Tag Archives: mast cells

Liberate me from the liberators!

I rarely talk about food on my blog these days.  For the first 2 or 3 years it was all I could talk about because I’d spent 18 months battling severe reactions after eating, not to mention after any kind of medication, and honestly thought I’d die so, naturally, the topic was all-consuming.  But my Histamine Intolerance and Mast Cell Activation Syndrome are, for the most part, under control now and have been for at least a couple of years so I’m happy to not have to think about every single thing I put in my mouth any more and the relief is HUGE.

Now and again, some lovely person out there in the Universe will leave some catty comment here on my site.  Something like “you’re talking shit” or “this site is a joke” which is hurtful considering how ill I am and the effort which has gone in to 6 years of writing twice weekly posts, not to mention the thousands of hours that have gone into research, putting together information, links and photographs, or all the recipes I’ve made available here for free, but not everyone in the world is nice or has manners so you just have to take it on the chin.  A couple of weeks ago, one of these kind people left a message on one of my histamine-related food pages to the effect that the information was out of date and I might like to sort that out.  I was taken aback, as I’d only revisited the page in January this year and hadn’t heard on the grapevine of any significant new information on histamine in food lately (or ever), so I asked the poster to please point me in the direction of said new information so that I could share it with all my followers.   She didn’t reply.  They rarely do when asked to provide proof to back up their claims.

I had some free time today and, despite the most god awful thumping bloody headache, I decided to do some digging to see if I could find any new information on histamine in foods.  I failed miserably, but I did find an abundance of low histamine food lists and every single one had a big list of “histamine liberators”, ie those foods not actually high in histamine themselves but capable of forcing mast cells to release histamine.  Things like egg whites, strawberries, ‘additives’ (unspecified), pineapple, peanuts, fish, pork, liquorice, spices (again unspecified), tomatoes and of course citrus fruits.  Seriously?  No, really.  Seriously?!  And then people have the gall to say that my painstakingly researched information on histamine in food is out of date!

I spent nearly a year researching histamine in foods and could find zero evidence for any food “liberating” histamine from mast cells.  If you don’t believe me, Google til your fingers bleed.  There is no such thing.

Hardly any of the low histamine foods lists, even really popular ones like SIGHI, reference the research on which they base their information.  Most freely admit it’s gathered from patients,  which is about as much use as a chocolate fireguard.  There is a reason we have laboratory tests and double-blind randomized controlled trials and it’s so there is a level playing field, all the participants have exactly the same disease and no other disease (like fructose intolerance, or coeliac disease, or an issue with nightshades), and the resulting information is accurate.

So where has this myth that egg whites, citrus fruits or strawberries liberate histamine from mast cells come from?  It took me ages to work that little puzzle out and eventually I realized that where research was cited on a low histamine food list it usually came from a single source: a paper called ‘Histamine and histamine intolerance’ by Laura Maintz and Natalija Novak in 2007 which was published in the American Journal of Clinical Nutrition, and their information came from various sources cited at the end of their paper.  I followed the trail and discovered that the myth about egg whites came from ‘research’ (and I use the term loosely) by Schachter and Talesnik in 1952 (!) that egg white releases histamine in non-sensitised animals when injected intravenously.    A 64 year old single animal research study which didn’t even involve the animals actually eating anything is the basis for everyone excluding egg white on low histamine diets – jaw dropping isn’t it?   And the myth about strawberries liberating histamine came from unpublished data by Schachter in the 1950s but the paper is so old and obscure no-one has actually been able to obtain a copy to see what it actually says! In the Jul-Aug 2005 edition of the Netherlands Journal of Medicine is a paper entitled ‘Mastocytosis and adverse reactions to biogenic amines and histamine-releasing foods: what is the evidence?’ in which the authors conclude “We could not find any study on histamine-releasing effects of most of the foods suggested of having histamine-releasing capacities.”  I rest my case.

Everyone is a lot more savvy and clued up on histamine these days and there are now dozens of sites giving information on low histamine diets………….and they are all, without exception, wrong.  I simply can’t understand why these myths linger or why sites that really should know better perpetuate them.

