Fatigue in MS – and what to do about it

Fatigue – that horrible overwhelming inability to do another thing, sometimes even to think straight, is one of the most disabling invisible problems of MS. When I took a poll of the top symptoms that people wanted to troubleshoot in a holistic way, Fatigue was top. So here goes:
fatiguedWhy do people with MS experience fatigue?

Fatigue in MS is  of 2 types. Motor fatigue, or ‘short-circuiting’ fatigue, is when the difficulty of transmitting the electrical nerve signal down demyelinated, or damaged nerves, overwhelm the body’s ability to produce  ATP ( the energy molecule). Fatigued muscles just have to stop; you feel as if you’ve run a marathon, it’s like hitting ‘the wall’ for an athlete, and you have to sit down. After a short while, energy is replenished, and you can go again.

The second type of fatigue is more of a  widespread, overwhelming all-over fatigue, described here by MS campaigner, Shoshana Pezaro in 2015:

“It’s an absolutely crushing physical and mental symptom that cannot be overcome through will-power. When fatigue hits, I feel like my plug has been pulled out. Physically my body suffers extreme weakness and heaviness and every tiny movement, even raising my hand, is like fighting through thick treacle. But the mental effects are worse. The world separates from my consciousness. My brain is shrouded in a deep fog. It is a dreamlike state where I can hear people and see people, but I somehow I cannot connect. Fatigue cannot be fought, only managed through rest and care.”

Lots of research and debate has been carried out about what causes this type of fatigue; an interesting study reported at this year’s ECTRIMS conference investigated whether fatigue was more strongly linked to lesions in the brain, or to inflammation. They found a strong correlation to inflammation as the driver of this type of fatigue.

So to address Fatigue, we need to address the MS itself, and take both a short and a long view. The good thing is, there is a lot you can do to address both MS itself, and the problem of fatigue.

Starting with the most simple, here’s my list:

  •  Obviously read all the MS Society  ( you can download here)

http://www.mssociety.org.uk/ms-resources/fatigue-ms-essentials-14  and

pace yourself, budget your energy, and:

  • Get your groceries delivered online
  • Call a family meeting, explain that fatigue is a physical problem in MS, and give the family information about it, set rules and boundaries and share out the chores!
  • Save your energy for the stuff that counts – if you can get a cleaner, do so!
  • Fluids – ensure you drink plenty of water
  • The drug  Amantadine can be tried for fatigue in MS but it only seems to help about 20% of people, and sometimes causes unpleasant side-effects

Sleep

Baby smiling in bed with eyes closed and arms out.

It seems obvious, but if your sleep is poor, you will have fatigue!

Sleep problems:

  • No caffeine drinks after 6pm
  • Consider having something to eat before bed to prevent low blood sugar
  • Try to get outside as early as possible (once the sun is up) in the day, and making sure you are outside for at least ½ an hour a day; this helps to set your body’s circadian rythm( wake-sleep cycle)
  • Address causes of waking if possible – eg bladder, worrying, spasm, pain
  • Consider natural sleep aids like ‘Nightall’ etc which are made from hops and valerian – check that its ok to take these with any medication you are on
  • Use the HeartMath technique, for 10 minutes every morning, plus whenever you experience negative or worrying thoughts, or mind is free, and when you’re going to sleep at night.

heartmath-pic

  • Lock into a positive emotion

  • Focus on heart area

  • Breathe in for 5 seconds and out for 5 seconds in one long continuous cycle

  • imagine blowing up a balloon in your belly as you breathe in – your abdomen should rise first, then abdomen squeezes in as you expel the last bits of air out.

HeartMath is wonderful – I can’t find a good website to make it simple; you can buy all kinds of gadgets to allow yourself to see how you’re doing and coach yourself further, but the basic technique is this simple, and it has powerful and far-reaching effects on your resilience to stress, amongst other things.

