This Is MS Multiple Sclerosis Knowledge & Support Community
Welcome to This is MS, the leading forum for Multiple Sclerosis research and support. Join our friendly community of patients, caregivers, and researchers celebrating over 20 years of delivering hope through knowledge. https://www.thisisms.com/forum/
In the book, which was on the NYT best seller list, Gary Taubes argues that the problem lies in refined carbohydrates, like white flour, easily digested starches, and sugars, and that the key to good health is the kind of calories we take in, not the number.
lyndacarol wrote:His latest book is Why We Get Fat.
Here's a lecture given by Gary Taubes discussing material from his book Why We Get Fat.
Are lectins causing the "auto"-immune diseases?
Posted: Wed Aug 14, 2013 8:56 am
by Leonard
I think that progressive MS is caused by lectins breaking through the gut barrier in combination with a broken BBB (due to many years of ccsvi). The first thing to do is to avoid lectins (and gluten).
As lectins are sugar-binding proteins, a low sugar diet works for diabetes II, and most likely for MS too. Fat is a factor too.
The "auto" reactive T-cells seen are normal T-cells that got a good training in the gut and that react to lectins on the vessel walls.
The working of the gut with important carry-on effects from a distorted enzyme driven small intestine (and lectin trained T-cells) to a bacteria driven large intestine (and vitamine production, CoQ10, Carnitine, micronutritients etc) is also compromised adding to the problems with mitochondrial functioning.
On the lectin role in immunity disease, quote from the links below:
Nature engineers, within all species, a set of defenses against predation, though not all are as obvious as the thorns on a rose or the horns on a rhinoceros. Plants do not have the cell-mediated immunity of higher life forms, like ants, nor do they have the antibody-driven, secondary immune systems of vertebrates with jaws. Therefore, they must rely on a much simpler, innate immunity. It is for this reason that seeds of the grass family, e.g. rice, wheat, spelt, rye, have exceptionally high levels of defensive glycoproteins known as lectins, which function much like "invisible thorns." Cooking, sprouting, fermentation and digestion are the traditional ways in which people, for instance, deal with the various anti-nutrients found within this family of plants, However, lectins are, by design, particularly resistant to degradation through a wide range of pH and temperatures.
Lectins are sugar-binding proteins and, through thousands of years of selectively breeding wheat for increasingly larger quantities of protein, the concentration of WGA lectin has increased proportionately.
This sketch of a new concept of MS is my best assessment of what is MS. It is based on our learnings over the last two and a half years, much of which can be found in the postings on this thread.
Venous obstruction in the drainage of the cerebro-spinal (CCSVI) is a birth defect. There is a certain genetic component that may pass from one generation to the next. Live in the shadow of the heavy metal industry, even of previous generations, is thought to be a contributing factor.
Many years of CCVSI will weaken the endothelium in areas closer to the outlet of brain and spinal column. But with the astrocytes and oligodendrocytes there is nothing intrinsically wrong – it is not genetic. And perhaps the most important thing is that the tissue of the BBB breaks.
With a broken BBB, an infectious agent may cause a blocking of receptors. The Cpn bacteria and the EBV virus which agents can be dormant for many years are known for a sudden outbreak and their ability to block receptors. If this happens, the equilibrium of the ion-pump cannot be maintained because mitochondria lack energy supply, the charging of the pump runs down. Motor functions get impaired and an acute relapse is the result. Cytokines are released, the immune system will signal that there is something wrong, an acute inflammation will arise, leukocytes will infiltrate the damaged region, removing the stimulus and repairing the tissue. This is RR MS. The time constant of the process just doesn't point to big biological changes..
In the progressive phase, a different mechanism underlies MS. As of mid-age (is entirely an age dependent phenomenon – not dependent on previous disease activity) the 'lining' of the gut breaks. The "leaky gut" will allow incompletely digested particles to be partially absorbed, including in particular gluten / lectins from wheat. Lectins are the natural defence of the plant against e.g. fungi. Some of these lectins leak into the blood stream, get carried to distant sites and have the capacity to bind to cell membranes in the vessel walls. The combination with sugar and fat seems particularly damaging and may cause "a double hit" in its inflammatory response.
