparagus
  • Yellow beans
  • Cabbage
  • Cauliflower
  • Carrots
  • Celariac
  • Chard

If you have symptoms after eating any of these foods it looks like it’s down to a problem not related to biogenic amines and therefore isn’t Histamine Intolerance.

There are some interesting foods on the ‘allowed’ list.  Bread contains yeast and yeast is banned from most low histamine foods lists, however from the research trawl I did for my Histamine in foods: the Evidence page, and from this research paper, baker’s yeast (ie the yeast used in bread) tested low for histamine, it was the yeast extract (a by-product of brewer’s yeast) found in marmite which was the problem.  Many low histamine food lists exclude nuts but most appear to be low in all amines so should be fine.  Soya beans are also excluded on all low histamine lists, yet tofu and soya milk tested low in all amines and soy beans tested low in histamine yet high in putrescine.  It’s the fruit which has shocked me the most though.  Berries, cherries, pears, plums and pineapple are all excluded from low histamine food lists yet all are low in histamine and most are low in all amines so I will be eating strawberries again before the week is out (I already eat blueberries and drink pear juice daily so knew I had no problem with them).

Although dairy foods weren’t looked at in this particular research paper milk, fresh cheeses like mozzarella (but not hard or blue cheeses!), butter, cream and yoghurt have all been found to be low in histamine, though I’m unsure of their other biogenic amine content – I’ll look into that when I’m not suffering from a sickening migraine, which I currently am :-/  Most fresh meats have also tested low for histamine, but again I’m unsure of their other amine content.  So, all in all low histamine diets don’t need to be anywhere near as restrictive as they are which really is great news 🙂

In light of recent evidence I’m going to totally re-vamp the low histamine food list on my blog when I have the time, energy and brain power.  I haven’t been following the list faithfully for a long time and am managing my HIT symptoms really well, so for me the list here on my blog is way too restrictive.  However, as I say all the time, my blog reflects my experience and yours may be totally different.

The new research paper talks about cooking methods and the fact that boiling vegetables reduced their histamine content, sometimes dramatically.  So, if you’re having an issue eating raw veg you might want to try boiling it and eating it cooked instead.

The other thing to mention while I’m on about food reactions is that Mast Cell Activation Disorder (MCAD) and Histamine Intolerance (HIT) are two distinct and separate illnesses.  Patients with HIT only have a problem with amine-related foods, while people with MCAD can react to just about anything so trying to control MCAD symptoms by a low histamine diet alone is fruitless.  The two diseases can sometimes occur together as in my own case, but many people ‘just’ have HIT and most people with MCAD ‘just’ have MCAD, so  when I talk about low histamine diets I’m exclusively talking about controlling HIT.  If people with MCAD find eating low histamine helps some of their symptoms too that’s great but it’s much more complicated than just diet for mast cell diseases.  If you’ve been religiously following a low histamine diet for more than 6 months and are still reacting to foods, or are reacting to foods low in biogenic amines, or are reacting to other things in the environment like heat or cold, your period makes your reactions worse, stress or strong emotions like excitement make your reactions worse and/or your hair is falling out, I would imagine you have more than HIT going on and it’s much more likely you have a mast cell issue.

Short ranty post

I feel dreadful this morning so this is just a short post to let off steam.  I recently saw this post on the ME Association’s Facebook page.  It’s research using hand grip strength  as a diagnostic biomarker for M.E.  Really?  Like……..really?!!  Can you imagine going in to the GP’s Surgery, shaking the Doctor’s hand and her saying “yes, you’ve definitely got cancer I can tell from how weak your hands are”.  I have never heard such utter tosh in all my life and the fact that money has been spent on this bollocks makes me livid.

I was chatting about it with my bestie at lunch on Sunday and we both agree that we are quite strong for girls.  In the years when I was doing up my little cottage I once bent a chisel.  My cousin, a builder, said “Jak, it’s not possible to bend a chisel” until I showed him mine, to which he replied “are you a fucking super human or just a freak?!”  The answer to which is probably just a freak, but a strong freak nevertheless.

