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Multiple sclerosis

A wide range of factors have been suggested as causes of multiple sclerosis (MS). It is likely that infectious [1] (and especially viral[2–5]),(Bains)

[1] Kurtzke JF, Heltberg A. Multiple sclerosis in the Faroe Islands: an epitome. J Clin Epidemiol 2001;54:1–22. [2] Warner HB, Carp RI. Multiple sclerosis etiology – an Epstein Barr hypothesis. Med Hyp 1988;25(2):93–7. [3] Simon J, Neubert WJ. The pathogenesis of multiple sclerosis: reconsideration of the role of viral agents and defence mechanisms. Med Hyp 1996;46, 537–43. [4] Asherio A, Munger KL, Lennette ET, Spiegelman D, Hernan MA, Olek MJ, et al. Epstein-Barr virus antibodies and risk of multiple sclerosis: a prospective study. J Am Med Assoc 2001;286(24):3083–8. [5] Tucker WG, Paskauskas RA. The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment. Med Hyp 2008;71:682–9.Central Florida; 1995.

- Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.1 Bains W Med Hypotheses Nov 2009; Download citation Affiliation Institute of Biotechnology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QT, UK. Abstract BACKGROUND: Multiple sclerosis (MS) incidence is higher among those who live at high latitudes before adulthood. This is usually attributed to lower levels of Vitamin D, caused by lower UV levels. However direct damage of the optic nerve by near-horizon sunshine is a possible alternative explanation. METHOD: Historical reports of MS from European populations in well characterised geographic locations where the numbers of cases and the target population were reported were collected, and the distribution of MS prevalence was calculated. Total UV, visible and infra-red exposure over a year as a function of latitude, and the fraction of time the Sun spends near the horizon as a function of latitude were calculated from geometric considerations, and were compared with the observed prevalence of MS. RESULTS: The observed distribution of MS prevalence fits well with the relative time that the Sun spends within 3 degrees and 8 degrees of the horizon, as calculated geometrically and summed over a year. Correlation with total UV exposure (without consideration of weather or shielding by clothing or buildings) was less satisfactory. CONCLUSION: I suggest that direct solar damage to the optic nerve may be a trigger for MS.

- Review Finds Marijuana May Help MS Patients - http://bit.ly/7ksqMT

Evidence of infectious cause

Sample PubMed cite2

Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.3

Non-MS autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body demyelination.4

Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. 5

Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.6

Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.7

Chlamydia pneumoniae infection of microglial cells in vitroA technique of performing a given procedure in a controlled environment outside of a living organism - usually a laboratory.: a model of microbial infection for neurological disease.8

Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid 9

Multifocal central nervous system lesions –multiple sclerosis or neuroborreliosis?10

MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.11

12 13 14 15

43. Granieri E, Casetta I, Tola MR, Ferrante P. Multiple sclerosis: infectious hypothesis. Neurol Sci. 2001;22:179-185. 44. Soldan SS, Jacobson S. Role of viruses in etiology and pathogenesis of multiple sclerosis. Adv Virus Res. 2001;56:517-555. 45. Steiner I, Nisipianu P, Wirguin I. Infection and the etiology and pathogenesis of multiple sclerosis. Curr Neurol Neurosci Rep. 2001;1:271-276.

Environmental risk factors for multiple sclerosis. Part I: the role of infection.16

Ascherio A, Munger KL. Department of Nutrition, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. aascheri@hsph.harvard.edu Although genetic susceptibility explains the clustering of multiple sclerosis (MS) cases within families and the sharp decline in risk with increasing genetic distance, it cannot fully explain the geographic variations in MS frequency and the changes in risk that occur with migration. Epidemiological data provide some support for the “hygiene hypothesis,” but with the additional proviso for a key role of Epstein-Barr virus (EBV) in determining MS risk. We show that whereas EBV stands out as the only infectious agent that can explain many of the key features of MS epidemiology, by itself the link between EBV and MS cannot explain the decline in risk among migrants from high to low MS prevalence areas. This decline implies that either EBV strains in low-risk areas have less propensity to cause MS, or that other infectious or noninfectious factors modify the host response to EBV or otherwise contribute to determine MS risk. The role of infectious factors is discussed here; in a companion article, we will examine the possible role of noninfectious factors and provide evidence that high levels of vitamin D may have a protective role, particularly during adolescence. The primary purpose of these reviews is to identify clues to the causes of MS and to evaluate the possibility of primary prevention. PMID: 17444504

Occupational exposure to UV light and mortality from multiple sclerosis. 17

Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases. 18

PMID: 19197935 [PubMed - as supplied by publisher]

Epidemiology and etiology of multiple sclerosis.19 Kurtzke JF.