As lectins attach to the cell membranes, nutritional problems follow for the mitochondria. This then will stimulate the release of cytokines and an immune response. T-cells that are well trained and multiplied in the gut recognise and remove these lectins. This process is often referred to as the aggressive T-cells that attack the myelin but it is a perfectly healthy reaction. But damage is done and more and more mitochondria will fail until the cell dies.
Problems spread through the body, other systems get affected like the parasympathetic nervous system with consequences on organs including the gut. The gut working will further detoriate establishing a vicious circle. There may also be important carry-on effects from the enzyme driven small intestine to the bacteria driven large intestine.
Micro-nutritions and vitamins then are insufficiently produced and absorbed in the large intestine causing a metabolic dysregulation, growing insulin/leptin resistance and further problems for the mitochondrial energy supply. More T-cells are drawn in and low grade inflammation and oxidative stress are created leading to a chronic hypoperfusion of the central nervous system, further induced mitochondrial energy failure, inflammation, a further neurodegeneration, oligodendrocyte apoptosis, myelin breakdown. Progressive MS is the result.
The "leaky gut" is the cause of many "auto" immune diseases, including diabetes type 2 and rheuma arthritis. But we suffer from MS symptoms because in our case the protective tissue of the BBB is broken.
At this stage MS will often be intertwined with a diabetes related peripheral neuropathy. In addition, typical RR effects caused by infectious agents (including at this stage infectious agents related to the sinus flora - dural sinuses empty in the blocked IJVs) followed by immune system repair will be superimposed on the steady progression course caused by mitochondrial failure.
The graph of the age of onset will show a double peak that is explained by the different underlying mechanisms that take effect over time. People who 'escaped' the MS diagnosis during the RR phase because they had a fairly mild version get diagnosed after mid-age when the bad gut develops...
Patients with MS may be affected in various ways depending on their genetic susceptibilities e.g. predisposition for diabetes type 2, the stress in their live and the Cortisol regulation/Adrenal fatigue, vitamin D / sun exposure during pregnancy of the mother and during adolecence that influences cell composition e.g. number of "vit D" gates / active membranes, the vitamin D and the natural anti-biotics in the gut balancing the gut flora, environmental factors such as exposure to heavy metals (even of previous generations) and related genetic factors of veins (Boston document, Texas study), the specific pattern of vascular insufficiencies of the draining neck veins.
Other factors may be the hormonal balances (e.g. the difference between men and women and a relationship with testosterone is a most clear indication that MS is metabolic related to cellular nuitrition), a lack of zinc to bind and store insulin thereby raising peaks and reducing insulin sensititity, even a vaccination for Hepatitis may be suspect, the mind-body connection (stress, distress, prolactin), etc.
The challenge is now to recollect all knowledge and expertise that is around and build a new more advanced model of what is MS and rapidly progress this matter for our cause.
... This autoimmune reaction produces specific findings within the small bowel as well as specific antibodies in the blood, both of which define the diagnosis of Celiac disease. Just in the last two decades, the estimated prevalence of this gluten-related autoimmune disease has gone from 1/6000 to 1/130 or even 1/100 people in the U.S..[1] At 1% of the population, celiac disease is not exactly a rare condition. However, celiac disease may be the tip of the iceberg when it comes to grain related disease and distress.
It turns out that not all Celiac sufferers have the typical symptoms, or any symptoms at all. Traditionally, Celiac disease is thought to result in diarrhea, intestinal cramping and bloating, malabsorption (often resulting in anemia), and weight loss. Yet, it has been more recently discovered that many people with positive antibody results and intestinal findings never complain of any symptoms. The term "silent celiac disease" has been coined to describe such cases.