Additional extras to consider.

mitochondria-2

Energy is created in our bodies by mitochondria, the ‘powerhouse’ of the cell. Each cell contains up to a thousand mitochondria. Mitochondria take fuel from the food we eat, and transform it into energy. They generate a chemical called ATP, which transports the energy for use by the body.

In order to function properly, mitochondria need the fuel of excellent nutrition and oxygen.

Dietary factors

  • Everything that we put in our mouths can either be pro-inflammatory or anti-inflammatory; what we eat has an impact on inflammation.
  • A study published in July 2016 showed improvements in fatigue over the course of one year,  in people with MS who adopted a low fat, plant-based diet

plant-based-diet

  • See www.overcomingmulstiplesclerosis.org  for this type of diet, which could be expected to reduce inflammation, www.fatfreevegan.com for recipes.
  • Also  have a look at the work of Terry Wahls, a medical doctor who reversed her own secondary progressive MS with advanced nutrition,  online. I prefer the overcomingms diet as above, but Terry’s extras like green smoothies and intense nutrition make sense to add in.
  • Be aware of food intolerances. More people with MS have full blown celiac disease than in the general population, but you can also have a milder food intolerance that is not picked up by clinical allergy testing. Experiment to find out if some foods worsen your fatigue, by excluding them for 3 weeks and then bringing them in and noticing. Common irritating foods are bread, cheese, dairy products, gluten grains, sugar, and sometimes beans, but many people have individual things that they don’t tolerate.
  • Vitamin D3 at least 5000 IU daily & consider minimal erythmal dose sunbed. Some people may need more to get into the optimal range of 150-200nmol per litre; you can get your blood checked at http://www.vitamindbloodtest.org.uk
  • A study published this year found a significant reduction in fatigue in people with MS who took 500mg of Co-enzyme Q10 daily.
  • Omega 3 fatty acids are found in oily fish, nuts, seeds and whole grains, and help to calm down and prevent inflammation, aswell as helping to store and retain energy. 20g daily can be supplied by 2 dessert spoons of cold pressed flax seed oil used cold, and make sure it’s fresh; one example; www.flaxfarm.co.uk
  • B vitamins – some people are deficient in these, which can mimic symptoms of MS; some people report these help with fatigue; probably when there has been some deficiency present.
  • Probiotics & fermented foods– very important to restore health of gut, especially after antibiotics, which contributes to health/ energy

Exercise  &  Oxygenation hyperbaric-chamber-10-person

  • Many people report that hyperbaric oxygen improves MS fatigue; if this isn’t possible, at least do deep breathing!
  • Just had great comment in response to this post by Frank:
  • “The very best thing for me has been taking Oxygen Therapy at the MS Centre. There are 56 centres to choose from so there’s almost bound to be one near you – unless you live in Northumberland or Cumbria. 
    With Oxygen Therapy and MS, lots of us find there there is an optimum pressure. The ascending protocol suggests that people should start at 1.5 ATA, move to 1.75 ATA and then try 2 ATA. After each session note down how you feel immediately afterwards and then again about 24 hours later. Once you’ve tried all three pressures you should know the one that suits you best.
    As you say, Miranda, it does not work for everyone, but then neither do any of the drug or dietary therapies – we are all different – however, I’ve found it great for reducing my fatigue and if I miss my weekly session, I certainly feel the impact. Some of my colleagues find they are really tired after the Oxygen Therapy but then feel full of energy the next day, others, like myself, feel the benefit within a few hours. Whatever your views, it’s definitely worth giving it a go.”
  • Regular cardiovascular exercise can help to raise oxygen and energy levels, in your own zone of tolerance. Exercise has been shown to be strongly anti-inflammatory – make it part of your daily routine in one form or another.
  • Some people with fatigue have reported improvement to fatigue by raising the head of their bed by 6 inches. Called ITB or inclined bed therapy – See New Pathways issue 62