Most of the people who write low histamine food lists are genuinely trying to be helpful and offer guidance to patients suffering from HIT and MCAS and it is nice to hear about other patients’ experiences of their safe, and not so safe, foods but it’s merely anecdotal and you simply can’t treat this kind of information as fact.  For example, buckwheat is listed on many lists as a safe food low in histamine, but I simply can’t tolerate it.  The truth is no-one has ever tested buckwheat for its histamine content as far as I’m aware and I have no clue where the testing figures or research information is that says it’s ‘safe’ for someone with HIT or MCAS to eat.

I could be wrong, of course.  There could be exciting new and accurate information on the histamine content of foods out there which I know nothing about and if so I hope one of you, my lovely readers, will tell me all about it. I’d like nothing more than to know which foods are safe to eat for someone with raging HIT and delinquent mast cells and which foods aren’t, but I suspect I’ll still be guessing by Christmas…………2030!

 

Histamine Testing

As regular readers know, last year I discovered a research team in Hong Kong who had a prototype testing device for measuring the histamine content of food.  They had made it predominantly to test for histamine in fish and seafood, but after I wrote to them explaining about our illnesses and the fact we were all desperate for a way to be able to test the histamine in other types of food they said it should be adaptable for our needs.  I was beyond excited and one of the researchers came over to the UK to demonstrate the device to me.  That was back in April, but despite saying they’d send me the prototype to try by early June I heard nothing from them.

Today I received an email from the lead researcher to say that unfortunately the company they’d approached to produce the prototype wanted $30,000 and there was no way that was affordable for them, so the project had been shelved 😦  I am absolutely and utterly gutted.

Not only has the project been shelved, but the lead researcher has left his post in Hong Kong to move to the UK in a different role so that is very much the end of that.  So my friends, we are still out in the wilderness in terms of being able to test our food for histamine and playing Russian Roulette as to whether we’ll go into anaphylactic shock or not on any given day.  Great.

A new perspective

Yesterday I read the most fascinating post by Jen Brea, author of the wonderful film Unrest.  For those that don’t know, Jen developed M.E. after a meningeal-type viral infection 8 years ago and has been severely affected ever since.  She also has dysautonomia/POTS (as many people with M.E. do), Mast Cell Activation Disorder (as many people with M.E. do) and has all the hallmark symptoms of hypermobile Ehlers-Danlos Syndrome only without the hypermobility (we hear this more and more, ie that people can appear to have connective tissue disease without having bendy joints!).

After being very ill for several years, Jen started not breathing when she lay down.  To cut a long story short, she turned out to have cervical cranial instability (CCI) and tethered cord syndrome, both of which are among several neurological and spinal problems seen in hEDS.  Jen admits she’s lucky enough to have access to one of a handful of specialists in the world who treats these diseases, and has the resources to fund surgery which she successfully had a few months ago.  She writes about the remarkable transformation the surgery has had on her health and in particular that she is now in remission from M.E.  That’s right, in remission from M.E. so severe she has been largely bedridden for 8 years!  She also says her POTS has vanished and her MCAD is getting better all the time.

Yet she had classic M.E.  No symptoms whatsoever before coming down with the meningeal-type viral infection back in 2011.  So how on earth can a viral infection, which is the precipitating factor in most cases of M.E., cause mechanical issues like CCI and tethered cord?  I’m no expert, but the obvious link is that the viral infection affects mast cells (which I’ve been saying for eons), which then weakens/affects connective tissue (as mast cells live in connective tissue) and this weakened connective tissue then doesn’t hold the spine in place properly.   Of course, weakened connective tissue can also affect veins (leading to POTS) and all the other symptoms we see in traditional hEDS including things like gastroparesis and chronic pain.  Having our spinal cord compressed would also account for brain fog, pins and needles, muscle twitching, vertigo and many of the other symptoms found in M.E.

So it looks like there may be two issues going on.  There are people, like myself, who were born with hEDS.  This may pre-dispose us to developing M.E. due to the issues having faulty connective tissue has on our mast cells, which are at some stage in our lives triggered by a viral infection.

