Share your experience!

I'd like to introduce you to a great website. Health Talk Online is run by the Health Experience Research Group at the University of Oxford.

The Research Group collects personal stories of health, illness and disability. As well as analysing these to use in academic publications, it makes the stories available on the website, as video or audio clips, so others with the same conditions can find support and information. There's a list of the conditions they've covered so far here.

At the moment, the researchers are looking for people with acquired conditions who live in London. Would you be interested in helping them? Contact details are here.They also want to speak to carers of people with MS, anywhere in the UK. Is that you, or do you know someone who is? Contact details are on the same page.

I know all and any help will be very gratefully received.

Research roundup December 2011: Blogger ate (most of) my post

This was going to be a lovely long, informative research roundup, full of interesting and groundbreaking stuff to take you through to the New Year.

Sadly, Blogger (the software on this site) decided to eat all my carefully saved links. And what with my terrible MS memory, I can only remember two of them!

Not to be daunted, I'm going to tell you about those two. I'm really sorry though. Hopefully I'll remember some of the others, and can add them to other roundups in the future.

I've often spoken before about vitamin D and MS. It's a very important area of research at the moment. Now a group of British and Canadian researchers have discovered a rare gene that seems to be linked to MS. The gene is called CYP27B1: a mutation in it affects a key enzyme, leading people with the variant to have lower levels of vitamin D.

They identified the mutation in CYP27B1 as being of interest, from looking at 43 people who came from families with 4 or more individuals affected by MS. Then they looked at over 3,000 unaffected parents of someone with MS. 35 of them carried one copy of the mutated version of CYP27B1 along with a copy of the normal version. In all 35 of these cases, the person with MS inherited the mutated version.

The likelihood of the gene's transmission being unconnected with MS are billions to one, the researchers claim. The very strong implication is that in these particular MS cases, low levels of vitamin D are directly connected to the disease.

It's always been thought that MS begins by attacking myelin in the inner layers of the brain, the white matter. Now American researchers have found that in fact the disease seems to move from the outer, cortical layers of the brain.

The next step for their research is to study these cortical lesions to identify new molecular targets for treatment, and to develop imaging techniques so that these lesions can be shown clearly.

And, well, that's it for December's roundup. Apologies again for the lack of content!

New blog

OK, first off, I'm still here, I'm not dead. Huge apologies for the long gap between posts. Looks like the November research roundup is going to be a December roundup...

Also, I just started a new blog. It's called The Spoonie Recipe Blog, and it's going to focus on recipes that don't need much energy to make, for people whose energy is limited by long-term illness. The first recipe - for the utterly toothsome Crispy Chicken - is here.

Back soon!

Disability: the bald truth

A few weeks ago, I thought I saw a squirrel running along the top of my front garden hedge. Turned out it was a bloke on the other side of the hedge with a really bad toupee. Truth.

Bad toupee                       Squirrel

But it reminded me of  a case about three years ago, when a Scottish teacher tried (and failed) to establish that being bald meant he was disabled. He'd been the victim of terrible harrassment from his pupils: if his baldness was a disability, he would have the protection of the Disability Discrimination Act to support his claim of constructive and unfair dismissal.

The judge in that case said that just because the teacher's baldness was used by others to taunt and harrass him did not make it a disability:

It seems to me it would be to take the definition of impairment too far. If baldness was to be regarded as an impairment then perhaps a physical feature such as a big nose, big ears or being smaller than average height might of themselves be regarded as an impairment under the DDA. That, to me, cannot be right

So what is a disability? The judge seems from that quote to use the words impairment and disability interchangeably. But are they?

The medical model of disability sees impairment and disability as closely linked: disability arises directly from impairment, which is a physical dysfunction of the body. Disability is therefore clearly the individual's "fault", may reduce their quality of life, and causes clear disadvantage to them.

In the social model of disability, by contrast, society is the main factor in disabling people. Impairment is a necessary factor for disability, but it doesn't lead to disability unless society fails to take regard of and include people regardless of their individual differences.

The legal situation in the UK is governed by the Disability Discrimination Act 1995 (now consolidated into the Equality Act 2010). It uses predominantly a medical model: disabled people are defined as people with certain conditions (someone diagnosed with MS, for instance, is automatically covered under the Act), or with certain limitations on their abilities.

But when it's placing requirements on employers and service providers, it uses the social model, requiring them to make "reasonable adjustments" to their premises, policies and practices to make them accessible.

What make an adjustment "reasonable" is not defined, and most court cases focus on this point. It could, for instance, be entirely reasonable for a large department store to install an entrance ramp in view of the shop's size and number of shoppers; it might not be reasonable to expect an office with only a few staff, rarely visited by members of the public, to do the same. On the other hand, someone from the office could perhaps go to visit a customer who can't access the premises at home. It's about...well, what's reasonable.

Some people are very militant about the issue, insisting that only the social model should be used. But really, you could have the most accessible environment, the most enabling society in the world, and I still couldn't take a full part in it because of my fatigue and pain - the main symptoms of my MS, for me. These are called impairment effects: they're not recognised by everyone working in the field of Disability Studies, but for those of us experiencing invisible symptoms, they are a major factor in our experience of disability.

So, what is disability? To me, it's a mixture of the dysfunctions of my body caused by lesions in my brain, and society's response (or lack of response) to me as a result of those dysfunctions. Others may have different answers, depending on their own particular experiences and understandings.

Perhaps, in the end, disability is one of those things that means something different to every one of us. But a bad toupee? That'll always be a bad toupee!

MS Research Roundup October 2011

There's been some very interesting research announced this month. Some of it is pretty technical, but once I've worked out what it means myself, I'll do my best to translate it!

American and Canadian researchers have developed an imaging technique using lasers that allows them to see the amount of damage the myelin sheaths around nerves have sustained. Previously, such measurements could only be obtained by removing the nerve and slicing it into layers - which was only possible once the patient was dead! So far, this research has only been carried out on animals, but it could in the future be used as a diagnostic tool for conditions like MS.

The body has developed what is generally a very effective barrier between the blood and the brain, to keep anything potentially harmful from moving between the two. While this is generally very useful, it can pose a problem with getting drugs into the brain to treat conditions like MS, Alzheimer's disease, and cancers of the central nervous system.