APS Therapy

At the MS Therapy Centre where I work we have now had many cases of people’s MS fatigue, including post relapse, responding very well to APS Therapy. This makes sense as the treatment stimulates production of ATP, and is a replica of the wave-form of action potentials ( the electrical nerve signal.)active-nerve-cells-29027134 It hasn’t worked for everyone that’s tried it; it seems to be more effecitve for fatigue in relapsing remitting, rather than progressive MS, and we are still collecting data about this, but the therapy is available privately ( see ‘my other work’ button)  and at 7 MS Therapy Centres:

Bedford, Portsmouth, Kent, Sutton & Croydon, Leicester, Berkshire and Hertfordshire and MS-UK’s Wellbeing centre, Joseph’s Court in Colchester.

Therapies

Lots of therapies, including Shiatsu, Reflexology, Yoga and ‘EFT’ tapping are found by people to improve wellbeing, energy and sleep which may then help with fatigue.

Remember that Disease Modifying Therapies (DMTs) all aim to reduce inflammation and relapses, and by doing so, can have a marked impact on reducing fatigue and improving how you feel. If you are eligible, but not on a DMT, review and reconsider the situation. If you’re on a DMT but still having relapses, request a review, as per the the MS Brain Health Campaign. And when choosing a DMT, ask about the common side-effects, explore how other people have responded, and choose one that fits best with your needs and aims.

happy

In summary, with both long and short term strategies, there are lots of things you can do to beat fatigue and enhance your energy. Some of the long term strategies take longer to bear fruit – but keep going; many people with MS can remember a time when they were so much more fatigued than they are now.

All the best

Miranda

 

Diet in Auto-immune disease

11.coverHow come other auto-immune diseases get articles like this in medical journals??

Even though this is about rheumatoid arthritis, it’s well worth reading if you have MS.

It confirms many things I’ve said here before. It is technical, and hard going but – scan it, and get the gist. For me, the low sat. fat diet is a cornerstone in MS, as per http://www.overcomingms.org. but I’m getting to think that individual intolerances can be wreaking havoc in some people, too. You read a lot of good discussions like this in natural health experts, but never in the medical literature for MS.

enjoy!  Reproduced from:

http://rheumatology.oxfordjournals.org/Diet therapy for the patient with rheumatoid arthritis?

In spite of the great advances that have been made in the development of new drugs for the treatment of rheumatoid arthritis (RA), many patients are interested in alternative treatments like dietary therapy. Although relatively few studies have been carried out on the possible impact of dietary therapy on disease activity in RA, interest in this matter is growing as our understanding of disease pathology and the effect of nutrients on immunity and inflammation increases.

Most clinical dietary therapy studies undertaken so far have focused on some form of dietary elimination. Scandinavian health farms have long promoted fasting and vegetarian diets for patients with rheumatic diseases.

In 1979 and 1983, Sköldstam et al. [12] carried out two studies to verify whether diet therapy could alleviate disease activity and symptoms in patients with RA. In one study, 16 RA patients fasted for 7–10 days and followed a lactovegetarian diet for the subsequent 9 weeks. There was a significant improvement in both objective and subjective disease symptoms during the fasting period, followed by rapid deterioration when the patients began on the lactovegetarian diet.

In the second study, 20 patients with RA completed a 7- to 10-day fast, followed by 3 months on a vegan diet (a diet without meat, fish or dairy products). Physician’s general assessment revealed that 11 patients had undergone subjective improvement, seven were unchanged and two were worse after the study period than before. Nineteen patients had lost weight and no improvement was seen in objective variables like erythrocyte sedimentation rate (ESR) and C-reactive protein during the dietary period. However, 5 (25%) of the patients showed both objective and subjective improvement. Several patients complained about the diet and only two patients had continued with a strict vegetarian diet after the study period. This confirms that many patients experience difficulty in implementing strict dietary changes.