There are also people who don’t have hEDS, but who develop a viral infection which affects mast cells, which in turn affects connective tissue.

So, one is the chicken and one is the egg but the end result is the same.

I have no doubt I have cervical cranial instability.  For a start my head feels like a bowling ball sat on top of my neck and is much of the reason I have to spend 17 hours of every day in bed – I simply can’t hold my head up all day.  Plus, if I’m sat upright and til my head backwards even a little way the room starts to spin, I get severe buzzy pins and needles throughout my entire nervous system, I develop palpitations, my brain feels like it’s cramping and just feel really, really, weird.  I have also suffered from lower back pain since I was 11 years old, which wasn’t cured following surgery for rare congenital spinal stenosis.  I can only assume I also have tethered cord or some other hEDS related spinal issue.  Not that I’m going to attempt surgery for either, as I don’t have the money or support, and can’t tolerate the drugs or analgesics used in surgery even if I did.

It’s all food for thought.  I’ve long suspected faulty mast cells to be at the heart of everything so, rather than going through the drastic step of surgery for CCI and other spinal issues, surely if we can inhibit mast cells that would stop the connective tissue from being weakened in the first place?  At least for people not born with hEDS.

For those who have genetically weakened connective tissue the issue is more complex, but even so if we can inhibit mast cells would that not theoretically make our connective tissue less unstable?

I don’t know if any of my thoughts on the mechanisms involved in M.E. are on the money – I’m so dizzy and have such severe brain fog today it’s a wonder I’m functioning at all 😉  I’m sure my less brain-fogged and more intelligent readers will share their own theories.

I’m so thrilled for Jen though.  She’s been to hell and back, yet despite that managed to make the best film I’ve ever seen on M.E. and promote it world wide.  She deserves to be well and I hope her recovery goes from strength to strength.

MCAD v HIT

I’ve noticed that whenever I talk about histamine and food here on my blog there is often confusion about the cause of food reactions, so I thought I’d write down my take on what’s happening.  I’m no expert, though, just a patient along with the rest of you so I could be well off the mark and I’m sure if I am someone will point it out 😉 .

I’ve had MCAD my whole life, but I have never reacted to foods.  I don’t have a nut allergy, or a gluten allergy, for example and have always been able to eat whatever I like.  I know I’m extremely lucky and many of my readers aren’t so fortunate.

I only started reacting to food when I was in my mid forties.  It came on gradually over a few years.  Bright red flushing after meals, increasingly itchy skin, hives which I’d never had before and out-of-control acid reflux.  Eventually in 2013 all hell broke loose and I started having anaphylactic reactions after I ate anything – severe palpitations, muscle spasms (particularly in my gut and back), weird head rushes that felt like I was having a stroke, anxiety (obviously the whole situation made me anxious, but the adrenalin fuelled anxiety from anaphylaxis is a different thing altogether), huge spikes then huge crashes in blood pressure, and eventually I’d just pass out.  It was terrifying and I had absolutely no clue what was going on.

To cut a very long story short I paid to see Dr Seneviratne at St Mary’s, who tested my DAO levels which were well below normal and he diagnosed me with Histamine Intolerance (HIT).  I’d never heard of the disease before so it was a steep learning curve!   Most foods contain small levels of histamine but some foods contain large amounts.  I don’t eat meat, and it turns out that many of the staple vegetarian foods I was eating every day (cheese, tinned tomatoes, soya beans, spinach, aubergiene) are all high in histamine :-/  Our bodies also produce histamine as part of the digestive process which is why I could react some days after drinking just water!   Fortunately we have a couple of enzymes in our bodes, DAO and HNMT, which ‘mop up’ the histamine we ingest so that it doesn’t cause us any problems.  For people with HIT, however, the enzymes are low or not working correctly so the histamine we eat in foods, and the histamine produced from digestion, accumulate in our bodies.  It’s a bucket effect – the more histamine we eat the more it builds up, and eventually the bucket overfills and we have a reaction.  No one specific food does this – it’s a cumulative effect.  I embarked on a low histamine diet and within 4 months my food reactions were under control – they hadn’t gone, but they were manageable.