Now a group of American researchers have found that a molecule called adenosine can help large molecules enter the brain. An existing drug called Lexiscan, which is based on adenosine and is used in heart imaging for very ill patients, briefly opens the blood-brain barrier. In MS, confusingly, research is also focusing on how to tighten the barrier, to stop destructive immune cells getting in to the brain and causing damage.

There's been a lot of research, and talk in the MS community, about the possible beneficial effects of taking fish oils for people with MS. Researchers from America looked at the effects of taking omega-3 fatty acid. They found that it had a significant impact on a molecule called matrix metalloproteinase-9 (MMP-9), which is associated with disruption of the blood-brain barrier, and immune system T cells getting into the brain. Their results suggest that taking Omega-3 supplements may benefit people with MS: they don't suggest amounts. That (as ever) will be for further research.

Another group of American researchers looked at how the body metabolises fatty acids. The speed of metabolism is controlled by an enzyme called carnitine palmitoyltransferase 1 (CPT-1). The researchers controlled the amount of CPT-1 in the animals they were working with, and found a reduction in disease severity as well as less inflammation and demyelination.This research is a long way from any clinical use, but it sounds a potentially useful therapeutic target for MS.

Certain steroids in the brain (neurosteroids) have a protective function. Canadian and Iranian researchers discovered that brain tissue from people with MS had much lower levels of neurosteroids than tissue from people without, particularly a neurosteroid called allopregnanolone.This was due to the action of a specific molecule called micro-RNA (miRNA).

They then treated mice with a disease similar to MS with injections of allopregnanolone and found that they maintained a better protective myelin coating on their spinal cords than mice receiving the placebo.They also had significantly reduced disease severity compared both with the mice receiving the placebo and their own symptoms before treatment.

Next, two treatment stories relevant to particular countries. The first North American stem cell trial for MS has been approved: as a Phase 1 trial it will assess the feasibility and safety of using the body's own stem cells to treat MS.

The procedure will consist of harvesting the patient's mesenchymal stem cells, culturing them in a laboratory, and then injecting them intravenously back into the patient. Mesenchymal stem cells have a wide range of effects, varying from lessening immune activity to encouraging tissue repair. Study participants will be closely monitored for six months after the procedure. If it's shown to be safe and feasible, an application may be made for a larger, controlled trial, including the use of a placebo procedure.

Fampridine (Fampyra) has just been launched in the UK. I did a separate post about this drug, which aids walking in some people with MS.

Finally for this month, an Italian research group have been researching treatments for fatigue in MS. They used neurocognitive rehabilitation techniques. The information I have about the research doesn't say what specific techniques they used, but neurocognitive rehabilitation can include things like occupational therapy and hand/eye coordination exercises.

The researchers found that both immediately after 5 weeks treatment and 6 months later less fatigue was reported. There was no difference in physical disability. They suggest that neurocognitive rehabilitation could be a useful strategy for treating people with MS.

That's the roundup rounded up for this month. What will the next month bring? Only time will tell!

Walking back to happiness?

Walking. It's such a significant ability, isn't it? Being able to walk is one of the markers of development from babyhood to childhood.

And to many of the general population in our culture, it's whether someone can walk or not that determines whether or not they're disabled. Many of us with MS quite rightly complain that our invisible symptoms disable us just as much, if not more, than mobility problems. Even so, we often resist using mobility aids such as sticks, crutches or wheelchairs for as long as possible: visible symbols of our disabilities.

The worst symptoms of my MS are fatigue and pain. Even so, any improvement in my mobility would make my life far easier! I'm currently able to walk very short distances, and use a power wheelchair outside the house.

That's why I've been so excited watching the trials of the new drug Fampridine (Fampyra), which was finally released in the UK this week.

Fampridine is a tablet taken twice daily. It's not like Beta Interferon, Copaxone or Tysabri - it has no effect on disease progression. It's effective for roughly 33-40% of people with MS with walking problems: when it does work, it gives an average 25% improvement in walking speed.

Back when it was in trials, I discussed Fampridine with my neurologist. She said that she would want to put me on it as soon as it was approved.

So far, so excellent. But like every medication, Fampridine has potential side effects. Some of these are relatively minor, and pass as you get accustomed to the drug. But some are potentially very dangerous.

Among these is a slight risk of seizures (fits). Now in general, for most people, that very small chance would be a risk worth taking. But I already have epilepsy. So although it's well controlled, anything that increases my seizure risk is not really very good news.

It's all about swings and roundabouts: balancing risks and benefits. At the moment I don't know if my neurologist will consider me suitable for Fampridine, given the seizure risk. I'm seeing her in 6 weeks, and will be asking about it.

But if she leaves the decision up to me, will a possible improvement in my walking be worth risking losing control of my epilepsy? If I have a seizure, I'll lose my driving licence for a year, and I really don't want that to happen. But easier walking would make my life so much simpler.

At the moment, I really don't know what my decision would/will be. I suppose I'm going to have to do some hard thinking over the next few weeks. And who knows? Pretty soon, like Helen Shapiro, I might be Walking Back to Happiness!

Book review: or how The Good Table bruised my toe

I was lucky enough to be sent this recipe book - The Good Table, by Valentine Warner - by the publisher, as a competition prize. The only condition was that I might like to write a review of it, here or on Amazon.

And truly, that's been no hardship to do, because overall this is a beautiful book to handle, look through, and read. The photographs of the finished dishes are stunning. The only complication really was that it somehow ended up tucked away under the sofa, at the furthest corner. (I blame the cat.)

I'm physically disabled, and inevitably that affects my perception of everything I do and experence.. The Good Table is a big book (hardback, nearly 12 inches tall,over 7½ inches wide and over an inch thick.). I just dropped it on my toe while I was moving it to go for a drink and it hurt like hell. Seriously.

For those of us with weak arms and hands, that can cause significant problems. It's very difficult for me to lift The Good Table at all! The binding does mean though that the book lies open at the chosen page, even if that's at the start or end of the book. A rare thing, and very useful for a recipe book.

As you can imagine, there are a huge number of recipes spread throughout its 368 pages, ranging in complication level from 'Boiled new potatoes with Stinking Bishop & spring onion' and 'Baked potatoes with garlic & cream' up to...well, I looked through the book for a dish that would be particularly complicated, and couldn't find one.