My besite is also strong for a girl.  We’re both quite masculine in our personalities, so maybe we have more testosterone than your average female, who knows?  My grip has definitely weakened over the last decade but that’s much more to do with pain and ligament weakness from my Ehlers-Danlos Syndrome than anything to do with my M.E.

My Dad has a weak grip, but then he has spinal issues – neurological diseases, of which M.E is one, tends to cause weakness.  My Mum also has a very weak grip, but then she’s had two lots of hand surgery for Dupytrens Contracture, also has hEDS and has survived Guillain Barre Syndrome which has left her with permanent nerve damage.  Anyone who is ill tends to be weaker than when they are well.  If you’ve been up all night puking with a tummy bug you’re going to feel pretty floppy the next day.  Since when is having a weak grip any indicator of a specific disease – it could be caused by sodding anything!

That a medical team would waste money, time and resources doing research like this drives me to despair when we are so much in need of an actual biomarker for this devastating disease.



Testing for Histamine – BIG news!

I was lying in bed this morning listening to BBC Breakfast news.  They were doing a review of the newspapers and my ears pricked up when they started talking about a mobile phone sensor which could test to see if a food is off or not.   I know enough to realize that food goes off because it produces biogenic amines, of which histamine is one, and I was suddenly sitting bolt upright in bed feeling very excited!

Unfortunately the news presenter didn’t say which paper the article was in, so I simply Googled ‘phone sensor histamine 2018’ and found the research the piece was based on, which is taking place at the City University of Hong Kong.  The researchers were looking mainly at ways to test for spoiled foods, but I wanted them to know there was a huge world-wide patient population desperate for a way to easily test for histamine in foods because they suffered from either HIT, MCAD or both so I emailed the lead researcher A. L. Roy Vellaisamy PhD to briefly explain about us all and tell him how vital his device could be for us.

I couldn’t believe my eyes when, just a few hours later and on a Sunday, Roy mailed me back to say he’d read my blog and learned loads about how big an issue histamine in foods is for us.  Not only that, but he asked if I’d be willing to test his mobile sensor as they were trying to fine tune the device.  Is The Pope Catholic?!  Of course I’d like to test the device!!  Being able to test for histamine in foods on a mobile phone would revolutionize not only my, but most of your, lives.

I’m now just waiting to hear back about the logistics and what I’d have to do – I’ll keep you posted 😀





Back in 2016 I became aware of a gene study in which researchers at the Institute for Neuro Immune Medicine were hoping to put together a genetic database of over 10,000 patients with ME/CFS so that genetic information would be available for researchers looking into the cause of the disease.  Luckily I’d had my genetic data mapped by 23andme years ago so I was able to participate in the study which simply involved filling out a questionnaire and sending off my RAW data via email.

I heard nothing for 2 years and then this week received a message to say that I had a MTHFR mutation and researchers were interested in studying this.  Up to 50% of the population may have a MTHFR mutation and it doesn’t mean you are going to develop a disease.  In fact it usually has no impact on health at all, though it may predispose people to certain illnesses if other environmental factors are present or mutations in related genes are found.

Amongst other things, the MTHFR gene is responsible for the conversion of folate (also called folic acid or vitamin B9) from the food we eat into activated folate.  When the MTHFR gene is mutated this conversion doesn’t work as well and can result in a folate deficiency.  Activated folate belongs to a group of ‘energy’ vitamins and a deficiency may produce fatigue and cognitive changes.

The new study would involve taking a L-Methylfolate supplement (the active form of folate) for 3 months to see if it had any impact on symptoms.  Unfortunately, however, as the research involves a blood draw it’s only available to people living in the United States so sadly that rules me out which is a shame as the fact it doesn’t involve taking drugs means it’s probably the one study I could have taken part in!