There are various reasons why, if we suffer from Histamine Intolerance, our DAO and/or HNMT levels could be low.  For example, they can be reduced by taking certain medications, in which case if you cease taking the drugs the enzymes should return to normal and the HIT would only be temporary.  In my case, however, I have no idea why my DAO isn’t as it should be – I wasn’t on any drugs, my diet was very healthy and I hadn’t had any major tummy bugs or infections.  For me, HIT seems to be a permanent problem and if I veer off my low histamine diet the anaphylactic reactions come back within a couple of weeks 😦

Because histamine build-up in HIT is a bucket effect, I can often have no problems eating my breakfast in the morning but I can quite often react to my dinner in the evening, because histamine has accumulated during the day.  So I tend to eat my main meal at lunchtime and just have a small snack at night.

The food issues faced by HIT patients are very different to the food issues faced by many Mast Cell Disease patients.  In MCAD the immune system is treating totally normal foods as a foreign invader and mounting a defence against them.  It could be any food and will differ from patient to patient.   It is not a build-up and the reaction comes on soon after the food is eaten (although some people do have mild, delayed reactions which muddies the waters!).  In MCAD our mast cells release chemicals including, but not limited to, histamine which then gives us an allergic-type reaction.   Our immune system doesn’t care whether the food is high in histamine or not – it can react to any food it likes which makes treating MCAD food reactions much harder than treating HIT food reactions!   For some people with MCAD the immune system is so over-reactive they are left with only a handful of foods that are ‘safe’ 😦

It’s important to note that in MCAD the immune system doesn’t just react to food – our mast cells can react adversely to just about anything in our environment.  My biggest reactions are to drugs – my mast cells hate them – but I also react to stress, hormones, some smells, pollen, my dog and often my own emotions.

The biggest difference between HIT and MCAD, is that HIT is a food issue only Stop eating high histamine foods and it is possible to get your HIT under control.  In MCAD the issue is much, much wider and not eating high histamine foods won’t alter the fact your mast cells react to hairspray, the smell of bleach or your hamster.

MCAD and HIT are totally distinct and separate illnesses – you can have HIT without having MCAD, and MCAD without having HIT.  However, if you’re unlucky enough to have both they can definitely affect each other and I think that’s where much of the confusion around food comes from.  I have people comment on my blog that they are following a low histamine diet but still reacting to all sorts of foods and of course they will if they suffer from mast cell disease.  Following a low histamine diet will only stop reactions after eating if you suffer solely from HIT.  It might reduce your symptoms if you have MCAD, because if your body is already over-whelmed by histamine adding to the load by eating lots of food high in histamine probably won’t help the situation, but a low histamine diet most definitely won’t cure all your symptoms which are caused by factors other than food.  At least that’s been mine and my friends’ experience.  So it’s important to know whether you’re suffering from HIT, MCAD or a combination of the two because management strategies will be very different, and you can only know this if you are tested by someone knowledgeable in both diseases (easier said than done I know, especially in the UK).

As far as I know there is no data available on whether HIT is more common in the mast cell disease population.  It would be interesting to know if there’s a link, because every piece of the puzzle is important when we’re trying to work out what causes disease and how to treat it.

 

Mast Cells & M.E.

Leading Doctors in the M.E. field are slowly coming to the realization that Mast Cell Activation Syndrome (MCAS) is common in their patients, with some finding issues with mast cells in more than 60% of the people they test (see this post by my friend and fellow blogger over at Rag & Bone Shop of the Heart).

Ever since I first learned about MCAS I knew, for sure, it was implicated in M.E. as I explain in my Canary post.  In particular it explains why POTS/orthostatic intolerance is almost universal in M.E. patients, why reactions to foods, drugs and the environment are so prevalent and why nothing is ever found on testing, despite some patients being profoundly ill (no-one has been testing for mast cell mediators!).