Certainly there are some that wouldn't be for novice or nervous cooks, but part of the stated aim of the The Good Table is to help restore the cooking skills of the country.The book includes a number of  'how-to' guides: for instance, how to put together a steak & kidney pudding. If less experienced cooks follow these, and move from less to more demanding recipes, Warner hopes that some of our lost cooking skills can be reestablished.

I haven't yet cooked anything from Warner's book: but some of the recipes sound so tempting, that I know I will very soon. How could anyone resist 'Floating islands with espresso caramel sauce'? And it's wonderful to have a recipe for chai.

Looking at the recipes from a disability point of view, things are a little more difficult. Many of the recipes are well within my capabilities, and I look forward to making them. There are however very many that would just be far too tiring: taking too long, or involving too much stirring or lifting, for instance. Others could possibly be risky because of chopping, cooker flames, and so on.

So speaking as a disabled person, I'm delighted to have won The Good Table. Would I pay out £25 for this heavy hardback version, with more than half of the recipes being ones I can't make? Well, no. I don't think I would, to be honest. But if you're able-bodied and you like cooking, or want to learn more about it, go for it. It's brill.

MS Research Roundup September 2011

Again, a short research review this month. My apologies.

First, an extremely interesting and important genetic study, that has received a lot of media attention. Researchers looked at more than 10,000 people with MS from 15 countries, as well as more than 17,000 healthy controls. We already knew about more than 20 gene differerences that may contribute to people getting MS. The large numbers involved in this study allowed them to find another 29 genetic variants that could contribute.

About half of all the gene variants known to be involved affect the immune system, and one-third have been implicated in other auto-immune diseases, such as Crohn's disease, coeliac disease, rheumatoid arthritis, lupus, and type 1 diabetes.Knowing which genes are involved in MS could potentially help new treatments be developed, including the possibility that treatments already in use for one auto-immune condition could be used for another.

I've mentioned the common herpes virus HHV-6 before. It causes the childhood infection roseola, marked by a chest rash and high fever. However very little is known about it, including how it manages to reach the brain to be implicated in causing conditions like MS, encephalitis and a form of epilepsy.

These American researchers found high levels of HHV-6 in the olfactory bulb (a part of the brain associated with smelling) and in nasal mucus, in over half of their samples. They also discovered that specialised cells connecting the nose to the brain are susceptible to infection by the virus. As ever, more research needed. It could be that infection entering the brain via the nose causes a different disease result from infection entering by another source. This is a really interesting study though.

It's well-known that MS, as well as other auto-immune diseases like lupus and rheumatoid arthritis, are considerably more likely to attack women than men, but it's never been clear why. Now American researchers have discovered a new type of immune system B cell: these make antibodies, which go on to bind to and attack the body's own tissues.

The researchers found higher levels of these cells in elderly female mice, young and old mice prone to auto-immune disease, and humans with auto-immune diseases. They are now seeking a way to treat these diseases by blocking production of the cells.

A very big MS-related story at the moment is vitamin D exposure. A group of American researchers compared vitamin D exposure between childhood (whether the individual had been given cod liver oil) and disease onset (sun exposure in the previous winter) with how rapidly they were progressing.

They found a close link between a low level of vitamin D exposure before disease onset and slower disease progression. They were working only with people with progressive MS, and with quite a small group, so research is needed with a larger group and with people with the relapsing remitting form as well to see if the same results are seen. A really worthwhile and interesting study though.

Daclizumab (Zenapax) is a monoclonal antibody, currently going through trials. In this recent global trial, where daclizumab was injected every four weeks, it reduced relapse rates by around half compared to taking a placebo. There was however an increased risk of infections. Daclizumab is now in phase 3 trials, where it's being compared with beta interferon 1a.

Finally, news on two treatments for MS symptoms. First, the Irish Medicines Board has given approval to the use of Botox for urinary incontinence for MS following the biggest ever clinical trial of Botox for neurogenic overactivity of the detrusor muscle. The study demonstrated that treatment was effective within a couple of weeks and lasted for 8-10 months.

Botox is already in use in the UK, and this large study just confirms its utility. It's an important step towards gaining licences in those countries where it's not yet used.

Many of us with MS, diabetes or shingles know the terrible, ongoing problem caused by nerve pain. Current drugs may not help at all. Now British researchers have discovered that a gene called HCN2 is involved in causing the excessive "firing" of pain-sensitive nerves.

In experiments with mice genetically modified to have the gene removed, disabling the gene was found to relieve chronic and inflammatory pain, but without reducing reactions to acute pain, the type caused by a sudden injury. This is crucial: responses to injuries can be vital to our survival. The researchers hope that they'll be able to develop a drug to block the protein produced by HCN2, so the same effect can be seen in humans.

That concludes this month's research review. Again, apologies for the limited number of items covered, but I hope you'll agree there are some really interesting studies in there.

See you next month!

The right model for killing yourself

"Martin" is 46 and has locked in syndrome He's asking the courts to clarify the law so that doctors and other medical staff who might help him end his life would not  be prosecuted.

This is an extension of Debbie Purdy's case, from two years ago. Purdy successfully argued in court that it was a breach of her human rights not to know if her husband would be prosecuted for assisting her suicide if he accompanied her to a clinic in a country where assisted suicide is legal.

"Martin's" case extends this to doctors and other medical staff, rather than lay-people. His wife has accepted his decision, but does not feel able to assist him.

At least 10% of suicides in the UK are by people with a chronic or terminal illness, and coroners believe that people are increasingly killing themselves at a younger age rather than wait until they are in severe pain. Some coroners avoid probing into what they suspect might be a case of assisted suicide, to avoid causing problems for those left behind.

So why do all these people with long-term illnesses feel that the appropriate response to their circumstances is to kill themselves? (Either with or without help). Opinions, inevitably, differ.

Some argue that the decision is made because the condition - the illness, the disability, whatever - has become too much to bear. Others say that these feelings are often because the individual has not had the chance to live as independent a life as possible within society at large.

The individual's condition on one side and society on the other. That sounds very familiar. And yes, it's our old friends the medical and social models of disability again.

Which is more important in an someone's decision whether they want to live or die?  The way their physical disability affects them as an individual, or how easy it is for disabled people to be part of mainstream society?

