In this and later sections, I'd like to explore some of the ways that multiple sclerosis has been observed to affect people. Much of this information is derived from statistical data and, as such, is subject to the vagaries and uncertainties inherent to statistics. In a later section, I shall explore the relationship between MS and statistics.
So who does get MS, then?
This would be a much easier question if it were known what causes MS, but since that knowledge remains elusive, we can only look at the distribution of the disease around the globe and at the people who actually have it.
World map of prevalence of MS
MS is predominately a disease of temperate latitudes and of the western hemisphere. Principally, it is a disease prevalent in Europe, North America, Australia and New Zealand. Although MS is found in Japan, China and some other temperate, eastern countries, it is very much rarer than it is in the West. Regions north of 40 degrees latitude have a markedly higher incidence than those south of this divide. Within Europe, Scandinavia, The British Isles, the Low Countries and Germany have very high rates. Canada, northern USA and New Zealand have an equivalently high prevalence. Within these areas, certain localities such as the border areas of Scotland (203 per 100,000), Crowsnest Pass in Alberta, Canada (217 per 100,000), the northern-most province of Sweden (253 per 100,000) and others have been found to have extremely high incidences of the disease.
Table of prevalence of MS by country
So why is MS more common in some areas than others?
Why MS is distributed around the world the way it is is not well understood. There are two main features of the prevalence data for MS that need to be explained. The unequal temperate/tropical distribution of the disease and the much higher rates in Western Hemisphere.
The temperate-tropical divide
Understanding why MS is so rare in tropical climes and so common in temperate ones is a crucial piece of the jigsaw of understanding why people get the disease. Population genetics, which I shall discuss later, provides some of the answers but not the whole picture. There is clearly one or more environmental factors involved in the development of multiple sclerosis and one or more or these has a geographic element. There are several theories as to what this may be.
One theory explains the uneven distribution of MS by focusing on the differences in the pathogens (viruses, bacteria etc.) that affect people in the tropics versus those that affect people in temperate lands. A currently popular theory for autoimmune diseases is called molecular or epitopic mimicy. This suggests that people with MS have previously been infected with a very common pathogen. The immune response that they have developed against that is also reactive against some part of the myelin-oligodendrocyte complex and, as a consequence, they mount an immune attack against themselves in the form of MS. Many pathogens have been examined, including Epstein-Barr virus (EBV), Human Herpes Virus 6 (HHV-6) and various other viruses, although, as with all pathogen work related to MS, it has produced many dead ends.
Sunlight and seasons
Some researchers suggest that multiple sclerosis is common in temperate regions due to the seasonal fluctuations in daylight affecting body chemistry. Research has shown that both disease onset and relapses are more common in the springtime and least common in the winter [Jin et al, 2000]. Levels of vitamin D3, melatonin and other biochemicals have all been shown to vary with the seasons and some of these have been shown to be immunologically or neurologically active [Embry et al, 2000, Timonen TT, 1999; Hayes, 2000, Nelson et al, 2001, Prendergast et al 2001].
If these biochemicals are related to the development of MS, do they also affect its course after onset? If they do, should therapies involving them concentrate on increasing their absolute levels in the body throughout the year or should we attempt to load our levels only at the times of the year when they are at their lowest? Studies in other diseases suggest that this may be a fruitful therapeutic line [Yamashita H, 2001; Guillemant J, 2001; Duhamel JF, 2000; Pawlikowski M et al, 2002 and many others].
Other theroies have addressed dietary habits.
One study has shown that the incidence of MS in coastal regions of Norway is lower than for the rest of the Norwegian population [Larsen et al, 1985]. Some have argued that this is due to the higher levels of fish consumption in coastal regions. The same study also showed a higher incidence of MS in urban areas and a degree of clustering in rural areas leading other commentators to suggest the involvement of an infective agent. Why might a diet rich in fish products be protective against MS? Fish is high in vitamin D3 and omega-3 fish oils, and it is possible that either or both of these might play a part. In any event, there is a lot of unrelated research that implies that a diet rich in fish is protective against a whole variety of diseases. Of course, this provided that you can get hold of fish that has not been polluted by PCBs, dioxins, lindane and other by-products of modern agri-business.
Other studies have found that the incidence of MS is higher in areas of high consumption of dairy produce [Malosse et al, 1993, Malosse et al, 1994, Sepcic et al, 1993, Butcher, 1986 , Butcher, 1992]. Other work has linked dairy proteins to multiple sclerosis at the cellular level [Dosch et al, 2001, Dosch et al, 2001, Stefferl et al, 2001]. Although this work is tantalising, larger studies are needed both to confirm these conclusions and to better explain what is going on. These studies have been cited to support a therapeutic dietary regime called the Paleolithic diet.