Where I disagree with most clinicians looking at the link between mast cell activation and M.E. is that doctors think it only applies to a sub-set of patients, while I think it is implicated in the disease in all patients.

I am convinced I was born with MCAS.  I think it can either be congenital (in my case it seems to be linked to my hEDS) or acquired later in life due to an immune event like a virus, vaccination or surgery.  I have photos of myself as a baby flushing my cute little face off and have had dermographism ever since I can remember, but I had no clue I had MCAS until I was in my mid forties because it wasn’t a problem until the peri-menopause set it off.  My point being it can go undetected in the majority of patients until something happens to rocket it into orbit.

For a decade I was life-threateningly ill with M.E., yet I could eat whatever I liked, take most medications without a problem, didn’t have hives, asthma, itchy skin or any of the other symptoms associated with MCAS.  But that didn’t mean it wasn’t there, lurking.

Looking back I’d flushed all my life (I didn’t know it was flushing, I had no idea why I went bright red all the time!), I could skin write and I’d been unable to drink alcohol without my face swelling or passing out since developing M.E (which I now know is grade III anaphylaxis), but other than that there were no obvious signs of mast cell mediator release.

In my mid thirties, after having M.E. for ten years, I started to become allergic to medications, many of which like paracetomol (tylenol) and travel sickness tablets I’d taken all my life.  I developed a tight chest around certain smells and the print ink off newspapers made me wheezy.  I also developed severe migraines almost out of the blue, hay fever each spring which I’d never had before in my life and started getting itchy lumps on my bum which I had no idea were hives.  I also had what doctors called either “A-typical seizures” if they believed in M.E., or “panic attacks” if they didn’t believe in M.E., but which I now know was anaphylaxis.

In my mid forties I started peri-menopause and all hell broke loose virtually overnight.  It was then I began reacting to all medications and nearly every food I put in my mouth, to the point where I honestly believed I’d die.  I’d had M.E. for 18 years at this point though and although there had been hints all along if I’d known to look for them, my mast cells hadn’t gone berserk enough for me to be really troubled by them or to link them to my M.E. in any way.

All my friends with M.E., without exception, have an allergy of some kind and the more severely affected by M.E. they are the more allergic they seem to be.  My best mate has never been severely affected, yet still has asthma, hay fever, POTS and auto-immune diseases (confirmed Coeliac in her thirties despite having no symptoms whatsoever at the time and confirmed Palindromic Rheumatism in her forties after suddenly developing swelling joints and skin problems).  It’s way too much of a coincidence that nearly all long term M.E. patients have, or develop, allergic reactions, many have auto-immune diseases and all have some kind of orthostatic intolerance.  There has to be some kind of missing link and, for me, that’s misbehaving mast cells.

It’s the only thing which fits.  It’s the only thing which causes seemingly unrelated systemic symptoms like insomnia, back pain, diarrhea, migraine, food allergies, breathing problems, fatigue, that tired-but-wired feeling, nausea, inflammation and on and on and on.  And of course no-one has been testing for it, which is why no-one has been able to find a test for M.E.

So if mast cells underly M.E. why don’t all patients tested have evidence of mediator release?  I’m just a patient and no kind of expert but I do have a couple of theories:

  • Because there is no test for M.E. lost of people are diagnosed with the disease that don’t actually have it.   I know this because of all the ‘cured’ stories I read in the press from people who clearly didn’t have M.E. in the first place, yet were diagnosed by GPs because the disease has become a dumping ground for anyone with unexplained fatigue.
  • Despite being seriously ill, having anaphylaxis every time I ate and having a bum covered in hives my histamine test when I saw Dr Seneviratne was still within the normal range!  Very high but not quite high enough to be considered abnormal.  I didn’t have any other tests, like leukotrienes and chromoglanin A, done because five years ago these weren’t available in the UK and I was only diagnosed with ‘probable’ MCAS based on my history and symptoms.  So it doesn’t take a rocket scientist to work out that the current mediator release tests simply aren’t sophisticated enough.  They’re looking for acute mediator release, not the chronic mediator release experienced by MCAS sufferers.  Maybe we need to re-think what the maximum levels are, or maybe we need to repeat test weekly over a period of say a month or two?  I’d love to be tested while I’m having my period because my reactions are so much worse then.