In 1983, Panush et al. [3] conducted a study of the then popular Dong diet (which eliminated dairy products, red meat, citrus fruits, tomatoes, alcohol and coffee). This was an elegantly performed clinical dietary study with a double-blind, placebo-controlled design. Twenty-six patients took part, 11 on the experimental diet and 15 on a control diet. Although there was no statistical difference between the experimental and placebo diet groups, two patients in the experimental group improved noticeably. One patient experienced disease exacerbation after eating dairy products and the other after eating meat, spices and alcoholic beverages.

In 1986, Darlington et al. [4] published the results of a single-blinded, placebo-controlled study of 6 weeks of dietary manipulation in 53 patients with RA. During the first week, the patients were only allowed to eat foods they were unlikely to be intolerant to. In the article, it is not stated which food items these were. Other food items were then reintroduced one at a time to see whether any symptoms were elicited by the dietary challenge. Foods producing symptoms were then excluded from the diet. Both objective and subjective variables improved significantly, and a subgroup of 33 patients were graded as good responders. However, the patients were only observed for 6 weeks, which is a weakness in a study undertaken on patients with a chronic disease.

In 1991, we published the results of a single-blinded controlled clinical trial testing the effect on disease activity in patients with RA of dietary elimination combined with the vegetarian diet traditionally practised on Scandinavian health farms [5]. Fifty-seven patients took part in the study, 27 in the diet group and 26 in the control group. The patients were followed for 13 months, making this by far the most comprehensive study undertaken with regard to dietary therapy in RA.

We found statistically significant improvement in both objective and subjective disease variables in the diet group compared with the control group. Twelve patients (44%) in the diet group were responders, according to the Paulus criteria, compared with 2 (8%) in the control group [6]. Ten patients (37%) in the diet group reported aggravation of symptoms after reintake of one or more food items. Eight of these belonged to the responder group.

After 2 yr, we conducted a follow-up study on the same patients and found that the responders had continued with the diet and still had a significant reduction in all clinical disease variables and ESR [7]. In this study, 13 patients (59%) in the diet group reported an increase in disease symptoms after intake of meat, and 10 patients (45%) after intake of sugar and coffee. Of the 10 responders examined in the follow-up study, eight reported an increase in disease symptoms after intake of different kinds of meat, and six after intake of coffee, sweets and refined sugar.

Fasting has been documented to have beneficial effects on both clinical and laboratory variables reflecting disease activity in RA [158]. It thus serves as a useful model for studying the biological changes associated with simultaneous improvement in disease activity. Previous studies in healthy subjects have revealed that fasting decreases mitogen- and antigen-induced lymphocyte proliferative responses [9], and suppresses interleukin-2 (IL-2) production [10]. We have recently shown that a 7 day fast in RA patients also decreases CD4+ lymphocyte activation and numbers, suggesting transient immunosuppression [11]. We also found an increase in IL-4 production from mitogen-stimulated peripheral blood cells. Thus, further studies should be carried out to clarify the immunomodulatory mechanism behind fasting.

Evidence suggesting that food allergy, defined as an immunological response to food antigens or to intestinal bacterial flora, might be involved in disease pathology in most patients with RA is weak. However, it is possible that an exogenous agent like a food antigen can initiate a pathological immune process in a genetically susceptible individual [12].

Food antigens, food antibodies and their complexes have been detected in the systemic circulation of healthy subjects [1314]. Animal models indicate that the gut is an important trigger of and pathway for the immune response. Encounters with complex proteins, like gluten and milk proteins, lead to either oral tolerance or sensitization and possible loss of self-tolerance to cross-reacting epitopes [15].

An association between a special food item and disease activity has been reported by patients with a variety of rheumatic diseases, such as palindromic rheumatism [1617], systemic lupus erythematosus [1819], Sjögren’s syndrome [20] and juvenile RA (JRA) [2122]. Case reports describing an association between diet and disease activity in RA include both seropositive and seronegative disease [2325]. Although the extent of food allergy involvement is still not known, it has been suggested that between 5 and 30% of patients with RA may be affected [2627].

