Frequently Asked Questions

There is a lot of controversy about the oils in coconut and their effect on health. While some reputable authorities like Udo Erasmus argue that the short chain fatty acids in coconut may be quite healthy, Swank was very clear in eliminating coconut from the diets of those in his landmark study. We know that most of the fats in coconut are saturated fats. One of the key issues with saturated fats is their melting point. If the melting point of a fat is above body temperature, then that fat will essentially behave in body cell membranes like a solid fat at body temperature, making cell membranes rigid, inflexible and sticky, thereby encouraging degeneration and inflammation. It is worth noting that the melting points of the common fats in coconut are as follows:

Lauric acid (12:0 carbon chain) 44.2C
Myristic acid (14:0 carbon chain) 53.9C
Palmitic acid (16:0 carbon chain) 63.1C.

These fats are solid at body temperature and are likely to significantly worsen MS. We do not recommend them in any quantity.

They all appear to contain the offending protein butyrophilin, as per this old piece of research:

Lipid globule membranes were isolated from human and bovine milk and from the milk of sheep, goat, pig, rat and guinea pig, and their polypeptide compositions were analyzed. The major polypeptides with molecular weights similar to that of bovine butyrophilin were separated by gel electrophoresis, isolated and characterized with respect to isoelectric point, molecular weight, immunological cross-reactivity and peptide composition after proteolytic cleavage. We show that in all species examined these proteins are similar to bovine butyrophilin in (i) their relative insolubility in buffers of low and high ionic strength and in non-denaturing detergents, (ii) the occurrence of several isoelectric variants, and (iii) patterns of peptides obtained by protease digestion. It is concluded that closely related proteins are major constituents of the cytoplasmic coat structures associated with milk lipid globule membranes of many species, and we propose the name butyrophilins for this group of proteins. Bovine and human butyrophilins are glycosylated with relatively large amounts of glucosamine, mannose, glucose and galactose but little fucose, sialic acids or galactosamine. Most if not all of the sugar residues are associated with an acetone-soluble peptide fragment of Mr 12000-16000 focusing at about pH 4.0. We suggest that this fragment contains a membrane-spanning peptide sequence and is involved in the attachment of the cytoplasmic coat to the membrane of the milk lipid globule.

Reference
Heid HW, Winter S, Bruder G, Keenan TW, Jarasch ED. Butyrophilin, an apical plasma membrane-associated glycoprotein characteristic of lactating mammary glands of diverse species. Biochim Biophys Acta 1983;728:228-38

Sounds like you are doing fantastically well. You are not getting anything wrong. Your issue is clearly your family history of hypercholesterolaemia. That means that you have a genetic predisposition to making more cholesterol in your own body. The good news is that all the things you are doing are preventing it from being higher. The only slight change that might help bring it down would be to increase omega 3 supplements. You are only taking 4000mg at this stage (ie 4 caps). Remember I recommend 20. But would add them as pure liquid flaxseed oil, spooned over dinner (pasta, salad, baked potatoes, etc). I would increase that to perhaps 30mls a day. That should make a difference. But remember, the aim is to stay well, and you are! These are just numbers.

We have had success with SLE (lupus), Sjogren's Syndrome and Rheumatoid Arthritis. The diet and supplements, sunlight, meditation and stress management are very anti-inflammatory and so are helpful for most immune based conditions. They are also anti-degenerative and you would expect to get some benefit in degenerative conditions like Parkinson's Disease, dementia, macular degeneration and so on.

My suggestion would always be to use therapies that have been shown in trials to be helpful in MS, or that have shown equivalence with such therapies in well-designed clinical trials. For the NZ green lipped mussel extract (Lyprinol), it is too early to tell, as most studies are in experimental models rather than patients, but the effect is likely to be small.

There is a lot of discussion about whether flaxseed oil is 'as good' as fish oil. Given that our oceans are gradually becoming more polluted, particularly with heavy metals like mercury, and that heavy metals are known to cause neurological problems, it would be good if a plant-based oil like flaxseed oil could provide all our omega-3 needs.