Just to be upfront, I have no intention (in the foreseeable future) of seeking assisted suicide. But as I've told you in a couple of posts recently, I've been having major problems getting out because of physical problems. At the moment, the accessibility or otherwise of society is kind of irrelevant to me, and my physical impairments are totally primary. At other times, or for other people, the physical problems may be secondary to accessibility, housing problems or employment discrimination.

So overall, I think sometimes the medical model is the right one and sometimes the social model. Or, at least, there's a continuum. At one end is "pure" medical model thinking, at the other end is "pure" social model thinking. Most of us are somewhere in the middle, and we move back and forward along the continuum depending on circumstances. (It's made of nice slidey material. Makes it easy.)

The vast majority of us could never kill ourselves, in any circumstances. And if someone is considering it, whether that decision is rational or irrational is a whole other packet of Jaffa cakes. For those few who have decided to seek assisted suicide though, reasons differ. And that fact must be acknowledged by the disability community.

Not going out

For the last couple of months, I've been having real problems in getting out. Not because of agoraphobia: I'd love to get out. Because of physical difficulties, and complete and utter lack of spoons. I just haven't had the energy to go out.

I used to be - well, not exactly a party animal (though I've had my moments!), but I went out a fair bit. Part of it was day-to-day getting out, of the going-to-the-shops, paying-the-bills type. And of course work, back when I was still able. In these teched-up days, the internet offers alternatives to much of that kind of going out, for those who want them.

But part of it was the joyous, wonderful kind of going out: meeting your mates, going to the pub, going to gigs. Falling in love with the band who were supporting the one you'd actually gone to see. Your table in the pub laughing so loudly that the landlord has to ask you to quieten down. An evening at the fair, throwing balls at coconuts to win teddy bears.

It's that kind of going out I miss so much. I have wonderful friends I'm in contact with online, by text or by phone: but it's just not the same as when I meet up with them in real life.

And even the boring, everyday kind of going out means you're still part of the community at large. You're still "normal" (whatever the hell that means!) rather than stuck permanently indoors.

So I'm still hoping I'll beat these damn recurrent infections, and get enough energy back to do some going out again. Because this not going out is really getting me down.

Revolting disabled people

Over the last week, we have all been horrified by the scenes of violence and criminality shown in Tottenham, Ealing, Hackney, Croydon in the London area, as well as further afield in England, in cities including Manchester, Birmingham, Nottingham and Bristol.

Those responsible are now being arrested and dealt with through the justice system. Everyone, and his dog in many cases, has spouted forth his or her opinion of the causes of the rioting. One factor frequently cited by the chattering classes (much like myself, you might say. And probably rightly) is the alienation of young people, and of the "underclass" that has developed under this and other governments, brought to a head by the savage programme of cuts introduced since the last General Election.

This may be true. The official inquiry into the causes of the rioting might look at such things - I hope so.

But there are other groups, equally alienated by their treatment by successive governments, and equally if not more affected by government cuts. Why weren't they out there rioting, looting, and setting fire to things?

They? I mean us. Disabled people.

Yes, things are better than they were in relation to accessibility, job opportunities and so on, but they're not improving nearly fast enough. Disability hate crime is still a regular occurrence and not taken nearly seriously enough. And we're facing frightening, ideologically motivated cuts to our benefits. Why shouldn't we be out there rioting?

Well, first of all, there's the practicalities of the matter. Few of the shops being looted looked very wheelchair accessible - through the windows at least. And wouldn't the glass puncture the tyres? For those of us who have disabilities that are also illnesses, it's difficult to do anything spontaneous like that. And what about if you need a PA to get out?

Then there's the age profile of the rioters. Overwhelmingly, those charged with riot-related offences are young, about 3/4 being under 25. Disabled people, on the other hand, tend to be older than the general population: although of course there are disabled children and young people, many disabilities only come on with age, so the number of disabled people in the population increases with age. With age comes...well, let's call it wisdom. Or maybe it's apathy. Something like that, anyway.

I think all of us, even living in our own homes rather than in care or nursing homes, undergo a kind of "institutionalisation" - to be placid and well-behaved little crips. It's hard to break out of that, to fight against it either physically or with your words.

This, along with the physical and logistic problems, is why it was such an impressive achievement when thousands of disabled people participated in the Hardest Hit march in May, protesting against cuts to disability benefits and services. It's a real shame that their strength and commitment got so little media coverage, in comparison to that given to a few trouble-making idiots on the TUC March For The Alternative.

So. Why weren't disabled people rioting? Some of the rioters probably were disabled of course, as not all disabilities are visible...but in general?

For most of us, I imagine it's because, the same as me, we know what's right and what's not. In other cases, it's just too damn difficult! Maybe some people don't feel national politics affect them?

A whole range of reasons, then. Just like there's a whole range of disabled people. And probably, like there's a whole range of reasons for what the rioters did.

Damn. Wouldn't it have been easy if there was one nice easy knee-jerk cause and solution?

"I'm better"

For the last month or so, I've really not been well. A succession of UTIs, along with the increase in MS symptoms they bring with them. Antibiotics would stop the symptoms of the infection during the course: but then, soon after, it would return.

Then, at the stage when my wee looked like creosote and smelt like something had died in it, I could barely stand, and was really just hoping I would die quickly...I discovered (/my doctor prescribed) nitrofurantoin. This seems to be the latest thing for persistent UTIs, as a friend has just been given it for the same thing. And you know the best thing? It works. Well, so far at least.

So, it seems I no longer have a UTI. I'm better.

Better.

What does that word mean to someone with a long-term illness? I'm never going to be really "better". I have a progressive condition. I'll always have dreadful fatigue. I'll always have cognitive impairment, and all my other symptoms. I can take tablets or injections to help with some things, or work around them, but they're always going to be there.

It seems to me we redefine what "better" means, for us, in our personal circumstances. I'm better because my UTI has gone away: in terms of my symptoms, I'm less worse.

Similarly, we redefine the words describing how we are. I can say "Yeah I'm good", even though I'm in pain and exhausted, because for me, in my terms of reference, that's good.

So...yeah, I'm better. Which is great!

MS research roundup August 2011

First this month, I have to apologise for the complete lack of posts since the last roundup. I've been a bit MSified - and in the less bad bits, I've been attempting to do some "real work". I have told myself off severely, and promise I will blog more this month. Honest.

