Med Hypothesesp(2009 Nov 9)
We have several members who are recovering on the Marshall Protocol who have a diagnosis of Multiple Sclerosis. One who is back to work after 15 years and another who is running a marathon.
I started the MP in 2009. My history is one of multiple sclerosis(1997) and chronic hepatitis (2004) because of (regular) medication.
My chronic hepatitis disappeared almost immediately after starting the MP.
My MS is improving, objectively shown by MRI.
In the last 15 years I have had a few parttime jobs, most of that years I wasn't able to work much.
Last month I started a new job for 32 hours per week. Most surprising to me: I don't get tired of working, on the contrary, it gives me new energy.
I think this is what health is!
I'm not where I want to be yet regarding my health, but this is a big step forward!
These also present the treatment of Multiple Sclerosis with the Marshall Protocol.
First: Greg Blaney gives two MS case histories 6 years ago…
Next: Dr Roswitha Goetze-Pelka, a German Neurologist, describes an MS case history in 2011:
Finally: Our simplified article in the recent “Current Opinion in Rheumatology” - a prestigious journal Doc should recognize.
A wide range of factors have been suggested as causes of multiple sclerosis (MS). It is likely that infectious  (and especially viral[2–5]),(Bains)
 Kurtzke JF, Heltberg A. Multiple sclerosis in the Faroe Islands: an epitome. J Clin Epidemiol 2001;54:1–22.  Warner HB, Carp RI. Multiple sclerosis etiology – an Epstein Barr hypothesis. Med Hyp 1988;25(2):93–7.  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.  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.  Tucker WG, Paskauskas RA. The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment. Med Hyp 2008;71:682–9.Central Florida; 1995.
Chronic inﬂammatory diseases of the intestine, such as inﬂammatory bowel disease (3) and celiac disease (4), are characterized by a leaky intestinal barrier…. Breakdown of the intestinal barrier is also implicated in immune reactions that target organs outside the digestive tract, leading to diseases such as IgA nephropathy (7), nonalcoholic hepatic steatohepatitis (8), and multiple sclerosis in the brain (9). Furthermore, entry of unwanted antigens can lead to systemic inﬂammatory response syndrome, characterized by a whole body inﬂammatory state, and multiple organ failure (10).
3. Suenaert P, Bulteel V, Lemmens L, Noman M, Geypens B, Van Assche G, Geboes K, Ceuppens JL, Rutgeerts P. Anti-tumor necrosis factor treatment restores the gut barrier in Crohn’s disease. Am J Gastroenterol. 2002;97:2000–4. 4. Vogelsang H, Schwarzenhofer M, Oberhuber G. Changes in gastrointestinal permeability in celiac disease. Dig Dis. 1998;16:333–6. 5. Damci T, Nuhoglu I, Devranoglu G, Osar Z, Demir M, Ilkova H. Increased intestinal permeability as a cause of ﬂuctuating postprandial blood glucose levels in Type 1 diabetic patients. Eur J Clin Invest. 2003;33:397–401. 6. Watts T, Berti I, Sapone A, Gerarduzzi T, Not T, Zielke R, Fasano A. Role of the intestinal tight junction modulator zonulin in the pathogenesis of type I diabetes in BB diabetic-prone rats. Proc Natl Acad Sci USA. 2005;102:2916–21
- 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.
Sample PubMed cite2)
Non-MS autoimmune 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)
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. firstname.lastname@example.org 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. email@example.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.
http://www.sciencedaily.com/releases/2009/09/090914111535.htm Curr Opin Neurol. 2009 Jun;22(3):201-6. Epstein-Barr virus and multiple sclerosis.Salvetti M, Giovannoni G, Aloisi F. Department of Neurology and Center for Experimental Neurological Therapy, S. Andrea Hospital, University of Rome La Sapienza, Rome, Italy. AbstractPURPOSE OF REVIEW: Recent studies have revived interest in the long-scrutinized association between Epstein-Barr virus (EBV) and multiple sclerosis (MS). We review this evidence and discuss it in relation to MS pathological and clinical features and patients' response to immunosuppressive therapies. RECENT FINDINGS: Serological evidence of previous exposure to EBV in children with MS supports a role for EBV infection early in MS pathogenesis, as already indicated by prospective studies in adults. Higher antibody titers and T-cell responses to EBV in patients compared to healthy EBV carriers indicate possible continuous viral reactivation, whereas there is some evidence that EBV could break immune tolerance to myelin antigens through molecular mimicry. Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated immunopathology in MS are the consequence of a persistently dysregulated EBV infection. Accordingly, targeting T-cells and/or B-cells with monoclonal antibody therapies ameliorates MS. Whether EBV has a causative or pathogenic role in MS can now be addressed in relation to genetic, hormonal and other environmental influences that may affect EBV-host interactions. SUMMARY: By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments.