Being one of the first people to talk about the link between mast cells and M.E. I am delighted that the medical profession finally seem to be catching on and that M.E. patients in America at least are now being more routinely tested for MCAS.  We really need a large scale study of severely affected patients though, and much more sophisticated tests to check for chronic mediator release, but at least we finally seem to be making a start.  “The journey of a thousand miles begins with one step”.

Mast Cells in M.E.

This month a two day summit was held in America for clinicians working in the field of CFS/M.E. and long-time advocates and ME Doctors David Kaufman, Charles Lapp and Susan Levine all discussed the fact that they are now suspecting mast cell activation as either a cause, effect or perpetrator of the disease – their views are outlined in this piece from Medscape.  Having thought this for five years now I hate to say “I told you so” but……..well…………I told you so 😉

All joking aside, I am as convinced as I can be that mast cells play a role in M.E.  Having followed research on the illness now for a quarter of a century it’s the only theory I have come across that even remotely fits every aspect of the disease as outlined in my Canary post.  And in my world, if it looks like a duck and quacks like a duck, chances are it’s probably a duck.  I may be proved completely wrong, but at the moment with the knowledge we have my feet are firmly in the mast cell camp.

The link to the Medscape article was posted on the ME Association’s Facebook page and seemed to ring a bell with quite a few patients.  They all then, naturally, wanted to get tested for mast cell disease in the hopes they would be cured.  I wish it were that simple.

Although I believe mast cells are implicated in M.E. that does not mean I think M.E. is just another name for Mast Cell Activation Disorder.  MCAD is a distinct disease entity.  You can have MCAD on its own, you can have MCAD alongside other diseases like Ehlers-Danlos Syndrome or M.E., of if you’re unlucky you can have both or in my case all three.  Treating the symptoms of MCAD (there is no cure) will do nothing to help your M.E., at least not in my experience.

If mast cells are implicated in M.E. why doesn’t treating the underlying mast cell disease help?  Good question.  I’m not a Doctor or a Research Scientist and even if I were I probably still wouldn’t know the answer.  MCAD was only discovered as a disease a decade ago and we currently know very little about it.  Treatments are available but they’re crude and even leading Doctors in the MCAD field admit they are limited in the ways they can help.

The focus is often on Histamine in respect of MCAD, but it’s only one of 30 chemical mediators expressed by mast cells so is only a tiny part of the MCAD puzzle.  We currently only have the capability to test for half a dozen of the 30 mediators (and in the UK only have the means to test for a couple), so we have a very long way to go in being able to accurately test for mast cell activation.  Even if excess histamine is found to be present it binds to four receptors in the body (at least, we only currently know about four) and we only have drugs to target two of those receptors (H1 and H2), so if H3 or H4 receptors are implicated in M.E. we can’t currently do anything about that.

Being treated for MCAD probably saved my life, but it had little effect on my M.E. with two notable exceptions.  The horrendous insomnia which has plagued me for the 24 years I’ve been ill was helped dramatically when I no longer had stimulating histamine in my brain, and the back pain from which I’d suffered for 30 odd years improved by about 60%.  But I still have M.E. in all its fluey, achey, brain fogged, POTSy, sore throated, weak muscled, post exertional malaise glory.  It’s a bugger.

It’s hugely difficult to get an official MCAD diagnosis here in Britain and most people end up having to go down the very expensive private route as MCAD still isn’t officially recognized here in the UK so isn’t funded on the NHS.  There are a couple of NHS Consultants who might see you but in practice only if you have severe disease and have classic MCAD symptoms like flushing, hives and a history of anaphylaxis which has been confirmed isn’t due to allergies.  Having received your diagnosis, treatments are limited and in my case the very fact I have MCAD and my mast cells reject drugs on a grand scale means I have anaphylaxis to the tablets needed to treat my anaphylaxis, which would be hilarious if it weren’t so scary.