The problem is that the fatty acid in flaxseed oil, alpha linolenic acid (ALA), needs to be converted in the body to the fish oil fatty acids, eicosapenanoic acid (EPA) and then docosahexanoic acid (DHA). I have seen various figures put on this conversion, mostly up to 10% of it being converted, dependent on general health, saturated fat consumption, alcohol consumption, and a number of other variables. Udo Erasmus in his excellent book 'Fats that Heal, Fats that Kill' does the best calculation I have seen on this. Erasmus quotes a figure of 2.7% per day of the ALA being converted to EPA. He says that this figure is likely to be higher for people getting all the essential nutrients from diet and supplements. As most people's fat deposits contain about 2% ALA (quite a bit higher for those following the diet and supplements here), this is about 200g of ALA, which could make about 5400mg of EPA (as there is 180mg EPA in a 1000mg capsule of fish oil, this is equivalent to about 30 of the 1000mg capsules of fish oil).

If there is no ALA in your fat deposits at all (if you had been taking no omega-3s in your diet whatsoever), then just taking two tablespoons of flaxseed oil would supply enough ALA to make about 378mg of EPA, equivalent to what is in two 1000mg fish oil capsules. But as can be seen from the above calculation of body stores, most people have enough stored if they are supplementing every day, to make quite adequate amounts of EPA and DHA.

The advantage of doing it this way rather than taking it as fish oil is not only related to chemical toxins like mercury in fish oil, and to questions about the sustainability of our fish stocks, but also that the EPA made this way is fresher, in the body every day. There is also the bonus that there is minimal saturated fat intake this way, as fish oil contains quite a bit of saturated fat. I prefer to take two dessert spoons of flaxseed oil a day (20mls) on the days when I don't eat oily fish.

It is incorrect to say there is no evidence for diet in MS. Swank's 34 year study of a low saturated fat diet supplemented with polyunsaturated fatty acids was a landmark study in MS.¹ Naturally, given that the study began in 1949, it was not a randomized, controlled trial, as these had not yet been devised. It was however a prospective clinical intervention study supported by grants from the MS Society of Canada, the Montreal Neurological Institute, the Department of Health and Welfare of Canada, the MS Society of Portland and other sources. Data collection on diet was meticulous over 34 years, only 6 of 150 people entering the study dropped out, and the differences in outcomes between those who adhered to the diet and those who did not were astounding. People on the diet essentially did not deteriorate significantly over 34 years. No other treatment has come close to the magnitude of this effect.

But Swank is only part of the diet story. We have strongly supportive data from laboratory and animal research, epidemiological research, case-control studies, observational cohort studies and a randomized controlled trial to support the view that this diet profoundly modifies MS progression. Indeed, I can find no literature that is in conflict with these data. The evidence base behind these and other lifestyle approaches to MS is covered in much more detail in my book 'Overcoming Multiple Sclerosis'.

Many people fall into the trap of asserting that there is no evidence base for this approach. As one of the key figures in the development of evidence- based medicine stated: "Evidence-based medicine is not restricted to randomized trials and meta-analyses. It involves tracking down the best external evidence with which to answer our clinical questions.....if no randomized trial has been carried out for our patient's predicament, we follow the trail to the next best external evidence and work from there".² The literature supporting diet in MS is wide-ranging, congruent and highly persuasive.

It is disappointing to see people occasionally saying that a dietary approach to MS just gives people false hope. There is no such thing as false hope. If one person can be diagnosed with MS and live a long, healthy life without further problems, then that is all that is needed for anybody else to have genuine real hope that they too can be like that person. The real problem is that often MS societies and doctors give us 'false no hope', that is they make us believe that all of us will be disabled eventually. I prefer to have hope that I will be like others before me who have remained well, many of them in Swank's study. It is entirely reasonable to have the real hope that diet and other therapies may stop the disease progressing; disease progression in MS is far from inevitable.