Still other commentators suggest that the differences in concentrations of minerals in temperate soils versus tropical ones affect the human intake of these chemicals through the plants we eat and the water that we drink. It is suggested that these variations make people more susceptible to the disease. Copper, iron, vanadium, lead, nickel, selenium, zinc, chromium, molybdenum, cobalt, boron, manganese and chloride, sulfate, nitrate and nitrite salts have all been looked at in this respect but satisfactory explanatory mechanisms are missing.
Different geomagnetic fields across the globe, variations in industrialisation and many other possibilities have all been proffered as potential explanations. Some of these are more worthy of further study than others.
Several studies show that people who migrate from one area of the globe to another at some stage before puberty, take on the incidence of the area to which they migrate. On the other hand, people who move after this point carry with them the incidence of the area from which they migrated. Countries like Israel and South Africa have a much higher incidence than would be expected from their latitude, presumably because they have such high immigration levels of first generation Europeans [Acheson, 1977; Alter M et al, 1966, 1971, 1978; Dean & Kurtzke, 1971; Kurtzke et al 1976 & 1985; Detels R et al 1978; Dean G et al 1997]. Conversely, first generation African, Afro-Caribbean and Indian immigrants to Britain have a much lower incidence of multiple sclerosis than their second generation counterparts [Elian M, 1990].
Contradicting this work is a more recent study of British and Irish born immigrants to Australia. This suggests that the age/geographical risk for developing multiple sclerosis spans a larger timescale than just the first 15 years of life [Hammond SR et al, 2000].
At whatever age the risk factors for multiple sclerosis fall off, if indeed they do, it is clear from other studies that the disease is active sometime before people with MS actually develop clinical symptoms.
This seems to me to be a huge clue towards the understanding of multiple sclerosis. We need to be looking at the earlier lives of PwMS and at the children of families with a high incidence of the disease and who are at a relatively high risk of the disease. Whatever is going on with this disease is starting a while, in my opinion years, before it actually manifests itself.
I am unaware of any studies which examine whether people with multiple sclerosis living in tropical regions have a less severe disease course than those living in temperate regions. If such a study has not been carried out, then it is my opinion that one should be done.
The west-east divide
The explanations for the west-east MS divide are more convincing than those of the tropical-temperate divide. There could, of course, be something different in the soils or diets of oriental peoples than those of occidentals, but by and large, the temperate Western hemisphere has many more similarities to the temperate East than either do to the tropics. The best explanation for why MS is relatively rare in the Orient and relatively common in the Occident is the genetic make up of their peoples.
So what does it matter what racial group a PwMS comes from? In terms of having the disease, treatment, support etc. the answer is nothing - it does not matter. I would like to make it clear that MS is every bit as serious a disease for a person of one genetic make-up as it is for any another. There are people of almost all major racial groups who have MS and I do not wish to downplay what anyone with this disease suffers in any way. In fact, in many ways, PwMS from groups in which it is rare, may find that getting a diagnosis is harder and that the support networks are not as fully developed within their own communities. However are all people with MS and, in the main, we have a awful lot in common with each other. In my opinion we would be much better off politically by emphasising our unity across racial, sexual, religious and national boundaries. I write this only to get a better understanding of the disease.
It is clear that there is a genetic component to the disease but the actual genes themselves remain unidentified. It is likely that there are a number of genes involved working in tandem and it is also possible that more than one combination of genes could result in a predisposition to develop the disease. As already mentioned, identical twin studies show that, when one twin has the disease, the other has only a 30% chance of developing the disease. MRI scans confirm that the identical twins without MS have no lesions. This means that for every person with the disease there are two with the genetic predisposition for the disease who have never contracted it. This makes locating the genes involved extremely difficult because it is virtually impossible to ensure that the control group (those confirmed not to have MS) do not have a genetic predisposition to contract the disease. Many candidate genes have been studied, but as yet, none have been positively identified, although, as is usual with this enigmatic disease, lots of vague correlations have been shown.
Despite the failure to identify which genes are involved, it is still a very reasonable hypothesis to say that a genetic configuration that conveys a predisposition to get MS is more common within some population groups than it is within others. Studies done in Scotland and Canada have shown that MS has a particularly high prevalence within peoples of European descent - British and Scandinavian especially. Within peoples of British descent, it is particularly common in those of Celtic descent. It is unknown within Innuit peoples. It is rare in Japanese and Chinese peoples, and many of those who do get it, get a more aggressive, Asian form, although the European form is known. The descendants of Africans migrating to the US and Britain from Africa are less likely to get MS than the descendants of those migrating from the Caribbean, many of whom have some European ancestry.
We can use the relative rarity of MS within certain population groups to attempt to devise better control groups and perhaps get closer to identifying what genes are involved. Isolating the genetic component of MS is likely to be a major step to discovering the cause, better treatments and even ways of preventing the disease.
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