Clin Microbiol Rev. 2004 Apr;17(2):323-47.Invasion of the central nervous system by intracellular bacteria. Drevets DA, Leenen PJ, Greenfield RA.
Department of Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma 73104, USA. firstname.lastname@example.org Abstract
Infection of the central nervous system (CNS) is a severe and frequently fatal event during the course of many diseases caused by microbes with predominantly intracellular life cycles. Examples of these include the facultative intracellular bacteria Listeria monocytogenes, Mycobacterium tuberculosis, and Brucella and Salmonella spp. and obligate intracellular microbes of the Rickettsiaceae family and Tropheryma whipplei. Unfortunately, the mechanisms used by intracellular bacterial pathogens to enter the CNS are less well known than those used by bacterial pathogens with an extracellular life cycle. The goal of this review is to elaborate on the means by which intracellular bacterial pathogens establish infection within the CNS. This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens.
Curr Opin Neurol. 2009 Jun;22(3):201-6. Epstein-Barr virus and multiple sclerosis. Salvetti M, Giovannoni G, Aloisi F. Department of Neurology and Center for Experimental Neurological Therapy, S. Andrea Hospital, University of Rome La Sapienza, Rome, Italy. Abstract PURPOSE OF REVIEW: Recent studies have revived interest in the long-scrutinized association between Epstein-Barr virus (EBV) and multiple sclerosis (MS). We review this evidence and discuss it in relation to MS pathological and clinical features and patients' response to immunosuppressive therapies. RECENT FINDINGS: Serological evidence of previous exposure to EBV in children with MS supports a role for EBV infection early in MS pathogenesis, as already indicated by prospective studies in adults. Higher antibody titers and T-cell responses to EBV in patients compared to healthy EBV carriers indicate possible continuous viral reactivation, whereas there is some evidence that EBV could break immune tolerance to myelin antigens through molecular mimicry. Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated immunopathology in MS are the consequence of a persistently dysregulated EBV infection. Accordingly, targeting T-cells and/or B-cells with monoclonal antibody therapies ameliorates MS. Whether EBV has a causative or pathogenic role in MS can now be addressed in relation to genetic, hormonal and other environmental influences that may affect EBV-host interactions. SUMMARY: By shedding light on the involvement of EBV in MS, these findings will pave the way to disease prevention and increase the therapeutic index of future treatments.
PMID: 19359987 [
From: edj2001 Date: 2011-12-30 20:49:17 Reply: http://www.marshallprotocol.com/reply.php?topic_id=14494
Add vitamin D to Scotland's food – experts, Dosing whole population would help cut levels of multiple sclerosis, say scientists Sarah Boseley, health editor guardian.co.uk, Friday 23 December 2011 15.30 EST Article history The following is a letter from Professor Stewart Fleming, University of Dundee to the Guardian in regard to above article:
“guardian.co.uk, Wednesday 28 December 2011 16.00 EST Article history
Your report (24 December) on the proposal that there should be artificial supplementation of Scotland's food by vitamin D to reduce the frequency of multiple sclerosis did not address the two main questions of whole-population interventions. Is it effective? Is it safe?
Current evidence strongly supports a role for low levels of vitamin D in the development of MS, as your article says. However, other factors are also involved. There are no population-based clinical trials supporting the effectiveness of artificial dietary supplementation by vitamin D in lowering the frequency of MS.
On the matter of safety, vitamin D supplementation should have no adverse effect on healthy individuals. However, whole-population medication also affects the frail, elderly and ill. There are a number of illnesses in which vitamin D supplementation is potentially harmful. These are diseases associated with elevated blood calcium and include hyperparathyroidism, myeloma, lymphoma, tuberculosis and sarcoidosis.
How common are these conditions? In Scotland hyperparathyroidism alone affects 6 per 1,000 of the population – it is several times more frequent than MS. So while we need to examine this issue carefully, mass medication with no published evidence of benefit, and with the risk that more people could be harmed than are likely to benefit, would be irresponsible.”