My only concern with much of the current research into ME/CFS is that it focuses on fatigue, and while fatigue is obviously a large part of the disease ME is not chronic fatigue.  It’s characteristic symptom is post exertional MALAISE.  I feel ill when I’ve done too much (in fact, I feel ill most days of my life) and it’s this researchers need to study.  If I’m on the computer for too long I start to get a sore throat and if I walk too far I start to feel fluey – I’m not simply ‘tired’.  As there is no diagnostic test for ME many people with chronic fatigue of unknown cause have been diagnosed with it and it’s sadly become a bit of a dumping ground which can only muddy the waters for researchers.  If you take a L-Methylfolate supplement and suddenly feel loads better you didn’t have ME in the first place, you had a folate issue.

While the MTHFR gene has other functions and may be implicated in cardiovascular disease, I personally don’t think MTHFR mutations are going to be the answer to ME, at least not unless they have some kind of massive impact on people’s immune systems we as yet know nothing about.  That’s my take on the situation anyhow but then I am a cynical old timer 😉  In fact, I wrote a post about MTHFR back in 2015 which states my views on the whole MTHFR issue – be warned, I’m not exactly on board the MTHFR band wagon.

ME aside, if having a MTHFR mutation can make you tired that’s obviously not a good thing when you already feel like the walking dead.  Luckily folate rich foods naturally contain the active form of folate and studies have shown that a folate-rich diet can match the homocysteine-lowering effects of a L-Methylfolate supplement.  My diet is already quite rich in high folate foods, such as beans, lentils, broccoli and mangoes though if you have a MTHFR mutation and are unable to eat folate rich foods it might be worth taking a L-Methylfolate supplement but be warned they can have side effects which you can read about here.  Personally I’m not giving the whole MTHFR mutation a second’s thought, that’s just my personal choice.

If any of you would like an informative, easy to read guide on MTHFR there is a decent one here.


The Heart in M.E.

I am a sun worshipper, probably because I live in the wettest place in England and we don’t see much of it, so the second the sun does come out I’m there basking like a lizard on a stone.  However, although it reduces my pain levels and makes me feel mentally good it kills me physically.  I can’t sit directly in the sun because I start to sweat, then my heart has to start pumping harder to cool me down and very shortly I feel like I’ve been hit by an express train – weak, brain fogged, fluey, achey and just generally ill.  When I was severely affected with M.E. I couldn’t go outside in hot weather at all.  After just half an hour I felt so poorly I would have to crawl my way back to bed and it would take hours for me to recover.

There’s been lots of research which has looked at energy metabolism and muscle dysfunction in M.E., but just lying reclining on a sun lounger doesn’t require mental or physical exertion or muscle energy expenditure.  Sweating, however, requires an increase in cardiac function.

I don’t know why in all these years I haven’t thought about that before.  It just came to me the other day when I was outside in the little mini heatwave we’re having, wanting to lie with my head in the lovely sunshine but knowing I couldn’t because if I did I would get too hot and feel like I’d been run over by a bus and I’m not alone.  The majority of my friends with M.E. find hot weather makes them worse and none of my severely affected friends are able to sunbathe.  The same goes for hot baths, which are hugely beneficial for my muscle spasms and pain levels but make me feel absolutely rubbish in every other way.

When I’ve given it thought before I always assumed it was a dysautonomia problem.  Heat causes your blood vessels to widen, which causes more blood pooling in the feet and less blood reaches the brain, and while I’m sure that’s still part of the issue it’s not the full picture.  I get ill lying down in the sun so the POTS theory doesn’t really fit.  It suddenly dawned on me that the only thing having to working extra hard when I’m hot is my heart.

M.E. is a disease of exercise intolerance.  Having a shower, for me, is like climbing the north face of th Eiger and leaves me absolutely and utterly knackered.  I haven’t run in over two decades and doing any activity which elevates my heart rate flaws me.   You would think there absolutely has to be a cardiac problem involved in M.E.