To anyone reading this who wants to rush out to see an MCAD specialist trust me when I say you’re heading down a difficult and potentially expensive road with no real destination, so think carefully about whether or not you want to spend your energy doing that before you start.  I’m not saying don’t, just that it’s probably not going to help your M.E. so unless you have clear symptoms of MCAD and are debilitated by those it will all be a bit pointless.

Having said all that I’m still hugely excited by the fact that Doctors are picking up on the fact that M.E. and MCAD might be related.  It’s no coincidence that Doctors seeing Hypermobile Ehlers-Danlos patients were finding that a large sub-section of those also had MCAD, and it’s no coincidence that many of those also had a diagnosis of M.E.  The hEDS/POTS/ME triangle is well known about in the patient population and the underlying common denominator appears to be mast cell activation.

 

Christmas roundup

Christmas Eve.  I can’t get my head round that.  It seems like days ago that I had my 50th birthday, not 3 months.  Seriously, a time thief lives in my house 😉

I’ve had a lovely, calm, peaceful week.  Looking back I have no clue what I’ve been doing but it seems to’ve involved eating lots of Pringles and Wine Gums which I’m going to regret when I finally get out of my elastic waist trackie bottoms and into my jeans in the New Year!

I went with my Dad to get the results of the MRI scan he had done on his back.  The good news is there is no stenosis.  The bad news is there are multiple bulging discs which are compressing the nerves, hence the pain and weakness in his legs.  Treatment begins with “conservative management” ie physio to strengthen the muscles.  I can’t see it working because until four months ago when his leg started to give way he walked 6 miles up the fells every week and has done for the past twenty years, so he has the strongest legs of any 80 year old I know.  A few stationary bike exercises are going to be child’s play to my Dad.  But you have to play the game and do what the doctor suggests before he’ll consider referring you on to a specialist.

Both my dog walkers are now on holiday until the new year, which means I have to take Bertie out twice a day.  It’s a killer, even going on my scooter.  I have to get bundled up like I’m going on an expedition to the North Pole, uncover and unchain my scooter, get Bert’s harness and lead on, actually go on the walk, recover and rechain my scooter, get all my kit back off again and wipe Bert’s paws (the mud in my village atm is ridiculous), which takes a good hour for a half hour walk.  And repeat five hours later.  It’s exhausting  and I come back with my brain so foggy I can’t form a thought, not that the mutt cares 😉

Today I am making some mushroom soup and a lemon meringue pie for our Christmas lunch tomorrow.  I gave up doing a huge roast dinner several years ago because neither my Mum nor I are up to it, so we have soup, sanis and a pudding on Xmas day and then go out for our roast dinner on Boxing Day to a lovely restaurant.  It works for us.

I shall leave you with my annual carol, sung to the tune of Once In Royal David’s City.  Whatever your Christmas holds I hope it’s filled with love and laughter 🙂

Once in snowy North West England,
Lived a lonely, country girl
Mast cells that were sorely rampant
histamine that made her hurl
Jak she was that poorly child
M-CAD was that illness vile.

Subluxations sent to try her
Joints all wandering out of place
Splints and braces plus her scooter
helped her join the human race
Jak she was that poorly childmistletoe
E.D.S that illness vile

Monthly torture from her cycle
makes her feel that she is cursed
Menopause that drives her crazy
She’s not sure yet which is worse
Jak she was that poorly child
Endo is an illness vile

Nervous system going bonkers
Pins & needles all the time
She would kill to just get tipsy
she’s allergic to the wine
Jak she was that poorly child
POTS doth make an illness vile

She is tired beyond all reason
Half her life is spent in bed
That Hugh Jackman is her Carer
fantasies just in her head
Jak she is that poorly child
M.E. is an illness vile.

Doctors told her she was crazy
symptoms were all in her head
She just hoped they’d catch her illness
or that they would drop down dead
Jak she was that poorly child
Chronic illness truly vile.

Blood tests showed she’s truly sickly
She had known this all along
Blew a raspberry at the doctors
who all said there’s nothing wrong
Jak she is that poorly child
She has proof now she can smile!