Some interpret my strong support of diet (and other lifestyle approaches) in MS management as being somehow in conflict with drug therapy. I do not see any conflict. Why would people not do everything possible to stop the progression of this serious illness? To imply that drug therapies are proven, effective therapies, and diet is not, is to ignore the serious methodological problems with the drug trials, particularly the interferon studies. Because of easily detected side effects, these studies were essentially unblinded studies, and they did not account for drop-outs, which when analysed, were mostly due to the disease worsening. This failure to perform intention-to-treat analyses seriously weakens the studies. And the studies were drug company sponsored; we know that drug company sponsored studies are more likely to be favourable to a company's product than independently conducted research³; authors of company-sponsored research are more than five times as likely to recommend the company drug as independent authors, regardless of results⁴; and researchers with industry connections are far more likely to favour company products.⁵ Importantly, the trials have not been at all convincing in showing any effect on disease progression.

It has been said that there is no plausible biological mechanism by which diet works in MS. There is too large an evidence base on the anti-inflammatory effects of vegan diets and the neuroprotective effects of PUFA supplementation to be covered here. In short, the effect of essential fatty acid intake on eicosanoids has been studied in great detail in people with MS. Gallai and co-workers showed that there was a marked decrease in pro-inflammatory chemicals after only four weeks' supplementation with fish oils.⁶ IL-1beta, IL-2, IFN-gamma and TNF-alpha were significantly decreased. The decreases were more pronounced after three and then six months. The pro-inflammatory eicosanoids PGE2 and LTB4 were also decreased. These eicosanoids have been shown to be involved in causing relapses in MS patients.^7,8 McCarty proposes a number of theories why vegan diets plus fish oil and vitamin D may be of wide-ranging benefit to people's health, largely through their effects on the immune system ^9,10, and UK scientists have added new experimental evidence for the benefits of fish oil in regulating inflammation.¹¹ Das has also published extensively on the anti-inflammatory effects of fish-based Mediterranean type diets.^12-14
It is quite reasonable for people with MS to use diet in their quest for health, and enthusiastically embrace the potential of staying well through their own efforts, with real hope, and confidence in their futures.

References

1. Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet 1990; 336:37-39
2. Sackett DL, Rosenberg WM, Gray JA, et al. Evidence based medicine: what it is and what it isn't. BMJ 1996; 312:71-72
3. Bodenheimer T. Uneasy alliance--clinical investigators and the pharmaceutical industry. N Engl J Med 2000; 342:1539-1544
4. Als-Nielsen B, Chen W, Gluud C, et al. Association of funding and conclusions in randomized drug trials: a reflection of treatment effect or adverse events? JAMA 2003; 290:921-928
5. Stelfox HT, Chua G, O'Rourke K, et al. Conflict of interest in the debate over calcium-channel antagonists. N Engl J Med 1998; 338:101-106
6. Gallai V, Sarchielli P, Trequattrini A, et al. Cytokine secretion and eicosanoid production in the peripheral blood mononuclear cells of MS patients undergoing dietary supplementation with n-3 polyunsaturated fatty acids. J Neuroimmunol 1995; 56:143-153
7. Calabrese V, Bella R, Testa D, et al. Increased cerebrospinal fluid and plasma levels of ultraweak chemiluminescence are associated with changes in the thiol pool and lipid-soluble fluorescence in multiple sclerosis: the pathogenic role of oxidative stress. Drugs Exp Clin Res 1998; 24:125-131
8. Toshniwal PK, Zarling EJ. Evidence for increased lipid peroxidation in multiple sclerosis. Neurochem Res 1992; 17:205-207
9. McCarty MF. Upregulation of lymphocyte apoptosis as a strategy for preventing and treating autoimmune disorders: a role for whole-food vegan diets, fish oil and dopamine agonists. Med Hypotheses 2001; 57:258-275
10. McCarty MF. A moderately low phosphate intake may provide health benefits analogous to those conferred by UV light - a further advantage of vegan diets. Med Hypotheses 2003; 61:543-560
11. Flower RJ, Perretti M. Controlling inflammation: a fat chance? J Exp Med 2005; 201:671-674
12. Das UN, Ramos EJ, Meguid MM. Metabolic alterations during inflammation and its modulation by central actions of omega-3 fatty acids. Curr Opin Clin Nutr Metab Care 2003; 6:413-419
13. Chrysohoou C, Panagiotakos DB, Pitsavos C, et al. Adherence to the Mediterranean diet attenuates inflammation and coagulation process in healthy adults: The ATTICA Study. J Am Coll Cardiol 2004; 44:152-158
14. Zampelas A, Panagiotakos DB, Pitsavos C, et al. Fish consumption among healthy adults is associated with decreased levels of inflammatory markers related to cardiovascular disease: the ATTICA study. J Am Coll Cardiol 2005; 46:120-124