Several small scale studies have been done on heart function, mainly by the CFS research team at Newcastle University in the UK, and although they’ve found some abnormalities in short QT waves and output nothing major which affects all patients has ever shown up.  Something catastrophic is happening inside our bodies but no matter how hard researchers look so far they haven’t been able to figure out what’s going on, which is the main reason the disease has always provoked such controversy.

Decades of research has now been carried but IMHO we’re realistically no further forward in finding out the cause of M.E.   Little clues here and there but nothing concrete or definitive.  I wonder when, or if, that’s ever going to change?



Jen Brea’s wonderful docu-film on M.E. ‘Unrest’ is still being shown around the world and if you haven’t seen it yet and suffer from chronic illness or care for someone who does you absolutely should, whether you have M.E. or not.  It was recently screened at UC Berkley and there followed a panel discussion with some of the leading M.E. researchers in the world which is available to view for free here.  I learned nothing from the discussion that I didn’t already know but it made a refreshing change to hear Ron Davis’ honest point that we have no idea as yet what causes the disease and I was heartened to learn that he shares my hypothesis that it is a single entity and will turn out to be something very simple.  M.E. causes widespread symptoms, the severity of which differs between patients (as happens in other neuro-immune diseases such as Multiple Sclerosis) but the causal trigger will be the same mechanism for everyone and IMHO will be an issue with our immune system.  I will not be swayed from this view so don’t bother trying 😉

One of the points that I took away from the discussion, which involved questions from patients, is how we all have our own bias when talking about M.E., myself included.  Erik Johnson, a long term advocate of CFS, believes his and many other people’s illness was triggered by Sick Building Syndrome/mould.  Another patient asked about EMF (electromagnetic fields) and their role in the disease.  I read lots of comments online from patients who are convinced they know the cause of M.E. and it’s x, y or z depending on how their own illness developed, none of whose views I share.

My own illness was triggered by a viral infection but later made significantly worse by travel vaccinations, however I don’t blame the vaccine or any component of it such as preservatives or heavy metals for making me ill – I blame my immune system for not responding appropriately to the injection.  Just like I blame Erik’s immune system for not responding appropriately to mould, not the mould itself.  As I said earlier I’m convinced that a breakdown in the functioning of part of our immune system will turn out to be the cause of M.E. and the triggers will vary – for some it will be vaccinations, for others mould exposure, for others viral infections and so on.  It’s the only model which fits everyone.

M.E. can, and does, run in families so of course the subject of genes came up.  I’m not convinced by the genetic argument or that genes are particularly implicated, at least not at the level we currently understand.  What I do think is that our immune system is genetically influenced, for example parents with allergies often have children prone to allergies, so it stands to reason that the potential for the immune system to be dysfunctional can be genetically inherited but again the environmental trigger for that dysfunction will differ from person to person.  I’m unconvinced, however, that the conclusion is going to be that ‘gene x mutation predisposes towards M.E.’.  The answer is going to be simple but not that simple.

The one thing I am utterly convinced about is that M.E. is treatable, no matter how seriously ill a person is, and that full recovery is absolutely possible.  It may be that we need to take medication for the rest of our lives to keep our immune system functioning healthily but I know I have glimpsed almost full remission following changes in my immune system (when starting with a cold for example) and if we can replicate these changes using drugs returning to full health is not beyond the realms of possibility.  In fact, it’s a certainty.  Having said all that, decades of illness will have affected our bodies and things like heart disease and osteoporosis from years of inactivity will be a lingering legacy.

‘Unres’t is available to view on DVD, Netflix, iTunes, Google Play, Vimeo and other platforms.





Research trends

I’ve mentioned recently my frustration at the current research trend in the M.E. world to focus on energy production when, as a sufferer, I know that the ‘fatigue’ (for want of a better term) I experience is merely a symptom of immune activation not the root cause of my disease. Researchers have been studying energy production, in particular the mitochondria, as a cause for M.E. for over 20 years now and still haven’t found anything, which leads me to conclude there is nothing to find.  I’m not suggesting that mitochondrial dysfunction isn’t part of the disease picture but it’s definitely not the cause.  I wish these people would talk to patients more, especially we old timers who’ve lived with the illness for decades!