My poorliness in July also meant that I wasn't keeping my usual eagle eye on what research results were being reported. Sorry and all for the low number of results I discuss in this post.

So on to the research...and more evidence for a link between MS and current vitamin D levels. British researchers compared average vitamin D levels among people in Scotland with MS, and their admission to hospital for things like relapses and infections. They found that the two factors were linked: hospital admissions were highest in spring (April-June) when vitamin D levels were lowest.

This suggests that vitamin D levels are associated with whatever it is that causes people with MS to be admitted to hospital. We already know that vitamin D affects the immune system: being deficient can increase the risk of infections and probably relapses.

Australian researchers have found that past infection with Epstein-Barr virus (EBV), the virus which causes glandular fever (mononucleosis) can combine with genetic variations to increase the risk of developing MS by up to 20 times. There was no evidence that a current infection with EBV could bring on MS.

Not research, but a discussion...a group of researchers held a session on cognitive (thinking) dysfunction in MS, and the problems of developing longitudinal tests and standardising data for the effects of MS on the mind. The researchers gave the contrasting example of Alzheimer's disease: the cognitive decline caused by that disease is faster and more certain than in MS, where cognitive decline affects about 6% of patients each year.

As far back as 2002, researchers published a consensus paper agreeing a battery of tests to be used to measure cognitive decline in people with MS. According to this discussion, it is time to update the consensus to 2011 standards.

Disappointingly for those of us who have followed its progress, the UK National Institute for Health and Clinical Excellence (NICE) has issued a draft recommendation that Gilenya (fingolimod) should not be prescribed on the NHS. This is because NICE feel that it has not been trialled against the correct drugs: it has been compared with a placebo and with Avonex, while NICE argue that it should be compared with other beta interferons as well as Avonex, and with Tysabri.

Gilenya is licensed for adults with highly active relapsing-remitting MS, who have had either one relapse in a year despite being treated with beta interferons, or two disabling relapses regardless of their treatment. The evidence Novartis submitted to NICE mainly dealt with a subset of the first of these two groups.

People with MS, healthcare professionals and others are invited to comment on this decision. However, it really sounds to me like the ball is in Novartis's court, to submit further trial evidence.

One interesting study that reported recently was carried out by an international group of researchers. They found that health-related quality of life, depression, fatigue and thinking all improved when people took Gilenya. However again the comparison was with a placebo, not with an existing treatment.

Finally for this month, exciting news of an upcoming major stem cell trial. British researchers plan to collect participants' own stem cells from their bone marrow, grow them in the laboratory, then reinject them into their blood. The cells will then make their way to the brain where it is hoped they will repair the damage done by MS.

The research is part-funded by the MS Society, which is concerned by the availability of unproven stem cell treatments. At present, there are no proven stem cell treatments, but many people with MS have been attracted to overseas stem cell clinics offering expensive "cures".

So, that's it for this month. See you in September!

MS research roundup July 2011

First this month, a very exciting discovery (for researchers and science geeks like me, anyway). Until now, MS researchers working in the very early stages of a project, when animals must be used, had only been able to use non-human primates when the illness had been artificially induced. Now a naturally occurring disease in Japanese macaques has been found by researchers in America.

This can give many more clues about the causes and development of the disease. It has already been discovered that the condition is associated with a herpes virus - linking in with previous research suggesting that MS in humans may be linked to previous infection with the herpes strain Epstein-Barr virus, which causes glandular fever (mononucleosis).

More herpes news. A Taiwanese research group have found that there may be an increased risk of MS in the year following an attack of shingles, caused by the herpes zoster virus, which also causes chickenpox. The study followed very large groups of people with and without shingles, and found that those with were almost 4 times as likely to develop MS as those without. This is a very interesting study, well designed and with a very large sample group: however it was limited almost entirely to Chinese patients, and Asian populations have considerably lower rates of MS than Western. This work needs to be repeated on other ethnic groups.

Now a piece of research that may not be news to many of us (including me!). American researchers have discovered that fatigue is the first symptom of MS in nearly 30% of cases, often months or even years before any demyelination can be observed. I can certainly remember multiple visits to my GP complaining of fatigue, when I was either told "But everyone gets tired." ("No this isn't NORMAL tired!") or offered anti-depressants. Not particularly helpful.

The group is planning studies to see if unexplained fatigue can be used as a predictor of MS, and another to see if people whose first MS symptom is fatigue differ in any other way from those who have multiple MS-related symptoms.

It's been known for some time that women with MS who become pregnant have a higher than normal likelihood of experiencing a remission during pregnancy, and then experiencing a relapse after the birth. Now Canadian researchers have looked at the effect of MS on the actual pregnancy. They found overall that pregnancy was safe for women with MS, with no significant difference in gestational age, birth weight or type of birth (vaginal or caesarian).

Women with a greater level of disability were more likely to have adverse birth outcomes, but these did not reach statistically significant levels. The researchers also found that women with MS were more likely to be overweight, which is associated with greater risk during pregnancy and birth.

Now, on to treatments, and first some news about existing drugs. I've spoken before about the highly promising treatment Tysabri.  Getting Tysabri carries the risk of developing the rare but severe condition progressive multifocal leukoencephalopathy (PML). PML is more likely if you have previous been exposed to (and therefore have antibodies to) anti-JC virus (JCV).

From now on, all patients in the EU will be tested for JCV antibody status before starting on Tysabri, and JCV antibody status will be included as a risk factor in Tysabri labelling. The risk of PML is still there, but it should be greatly reduced if people with antibodies to JCV do not take the drug.

Another existing treatment, of longer standing, is Copaxone(glatimer acetate). A group of Canadian researchers found that after a year patients receiving a new oral drug, teriflunomide, along with Copaxone, had only about 1/3 the number of lesions of a control group who took Copaxone plus a placebo tablet.

Teriflunomide has previously been tested with interferon: that trial also showed impressive results. It operates by stopping certain immune cells from dividing. This sounds like a very promising adjunct treatment. I hope it's trialled in larger groups, and against other therapies, as soon as possible.

American researchers have developed a very promising new approach to identifying the "self" proteins our bodies attack in auto-immune diseases like MS, rheumatoid arthritis and diabetes. Their new technique, called phage immunoprecipitation sequencing, allows the identification of any interaction between an autoantibody in the cerebrospinal fluid and the self-protein that drives the autoimmune response. This work is at very early stages, but could eventually be developed into diagnostic tests and even treatments.