There is abundant calcium in this diet. The real problem with calcium in western societies is lack of sunlight. Sunlight results in vitamin D being produced in the body, and vitamin D's main job is to absorb calcium from the diet. A whole calcium supplementation industry has grown in western countries as a result of sun avoidance. Foods such as dairy are heavily promoted as being healthy because they contain calcium, ignoring the real health problems they may cause. With adequate vitamin D, from sun or supplements, there is no problem with inadequate calcium. Osteoporosis is unlikely too for people who get enough vitamin D.

There is sufficient iron in this diet to keep most people from getting anaemic although women with heavy periods may find they get iron deficient. Iron is found in a variety of vegetables. It is possible to get tested at the local doctor for iron deficiency if it is suspected. If low, a natural herbal iron replacement like Floradix is recommended.

It is important for optimal health to have both omega-3 and omega-6. These are essential fatty acids, that is, health cannot be sustained without them. The right balance is about 2-4:1 omega-6 to omega-3. This is much lower than the current ratio in our society of about 16-25:1.

Most people actually find that they feel better, but the real effect is on reducing the rate of relapses. This only becomes clear with time. It took people in Swank's study 3-5 years to stabilise on the diet, that is, get their relapse rates down to a minimum, although there was a big difference by about 9-12 months.

There is a number of researchers who contend that, in an evolutionary sense, legumes, and gluten in cereals, are relatively recent additions to the human diet. These protein-rich foods may be implicated in a host of auto-immune diseases including MS. The most severe form of gluten intolerance is coeliac disease. Here, people develop serious digestive system disorders due to an immune response to the gluten in wheat. One might expect, if gluten was a key ingredient in the diet to avoid in MS that people with MS might have a higher than usual incidence of coeliac disease, or vice versa, that people with coeliac disease might have a higher than expected incidence of MS. A major population study published in mid-2007 examined 14 000 people in Sweden with coeliac disease and compared them with 70 000 other people without the disease acting as controls.¹ One would have expected a higher rate of MS (or other CNS degenerative disease) in those people with coeliac disease than controls if gluten was involved in causing these diseases. In fact the researchers found no statistically significant association between coeliac disease and subsequent multiple sclerosis, Parkinson's disease, Alzheimer's disease, hereditary ataxia, the symptom ataxia, Huntington's disease, myasthenia gravis or spinal muscular atrophy. This is very strong evidence that there is no link with gluten.

If there was indeed a link, one should at least expect to find in people with MS antibodies to gluten which indicate intolerance. In fact, Italian researchers looking at 95 patients with MS found not a single patient with elevated antibody levels.² UK researchers tested 49 patients with MS for their antibody levels and found 12% had raised levels; however this compared with 13% of unselected blood donors, so it was unlikely that people with MS had any special sensitivity to gluten.³ Iranian researchers tested 166 people with MS for antibodies and compared them to people without MS.⁴ They found no difference in antibody levels.