Professor Stewart Fleming
University of Dundee
21697250. Kimball, S., R. Vieth, et al. (2011). “Cholecalciferol plus calcium suppresses abnormal PBMC reactivity in patients with multiple sclerosis.” The Journal of clinical endocrinology and metabolism 96(9): 2826-2834. CONTEXT: The active metabolite of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)(2)D], is a potent modulator of immune cells in vitro. OBJECTIVE: Our objective was to determine whether the sun-dependent nutrient, cholecalciferol, can alter disease-associated cellular immune abnormalities in patients with multiple sclerosis (MS). DESIGN: This was an open-label, 12-month, randomized controlled trial. SETTING: Patients with MS were recruited from the MS Clinic at St. Michael's Hospital, Toronto. PATIENTS: Forty-nine patients were matched (for age, sex, disease duration, disease-modifying drug, and disability) and enrolled (treated n = 25; control n = 24). Four patients were lost to follow-up (n = 2 from each group). INTERVENTION: Treated patients received increasing doses of cholecalciferol (4,000-40,000 IU/d) plus calcium (1200 mg/d), followed by equilibration to a moderate, physiological intake (10,000 IU/d). Control patients did not receive supplements. MAIN OUTCOME MEASURES: At enrollment and at 12 months, peripheral blood mononuclear cell (PBMC) proliferative responses to disease-associated, MS-relevant, and control antigens were measured, along with selected serum biochemical markers. RESULTS: At 12 months, mean serum 25-hydroxyvitamin D [25(OH)D] concentrations were 83 +/- 35 nmol/liter and 179 +/- 76 nmol/liter in control and treated participants, respectively (paired t, P < 0.001). Serum 1,25(OH)(2)D did not differ between baseline and 1 yr. In treated patients, 12-month PBMC proliferative responses to neuron antigens myelin basic protein and exon-2 were suppressed (P = 0.002). In controls, there were no significant changes in disease-associated PBMC responsiveness. There were no significant differences between groups in levels of selected biomarkers. INTERPRETATION: MS-associated, abnormal T cell reactivities were suppressed in vivoA type of scientific study that analyzes an organism in its natural living environment. by cholecalciferol at serum 25(OH)D concentrations higher than 100 nmol/liter.
High-dose vitamin D also was not associated with a significant difference in change in total volume of T2 lesions, with median changes of −330 mm3 compared with a change of −95 mm3 for low-dose vitamin D (P=0.6), the investigators reported in the October 25 issue of Neurology.
22025459. Stein, M. S., Y. Liu, et al. (2011). “A randomized trial of high-dose vitamin D2Form of vitamin D created by plants and fungi. When ingested the secosteroid is (sometimes) converted into 25-D. Also known as ergocholecalciferol. in relapsing-remitting multiple sclerosis.” Neurology 77(17): 1611-1618. OBJECTIVE: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS. METHODS: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months' double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130-175 nM. All received daily low-dose (1,000 IU) D2 to prevent deficiency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses. RESULTS: Twenty-three people were randomized, of whom 19 were on established interferon or glatiramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p = 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p = 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p = 0.04). CONCLUSION: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation. Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (targeting 25OHD 130-175 nM), compared to low-dose supplementation (1,000 IU/d), was not effective in reducing MRI lesions in patients with RRMS.
High-dose vitamin D may not be better than low-dose vitamin D in treating MSST. PAUL, Minn. – Low vitamin D levels are associated with an increased risk of developing multiple sclerosis (MS), but the first randomized, controlled trial using high-dose vitamin D in MS did not find any added benefit over and above ongoing low-dose vitamin D supplementation, according to a study published in the October 25, 2011, issue of Neurology®, the medical journal of the American Academy of Neurology. “We did not find added benefit from high-dose vitamin D over and above ongoing low-dose vitamin D supplementation, but these results need to be confirmed with larger studies,” said Mark S. Stein, MBBS, PhD, FRACP, of The Royal Melbourne Hospital and The Walter and Eliza Hall Institute of Medical Research in Parkville, Australia. The six-month study involved 23 people with the relapsing-remitting form of MS. All of the participants received low-dose vitamin D (1,000 international units daily) to prevent any vitamin D deficiency. Half of the participants also received high-dose vitamin D2 to elevate their blood vitamin D to high levels (with a target serum 25-hydroxyvitamin D level of 130-175nM). The other half received a placebo high-dose. MRI scans of the participants' brains were performed at the start of the study and again after four, five and six months. There was no significant difference between the two groups in the number of new abnormalities that had formed in the brain after six months and no significant difference in the change in the total volume of brain abnormalities. Four of the 11 people taking the high-dose vitamin D, or 37 percent, had a relapse where their MS symptoms worsened during the study, while none of the 12 people taking only low-dose vitamin D had any relapses. Stein noted that the study involved people who had MS for an average of six years. “It's possible that studies of high-dose vitamin D at an earlier stage of MS may lead to different results,” he said.