Meanwhile, British researchers have discovered a synthetic chemical compound which both reduces the inflammatory response in the body and stimulates the body to produce interferon-beta, an anti-inflammatory molecule commonly given to people with MS. Together, these effects cause significant reduction of inflammation in an animal model of MS. The researchers also found that immune system cells from people with MS were more sensitive to the drug than immune system cells from people without the condition.

Excitingly, a joint research group from Britain and the USA have discovered a new molecule that they believe may lead to a drug able to repair myelin by stimulating stem cells. Again, this is very early stage research. Hopefully it will move to clinical trials and ultimately to some form of treatment, probably within 10-15 years. That would repay all the work that's being going on in myelin repair research.

So, that's what happened in June. Some really exciting news this time! See you, same place next month?

The superhighway to friendship

My computer network has been acting up, for a week or so. Or possibly it's my computers. But both of them at the same time? And my shiny new smartphone as well? No, it's the network, I'm pretty sure.

I can get online. But not wirelessly. And I can only access certain websites.

I've gone through a lengthy process of:

1. Swear
2. Hit side of computer
3. Reboot computer
4. Restart router
5. Change settings on router
6. Change them back again when that didn't work
7. Panic when I think I've changed them back wrong
8. And repeat

Now I think I may have to resort to Getting A Man In, which I really resent. I'm a long way from being a tech-head, but I can sort out most things that mess up on the computer. This, however, seems to have defeated me.

Anyway, it's got me to thinking. Since I became disabled, I've spent far more time at home than ever before. In such a situation, it's very easy to become socially isolated. You possibly can't get out as often or as easily to meet friends, you quickly lose contact with work acquaintances, family may begin to resent always having to come to see you instead of travelling being shared.

Access to the internet opens up a huge range of existing and new social contacts: whether it's the ease of emailing, without needing to get out to a postbox; Skype or other free voice chat with someone on the other side of the world; making contact with other people with the same condition, in a chatroom, on a Facebook group, or through a Twitter hashtag; even just, as I did this morning on Twitter, discovering that someone I already chatted to also endures severe pain (we fell on each others' necks like twins separated at birth).

Disabled people are less likely to be online than non-disabled, and that's a real shame. I think we really need it, and for more things than ordering pizzas and viewing porn. Valuable as those activities are...

Rant

I just popped out, down to the local shops. At the final road junction before I got there, a woman had parked across the dropped kerb, and was still sitting in the car. I asked her, very politely, to move.

It pains me to report to you that I was greeted with a load of swearie-words. About the only bit I can repeat to your tender ears (/eyes), reader, is:

"How was I supposed to know you'd be here?"

Well you know what, love? THAT'S THE WHOLE BLOODY POINT! If it was just a case of "Margo'll be along at 12.57, Sunday lunchtime", you could roll your car out of the way for the moment and then roll it back. But it's not. I could be along at any time. (Well, not early mornings, to be fair. I do have MS.) So could any other wheelchair or scooter user, or someone pushing a buggy.

That's why we need the dropped kerb to be free. That's why the powers that be, in a rare example of common sense, have demarcated it with a double yellow line.

So don't fecking park your car across it in the first place. OK? OK, good. I'm glad we've got that sorted.

Bread and circuses

Last Thursday, the House of Commons spent some hours debating whether the use of wild animals should be banned in circuses. It was quite a heated debate. (Personally, I can't see the issue. Of course it should be banned. Duh.)

Meanwhile, I spent the days leading up to yesterday (B for Benefits Day!) living off bread and cheese. I ran out of butter on Wednesday, so it was dry bread from then on.

For now I have money. And food. But the cost of living keeps going up, and my income doesn't, or not enough. Many, many others are in the same situation as me. Thousands of them are hard-working people, who happen to be in low-paid jobs. Others are deeply vulnerable people, unable through no fault of their own to work. They may have a physical disability or learning difficulty, they may have mental health problems, they may be carers for a loved one.

Of course it's important to ensure the welfare of circus animals. But don't you think it would be more important to make sure that everyone in the country has enough money to live on? As opposed to the current government proposals, which seem aimed at reducing our incomes still further..

Bread and cheese, anyone?

Selecting disability, naturally

A hundred years ago or so, most of us disabled people wouldn't have had the lives we do today. I know we complain about welfare reform (and we're right to do so) but back then, we'd have been in workhouses. And that's if we were alive at all. Natural selection - evolution - might have had a word to say about our continued existence.

According to Darwin's theory of natural selection, a characteristic (let's say being taller) becomes more or less common in a population depending on whether it makes the individuals with it more reproductively successful or not. That is, if being taller means they have more offspring, the genes that gave rise to that characteristic are passed on to a larger group, and become more common. If they have fewer offspring, they don't.

All very interesting (for sad science geeks like me, anyway). But how does it relate to disability?

Many disabilities are caused, or at least influenced, by genes carried by the individuals concerned. Those genes are as controlled by the rules of natural selection as any others. If the gene for a disability means more offspring, it should become more common, along with the disability. If it means fewer offspring, it should become less common, and ultimately be eliminated from the population. "Fewer offspring" could arise through the individual dying before reproductive age.

However (predictably) it's not always quite as simple as that. Sickle cell anaemia is a genetic blood disorder where the red blood cells take on a sickle shape. This decreases the cells' flexibility and increases the risk of various complications. It occurs most commonly in people (or their descendants) from tropical or sub-tropical regions where malaria is or was common.

Sickle cell is a recessive condition: that is, both parents have to be carriers, and the child has to inherit a copy of the sickle cell gene from each of them. Being a carrier (known as "sickle cell trait") appears to give some protection against malaria. So natural selection seems to have provided a play-off between the parents having protection against malaria, and each of their children having a one in four chance of developing sickle cell disease with its severe complications and likelihood of dying young.

Kin selection is a theory explaining why individuals behave in ways that favour their relatives rather than themselves, even at a cost to their own survival and/or reproduction. The classic example is a beehive, where asexual drones work for the benefit of the all-powerful queen bee. The kin selection theory states that they do this in order to help pass on the queen's genes, which are so close to their own.