Italian researchers used an alternative approach to investigate this problem. They fed a gluten-free diet to animals with the experimental form of MS, EAE. The animals on the gluten-free diet initially had a more severe disease course.⁵ Later, they seemed to be doing better than those animals eating gluten. The study in my view provided an indeterminate result.

The molecular mimickry theory of MS causation is perfectly valid, and probably explains why cow's milk protein for example sets off the chain of events leading to myelin attack by the immune system. We now have good evidence from the laboratory that a segment of cow's milk protein is identical to a segment of myelin oligodendrocyte glycoprotein. The immune system, in setting up defence against this foreign protein, is 'tricked' into also attacking this part of myelin. Whenever something like this is proposed as an explanation for the immune attack on myelin,  it is important to validate it against what we actually see in human populations.

For cow's milk, this is easy. The world map of MS distribution is almost exactly the same as the world map of cow's milk consumption. That is, there is almost a direct correlation epidemiologically between cow's milk consumption and MS incidence. This is a kind of 'cross check' if you like, that the theory is correct. As a result, I strongly advise people to avoid cow's milk.

For gluten for example (or tomato for that matter), there are several major problems with the theory. Firstly, there is no clear biochemical similarity between part of the gluten compound and myelin as far as I am aware. Secondly, when we run the epidemiological cross-check, populations that consume wheat do not appear to have a higher incidence than other populations. A further cross-check is to see whether people who do develop auto-immunity to wheat (those with coeliac disease) also get auto-immunity to myelin; the data show that there is not a higher incidence of coeliac disease in those with MS or vice versa. And finally, the animal data don't support a link either.

So I advise people that gluten should be relatively safe. It is important to try to base these recommendations on evidence, not just theory, and I feel comfortable that the evidence does not support a link with gluten sufficiently to make a recommendation to avoid it. Overall, the evidence of any effect of gluten in MS is not convincing enough to warrant changing my own diet to exclude wheat products.

References

1. Ludvigsson JF, Olsson T, Ekbom A, et al. A population-based study of coeliac disease, neurodegenerative and neuroinflammatory diseases. Aliment Pharmacol Ther 2007; 25:1317-1327
2. Salvatore S, Finazzi S, Ghezzi A, et al. Multiple sclerosis and celiac disease: is there an increased risk? Mult Scler 2004; 10:711-712
3. Pengiran Tengah CD, Lock RJ, Unsworth DJ, et al. Multiple sclerosis and occult gluten sensitivity. Neurology 2004; 62:2326-2327
4. Borhani Haghighi A, Ansari N, Mokhtari M, et al. Multiple sclerosis and gluten sensitivity. Clin Neurol Neurosurg 2007
5. Di Marco R, Mangano K, Quattrocchi C, et al. Exacerbation of protracted-relapsing experimental allergic encephalomyelitis in DA rats by gluten- free diet. Apmis 2004; 112:651-655

No. The problem with chocolate is the cocoa butter which is very high in saturated fat. Worse, there is an allowable limit of 15% altered fats in cocoa butter. Chocolate is just cocoa (which is a good, healthy product) turned into junk food.

These fats are cooked and ideally, it is best not to eat cooked and therefore altered fats. I think they should be avoided. Nuts (preferably uncooked) make a good snack.

Because, knowing that saturated fat is a real problem for people with MS, why take any in at all if you can avoid it. After a while, most people don't miss meat at all.

It is a good idea to start out taking fish oil and flaxseed oil until body fat stores are saturated with alpha-linolenic acid. That takes about nine months. After that, you can get all your omega-3 from flaxseed oil, but it needs to be fresh.

Yes. Fish, scallops, lobster, prawns, calamari, mussels, yabbies.