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
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
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.
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
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.
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.”
Combination Therapy Appears Safe, Effective in Small MS Study
The Shreveport Times
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.
Dr Marshall wrote:
Here is a paper on cytokine 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 immunopathology 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:
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.
Here is the paper by Hector DeLuca's group, no less, the official inventor of 1,25-D….
Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6418-23. Epub 2010 Mar 22. UV radiation suppresses experimental autoimmune encephalomyelitis independent of vitamin D production.20) Becklund BR, Severson KS, Vang SV, DeLuca HF. Department of Biochemistry, University of Wisconsin, Madison, WI 53706, USA. Comment in: Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):E130; author reply E131. Abstract Although the exact cause of multiple sclerosis (MS) is unknown, a number of genetic and environmental factors are thought to influence MS susceptibility. One potential environmental factor is sunlight and the subsequent production of vitamin D. A number of studies have correlated decreased exposure to UV radiation (UVR) and low serum 25-hydroxyvitamin D(3) [25(OH)D(3)] levels with an increased risk for developing MS. Furthermore, both UVR and the active form of vitamin D, 1alpha,25-dihydroxyvitamin D(3), suppress disease in the experimental autoimmune encephalomyelitis (EAE) animal model of MS. These observations led to the hypothesis that UVR likely suppresses disease through the increased production of vitamin D. However, UVR can suppress the immune system independent of vitamin D. Therefore, it is unclear whether UVR, vitamin D, or both are necessary for the putative decrease in MS susceptibility. We have probed the ability of UVR to suppress disease in the EAE model of MS and assessed the effect of UVR on serum 25(OH)D(3) and calcium levels. Our results indicate that continuous treatment with UVR dramatically suppresses clinical signs of EAE. Interestingly, disease suppression occurs with only a modest, transient increase in serum 25(OH)D(3) levels. Further analysis demonstrated that the levels of 25(OH)D(3) obtained upon UVR treatment were insufficient to suppress EAE independent of UVR treatment. These results suggest that UVR is likely suppressing disease independent of vitamin D production, and that vitamin D supplementation alone may not replace the ability of sunlight to reduce MS susceptibility. PMID: 20308557
Ask your Questions Here > Verena's Questions
From: Verena Date: 2010-07-07 15:47:41 Reply: http://www.curemyth1.org/reply.php?topic_id=2490
Just home from MRI and “after party”. I have no new lesions and some old ones have disappeared or one can see just a shadow :D:D:D
When include link to this article from “incidence and prevalence”:
J Neuroimmunol. 2011 Jan 28. [Epub ahead of print] The impact of parasite infections on the course of multiple sclerosis. Correale J, Farez MF. Abstract Previously, we demonstrated that helminth-infected MS patients showed significantly lower number of relapses, reduced disability scores, and lower MRI activity compared to uninfected MS subjects. In the current study, 12 patients with diagnosis of relapsing remitting MS presenting parasite infections were prospectively followed during 90months; due to exacerbation of helminth-infection symptoms after 63months of follow-up, 4 patients received anti-parasite treatment. Helminth-infection control was associated with significant increase in clinical and radiological MS activities. Moreover, these patients showed significant increase in the number of IFN-γ and IL-12 producing cells, and a fall in the number of TGF-β and IL-10 secreting cells, as well as CD4+CD25+FoxP3+ Treg cells evident 3months after anti-helminth treatment began. These new observations on parasite infections associated to MS indicate that parasite regulation of host immunity can alter the course of MS. Copyright © 2011 Elsevier B.V. All rights reserved.