I’m equally unconvinced by the current trend to put every ailment known to man down to gut issues (SIBO, flora, bacteria etc) – it just feels like the current ‘hot new thing’ in a very long line of ‘hot new things’ on which to pin disease.  My Dad excitedly kept an article out of his newspaper for me this week which touted “answer to chronic fatigue syndrome found in the gut” and, much as I love him, I just sighed.  Here’s the thing: most cases of M.E. start with some kind of viral or toxic event (OP poisoning, vaccinations) but the event is different in all of us – mine was a tummy bug, yours might have been glandular fever, someone else’s a Hep B vaccine.   If we’d all started with a tummy bug then I’d be much more open to the disturbed gut theory, but we didn’t.  The one thing we share is immune activation, so for me the answer has to lie in the immune system and in particular its response to viral or toxic trauma.  As I’ve said before, if researchers studied why people with the flu are so weak and exhausted they can barely get out of bed they’d go a long way to finding out the cause of M.E.  In fact, it gobsmacks me that no-one has looked at that before now!

No offence to my American friends, but there is a mould trend going on in the States with everyone convinced that mould is the root cause of their issues and it makes me want to chuckle.  Northern England is wet for 10 (sometimes 12) months of the year, humid in summer, we mostly live in houses which are at least 100 years old and inherently damp, so I’m sure mould is everywhere.  We couldn’t escape it if we tried.  Yet not every Brit you meet is sick and we don’t have a larger M.E. population than any other country as far as I’m aware.  Obviously rampant mould growth, where you have black stuff growing on your ceiling, is hazardous to health and must be dealt with but other than that we in the UK don’t give mould a second’s thought – it’s been around a lot longer than we have and as a species we’ve managed to survive.

I’m just as cynical about the current inflammatory trend.  Inflammation, it seems, is everywhere and is causing total havoc.  Only of course it’s almost impossible to measure inflammation or to say, if inflammation is present, why it’s there and whether it’s a good thing or a bad thing.  When we cut ourselves the wound is immediately inflamed which is a painful, but absolutely necessary, part of our body’s response and vital for healing.  And before anyone comments, yes I know there’s a difference between acute and chronic inflammation but who’s to say chronic inflammation isn’t just as protective as acute?  It’s got to be there for a reason and we’d do better to find out why our bodies are enlisting our inflammatory response, rather than blaming the inflammation itself.

Going off-topic slightly, the trend of foods purportedly giving you every disease from cancer to Alzheimer’s drives me insane.  We have no idea what causes Cancer and even less idea what causes dementia, so for anyone to say “burnt sausages give you cancer” or “broccoli reduces your risk of Alzheimer’s” is absolutely absurd and makes me furious.  In fact, I’d go as far as to say researchers who tout this nonsense should be prosecuted.  The same goes for anti-inflammatory foods.  If we have no accurate way of measuring inflammation, how do we know what foods affect it?!

There have been articles in the newspaper this year saying “exercise staves off dementia” and “lack of sleep increases risk of dementia” and I think “what a crock of shit!”  My Dad, who is 78, still walks 8 miles a week up a mountain and, as a former marathon runner, has exercised vigorously his entire life.   He’s never had insomnia and sleeps 9-10 hours a night without a problem, yet has dementia.  My Mum, on the other hand, hasn’t exercised since she was a child and wakes at least twice a night every night, yet she is totally mentally on the ball (when she’s not drunk!).  All these articles do is play on people’s emotions.  We don’t have a clue what causes Cancer or Alzheimer’s and that lack of control scares us, so we focus on what we eat or how much we exercise because those are two things we can control and it makes us feel better.