Neurology Service, Veterans Affairs Medical Center, Washington, DC, USA. kurtzke2@aol.com

The author believes that the Faroese saga provides major insight into what seems to him to be the essential nature of MS: There is a specific, widespread, but unidentified, infection that we call the primary multiple sclerosis affection (PMSA). PMSA is a persistent infection that is transmitted from person to person. A small proportion of persons who has PMSA will develop clinical neurologic multiple sclerosis (CNMS) years later. Prolonged exposure is needed to acquire PMSA. Acquisition follows first adequate exposure. Susceptibility to PMSA is limited to approximately age 11 to age 45 at start of exposure. CNMS is not transmissible.PMSA transmissibility is limited to a period that is less than the usual age of onset of CNMS. On the Faroe Islands, this period is approximately from age 13 to age 26. The existence of PMSA now must be inferred from the presence of CNMS.

Read more:

Notes and comments

===== Symptoms ===== ===== Management ===== ===== Other treatments ===== ===== Tests ===== ===== Diagnosis ===== ===== Epidemiology ===== ===== Types ===== ===== Evidence of infectious cause===== ===== Role of vitamin D metabolism ===== ===== Politics ===== ===== Patient interviews ===== ===== Presentations and publications=====

REVISE Please note that some of the links listed were to non-MS topics (foods), eg s315a = Artificial sweeterners, whereas non-listed s315 = Member experience with MS, and I copied that content instead. However, some of these alternate content links came up “Topic not found” on the legacy index in the orange-header wiki. I also noticed some other MS topics on the legacy index that were not listed as content to be added here. I think this article needs mega mega revision and I don't believe all the intended content has been added. –Dody 2/22/09

  • e243 = MS as a bacterial infection.

Note: There is an internal link called Multiple sclerosis but I don't know how to draw in that material–dody 2/22/09

Interesting new abstract about MS as an infection

Epidemiology and etiology of multiple sclerosis. Phys Med Rehabil Clin N Am. 2005 May;16(2):327-49. PMID: 15893675

s317a:

Myelin sheath

We see nerves regenerate when peripheral neuropathy resolves for folk on the MP, so I see no reason the myelin sheath needs to be protected more than any other part of the body. Yes, I know that the MS researchers have focused on myelin, but so have the Alzheimers researchers focused on amyloid. They are both incorrect, IMO. They are looking at what is visible, but the intra-cellular changes are what are causing, and exacerbating, the illness.

s311a:

Low carbohydrate diets

The media is reporting that the low carb is dead but surveys show that as many people are eating low carb now as were eating low carb a year ago.

Carb-controlled diets have expanded past Atkins, Protein Power, CAD, and South Beach (which likes to claim it's not low carb, but about “good carbs”). Lowcarbing has many variations; from Atkins Induction, to people who are simply adding more protein and healthy fat, while cutting out sugar, white flour, and other highly processed carbs – with a big range of carb control in between. There are many people who insist they “aren't doing low carb” – but now eat eggs for breakfast instead of a muffin, and meat and vegetables for supper instead of pasta. (Do you know anyone who builds a dinner party around nothing but pasta anymore?)

There are two competing diet theories; low carb and low cal. The low calorie theory fails to take into account the facts that what kind of foods we eat influence how many calories we burn, and that eating more protein and fat and less carbohydrate has been demonstrated to reduce appetite too – it's hard to keep calories under control when you're ravenous.

On the other hand, some low carbers have gotten the idea that so long as they keep their carb count very low they can eat unlimited calories. I know of no studies that show this is so, only that the increase in metabolism and reduction in appetite means we can eat enough calories to be *comfortable*. (Most clinical studies show that low carbers lose weight at between 1800-2200 calories per day.)