There is a general problem with pollution in our oceans like our land. The oceans are increasingly becoming polluted, particularly with heavy metals like mercury. Mercury is concentrated in the flesh of fish that eat smaller fish higher up the food chain. So the bigger the fish the more mercury in general. In some parts of the world, they have banned eating shark for instance because of the very high levels of mercury. In smaller fish like sardines there is much less problem. Some people may feel it is safer to get their omega 3s from flaxseed oil, and that is quite reasonable after an initial period of say 9 months eating fish or taking fish oil as well, so as to get good tissue levels of the important fatty acids EHA and DPA.

Yes. All types of alcohol are OK in moderation. Moderation means not more than two standard drinks a day, with at least two alcohol-free days a week. Alcohol is harmful to health in excess. Moderation is required for reasons other than MS.

There is very little clinical trial evidence to support this claim. The Women's Health Initiative study¹ reported a small increase in kidney stones in postmenopausal women aged 50 to 79 years whose daily vitamin D(3) intake was 400IU (the reference intake for 50 to 70 years, and below the reference intake for > 70 years) combined with 1000 mg calcium. The increase in renal stones corresponded to 5.7 events per 10,000 person-years of exposure. The women in this trial had higher calcium intakes than is seen in most post-menopausal women. But it is so difficult in this study to determine the effect of vitamin D because the supplements were so small, and they don't provide details of the vitamin D levels of those who got stones and those who didn't. It is not possible to reach any conclusions about risk of kidney stones with vitamin D supplements from this paper.

In another paper² which reviews the literature and references the WHI trial, the conclusion is reached that high calcium intake probably caused the effect of kidney stones seen in the trial. There is little evidence from any trials that vitamin D above current reference intakes is harmful. In most trials, reports of hypercalcemia and hypercalciuria were not associated with clinically relevant events. It was concluded that Vitamin D intake above current dietary reference intakes is not associated with an increased risk of adverse events.

A good review of what consitutes a safe dose of Vitamin D was published in 2009³. Evidence from clinical trials show, with a wide margin of confidence, that a prolonged intake of 10,000 IU/d of vitamin D(3) poses no risk of adverse effects for adults, even if this is added to a rather high physiologic background level of vitamin D.

References

1. Rebecca D. Jackson, M.D., Andrea Z. LaCroix, Ph.D., et al. Calcium plus Vitamin D Supplementation and the Risk of Fractures. NEJM 354(7):669-683 February 16, 2006.
2. Cranney A, Horsley T, et al. Effectiveness and safety of vitamin D in relation to bone health. Evid Rep. Technol Assess (Full Rep). 2007 Aug:(158):1-235.
3. Vieth R. Vitamin D and cancer mini-symposium: the risk of additional vitamin D. Ann Epidemiol. 2009 Jul;19(7):441-5. Epub 2009 Apr 11.

Everyone needs a one-off megadose to get vitamin D levels up immediately if levels are initially low as they usually are. It takes ages for the hormone to accumulate in fat stores (it is fat soluble), so supplementing takes many many months to raise levels. At a level of 70nmol/L you remain at risk of relapse. I would take a one-off supplement of 150,000IU (30 capsules of the 5,000IU) immediately. That will get your level to around 150 or so overnight. Then 5,000IU a day should keep it there, although many people need more than that. Many people take 10,000IU a day to keep the level there. Get it checked again in six months.

Any doctor can order a vitamin D level. For people with MS, I recommend keeping around 150nmol/L. In the tropics, where there is little MS (because of the abundant sunshine), people often have levels of the order of 200-220nmol/L.

Yes. UVB penetrates water.

No. Glass filters out UVB (the wavelength required to make Vitamin D).

Sunscreen blocks the absorption of UVB which is responsible for vitamin D production. So, if spending a short amount of time in the sun, avoid sunscreen. If out for longer, it is sensible to get sun on unprotected skin for the first 10-15 minutes (depending on UV index), then apply sunscreen.

10-15 minutes of all over sun on a UV index 7 day. More if the UV index is lower (so 20-30 minutes if the index is 3.5) and less if the index is higher (so 5-7.5 minutes if the index is 14). Staying out longer than that doesn’t make any more vitamin D.