We found an increase in humoral response in all patients with RA, with a general increase in IgG, IgA and IgM antibodies to various food antigens, like gluten and milk proteins. However, the elevated concentrations of specific immunoglobolins could not be used to predict which food items would aggravate the disease symptoms [28].

Wheat and other rough grain products can elicit an allergic T-cell response through their lectin structures. Lectins are glycoprotein molecules that bind to carbohydrate-specific receptors on lymphocytes with high affinity and thus elicit a significant immune response. Lentils and grain products have a particularly high lectin content. Lectins are fairly heat resistant; for example, lentils have to be cooked for a long time to inactivate the lectins.

While the results of a questionnaire-based survey revealed that 37–43% of patients with rheumatic diseases experienced an increase in disease symptoms after intake of certain food items, no difference could be found between the various diseases [29]. This suggests that diet may influence the inflammatory process in general and is not a specific feature of RA.

One of the mechanisms involved may be the release or secretion of vasoactive amines (bioactive amines) like histamine and serotonin [30]. Several of the food items reported to cause disease aggravation have a high histamine content, like pork and beef sausage, meat, tomato and spinach. Since no immunological response to pork and other meat has been demonstrated, a pharmacological response would explain the often reported increase in symptoms resulting from these foods [31]. Other foods like shellfish, strawberries, chocolate and fish can cause a release of histamine.

Citrus fruits, which contain other vasoactive amines (octopamine and phenylephrine), are often said to aggravate symptoms [30]. Consumption of both coffee and alcohol has been shown to liberate adrenaline and/or noradrenaline, which suggests that they have a pharmacological effect [3032]. Consumption of alcohol can also result in the release of histamine, and certain red wines have in addition a high concentration of histamine, which may explain the frequently reported intolerance.

A pharmacological reaction would also explain why the patients reported immediate reactions to these food items, as opposed to the more delayed reactions to dairy products and gluten. This may mean that a different mechanism is involved in symptom aggravation. The reported aggravation of symptoms after intake of refined sugar and sweets in patients with RA may have a metabolic explanation, such as an increased concentration of blood glucose due to impaired glucose handling [3335].

Gut involvement in the pathogenesis of rheumatic diseases was proposed by Rea Smith [36], who reported that surgical removal of intestinal segments with focal infection had a beneficial effect on disease activity. Monroe and Hall [37] reported differences in the stools of 142 patients with chronic arthritis as compared with controls. Månsson and Olhagen [38] found not only an abnormal faecal flora, with an increase inClostridium perfringens in patients with RA, systemic lupus erythematosus and psoriatic arthropathies compared with healthy controls, but also a higher level of alpha-antitoxin in the serum of these patients. Alpha-toxin (phospholipase-C) is produced by a special strain of C. perfringens often found in RA patients. Månsson and Olhagen [38] found a rise in alpha-antitoxin titre in 75% of the patients with RA in the study, but in none of the controls.

A significantly higher carriage rate of C. perfringens in patients with RA than in healthy controls has also been documented by Shinebaum et al.[39]. An altered intestinal bacterial flora has been reported in patients with seropositive erosive RA compared with patients with seronegative RA and controls [40]. An increased concentration of antibodies to Proteus has been described in patients with active RA [4142] and to Klebsiella in patients with ankylosing spondylitis [43]. Several of these reports have suggested that RA and ankylosing spondylitis could be mediated by cross-reactivity between self and bacterial antigens.

The intestinal bacterial flora is known to be affected by diet [4446], and it has been suggested that a diet which could alter the intestinal flora might have an effect on disease activity. This theory was supported by the finding that changes in disease activity correlated with alterations in the intestinal flora measured in patients who switched from an omnivorous to a vegetarian diet [47]. The effects of the intake of functional foods (i.e. food as medicine; in this case, food which promotes the growth of health-promoting bacteria in the intestine or food items that contain natural healthy intestinal bacteria) should be an interesting field for further research.

