Causes of MS
What causes MS? We know that MS is a ‘modern’ disease. Textbooks are not definite about when it appeared but it seems that we first got descriptions of the disease in the mid-1800s. Swank in his Multiple Sclerosis Diet Book says the first case recorded in the literature was that of Augustus D’Este who suffered an attack at the age of twenty-eight, followed by remission, at the beginning of the 19th century. He then documented in his diary a series of relapses and remissions which, to those now familiar with MS, are characteristic of the disease. Swank points out that by the turn of the 20th century, the disease was commonly recognised throughout Europe.
It is very likely that the incidence of the disease is increasing. A 1922 review from the US showed that the incidence had increased over the preceding twenty years.1 Swank cites a 1952 report which indicated that the incidence of MS had doubled in Europe early in the 20th century, and he presents other data from his own health system in Montreal documenting a 50 per cent increase from 1935-1958. More recently a 2005 study from Sardinia, a high risk area for MS, showed that the incidence of MS in the area had increased more than five fold over the 30 years to 1999.2 A major study from Canadian Collaborative Study Group in 2006 showed that the sex ratio of females to males with the disease in over 27,000 Canadian people with MS had changed significantly over the previous 50 years.3 The ratio was now over 3.2 women for every man with MS. The significance of the finding was two fold. First, it implies that incidence of the disease is increasing, but more importantly it shows that environmental factors play the major part in the risk of getting the disease, and therefore, that the majority of the disease is preventable with changes to these factors. It is clear that these factors mostly relate to lifestyles we have adopted in Western society.
It is very likely that the incidence of the disease is increasing. A 1922 review from the US showed that the incidence had increased over the preceding twenty years.1 Swank cites a 1952 report which indicated that the incidence of MS had doubled in Europe early in the 20th century, and he presents other data from his own health system in Montreal documenting a 50 per cent increase from 1935-1958. More recently a 2005 study from Sardinia, a high risk area for MS, showed that the incidence of MS in the area had increased more than five fold over the 30 years to 1999.2 A major study from Canadian Collaborative Study Group in 2006 showed that the sex ratio of females to males with the disease in over 27,000 Canadian people with MS had changed significantly over the previous 50 years.3 The ratio was now over 3.2 women for every man with MS. The significance of the finding was two fold. First, it implies that incidence of the disease is increasing, but more importantly it shows that environmental factors play the major part in the risk of getting the disease, and therefore, that the majority of the disease is preventable with changes to these factors. It is clear that these factors mostly relate to lifestyles we have adopted in Western society.
Any disease that appears like that in recent times, such as coronary heart disease, and increases rapidly in incidence, is very likely to be caused or at least precipitated by lifestyle changes that the human race has made due to the industrial and technological revolutions. Most of these lifestyle changes centre around diet and exercise. A really good account of the changes in foods and diet over recent years is provided by Dr Artemis Simopoulos in her book The Omega Plan (The Omega Diet in the US).4 This book also details much of the current knowledge of fats in the genesis of modern degenerative diseases. Our changing diets with respect to fats play a major role in the development and progression of MS.
There are many theories as to what causes MS. Most of the theories revolve around a problem with the immune system which is tricked into initiating immune attacks on its own nervous tissue. In effect, somehow the immune system seems to ‘see’ the myelin in the CNS as a foreign invader and, like overcoming an infection, it tries to get rid of it by attacking it. This is called autoimmunity. A virus or viruses may somehow trigger the process in susceptible people. Alternatively, the immune system may be tricked in a process called molecular mimickry, where part of some foreign molecule looks just like part of myelin. The immune system may mount an immune reaction against this molecule, and later be tricked into doing the same against myelin, seeing it as foreign. A number of different molecules have been suggested as mimicking myelin, including dairy protein 5,6 and gut bacteria7.
In addition to autoimmunity being a cause of MS, there are almost certainly several other multiple sclerosis causes. There has been a lot of discussion about MS also being a degenerative disease, like Parkinson’s Disease and Alzheimer’s Disease.8-10 Recently, renewed emphasis has been placed on other multiple sclerosis causes. The MS-initiating role of diet, particularly fats, has long been suspected. These may be involved because of their role in production of immune system chemicals, and the integrity of cell membranes. There has also been a lot of interest in the proteins in cow’s milk, which look in part like myelin to the immune system. And there is now a convincing case for lack of sunlight being one of the multiple sclerosis causes, given the unusual geographical distribution of the disease. A number of other factors have been proposed including exposure to organic solvents (one study found painters had about twice the risk of other workers11), dental amalgam, heavy metals, and others, but the evidence for these is far from compelling.
Poser, a world authority on MS, has recently proposed a plausible theory about how these various factors interact to become what causes MS in susceptible people.12 He proposes a systemic condition called the multiple sclerosis trait (MST) which basically results from a challenge to the immune system of a genetically susceptible person that doesn’t cause damage to the nervous system and may never evolve into full blown MS. However that individual is now primed so that if a certain environmental event then occurs, it can turn the trait into MS. This event could be any of the lifestyle factors discussed on this website, including infection, vaccination, exposure to saturated fat over a long period or food antigens like cow’s milk, inadequate sun exposure, and so on. The person may then develop symptoms of MS, remain symptom-free, or perhaps even only have lesions on MRI with no noticeable effects for the patient.