Yet, silent celiac disease is not truly silent. Individuals with the silent version of the disease are just as likely (or even more likely) as those with symptomatic celiac disease to develop or have osteoporosis, lymphoma of the small bowel, and other autoimmune diseases like rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, psoriasis, Hashimoto's thyroiditis (hypothyroidism), and perhaps even dementia[2],[3],[4],[5],[6],[7],[8]. …
Before you consider the possibility, or the likelihood, that you have gluten sensitivity and alter your diet, there is still more to the story. It turns out that gluten, the common term for several different proteins in wheat, rye, barley, and oats, may not be the only cause of the adverse health effects from these foods. Grains contain molecules called lectins. For instance, wheat contains wheat germ agglutinin (WGA) and it has been proposed that celiac disease and gluten sensitivity results from a gluten-lectin combination effect. Indeed, many celiac patients also test positive for antibodies against WGA.[22] ...
While lectins are prevalent in nearly all plants and animals, grains contain very high concentrations of lectins. Additionally, genetic modification of some grains has intentionally increased their lectin concentration in order to improve pest resistance. Therefore, if lectins cause health problems, we would expect those problems to be most strongly associated with grain consumption. However, studies have shown that wheat germ agglutinin (WGA) can have adverse effects on the intestinal cells even at extremely low "nanomolar" concentrations[23].
The wheat kernel is composed of hundreds of potentially antigenic protein components, of which gliadin (water soluble glutens) makes up only a small proportion. There is an array of protein, enzyme and peptide antigens namely glutens, opioids, lectins and enzymes. ...
Diagnosis is recommended for patients who [among others] may suffer from blood brain barrier permeability...
And we know that we have a problem with our blood brain barrier that was at least partly compromised because of many years of ccsvi.
I am trying to get a better understanding of the gluten/lectin complex of things.
The above links provide some interesting information but I am sure there is much more to be said.
I invite all of you to add if you have more information or knowledge or other perhaps broader perspectives.
Re: A new concept for MS
Posted: Tue Sep 03, 2013 8:21 am
by lyndacarol
Excellent information! Thank you for posting this, Leonard.
gut permeability
Posted: Fri Sep 06, 2013 12:18 pm
by Leonard
is this how it works?
the gut becomes permeable because of gliadin (gluten) / lectins http://www.ncbi.nlm.nih.gov/pubmed/16635908 and then lectins leak into the bloodstream (if not caught by the immune system on inner epithelial wall) and bind to the cell membranes disrupting the membranes and damaging the cells. this then initiates a cascade of immune and "auto"immune events leading to cell death. and all the rest follows..
I found the reference in the book of William Davis on the Wheat Belly.
Just finished reading the book, very convincing book about the bad effects of modern commercial wheat from an expert...
it neatly fits the broader picture that is emerging here.
the "auto"immunity should be read as a reaction due to compromised cellular feeding condition.
A new concept of MS -2
Posted: Sat Sep 14, 2013 3:50 am
by Leonard
A new concept of MS - 2
Our biological center is the gut. The gut microbiome is 100 times larger than the human genome. The gut is where ‘foreign’ is processed to ‘own’, where nutritions and vitamins are absorbed and some even produced. Some people have gone so far as to say that the human body is nothing else than a big incubator for our gut. Obviously, an incubator that is under our control in the sense that we decide where we take it, how we feed it..
If things go wrong in this biological center, a plethora of things can go wrong in the incubator, including lesions that results from poor mitochondrial feeding. Ccsvi is also a factor that affects various flows in the brain and that can cause damage. MS then is just a collection of symptoms, an MS centric view of things is just wrong. For long time, we have seen the cause of poor cellular feeding as a problem of the veins, marked by increased insulin resistance and leptin resistance. But evidence now shows that the root of the problem lies elsewhere, not downstream but upstream, in the gut. Patients who remove all wheat products from their diet change from diabetic to non-diabetic. Fecal microbiota transplantation (FMT) raises the insulin sensitivity of cells by more than a factor 2 in just 6 weeks time, turning patients from diabetic to non-diabetic state.