Much interest has been taken in recent years in the immunomodulatory effects of polyunsaturated fatty acids (PUFAs) and their therapeutic potential as anti-inflammatory agents [48]. Both clinical and in vitrostudies have established that long-chain n-3 and n-6 fatty acids inhibit T-lymphocyte function [4952].

Research suggests that manipulating the balance of dietary fatty acids in favour of increased n-3 fatty acids and decreased n-6 fatty acids may have a beneficial effect on disease activity in RA [495356]. These studies have shown that long-chain n-3 fatty acids can diminish peripheral blood mononuclear cell proliferation and reduce the production of IL-1, IL-2, IL-6, tumour necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). However, clinical studies on supplementation of ω-3 fatty acids have not supported the expectations raised by the laboratory findings [5357].

The balance between unsaturated and saturated fatty acids may also affect lymphocyte proliferation (in vitro) [58]. The practical implications of these observations for the in vivo situation are currently unclear, but suggest that a diet which is high in unsaturated fatty acids and very low in saturated fatty acids may have a stronger immunosuppressive effect than that obtained by only n-3 fatty acid supplementation.

In this respect, the Mediterranean diet, with a low content of red meat and a high content of olive oil, is of interest. Olive oil has been shown to reduce lymphocyte proliferation, natural killer cell activity, adhesion molecule expression on lymphocytes and the production of pro-inflammatory cytokines in animal models [59]. In an intervention study in which dietary saturated fatty acids were partly replaced by olive oil, mononuclear cell expression of ICAM-1 was found to be significantly reduced [60].

It has also been reported that a very low intake of saturated fats is beneficial in multiple sclerosis, where, as in RA, CD4+ lymphocytes are thought to play a pathogenic role [61]. It is thus worth investigating whether a diet low in saturated fats, with a high content of olive oil and with n-3 supplementation, could have immunosuppressive effects in vivoand could thus be of benefit in the treatment of RA.

The pathological hallmark of RA is persistent destructive inflammation in the synovial membranes of joints, which leads to a gradual destruction of the supporting structures of the joints, such as bone and cartilage. Although the aetiology is still unknown, the inflammation resulting from the immunological reaction is quite well described. It is known that neutrophil granulocytes, macrophages and lymphocytes are activated, and that oxygen free radicals are produced [62]. Hence, a low concentration of antioxidants may perpetuate tissue destruction in RA. Free oxygen radicals and oxidative stress may also be of importance for the aetiology and chronicity of the inflammatory rheumatic diseases [6364]. Two epidemiological studies have recently suggested that antioxidants may play a protective role [6566].

The most important antioxidants known today are vitamin A, vitamin E, vitamin C, beta-carotene, the bioflavonoids, zinc and selenium. The antioxidant properties of vitamin A and vitamin E lead to a reduction in the oxidation catalysed by free radicals [67]. Vitamin E functions as a physiological antioxidant for the cell membrane and is the most important fat-soluble antioxidant in the cell membrane lipids [6468]. Zinc plays a significant role in antioxidant protection and immunity because it is a constituent of the cytoplasmic enzyme superoxide dismutase [69]. Selenium, on the other hand, is part of the glutathione peroxidase enzyme, which can react with peroxides formed during inflammation. Beta-carotene is a fat-soluble, chain-breaking antioxidant and a quencher of singlet oxygen, and is known, along with alpha-tocopherol, to be the most important element of the non-enzymatic antioxidant defence in biological systems [7071].

Low serum concentrations of selenium and zinc in RA patients were reported as early as 1978 [72] and were further investigated by Tarp et al.[7375]. Mezes and Bartosiewicz [63] found reduced plasma vitamin A content in patients with RA. Honkanen et al. [76] found lower serum levels of vitamin A and E in patients than in healthy controls. Sklodowska et al.[64] found lower vitamin E concentrations in plasma in children with JRA than in controls. Studies have also shown reduced concentrations of zinc and selenium in children with JRA [7778].