The quality of every calorie counts. Vegetables are the best of the “good carbs” and whole grains, no matter how highly touted, are the least beneficial of the acceptable carbs, completely inessential in the human diet, and apt to cause bad reactions in many people.

Whether you are a true low carber or just one of those who has simply realized that bagels for breakfast, a sandwich for lunch, and pasta for dinner is *not* a healthy diet, you will benefit by making sure that all your food is NUTRITIOUS – no empty calories (nor empty carbs). Then every food you eat will promote good health ~Dana Carpender

HoldTheToast Press (Dana Carpender's website)

Did you want s311 instead (dody): Bacterial etiology of MS–but that link comes up empty (“topic not found”) in the legacy index on the orange-header wiki

s316a:

Fruits lowest in sugar:

· Rhubarb · Strawberries · Cranberries · Raspberries · Blackberries · Blueberries · Grapefruit · Melons · Apricots · Plums · Peaches · Pears · Guava · Cherries · Apples

These are fairly high in sugar:

· Grapes · Tangerine · Oranges · Pineapple · Kiwi

The following fruits are very high in sugar and generally going to be very infrequent visitors to the low carb diet:

· Bananas · Dried Fruit · Mango · Papaya

Did you want s316 instead (dody): Genetic etiology of MS disputed?–but that link comes up empty.

s310a: Not found on legacy index–dody

Did you want S310?–dody Titled Minocycline and MS–but link comes up empty

s318a: is Protein Primer, I did not copy it–dody

Did you want s318 instead? (dody):

Antibiotics 'could help slow MS'

BBC News Tuesday, 11 December 2007

Adding antibiotics to standard drug therapy may slow down the progress of multiple sclerosis, research suggests.

Patients showed fewer symptoms and fewer signs of tissue damage when they took the antibiotic doxycycline alongside the MS drug beta interferon.

Louisiana State University researchers believe the antibiotic may block the action of enzyme that destroy certain cells in the nervous system.

Archives of Neurology reports the study involving 15 patients on its website.

However, UK experts warned the study was small, and no comparison was made with patients who did not take doxycycline.

“Antibiotics are cheap and easily available, which would make them an attractive treatment for MS if they were shown to be beneficial” Dr Laura Bell MS Society

The 15 patients who took part in the study all had relapsing-remitting MS - the most common form of the disease.

Typically, this causes attacks of symptoms such as muscle weakness and spasms, followed by periods of remission.

The attacks result from damage inflicted on the body by its own immune system, which turns in on itself, attacking the nervous tissue.

It is thought that these attacks may be triggered by an inappropriate response to viral or bacterial infections, or another potentially disease-causing agent.

They are certainly very unpredictable, and symptoms come and go, often seemingly randomly.

Many patients with relapsing-remitting MS take the drug interferon, which helps to suppress the immune system, and keep it working more normally.

However, they are still prone to attacks which cause damage to the tissue of the brain.

Brain scans

The study focused on patients who had been taking interferon for at least six months, and who were still experiencing symptoms, and developing new tissue damage in the brain.

For four months the patients took 100mg a day of doxycycline alongside their regular dose of interferon.

At the end of this period brain scans revealed that brain tissue damage was reduced by at least 25% in nine of the patients.

There were also signs that disability levels had improved.

The researchers believe that doxycycline, a member of the tetracycline family of antibiotics, may block an enzyme which destroys nerve cells, thus protecting the brain and increasing the effectiveness of the immune system.

Dr Laura Bell, of the MS Society, said: “Antibiotics are cheap and easily available, which would make them an attractive treatment for MS if they were shown to be beneficial.

“However this study is very early stage in only 15 people with MS and no firm conclusions can be drawn at this stage.”

Chris Jones, chief executive of the MS Trust, agreed that the study was small, and had only covered a short period of time.

“A longer trial with more people will be needed before we can properly gauge the value of this combination for people with MS.” Helen Yates, of the MS Resource Centre, said the condition was complex and difficult.

She said other work was examining the possibility that MS was linked to an infection of the bacterium Chlamydia pneumoniae - more commonly associated with respiratory disease - in the brain.

“The growing interest in combination therapies is producing some good results, in particular for those people for whom single therapies have not worked.”