As much as modesty allows. The more that is exposed in a given sitting, the more vitamin D is made, but only up to a certain maximum (about 10,000 to 15,000IU). No more is made by staying out longer, and it raises the risk of skin cancer.

If you feel better when you have finished you are doing it right.

She urgently needs to check her vitamin D status, and should consider re-commencing breast feeding. Low vitamin D is closely correlated with depression. If it is low, she needs the usual mega-dose to get levels up urgently. It is also important to get some regular exercise, preferably outdoors, as this helps enormously with depression, and will also assist with getting adequate vitamin D. It might also be worth looking at getting some counselling regarding the depression.

Recent research confirms that breastfeeding is protective for the mother against further MS attacks while she is breastfeeding. It will also help her babies get their vitamin D levels up once she takes the megadose, through the breast milk. That will reduce the risk of the babies ever getting MS, and once the children stop breastfeeding, vitamin D supplements should start as per the instructions found on the website.

Swank noted in his study that there were no new cases of MS in families where everyone followed the same diet as those with MS. It is also easier to cook one meal only, but may be difficult to get agreement from family members, especially if they are older.

There is good evidence that taking even a low dose of vitamin D regularly substantially reduces the risk of getting MS. Children of people with MS should routinely be supplemented with vitamin D. See the section on Preventing MS in Family Members on this website for doses.

If you have MS, then your children are at much higher risk (40-80 times) than the rest of the population. The more people in the family with MS, and the closer the relationship, the higher the risk.

Another therapy which has had its proponents over the years has been beesting therapy. A 2005 study of 26 patients used live bees stinging patients with relapsing-remitting MS three times a week.¹ The researchers found no reduction in disease activity, disability, or fatigue and no improvement in quality of life, so this therapy is difficult to recommend. Others have tried immunising people with MS with bee venom extract. In a small study of nine patients, researchers found it to be safe but it did not seem to produce any benefit.²

References

1. Wesselius T, Heersema DJ, Mostert JP, et al. A randomized crossover study of bee sting therapy for multiple sclerosis. Neurology 2005
2. Castro HJ, Mendez-Lnocencio JI, Omidvar B, et al. A phase I study of the safety of honeybee venom extract as a possible treatment for patients with progressive forms of multiple sclerosis. Allergy Asthma Proc 2005; 26:470-476

There has been a lot of conjecture about whether getting immunised against hepatitis B increases the risk of getting MS. Hepatitis B vaccine is genetically engineered and has been available since the 1980s. It is considered to be well tolerated by people, although there have been many reports of increased risk of MS associated with the immunisation. A large case-control study from the US tested whether this was by chance, and found an alarming increase in the risk for several major autoimmune diseases, including MS. People getting hepatitis B vaccination were 5.2 times more likely to be diagnosed with MS than controls who were not vaccinated.¹ This is supported by a US case-control study which showed that people with MS were 3.1 times more likely to have been vaccinated in the three years prior to onset of symptoms than controls who did not have MS.² To confirm that this was a real effect specific to hepatitis vaccination, they checked whether tetanus or influenza vaccination resulted in any similar effect, and found none.

It seems likely that MS is not the only autoimmune disease which may be precipitated by hepatitis B vaccination. US researchers found significant numbers of people with other autoimmune disease after hepatitis B vaccination in a Vaccine Adverse Event Reporting System and the general medical literature.³ They concluded that it should be considered that there is causal relationship between hepatitis B vaccination and serious autoimmune disorders among certain susceptible people.

For people already vaccinated for hepatitis B there is nothing that can be done about it. But it may be worth considering this information if the question comes up of having close family members or children vaccinated for hepatitis B, given that they already have a much higher risk of developing MS than the general community.