The reduced serum concentrations of antioxidants found in patients with inflammatory rheumatic diseases do not appear to be a consequence of reduced dietary intake in these patient groups compared with healthy controls [7880]. They may, therefore, indicate a high turnover of antioxidants and an increased antioxidant requirement in these patients which is necessary in order to balance the higher production of free radicals.

Although studies of supplementation with a single antioxidant have not shown disease reduction in RA patients, it is still possible that patients with an inflammatory rheumatic disease will benefit from supplementation with a combination of several antioxidants or from a dietary intake that exceeds the recommended dietary allowances.

Studies of immunomodulation have revealed that nutrients other than food proteins and fats also have an impact. The effects of fatty acids, antioxidants and food proteins on immunomodulation need to be investigated further, and so should the question of the involvement of the gut in the aetiology and pathology of rheumatic diseases. More knowledge on the effects of dietary components upon immunological function is necessary if the potential use of dietary therapy as a tool in the treatment of RA is to be adequately assessed.

  1. 1.     M. Haugen
  2. 2.     D. Fraser and 
  3. 3.     Ø. Førre

 

MS Trust annual conference 2012

MS Trust conference – part 1.

In November I attended the MS Trust’s annual conference for healthcare professionals working in the field of MS.

I really enjoyed this year’s conference, and will summarise what I learned below.

The first speaker was Gavin Giovanonni, top MS researcher at Royal London Hospital. This is a pic from his blog, which you can follow at http://multiple-sclerosis-research.blogspot.co.uk/ http://multiple-sclerosis-research.blogspot.co.uk/. It includes ‘the mouse doctor’ (?) who is co-blogger.

vcm_s_kf_repr_150x126

to this talk resonated with everything I have been thinking for the last few years. You could sum it up as MS – which is more important – inflammation or degeneration? This argument has been recently explored in the article

‘Will the real MS please stand up?’ by Peter K. Stys, Gerald W. Zamponi, Jan van Minnen & Jeroen J. G. Geurts  – here’s a link to the full text article http://mssociety.ca/chapters/calgary/pdf/2012_Stys_507.pdf.

This article  weighs heavily on the side of looking at the importance of degeneration, so doesn’t really discuss the benefits of early aggressive treatment of inflammation.

Giovannonni’s blog calls this article ‘myopic ramblings’ ; it’s a dog-eat-dog world out there in academia, but Peter Stys has received funding from the MS Society of Canada to research progressive MS, which has got to be good news.

To illustrate what this discussion is about,  I’ve done a rough diagram based on one by Professors Coles & Compston Lancet. 2002;359:1221-1231

inflammation or degeneration

Basically, the tall skyscrapers represent inflammation –  relapses or new symptoms. They are the part of MS that pretty much all the research and medications for MS have always been aimed at; that’s why research trials always only want to recruit people with relapsing –remitting MS.

But the disappointment over the last few years has been realising that although the  disease modifying MS drugs can show a reduction in relapses, they have not been able to prove a reduction in the progression of MS.

The progressive element of MS is represented by the green block, and represents damage to and loss of axons, the long part of the neurons, or nerve cells.

The argument that Giovannonni presented, which is being mirrored by various thinkers around the world at present, is that perhaps research/pharmaceuticals have been focussing on the wrong part of MS. Perhaps the periods of inflammation in MS are the body’s reaction to a degenerative process that is going on.

As in this article, Giovanonni described his team’s interest in HERVs ( human entero-retrograde viruses – virus which are within the genes) and other virus which we can contract later in life; in particular, the Epstein Barr virus which causes glandular fever, and is part of the Herpes virus family. They want to see whether by suppressing these viruses, the driving force of the degenerative process might be taken out, and they have just received funding to do the preliminary research with anti-virals, which is great news.

It made me think again about looking into powerful natural anit-virals, and I’m going to speak to all the people who tried using some last spring to hear about  experiences and see how they’ve been doing since.