See also:

Combination Therapy Appears Safe, Effective in Small MS Study

The Shreveport Times

s306:

Does a virus (HHV-6A) cause MS?

The viruses are easy to find, and possibly involved in the infectious cascade, but they are just a red-herring.

I have (limited) data now, including MS folks who are already responding to the MP, but I have no doubt that MS will succumb to the MP.

Here is an example of the type of study which had initially side-tracked me into thinking viruses might play a part in MS http://www.primezone.com/newsroom/news.html?d=87395

But what these scientists are forgetting is that a monkey is not a human. Animal models have failed to predict human autoimmune disease time after time. So, while this study sounds very persuasive, it will fail to be replicated in man.

Note the sentence “an exceptionally strong, statistically significant association between HHV-6A and both multiple sclerosis and chronic fatigue syndrome (CFS) is consistently seen.” Well, we know they are 100% wrong with CFS, and the initial response of MS patients to the MP is showing them 100% wrong with MS as well.

There is a possibility I may be stating the lemma incorrectly, and HHV-6 variant-A might in fact be conditioning the immune system (through mutation) thus causing the CWD to run rampant. But the same outcome is in play - get rid of the CWD and you get rid of the disease.

..Trevor..

s309:

Dr Marshall wrote:

Here is a paper on cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. profiles in MS http://tinyurl.com/5pa9n

They concluded that the Th1 profile is predominant, except during pregnancy. That conclusion was erroneous, in my opinion, for the reasons I stated here http://tinyurl.com/6f6qr

however their raw data seem reliable, and it indicates Th1 is dominant.

The potential benefit of trying the MP is that it could cure the disease, the potential harm is that immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed. will exacerbate the symptoms and make life even less enjoyable for the patient. The problem I have with discussing applicability of the MP to ALS, or MS, or Diabetes, or even Parkinsons, is our current lack of understanding of how serious the immune system reactions might be, and in what form they might become manifest.

s307 = D-metabolite levels in MS–link comes up empty (“topic not found”) in legacy index

s308 = Diagnosis of MS–but link comes up empty (“topic not found”) in legacy index

s315a = Artificial sweeteners, I did not copy–dody

Did you want instead s315: Member experience with MS:

Member experience:

MS patient improves

also Dr. Greg Blaney wrote: I have several MS patients on the MP with good results so far. Like all MP patients, significant Immune reactions can occur which require informed supervision and treatment modifications

Interview with Ken L. of interest.

References

2) Marshall TG Vitamin D discovery outpaces FDA decision making. Bioessays. 2008;30:173-82.
3) García-Moncó JC, Miró Jornet J, Fernández Villar B, Benach JL, Guerrero Espejo A, Berciano JA [Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion] Med Clin (Barc). 1990;94:685-8.
4) Cikes N, Bosnic D, Sentic M Non-MS autoimmune demyelination. Clin Neurol Neurosurg. 2008;110:905-12.
5) Stratton CW, Wheldon DB Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. Trends Microbiol. 2006;14:474-9.
6) Sriram S, Mitchell W, Stratton C Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS. Neurology. 1998;50:571-2.
7) Sriram S, Stratton CW, Yao S, Tharp A, Ding L, Bannan JD, Mitchell WM Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis. Ann Neurol. 1999;46:6-14.
9) Brorson O, Brorson SH, Henriksen TH, Skogen PR, Schøyen R Association between multiple sclerosis and cystic structures in cerebrospinal fluid. Infection. 2001;29:315-9.
10) , 12) , 13) , 14) , 15) Drozdowski W [Multifocal central nervous system lesions --multiple sclerosis or neuroborreliosis?] Przegl Epidemiol. 2006;60 Suppl 1:39-45.
11) Agosta F, Rocca MA, Benedetti B, Capra R, Cordioli C, Filippi M MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis. AJNR Am J Neuroradiol. 2006;27:892-4.
17) Westberg M, Feychting M, Jonsson F, Nise G, Gustavsson P Occupational exposure to UV light and mortality from multiple sclerosis. Am J Ind Med. 2009;52:353-7.
19) Kurtzke JF Epidemiology and etiology of multiple sclerosis. Phys Med Rehabil Clin N Am. 2005;16:327-49.
Last modified: 05.31.2010
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