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There are many theories as to what causes MS. Most of the theories revolve around a problem with the immune system which is tricked into initiating immune attacks on its own nervous tissue. In effect, somehow the immune system seems to ‘see’ the myelin in the CNS as a foreign invader and, like overcoming an infection, it tries to get rid of it by attacking it. This is called autoimmunity. A virus or viruses may somehow trigger the process in susceptible people. Alternatively, the immune system may be tricked in a process called molecular mimickry, where part of some foreign molecule looks just like part of myelin. The immune system may mount an immune reaction against this molecule, and later be tricked into doing the same against myelin, seeing it as foreign. A number of different molecules have been suggested as mimicking myelin, including dairy protein 5,6 and gut bacteria7.
In addition to autoimmunity being a cause of MS, there are almost certainly several other multiple sclerosis causes. There has been a lot of discussion about MS also being a degenerative disease, like Parkinson’s Disease and Alzheimer’s Disease.8-10 Recently, renewed emphasis has been placed on other multiple sclerosis causes. The MS-initiating role of diet, particularly fats, has long been suspected. These may be involved because of their role in production of immune system chemicals, and the integrity of cell membranes. There has also been a lot of interest in the proteins in cow’s milk, which look in part like myelin to the immune system. And there is now a convincing case for lack of sunlight being one of the multiple sclerosis causes, given the unusual geographical distribution of the disease. A number of other factors have been proposed including exposure to organic solvents (one study found painters had about twice the risk of other workers11), dental amalgam, heavy metals, and others, but the evidence for these is far from compelling.
Poser, a world authority on MS, has recently proposed a plausible theory about how these various factors interact to become what causes MS in susceptible people.12 He proposes a systemic condition called the multiple sclerosis trait (MST) which basically results from a challenge to the immune system of a genetically susceptible person that doesn’t cause damage to the nervous system and may never evolve into full blown MS. However that individual is now primed so that if a certain environmental event then occurs, it can turn the trait into MS. This event could be any of the lifestyle factors discussed on this website, including infection, vaccination, exposure to saturated fat over a long period or food antigens like cow’s milk, inadequate sun exposure, and so on. The person may then develop symptoms of MS, remain symptom-free, or perhaps even only have lesions on MRI with no noticeable effects for the patient.
A study published in 2006 lent weight to this hypothesis. Italian researchers performed MRI scans on 296 first degree relatives of people with MS and people without MS.13 They chose those with MS from families where there was no recorded MS (sporadic cases) and where there was a history of MS (familial cases). All of these people had no symptoms of MS and had not been diagnosed with MS. Surprisingly, they found that 10% of relatives of familial cases had MRI brain lesions indistinguishable from MS. In the relatives of sporadic cases, 4% of people had such lesions. In people who were not related to someone with MS there were no lesions.
This strongly suggests that there is a susceptibility conferred by genetic make-up that requires the right set of environmental circumstances to develop into actual MS. The potential therefore exists, for parents worried about their children getting MS, that making lifestyle changes such as those discussed in this book can significantly affect their chances of developing MS. It also raises the intriguing possibility that, by reversing the various lifestyle factors which turned this MS trait into MS, it may be possible to somehow revert to this ‘carrier’ state, with a few MS lesions, but have no progression to further illness.
The most recent addition to the factors suspected as multiple sclerosis causes has been discovered by Italian scientists. They have discovered that MS may be the result of a chronic problem with venous blood not draining adequately from the brain, causing disruption to small veins and damage to the brain and spinal cord around these areas. This fits with what we know of the distribution of lesions in MS. The scientists scanned people with and without MS and found that those with MS all had these drainage problems, but none of the people without MS had them. Further they suggested that it might be possible to fix the problem with minimally invasive surgery. News reports have now revealed that some vascular surgeons are already doing these procedures on people with MS with good results although we await formal reporting of such results in the peer-reviewed medical literature before we can make any judgement about the real benefits of such therapy.
It is important to note that this new research of course does not negate all that we already know about the causes of MS. It may be that this venous insufficiency is actually the result of the viral infections that we know are associated with MS risk, like Epstein-Barr Virus. It is also important to note that the various lifestyle factors described on this site that we know influence the progression of MS will still be effective regardless of what causes MS, as they have been shown in qood quality research to be effective. Swank for instance, long hypothesised that his diet in fact worked by altering the blood vessels in the brain.
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This strongly suggests that there is a susceptibility conferred by genetic make-up that requires the right set of environmental circumstances to develop into actual MS. The potential therefore exists, for parents worried about their children getting MS, that making lifestyle changes such as those discussed in this book can significantly affect their chances of developing MS. It also raises the intriguing possibility that, by reversing the various lifestyle factors which turned this MS trait into MS, it may be possible to somehow revert to this ‘carrier’ state, with a few MS lesions, but have no progression to further illness.