Another big factor in his research is Vitamin D; for a long time he has been an advocate of high dose vitamin D3 supplementation. I’ve got previous posts about this so won’t go into the pro side of vitamin D, BUT…

vitamin D

The subject got pretty confusing later when Professor Carolyn Young, Consultant Neurologist and Honorary Professor of Neurology

Walton Centre for Neurology & Neurosurgery, Liverpool led an 

Update on Vitamin D.

The professor warned us that this would be a challenging session, and it was. This is really important, as high dose vitamin D has become a mainstay of treatment for anyone who’s had their ear to the ground in the last few years, and neurologists have started to also take it seriously and recommend it.

She introduced us to all the formative research on vitamin D and MS; the Nurse’s study, which is scientifically important and excellent due to the enormous size of the sample –  92,253 women followed from 1980 to 2000) and Nurses’ Health Study II (NHS II; 95,310 women followed from 1991 to 2001. This study showed that having higher vitamin D blood levels, and taking supplements containing vitamin D had a strong effect of protecting a person from developing MS.

The US army study; likewise, great numbers and scope of years, showing 7 million army recruits from 1992-2004 and compared the vitamin D levels with their risk of developing MS.18 They found 257 new cases of MS in the group. There was a significant decrease in risk with increasing vitamin D levels among white, but not black or Hispanic people, who had lower vitamin D levels than whites. Levels of around 100nmol/L or more seemed to be protective, with almost a two thirds reduction in risk for those with these higher levels.

A good factsheet summarising research on vitamin D and MS is on the MS Trust website at http://www.mstrust.org.uk/downloads/vitamind.pdf

She then gave feedback on 4 or 5 more recent studies, where vitamin D supplementation ( mostly D3 but one study used D2) was given at various doses, over various timescales, none of which showed any influence on annual relapse rate, or level of disability at all.

We then went on to discuss what to make of this?

One point was that an association is not necessarily a cause

For example, low levels of vitamin D in the blood are associated with relapses in MS – but maybe they do not go towards causing it – maybe the low level of vitamin D is caused by the relapse or inflammation?

One point was that it may not be possible to extract the active ingredient – whatever that is – from the foods in order to make an effective supplement, and that sometimes other helpful substances in foods are responsible for the absorption of a nutrient.

I asked whether there was a difference between getting your vitamin D from the action of sunlight on the skin and a supplement? I didn’t get the full answer I was looking for, but Prof Young did make the point that there are other actions that the sun has on the immune system and inflammation that are generally beneficial.

People wanted to know what we should advise ‘while the scientists work it out’. Prof Young’s advice was that she felt that 1000IU should be the top recommendation a healthcare professional makes to a person with MS, and that it chould be checked that the person doesn’t have any kidney problems, as if they do, high dose vit D could cause kidney stones.

I’m going to ask Giovannonni on his blog/twitter/whatever what his response to this is, and also check what George Jelinek has been making of it.

I think if I have any thoughts on this so far, they are that perhaps people with MS need to try to get a s much Vit D as possible from foods and from the action of sunlight on the skin. In this country that only works between April and October, and when the sun is high in the sky.

It makes me wonder about sunbeds, I haven’t gone right into this, but just asking around, apparently you can get vitamin d from using a sunbed, but it has to put out UVB rays.

( and obviously, use sensibly, don’t get burned or overdo it)

I think I’m probably going to carry on recommending 5000IU, due to all the other research I’ve seen, but will be keeping my ear to the ground.

I’ve got more from the conference and will post as soon as I get time to write it up!

We also had a great time at the gala dinner fancy dress night, so In the meantime, this is for the Bedfordshire people – if you ever wondered whether your MS nurses were arch rivals or accomplices in crime, here’s something to confuse you further….!

vcm_s_kf_repr_624x832

haha

it’s not my normal look…

but I did enjoy being Marylin for the night!