People with genes that lead to disability are part of a family. Whether or not they have progeny themselves, others in their family are likely to - and the genes for the disability are quite possibly hidden in their genomes too. As families support each other, they make it more likely that their genes, including "defective" ones, will be passed on.

And, of course, disabled people make many contributions to the humanity-hive. In paid or voluntary work; as children, siblings, lovers, spouses, and parents; as employers (or the reason people are employed); and as friends, giving emotional support. I'm sure you can think of many more.

The genes that code for disabilities may not always be helpful. But I don't think evolution will be eliminating them just yet. Factors like carrier status being beneficial, and kin selection, mean they are neutral at worst in their effect.

Juggling

I'm currently listening to music (the album A Curious Thing by Amy MacDonald, if you're interested), watching athletics on the telly, and attempting to write this. I used to be an ace multi-tasker. These days, my MS-ified self can barely cope with one thing at a time. So the fact that I've taken on three at once means that at least two of them are going to suffer. Life with MS is all about juggling your commitments, because of the effects it has on your cognitive skills.

Cognition is the term used to describe a person's "thinking ability". People will often realise they are starting to have cognitive problems when they begin to find it hard to read books or follow conversations. Cognition includes:

• focusing, maintaining and shifting your attention
• learning, remembering and recalling information
• understanding and using language appropriately and effectively
• performing maths calculations
• ‘executive function’ such as planning actions, performing tasks in the correct order, controlling one’s impulses, transferring learning from one situation to another, and working with abstract concepts

Mild cognitive problems are common in MS.It's thought that somewhere between 45% and 65% of people with MS have some degree of cognitive problem, though as with every symptom the degree and profile varies from person to person. It is most severe in people with secondary progressive MS. People with primary progressive MS seem to be rarely affected, possibly because this type of MS prefers to attack the spinal cord rather than the brain.

The most common problems are in:

• Learning and memory - almost always short term memory
• Attention, concentration and mental speed - it may be difficult to concentrate for long periods of time or keep track of what you're doing if you're interrupted, do several jobs at once or carry on a conversation if the TV or radio is on.
• Problem solving - planning, performing and evaluating tasks - you know what you want to do but find it difficult to know where to begin, or to work out the steps needed. Problems can lead to confusion and stress, which can in turn increase learning and memory problems.
• Word finding - particularly nouns, including abstract nouns. It can be difficult to take part in a conversation because it takes too long to express an opinion or find the correct word, and the discussion has moved on.

There seems to be little association between someone's level of physical disability and their cognitive problems. Cognitive changes can worsen with a relapse, or when the person is tired. People with MS rarely experience cognitive impairment as bad as that with (for instance) Alzheimer's disease, and then only in the very late stages of the disease.

The level of impairment can stabilise at any time rather than continuing to progress. Most people with MS who have cognitive impairment have mild symptoms.

Most of the ways of trying to deal with cognitive impairment are behavioural. They include things like:

• Writing everything down. Rely heavily on a diary, loose-leaf organiser and/or palm-held computer/organiser.
• Having a particular place for everything, always putting things back where they belong and encouraging others to do the same.
• Trying to focus your attention more keenly on the things that are important. Repeating important things that need to be remembered over and over in your head will often keep them there.
• Trying to jot everything down, including people's names and how they appear to you. Often just the act of writing something down will commit it to memory better. Pictures also help. These can be mental or drawn.
• Word recall is a problem that is often reported in MS. If you suffer from this, try not to get hung up about the exact word. People are often happy to chime in with the right word anyway - let them.
• Working slowly. Take your time to plan things and don't be rushed by anyone. Use paper and/or a calculator as necessary.

So, I've moved on to Snow Patrol's Eyes Open, the athletics are still on, and I'm thinking hard here about what my conclusions should be. But given my cognitive impairment, and my problems with pattern formation and word finding, I don't really have any. Except that I really should stick to one thing at a time...

Smoke gets in your eyes - or is it Optic Neuritis?

I've noticed, among people that I know, that a lot of people with MS seem to smoke. I've often wondered whether it's the smoking that causes their MS, or having MS that makes them not want to give up. Or is there a third factor that's related to both of them?

Incidentally, I should declare a conflict of interest here, being on day 3 of giving up smoking. If I should come over all sanctimonious ex-smoker, you have my full permission to kill me, OK?

Smoking is now accepted as a risk factor for MS (as is passive smoking), and it appears that it may also make the disease course worse, both clinically and on MRI. Heavier smoking seems to increase the risk. Smoking is also associated with the type of MS someone has. Current smokers are more likely to have primary progressive MS, and smokers progress from relapsing-remitting MS to secondary progressive MS faster than those who have never smoked.

In addition, people with MS who smoke are more likely to have other auto-immune conditions, such as lupus, Crohn's disease, or pernicious anaemia. It seems that nicotine can precipitate the inflammatory response. Having more than one condition affects the length of time between symptom onset and diagnosis, disability progression, and health-related quality of life.

Smoking is associated with disruption of the blood-brain barrier, which will make it easier for immune system cells to get through and cause damage, with more lesions, and with more atrophy (wasting away) of the brain.

Do smokers with MS get the same encouragement as others to give up? Several friends with MS have told me of their GPs saying, in as many words:

In your situation, if smoking makes you happy - carry on!

In other cases, people may feel that they're buggered physically anyway, so why go through the stress of giving up? One friend told me that she resented being told to give up smoking, something she enjoyed doing, when she'd already lost so much.

Many people with MS also smoke those special herbal cigarettes for people with MS.

Could the smoking of cannabis by people with MS (most often for the relief of pain or spasticity, or to help with sleep) be linked to the high levels of cigarette smoking? After all, many cannabis users smoke cigarettes.

So what conclusions can we reach? Yes, smoking is a risk factor for MS - as it is for many other conditions. There's no question that it would be sensible for us not to start smoking, and if we have started, to stop. But we're not necessarily sensible. There are all sorts of reasons people smoke, that can outweigh possible, statistical risks.

I'm not going to tell anyone to give up smoking. I smoked for many years when I was fully aware of the risks - not just for my MS, but everything else too. I'm giving up now because I think it's finally the right time, for me. We all need the facts though, to be able to make an informed decision about risks and benefits.

Now, back to Smoke Gets In Your Eyes:

(Smoke Gets In Your Eyes is a classic song, a standard, and very many people have recorded it. But being the age I am, this is the version I most remember, and one I love.)