I’m no psychologist, but much of the information currently touted as being bad for our health, or good for our health, is environmental – sleep, exercise, food and living conditions.  In other words, all things we can control.  We’re extremely fearful of the fact that Alzheimer’s or Cancer might be viral, bacterial, or genetic, or even worse some novel new thing we as yet know nothing about, and therefore outside of our control.  We’re fairly arrogant us humans and think that we have power over our bodies, when in fact life is mostly just random and shit simply happens.  If keeping mentally alert staves off Alzheimer’s how come author Terry Prachett developed it in his 50s?  If the phytoestrogens found in soya stave off breast cancer how come soy munching vegetarian Linda McCartney died from the disease?  How come my Mum, a lifelong smoker, couch potato and current alcoholic, is nearly 80 and has never had cancer and her non-smoking, tea-total, bike riding sister died from it?  None of it makes sense and that’s the very thing that scares us the most.

I have no voice

As I’ve mentioned in recent posts, when I first contracted M.E. I was determined to raise the profile of my illness.  Back in the early 1990s nothing was known about the disease, it wasn’t in the public or the medical professional’s field of consciousness, and only a handful of people world-wide were fighting for M.E. patients.  I took part in every study going.  I wrote articles in the press.  I wrote to any ill-informed doctor I ever saw, educating them on my disease.  I attended conferences even though the effort nearly killed me.  But it was all for nothing.  No-one was listening.

The cost of activism, in terms of symptoms and energy expenditure, was too much for me and I realized I had to focus on my health instead which I did for many years.  However due to the super-human efforts of exceptional patients like Jen Brea M.E. has lately received international attention, so I thought I’d have another go at getting my voice heard.

There are some exciting research projects going on in the M.E. world and I’ve written to the researchers, eg. Ian Lipkin, Ron Davis, offering my 22 years worth of M.E. riddled body for study. They haven’t afforded me the courtesy of even replying, let alone taking me up on my offer.  I was told by the ME Association that, due to the fact I took part in the world’s only longitudonal study of severe M.E. patients (the CHROME database), that my bodily fluids would be amongst the first to be collected and stored at the UK’s ME bio-databank, which has turned out not to be the case.  They are only collecting samples from severe M.E. patients in the London area to cut down on travelling costs even though I’m willing pay for sample collection here in the north and Fed-ex it to them down the M6.

Severely affected patients are excluded from almost every study ever conducted on M.E.  How shocking is that?  Would you study Cancer and only include people who have a small skin melanoma and not people with Leukaemia?  Would you study heart disease and only include people with angina, not those with congestive heart failure?  Would you study allergies and only include people with mild hay fever and exclude anyone who has life threatening anaphylaxis?  Of course not, because you’d have a very skewed picture and the treatments to cure a small skin melanoma would not be the same as the treatments needed to cure Leukaemia even though they are both cancers.

If you studied cancer, would you exclude anyone who had recovered?  Surely you’d want to find out why they’d recovered.  It’s very rare for someone as ill as me for as long as I have been to make any kind of recovery from severe M.E. yet here I am, OK not ‘better’ but a million times better than I used to be.  Yet no-one is interested in finding out why!  It makes me want to scream.

The only M.E. patients well enough to travel to hospitals for research studies are the mild to moderately affected.  The severely affected are in their beds too sick to crawl to the loo.  So, hey, let’s just ignore them – what can they tell us about the disease anyway right?!!  The longer you have severe M.E. the more health problems you seem to accumulate, yet long-term severe patients are the most ignored of all.  Going back to cancer as an example, would you only study people who had cancer for 6 months or people who had lived with the disease for 10 years and managed to survive?

The world may not want to listen to a sick old timer like me, but thankfully they are listening to Jen Brea who this week made the first TED talk on M.E.  I hope all her effort isn’t in vain.  I hope M.E. researchers finally wake up to the fact that the answer to this disease lies in the severely affected patient’s hands, particularly those who have been sick for many years, and makes an effort to reach out to us.