I can't envision mercury as a prime causal mechanism of MS, not even for some individuals. The stance of MS being a condition of autoimmunity is well established in my mind. Thus any causal factor must satisfy the process of the immune system attacking self. While mercury is toxic to humans, the biochemical process of autoimmunity does not allow for the molecular composition of mercury to be mistaken for self tissue. There is no evidence in I am aware of to compel one to think mercury shares the same molecular structure as self tissue. The mechanism of molecular mimicry
must be honored in order to postulate something as causal for MS.
bromley wrote:(i) How diet might contribute to the higher prevalence of ms in females.
This is a tough one. The speculations provided by Lisa and Melody are as good as I could offer.
bromley wrote:(ii) How diet might contribute to the onset of MS at different ages (the lowest age at which MS has been diagnosed is two and a half and some are diagnosed later in life (50s and 60s)).
I feel that MS and the "types" of MS are an interaction of a number of variables. Such factors of individual immune system aggressiveness, latitude of residence, degree of exposure to causal proteins, degree of exposure to protective factors, etc. The culmination of these are the determinant of age of onset and the degree of MS disability.
bromley wrote:(iii) Why some get Primary Progressive MS - does diet play a role in this form of MS?
As I stated above, the interaction of variables will determine the type of MS. At one end of the spectrum, consider the migrants from Great Britain to Queensland, Australia who enjoyed an 80% drop in risk of MS. I attribute this to an overwhelming amount of immunoregulatory vitamin D which negated the influence of the other factors.
I may have missed it, but do you have MS and, if so, for how long? If you have MS how as diet helped you?
Unfortunately yes. I consider myself to have had MS (optic neuritis as a teenager) for at least 25 years, most likely my entire life, although I was diagnosed 15 years ago when my RR morphed into chronic progressive. Diet revision has stopped the progress of my MS cold aside from when I contract a viral infection. Fortunately I've only had the flu twice in the past eight years since I revised my diet.
I still have neurological damage which impairs my right leg and arm but I feel very well and consider my overall state of being now, compared to pre-diet revision days, as I would day and night.
bromley wrote:Is there any data on those that follow the diet you suggest e.g. data on how they have done in relation to their MS?
No hard data for MS aside from heaps of anecdotal accounts. This why Direct-MS is trying to conduct a clinical trial testing the diet hypothesis. There are however other AI diseases for diet have been shown to be very effective. Celiac disease is of course the most prominent.
BTW I am nothing if not opinionated and I like to think I maintain my convictions unless I find valid reasons not to.
I don't think the rationale you mention for lupus eliminates foreign proteins. Molecular mimicry accounts for antibodies to both self and foreign proteins being present. Did the cases you allude to test for the presence of antibodies to not only self but for many different types of proteins identified as having a similar molecular composition to self. This would be an onerous undertaking for sure but the presence of anti-DNA antibodies to me does not preclude foreign proteins to be an instigator. On the contrary, I would expect it. Something though must compel the immune system to turn against self.
I've posted here before the study by Guggenmos et al (2004) who demonstrated that antibodies (agents of the immune system) found in the cerebrospinal fluid of a population of people with MS, were reactive to both brain tissue and cows milk. The authors found cross reactivity between a protein in cow’s milk (butyrophilin(CMP)) and brain tissue (myelin oligodendrocyte glycoprotein(MOG) in 34% of the 35 people with MS in the study, a rate significantly higher than in healthy controls.
This is not to say that butyrophilin is the cause of all MS'ers state of MS. It is but one of the many proteins found in cow's milk and dairy is only one of five possible food protein groups with the ability to be causal for autoimmunity. In the above example it happened to be the one third of the study group showed this particular protein to be causal. Consider what would have been the percentage had they tested for all of the proteins found in milk AND the other food proteins such as gluten (gliadin).
This work is critical evidence of molecular mimicry in action. -a display of immune activity against both self tissue and a foreign body.
With repect to the Faroes situation, this an excerpt from Multiple Sclerosis and Food Hypersensitivities
One of the most interesting and widely quoted epidemiological studies of MS is that of the greatly increased prevalence of MS in the Faroe Islands (North Atlantic, west of Norway) following the occupation by 1500-2000 British troops between 1941 and 1944 (Kurtzke, 1977, 1980, 1995). Kurtzke has classified this increase as an epidemic although other authors have challenged this view (Benedikz et al., 1994, Poser et al. 1988). Regardless, there can be no doubt that MS prevalence substantially increased in the Faroes following the British occupation. Furthermore, the relationship between MS in the Faroe islanders and the presence of British soldiers is strongly supported by the fact the cases of MS all occurred in islanders who lived close to British bases (Kurtzke, 1980, fig. 15). This is an extremely important constraint because it demonstrates that the environmental factor is not solely indigenous and can transported from one area to another. Any interpretation of the cause of MS must satisfactorily explain the sudden increased prevalence in the Faroes and the mobility of the environmental factor.
The devil they say, is in the details.