The most recent addition to the factors suspected as multiple sclerosis causes has been discovered by Italian scientists. They have discovered that MS may be the result of a chronic problem with venous blood not draining adequately from the brain, causing disruption to small veins and damage to the brain and spinal cord around these areas. This fits with what we know of the distribution of lesions in MS. The scientists scanned people with and without MS and found that those with MS all had these drainage problems, but none of the people without MS had them. Further they suggested that it might be possible to fix the problem with minimally invasive surgery. News reports have now revealed that some vascular surgeons are already doing these procedures on people with MS with good results although we await formal reporting of such results in the peer-reviewed medical literature before we can make any judgement about the real benefits of such therapy.
It is important to note that this new research of course does not negate all that we already know about the causes of MS. It may be that this venous insufficiency is actually the result of the viral infections that we know are associated with MS risk, like Epstein-Barr Virus. It is also important to note that the various lifestyle factors described on this site that we know influence the progression of MS will still be effective regardless of what causes MS, as they have been shown in qood quality research to be effective. Swank for instance, long hypothesised that his diet in fact worked by altering the blood vessels in the brain.
- Wesler IS. Statistics of multiple sclerosis. Am Med Assoc Arch Neurol Psych 1922; 8:59-63
- Pugliatti M, Riise T, Sotgiu MA, et al. Increasing Incidence of Multiple Sclerosis in the Province of Sassari, Northern Sardinia. Neuroepidemiology 2005; 25:129-134
- Orton SM, Herrera BM, Yee IM, et al. Sex ratio of multiple sclerosis in Canada: a longitudinal study. Lancet Neurol 2006; 5:932-936
- Simopoulos A, Robinson J. The omega plan: Hodder Rydalmere, 1998
- Stefferl A, Schubart A, Storch M, et al. Butyrophilin, a milk protein, modulates the encephalitogenic T cell response to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis. J Immunol 2000; 165:2859-2865.
- Winer S, Astsaturov I, Cheung RK, et al. T cells of multiple sclerosis patients target a common environmental peptide that causes encephalitis in mice. J Immunol 2001; 166:4751-4756.
- Westall FC. Molecular mimicry revisited: gut bacteria and multiple sclerosis. J Clin Microbiol 2006; 44:2099-2104
- Arnold DL. Changes observed in multiple sclerosis using magnetic resonance imaging reflect a focal pathology distributed along axonal pathways. J Neurol 2005; 252 Suppl 5:v25-v29
- Chaudhuri A, Behan PO. Treatment of multiple sclerosis: beyond the NICE guidelines. QJM 2005
- Hauser SL, Oksenberg JR. The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. Neuron 2006; 52:61-76
- Riise T, Moen BE, Kyvik KR. Organic solvents and the risk of multiple sclerosis. Epidemiology 2002; 13:718-720.
- Poser CM. The multiple sclerosis trait and the development of multiple sclerosis: Genetic vulnerability and environmental effect. Clin Neurol Neurosurg 2006
- De Stefano N, Cocco E, Lai M, et al. Imaging brain damage in first-degree relatives of sporadic and familial multiple sclerosis. Ann Neurol 2006
- Wesler IS. Statistics of multiple sclerosis. Am Med Assoc Arch Neurol Psych 1922; 8:59-63
- Pugliatti M, Riise T, Sotgiu MA, et al. Increasing Incidence of Multiple Sclerosis in the Province of Sassari, Northern Sardinia. Neuroepidemiology 2005; 25:129-134
- Orton SM, Herrera BM, Yee IM, et al. Sex ratio of multiple sclerosis in Canada: a longitudinal study. Lancet Neurol 2006; 5:932-936
- Simopoulos A, Robinson J. The omega plan: Hodder Rydalmere, 1998
- Stefferl A, Schubart A, Storch M, et al. Butyrophilin, a milk protein, modulates the encephalitogenic T cell response to myelin oligodendrocyte glycoprotein in experimental autoimmune encephalomyelitis. J Immunol 2000; 165:2859-2865.
- Winer S, Astsaturov I, Cheung RK, et al. T cells of multiple sclerosis patients target a common environmental peptide that causes encephalitis in mice. J Immunol 2001; 166:4751-4756.
- Westall FC. Molecular mimicry revisited: gut bacteria and multiple sclerosis. J Clin Microbiol 2006; 44:2099-2104
- Arnold DL. Changes observed in multiple sclerosis using magnetic resonance imaging reflect a focal pathology distributed along axonal pathways. J Neurol 2005; 252 Suppl 5:v25-v29
- Chaudhuri A, Behan PO. Treatment of multiple sclerosis: beyond the NICE guidelines. QJM 2005
- Hauser SL, Oksenberg JR. The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration. Neuron 2006; 52:61-76
- Riise T, Moen BE, Kyvik KR. Organic solvents and the risk of multiple sclerosis. Epidemiology 2002; 13:718-720.
- Poser CM. The multiple sclerosis trait and the development of multiple sclerosis: Genetic vulnerability and environmental effect. Clin Neurol Neurosurg 2006
- De Stefano N, Cocco E, Lai M, et al. Imaging brain damage in first-degree relatives of sporadic and familial multiple sclerosis. Ann Neurol 2006