MS research roundup June 2011

This month's research roundup includes several studies on treatments for MS, particularly Natalizumab (Tysabri). As usual, I'll do my best to arrange the post with risk factors for MS first, then symptoms, diagnosis and treatment.

It's still pretty obscure what causes MS, but researchers in the USA may have gone some way to finding out. It has long been suspected that there is a genetic component to MS, but the relationship is not simple. This study looked at the way a range of environmental factors such as metabolism and Vitamin D-3 levels interacted with four genes (interleukin-7 receptor-alpha, interleukin-2 receptor-alpha, MGAT1 and CTLA-4) to affect certain proteins that regulate the disease. They found that adding Vitamin D-3 or a simple sugar called GlcNAc could help to restore proteins to their normal functions. Sounds like a very promising line of research, and one that could potentially solve the mystery of MS causation.

Spanish researchers have looked at all previous studies investigating links between having been previously infected with Epstein-Barr virus (which causes glandular fever / mononucleosis) and MS, and confirmed that having antibodies to the virus means a higher likelihood of developing MS. The timing of the infection (how long ago) was not relevant. Further research is needed, though - ideally following a group of people from before any of them develop MS symptoms.

I've observed in the past that a high proportion of people with MS seem to be (cigarette!) smokers. A group of Swedish researchers have found that smoking interacts with two genetic factors, having a gene called human leukocyte antigen DRB1*15 and not having human leukocyte antigen A*02.Smokers with both genetic risk factors were 13.5 times as likely to develop MS as non-smokers with neither. The researchers believe that cigarette smoke acts in the lungs to "prime" the immune system and make MS more likely.

Many of us who have MS are fully aware that stressful life events can make our symptoms worse. But can stress cause MS in the first place? No, say researchers from the USA and Norway. They used data from two study of nurses' health, which started in 1976 and 1989. Participants were asked to report their level of stress at work and at home. The researchers found no link between self-reported stress and MS risk. As ever though, more research is needed.

We are used to MRI imaging being used to identify MS lesions, but Italian researchers have found that people with MS also experience atrophy (wasting away) of the brain and spinal cord. The amount of atrophy is linked to the degree of disability. They suggest that in the future MRI could be used to monitor response to treatment.

Now on to treatments, and as I said above several studies on Tysabri have reported this month. There have (quite rightly) been concerns about the risk of developing the potentially fatal brain infection progressive multifocal leukoencephalopathy (PML) while using Tysabri. PML is caused by the reactivation of a virus called Polyomavirus JC (JC virus) in the nervous system. JC virus is carried by many people, and is harmless unless the person has lowered immunity.

A number of different research groups gave conference reports on Tysabri and PML. One group has developed a blood test to check whether there has been previous infection with JC virus: it's thought that these patients will be at higher risk of PML when taking Tysabri, a risk that they must take into account when deciding whether or not to take the medication. Another study confirmed that having been on another immunosuppressant therapy at any point before Tysabri increases the risk of PML.

Although PML is unquestionably serious, survival rates among those who develop it while on Tysabri seem to be better than those with other conditions (such as AIDS), possibly due to the development of modern anteretroviral drugs. Most people with MS who develop PML will survive.

People of African descent who get MS typically have a more severe disease course than average, and are less likely to respond to treatment with interferon-beta. American researchers looked at data for Tysabri use in this group of patients, and confirmed that it worked well, reducing relapse rate by an average of 60% and lesion accumulation by 79%.

Because of the risk of PML, some doctors recommend breaks in treatment with Tysabri. A group of researchers in Canada found that disease activity (measured by relapse rate and lesion growth) returned very rapidly after Tysabri was discontinued, whether or not another treatment was started.

Two studies, in Holland and Germany, followed women who became pregnant while taking Tysabri. Both studies were small, as they included only accidental pregnancies: at the moment women on Tysabri are advised not to get pregnant. Out of a total of 37 pregnancies, 28 were completely normal, 5 ended in miscarriage and one woman had a termination: one child was born with an extra finger. These data are promising, but a much larger study is needed before it can be confirmed that Tysabri is safe in pregnancy.

The increased risk of developing PML while on Tysabri, which is highly successful at slowing disease progression, illustrates the need to balance the risks and benefits of any treatment. Australian researchers have found that MS patients are often prepared to take more risks than their doctors in terms of possible side-effects. This illustrates the importance of healthcare professionals listening to the priorities and views of their patients.

Now on to other treatments. The first treatment for MS, interferon-B, was developed and trialled in the late 1980s. A group of American researchers have tracked down participants in the original trials to see howthey had fared since then. The researchers found that those who received interferon-B were only half as likely to have died as those who received a placebo. It's not clear yet what accounts for this difference, as all the participants were likely to have been on other drugs subsequently. A very significant difference though, and one that needs to be investigated further.

There have been concerns about side-effects from the new oral treatment fingolimod (Gilenya), including a risk of lowered heart rate and a condition called AV block. An American study found that these effects were transient, and usually resolve within six hours without treatment. People should be screened for heart abnormalities before taking Gilenya, though, and carefully observed after the first dose.

Spanish researchers have found that Viagra dramatically reduces symptoms in animals with a condition similar to MS. They are hoping to begin clinical trials soon. I'll be interested to see the results. MS can cause sexual dysfunction, and many men with MS are prescribed Viagra. I've not heard of any of them having "miracle cures" from MS...

It's been found that less than half of people with MS are still consistently taking their disease-modifying drugs after 2 years, possibly because of side effects or people perceiving no benefit from them. What is needed, as we all know, is a cure. Excitingly, American and Chinese scientists have succeeded in making human stem cells convert into astrocytes, the cell type which promotes myelination. In my view, stem cell research is what will eventually provide a cure for MS, and this is a major step forward.

Finally - and, I'm afraid, rather depressingly - some British research into the use of antidepressants in MS. Although treatment with antidepressants was always preferable to no treatment, there was no definite evidence that quality of life was improved as a result. Depression is a very common symptom of MS, and it's important that people feel they can get an effective treatment when it's needed. More research is needed to discover whether some anti-depressants are more helpful in MS than others.

So, it was another bumper bundle this month. Does the reporting of research results slow down in the summer? Let you know in July!