Phillyguy: Probably explains one of the reasons why the incidence of autoimmune disease is lower in developing countries and infectious disease is higher. Interestingly, VDR generally increases the expression ofTregs, IL-10 and TGFbeta and represses IFNg and IL-12.
Inflammopharmacology. 2011 May 6. [Epub ahead of print] Paradigms in multiple sclerosis: time for a change, time for a unifying concept. Krone B, Grange JM. Source Institute of Virology, Centre for Hygiene and Human Genetics, University of Göttingen, Kreuzbergring 57, 37075, Göttingen, Germany. Abstract It has recently been suggested that, rather than being an autoimmune disease, multiple sclerosis (MS) is an example of a neurocristopathy, a pathological process resulting from a faulty development of the neural crest. Whilst several characteristics of the disease suggest a neurocristopathy, other aetiological factors require consideration, including hygiene-related factors that alter the immune responses to common pathogens resulting in an eclipse of immune reactivity that could protect against MS, the possible role of human endogenous retroviruses (HERVs) in pathogenesis and autoimmune phenomena, HLA polymorphism, vitamin D levels before and after birth and immune repair mechanisms. A postulated aetiological factor in MS, associated with altered vitamin D metabolism and abnormal HERV expression, is a long-lasting disturbed redox regulation in the biosynthesis of a melanoma-like melanin pigment. Although intensive further studies on melanin pigments in nerve tissue in MS are required, the known properties of a pathological form of such pigments in melanoma could explain a number of observations in MS, including the impact of light, UV-light, and vitamin D, and could explain the clinical manifestations of MS on the basis of an oscillating process of oxidative charge and discharge of the pigments and a threshold phenomenon with a change of the quasi-catalytic function of the pigment from destroying reactive oxygen radicals or species to transforming them to more harmful long-persisting highly reactive species. Taken together with the consequences of an adaptive process in partly demyelinated neurons, resulting in an increase in number of mitochondria, and the impact of stressful life events, these conditions are necessary and sufficient to explain the disease process of MS with its spatial (plaques) and temporal (attacks and remissions) characteristics. This suggested unifying concept of the pathogenesis of MS may open perspectives for prevention, diagnosis and therapy. In particular, prevention may be achieved by vaccinating against Epstein-Barr virus in early childhood.
PMID: 21547536 [
Friendly Gut Bacteria May Trigger MS
In an astonishing new study published in Nature today, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say.
Nature. 2011 Oct 26. doi: 10.1038/nature10554. [Epub ahead of print] Commensal microbiota and myelin autoantigen cooperate to trigger autoimmune demyelination. Berer K, Mues M, Koutrolos M, Rasbi ZA, Boziki M, Johner C, Wekerle H, Krishnamoorthy G. Source Department of Neuroimmunology, Max Planck Institute of Neurobiology, 82152 Martinsried, Germany. Abstract Active multiple sclerosis lesions show inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter. These pathogenic immune cells derive from progenitors that are normal, innocuous components of the healthy immune repertoire but become autoaggressive upon pathological activation. The stimuli triggering this autoimmune conversion have been commonly attributed to environmental factors, in particular microbial infection. However, using the relapsing-remitting mouse model of spontaneously developing experimental autoimmune encephalomyelitis, here we show that the commensal gut flora-in the absence of pathogenic agents-is essential in triggering immune processes, leading to a relapsing-remitting autoimmune disease driven by myelin-specific CD4(+) T cells. We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota. Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets. PMID: 22031325
A randomized trial of high-dose vitamin D2 in relapsing-remitting multiple sclerosisABSTRACT Objective: Higher latitude, lower ultraviolet exposure, and lower serum 25-hydroxyvitamin D (25OHD) correlate with higher multiple sclerosis (MS) prevalence, relapse rate, and mortality. We therefore evaluated the effects of high-dose vitamin D2 (D2) in MS. Methods: Adults with clinically active relapsing-remitting MS (RRMS) were randomized to 6 months’ double-blind placebo-controlled high-dose vitamin D2, 6,000 IU capsules, dose adjusted empirically aiming for a serum 25OHD 130–175 nM. All received daily low-dose (1,000 IU) D2 to prevent defi- ciency. Brain MRIs were performed at baseline, 4, 5, and 6 months. Primary endpoints were the cumulative number of new gadolinium-enhancing lesions and change in the total volume of