References

1. Geier DA, Geier MR. A case-control study of serious autoimmune adverse events following hepatitis B immunization. Autoimmunity 2005; 38:295-301
2. Hernan MA, Jick SS, Olek MJ, et al. Recombinant hepatitis B vaccine and the risk of multiple sclerosis: A prospective study. Neurology 2004; 63:838-842
3. Geier MR, Geier DA. A case-series of adverse events, positive re-challenge of symptoms, and events in identical twins following hepatitis B vaccination: analysis of the Vaccine Adverse Event Reporting System (VAERS) database and literature review. Clin Exp Rheumatol 2004; 22:749-755

Interest in this area stemmed from an early observation about the geographical distribution of MS. Ingalls, a doctor in Massachusetts noted that the incidence of MS seemed to follow the incidence of dental tooth decay.¹ Knowing that mercury (which forms part of dental amalgam in fillings) has been implicated in neurological disease, the theory was formed that perhaps the amalgam in fillings was causing MS. One of the difficulties with this theory is that the incidence of dental caries may just be a marker for some other factor which is really contributing to the development of MS. An interesting case control study from Leicester found that people with MS had more dental caries than those without.² It also found that people with more mercury amalgam fillings had higher mercury levels in their bodies, but it found no higher incidence of MS in those with fillings. So the association of dental caries with MS may just be a reflection of some other variable which is also related to dental caries, and not dental amalgam.

Although the issue remains contentious, a major 2001 review concluded there was no significant health risk from dental amalgam.³ A subsequent review in 2005 concluded that there was no evidence of any association of amalgam with neurodegenerative diseases or autoimmune diseases, but that more research is needed with regard to MS.⁴ A further systematic review in 2007 reported that there was a slight increase in the risk of developing MS for people with amalgam fillings which was consistent across studies but did not reach statistical significance.⁵

Although many people with MS have had their fillings removed as a result, there is as yet no evidence of any sort that I can find to indicate that this might be helpful. Critics of the technique will point out that MS has developed in many, many people who have no fillings or have dentures. On the other hand, many people approach their recovery from serious illness in a very holistic way, and feel that removing all possible toxic substances from their bodies and environment is essential. Removing their dental fillings may be part of this process. It certainly seems that people with many amalgam fillings have higher levels of mercury in their bodies.

I wouldn't advise people getting fillings replaced as a trial to see if it will help, if people are doing all the other things recommended here. Like asbestos roofs in houses, the hazardous material is probably safer left alone, where it will release much less of its toxicity than if drilled and removed. A reasonable approach would be to leave current amalgam fillings in place, but if any new ones are needed, to get them made from a different material.

References

1. Ingalls TH. Epidemiology, etiology, and prevention of multiple sclerosis. Am J Forensic Med Pathol 1983; 4:55-61
2. McGrother CW, Dugmore C, Phillips MJ, et al. Multiple sclerosis, dental caries and fillings: a case-control study. Br Dent J 1999; 187:261-264.
3. Wahl MJ. Amalgam--resurrection and redemption. Part 2: The medical mythology of anti-amalgam. Quintessence Int 2001; 32:696-710.
4. Mitchell RJ, Osborne PB, Haubenreich JE. Dental amalgam restorations: daily mercury dose and biocompatibility. J Long Term Eff Med Implants 2005; 15:709-721
5. Aminzadeh KK, Etminan M. Dental amalgam and multiple sclerosis: a systematic review and meta-analysis. J Public Health Dent 2007; 67:64-66

No. We are close to understanding how it occurs, but because there are so many factors involved, including a genetic predisposition, I don't see a cure being found for a long time. That doesn't mean it is not possible to stay well with MS. People following the guidelines on this website can reasonably hope to stabilise the condition. There is a great difference between healing and curing. Cure implies that some outside agent provides treatment, whereas healing is about optimal health, and comes from within.

Doing it manually is best, rather than with the automatic devices. It is important to warm the syringe to body temperature first by holding it in your clenched hand for a few minutes. It is also important to pinch a piece of skin and lift it up before injecting into it. Injecting with the skin flat means it often goes too deep.