- Exposure of the eyes to near-horizon sunshine may be a trigger for multiple sclerosis.1)
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.
suggested as causes of multiple sclerosis (MS)
Multiple sclerosis etiology – an Epstein Barr hypothesis. 2)
The pathogenesis of multiple sclerosis: reconsideration of the role of viral agents and defence mechanisms. 3)
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). some references follow
Anti-tumor necrosis factor treatment restores the gut barrier in Crohn’s disease. 4)
Changes in gastrointestinal permeability in celiac disease. 5)
Increased intestinal permeability as a cause of fluctuating postprandial blood glucose levels in Type 1 diabetic patients. 6)
Role of the intestinal tight junction modulator zonulin in the pathogenesis of type I diabetes in BB diabetic-prone rats. 7)
Multiple sclerosis or Lyme disease? a diagnosis problem of exclusion.8)
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.9)
Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. 10)
Multiple sclerosis associated with Chlamydia pneumoniae infection of the CNS.11)
Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis.12)
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.13)
Association between Multiple Sclerosis and Cystic Structures in Cerebrospinal Fluid 14)
Multifocal central nervous system lesions –multiple sclerosis or neuroborreliosis?15)
MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis.16)
Multiple sclerosis: infectious hypothesis. 17) Role of viruses in etiology and pathogenesis of multiple sclerosis. 18) Infection and the etiology and pathogenesis of multiple sclerosis. 19)
Part I: the role of infection. 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. 20)
Correlation of mollicutes and their viruses with multiple sclerosis and other demyelinating diseases.21)
The MSMV hypothesis: measles virus and multiple sclerosis, etiology and treatment. 22)
Epidemiology and etiology of multiple sclerosis.23)
Detection of EBV-infected B-cells in patients' brain raises the possibility that intrathecal B-cell abnormalities and T-cell-mediated 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. in MS are the consequence of a persistently dysregulated EBV infection. 24)
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.
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.
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. 25)
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. 26)
In a collaborative GWAS involving 9772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the Class I region. Immunologically relevant genes are significantly over-represented amongst those mapping close to the identified loci and particularly implicate T helper cell differentiation in the pathogenesis of multiple sclerosis. 27)
Antibiotic Use 28)
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:
bureaucratic blight on medical research
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
Occupational exposure to UV light and mortality from multiple sclerosis29)
“Cholecalciferol plus calcium suppresses abnormal PBMC reactivity in patients with multiple sclerosis.”30)
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).
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.
map from msrc.co.uk
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.
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)
2018 This review focuses on four main themes influencing current understanding of thermoregulatory dysfunction in MS 31)
2019 from Misgeld, Kerschensteiner. et al
• Cytoplasmic calcium accumulations predict axon degeneration in neuroinflammation • Release from the axoplasmic reticulum does not explain calcium accumulations • Calcium influx from the extracellular space drives axon degeneration • Nanoscale ruptures allow entry of calcium across the axonal plasma membrane
We have several members who are recovering on the Marshall ProtocolA curative medical treatment for chronic inflammatory disease. Based on the Marshall Pathogenesis. 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!
-Limburg
On starting MP Yomi posted I was diagnosed with Sarcoidodis in 2001. I have had manifestaions obviously in the lungs but later in the eyes (uveitis) the skin (granluoma) and most recently in the nervous system (neuropathy). I've got a decent case of lupus pernio pretty much all over my body. So these symptoms along with the neuropathy are taking its time as expected.
(questioned after 8 years how the lupus has responded)
It has some. The raised bumps on my face used to have a dark colored center. Now the bumps no longer have the dark colored center and aren't as swollen.
These also present the treatment of Multiple Sclerosis with the Marshall Protocol.
First: Greg Blaney some years ago… Two MS cases
Next: Dr Roswitha Goetze-Pelka, on MS patient in 2011: Case history by neurologist
Our simplified article in Current Opinion in Rheumatology 2013