T2 lesions. Secondary endpoints were Expanded Disability Status Scale (EDSS) score and relapses. Results: Twenty-three people were randomized, of whom 19 were on established interferon or glati- ramer acetate (Copaxone) treatment. Median 25OHD rose from 54 to 69 nM (low-dose D2) vs 59 to 120 nM (high-dose D2) (p 0.002). No significant treatment differences were detected in the primary MRI endpoints. Exit EDSS, after adjustment for entry EDSS, was higher following high-dose D2 than following low-dose D2 (p 0.05). There were 4 relapses with high-dose D2 vs none with low-dose D2 (p 0.04). Conclusion: We did not find a therapeutic advantage in RRMS for high-dose D2 over low-dose D2 supplementation. Classification of evidence: This study provides Class I evidence that high-dose vitamin D2 (target- ing 25OHD 130–175 nM), compared to low-dose supplementation (1,000 IU/d), was not effec- tive in reducing MRI lesions in patients with RRMS. Neurology® 2011;77:1611–1618
High-dose vitamin D may not be better than low-dose vitamin D in treating MS
ST. PAUL, Minn. – Low vitamin D levels are associated with an increased risk of developing multiple sclerosis (MS), but the first randomized, controlled trial using high-dose vitamin D in MS did not find any added benefit over and above ongoing low-dose vitamin D supplementation, according to a study published in the October 25, 2011, issue of Neurology®, the medical journal of the American Academy of Neurology.
“We did not find added benefit from high-dose vitamin D over and above ongoing low-dose vitamin D supplementation, but these results need to be confirmed with larger studies,” said Mark S. Stein, MBBS, PhD, FRACP, of The Royal Melbourne Hospital and The Walter and Eliza Hall Institute of Medical Research in Parkville, Australia.
The six-month study involved 23 people with the relapsing-remitting form of MS. All of the participants received low-dose vitamin D (1,000 international units daily) to prevent any vitamin D deficiency. Half of the participants also received high-dose vitamin D2 to elevate their blood vitamin D to high levels (with a target serum 25-hydroxyvitamin D level of 130-175nM). The other half received a placebo high-dose.
MRI scans of the participants' brains were performed at the start of the study and again after four, five and six months. There was no significant difference between the two groups in the number of new abnormalities that had formed in the brain after six months and no significant difference in the change in the total volume of brain abnormalities.
Four of the 11 people taking the high-dose vitamin D, or 37 percent, had a relapse where their MS symptoms worsened during the study, while none of the 12 people taking only low-dose vitamin D had any relapses.
Stein noted that the study involved people who had MS for an average of six years. “It's possible that studies of high-dose vitamin D at an earlier stage of MS may lead to different results,” he said.
New autoantibody found in MS
- Review Finds Marijuana May Help MS Patients - http://bit.ly/7ksqMT
Fish Oil Flops in MSBy Kristina Fiore, Staff Writer, MedPage Today Published: April 16, 2012 Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner 6 comment(s) Fish oil doesn't appear to be of any help in treating multiple sclerosis, Norwegian researchers found. In a randomized controlled trial, supplementation with omega-3 fatty acids had no effect on the number of brain lesions seen on MRI over two years compared with placebo, Oivind Torkildsen, MD, PhD, of Haukeland University Hospital in Norway, and colleagues reported online in the Archives of Neurology. Though the Norwegian diet is usually associated with high levels of fish intake, Torkildsen told MedPage Today that serum omega-3 levels in the placebo group were low to normal, “which indicates that their fish intake was not higher than would be expected in other populations,” and that those in the supplementation group did indeed see a rise in omega-3 levels while the placebo group did not. Smaller trials have found a potential benefit for omega-3 fatty acids, which may be active in MS because of their anti-inflammatory and neuroprotective properties. But controlled trials haven't been able to draw any definitive conclusions, the researchers said. Still, fish oils are the most common form of complementary medicine used by MS patients, they noted. So Torkildsen and colleagues conducted a randomized, double-blind, placebo-controlled trial at 13 public neurology departments in Norway totaling 92 patients ages 18 to 55 with relapsing-remitting MS. Patients were given either 1,350 mg of eicosapentaenoic acid (EPA) and 850 mg docosahexaenoic acid (DHA) every day, or placebo. After the first 6 months of the trial, all patients were also given 44 mcg of interferon beta-1a three times a week for another 18 months. The researchers found that at all time points – 6, 9