The gut is also the center of our immune system. Foreign particles that pass through the outer epithelial walls are arrested. The gut trains T-cells and is the home for the collective memory of vaccinations that we received during our lifetime making sure the right T-cells are ready when needed. If too many particles penetrate through the outer epithelial walls, the state of inflammation will be raised. If this is caused by wheat gluten, this is celiac disease, or silent celiac disease. In the last 20 years, the diagnosis of celiac disease among Americans has dramatically increased, from 1 in 6300 to 1 in a 100. Likewise, immune diseases and diabetes have sharply increased. Heavy fat and sugar are factors that, when absorbed by the gut, are thought to increase the permeability of the gut and cause a double hit in inflammatory response.
But the worst of all is wheat. The modern wheat plant has a multitude of invisible ‘thorns’ with WGA (Wheat Germ Agglutinin or lectins) being the smallest (in order of 30 thousand Daltons while the healthy goes to 1000 Daltons) and perhaps most potent defense against predation. In addition, there is this protein gliadin in gluten that triggers the release of zonulin that helps break the gut lining.
The WGA in the circulation binds to carbohydrate membranes of our cells, that is what mother nature has learned them to do, that is what hundreds of millions of years of evolution has produced. Fat and sugar are thought to affect the binding propoerties. This will block the feeding of the cells, the cells exhibit leukocytes which in my view is a normal reaction, an immune reaction that follows when cellular feeding goes wrong. The cells are then marked for attack by white blood cells, the T-cells that are ample available in the gut, well trained and that ‘know’ their lectins..
WGA does not necessarily directly transform the phenotype of our cells into ‘other’ but the cross-reactivity of antibodies to WGA with our own cells would nonetheless result in - what we then see as - autoimmunity. I think it is the strength of the lock, the irreversible lock of lectins with the cell membranes that damages the membranes. If enough membranes are damaged, the ion pump runs down and eventually the cell dies. Because of the specific lock, the T-cells can not remove the lectins from the receptors as if they were a virus or bacteria (something the T-cells can do in the RR phase when receptors are blocked by virus or bacteria which became possible after the BBB broke).
Some may argue that lectins pass through the BBB. The condition of the BBB is not so important anymore in the progressive phase. But for us, the problem there is that an already weak structure (endothelium and nerve conduct in brain and spinal due to ccsvi) gets weaker much faster than in healthy people. In addition, and perhaps the overriding thing at this stage, is that a serial neuropathy now kicks in of weakening nerve conduct in the peripheral nerves over and above the weak conduct in brain and spinal column. Unlike for RR where phenomena may be the loss of control of a hand, the progressive part typically starts from a weakening of feet and legs, the longest neurological pathways which is a most clear indication confirming such serial concept. Neurologists will no doubt be able to confirm (or deny) this because they best know where typical symptoms occur in RR relapses and the progressive course.
Fortunately, evidence accumulates that the process at the meta-level is reversible. Wheat is particularly bad but lectins are found in all food. The issue is then to stop eating wheat products and to stop the leaking gut as good as possible. This then should turn the negative balance of more cells that get disabled relative to new formed cells to a positive balance of new formed cells outweighing the number of disabled cells. [with a healthy gut, the normal rate of replenishment is good enough to overcome damage done by lectins] The process to reverse direction may take as much as a year or more; where it is important to start as early as possible because hidden damage is done.
The diet by Roger MacDougall (no gluten, low fat, low sugar, see a few postings above) seems a way to reverse the disease progression. Supplementation of Vit D and B may help to strenghten new cells with many active gates.
I would be interested in any views that you might have.
Lectins are proteins that are in plants. They are very small and easily leak through the intestinal wall into the circulation. They then attach themselves to cell membranes. The membrane of the cell is blocked and can not take up energy and falls into crisis.
The cell marks itself by cytokines. The immune system recognizes and sends T - cells that are well trained in the gut because they have seen many lectins there. The training occurs on the inner intestinal wall where foreign molecules are stopped as much as possible.
But once lectins are attached to the cell membrane, they do not loose, and the T-cell action destroys the membrane. The membrane is calcified and becomes inactive. Each cell has about 1500 to 3000 membranes. Slowly they 're all going to die and then the cell will die.
Slowly it becomes more difficult for the cell and the concatenation of cells to keep the neurological conduction mode - we say that the ion pump of the cell is declining (the ion pump works really very nice - is an act of God ).
This process of lectin leakage should be stopped as much as possible. Wheat is particularly bad. The kernel has both gliadines and agglutinin, these are the two important proteins. The agglutenin are the lectins we saw above. But gliadines are also very bad. They trigger in the gut a protein called zonulin that breaks the film of the intestinal wall and makes it much more porous.
Therefore the first thing you should do is stop eating wheat (celiac diet). Also, do not take sugar and go low in saturated fat. My explanation is that these also make the gut film more porous.
Slowly, your body will replace the cells. With proper nutrition, vitamins, minerals etc new good cells with many new active membranes will be formed, powerful cells. And very slowly, the neurological path will recover. The crux of the matter now is to make sure that the degradation by lectins, which can never be completely prevented, is going slower than the growth of new cells. The recovery is a matter of years, just as the disease has come.
The neurological path is a serial circuit of brains and spinal and the peripheral nerves. In the progressive phase all is involved, the entire path. But in the ccsvi / RR phase (there is a completely different mechanism underlying) the neurological path will be weakened in brains and spinal cord. Therefore in the progresive phase, we decline much faster than anyone else.
I think this could well be correct. I can not remember the earliest incidences of my own MS history because they are too long ago, and I did not know anything about MS at that time. But I do remember a very heavy pressure on my head and in particular on the sinus during my last serious flare; and if I remember well it occurred over several subsequent years, always in the Spring/early Summer. I explained it for myself as a hay fever, as if I was developing an allergy… But this happened at 45/46/47 where I did not have any such reactions before. I remember I found it all a bit weird at the time, but now it finds an explanation here…
If I remember well, I even asked the neurologist who diagnosed me at 47. He responded that MS has no relationship to the sinus. Just as he said that massive chocolate consumption (see earlier posting) has no relationship to MS. With the knowledge of today, how wrong can you be...
[I remember he even went away to ask the older neurologists in the local hospital. I don't blame them. In family psychology, it is referred to as the fate of generations, this time of the neurological family...]
I looked also a bit on the staphylococcal infection on Wikipedia. Besides the toxicity argument of the article, I found that these bacteria can also cause micro-blood clots. And in fact that could cause further energy problems for the mitochondria, in particular if the BBB is breached and the endothelium is already weak. I do believe that the sinus infection is a factor in MS although it is not clear to me whether the sinus infection is causal or whether the infection is part of a bigger syndrome caused by weakened endothelial conditions in a bigger part of the head...
I have included the sinusitis in the new concept for MS on the first page..
look at this!!
From http://en.wikipedia.org/wiki/Wheat_germ_agglutinin , note that the Wheat Germ Agglutinin (WGA or lectins) bind to the cartilage, in our case to the lining of the inner nose! For others, it may be the cartilage between the joints. So far, MS and rheuma arthritis are the same disease, have the same cause. In the case of arthritis, the perfusion of the cartilage through the joints is low; for MS, the perfusion through the cartilage in the head (the sinus, the dural sinuses) is low.
Why is the perfusion through the dural sinuses low? Because they empty in the Internal Jugular Veins which in our case are blocked.
That is why the second stage of MS (the progressive stage induced by the leaky gut) starts with the very heavy pressure on the sinus. This was the case for myself. But apparently many others experience this problem (see above article in the box from Frederick Gay).
The article from Gay then suggests that Anti-staphylococcal antibodies detected antigen co-locating with IgG/C3d immune complexes in pre-demyelinating and in primary lesions. Where I would question whether these are really 'anti-staphyloccal' antibodies or antibodies fighting something else e.g. WGA.
What follows seems reasonable .. points to the involvement of a cocktail of transportable antigens leaking in a similar manner into the CNS from the paranasal sinus mucosal tissues where these molecules are conserved by the resident flora to manipulate and subvert the normal processes of local and systemic immunity.
Hence, the heavy pressure on the sinus that people apparently experience with the onset of their MS (as I did, my MS set on in the second progressive stage) can be seen as a confirmation of the New concept of MS with WGA/lectins breaking through the epithelial wall into the circulation and binding to the Cartilage in the head! The spill-over from the sinus immune complexes into the CNS does the rest. Clearly the broken BBB due to years of ccsvi is a necessary condition...
wow, another mystery uncovered...
The lectin connection
Posted: Sun Sep 29, 2013 10:50 am
by Leonard
What is the difference between a 35KDa (not-bacterian) antigen (Gay, 2013), a "small diffusible protein" (Gay, 2013) and a 38,000 Dalton WGA (Wikipedia on WGA)? Nothing! I think it is one and the same thing.
The meta-analysis by Frederick Gay in the above posting has under the introduction and the discussion strong evidences and useful leads.
The bacterial toxin hypothesis (Gay, 2007) postulates that MS is caused by the leakage of a cocktail of bacterial transportable toxins, intermittently released by the mocusal flora of the posterior paranasal sinuses into the extracellular fluid compartment (ECF) of the central nervous system. The sub-mocusal structures of ethmodial and spenodial cells not infrequently lie on optic nerve and contiguous basal dura without the protection of intervening bones (Gay, 2007).
The currently available data from genetic analysis of MS clearly points to a polygenetic susceptibility to immune dysregulation. But the failure to identify the specificity of the immunoglobulins or to link to any virus makes the matter intriguing.
In addition to the immune deviations, a remarkable miscellany of small diffusible proteins are produced that are directly toxic for neurons and oligodendrocytes by attacking membrane ion channels and a variety of membrane components to induce apoptosis (Dinges, 2000). Gay argues that recent analysis of the immunoglobulin variable region in B-cells, obtained from MS lesions, provides powerful evidence of an antigen-driven response and reinforces the hypothesis that unknown anti-genic targets, with specific aetiological relevance to MS, are implicated even in the earliest stages of the disease.
The discussion of the article explains the frequent proximity of MS plaques to the walls that has led many neuropathologists to speculate that demyelination could be related to a toxic agent with IgG/C3d immune complexes causing cellular activity. But the toxic agent was found not to be a bacterian antigen.
I think the WGA/lectins breaking through the epithelial walls are the missing piece of the puzzle. These small particles link first to the cartilage of the nasal tissue but then affect wider CNS compartments. In other words, the "small diffusible protein" in the meta-analysis of Frederick Gay may point to a complicity of lectins in the pathogenesis of MS
Lectins: a new dimension
Posted: Tue Oct 08, 2013 1:22 am
by Leonard
Are cancer and MS two sides of the same coin?
WGA/lectins attack membranes by forming a ring in the membrane. Some of the damage done is irreparable. This leads to a free diffusion of molecules in and out of the cell, and if enough poores are affected, the cell will not survive. This is called lysis. http://en.wikipedia.org/wiki/Membrane_attack_complex
The case of MS and a significantly reduced risk of cancer, and in particular colon cancer with an abundance of lectins available in the gut (before the blood passed and was processed by the liver), could point to an important role of lectins and the lysis/innate immunity to control cancer. The results of these studies, when taken together, are of epidemiological nature and thus very powerful. http://www.medicalnewstoday.com/articles/247220.php http://www.oncologypractice.com/oncolog ... 27a40.html
[The relationship of cancer with Type 2 Diabetes Mellitus is less clear, and results may be obscured because T2DM typically develops when people get older, just as cancer. http://www.biomedcentral.com/1471-2458/12/567 ]
This leaves me puzzled with a number of questions:
- Is there something (e.g. carbohydrates, cytokines) that is more expressed in cancer cells because they need an abundance of nutrition? Is this triggering the lectin mechanism to attack to kill the cancer cell, in its early stage?
- Likewise, are some (neuron, oligodendrocytes, myelin, Schwann) cells in MS patients in desperate need of nutrition, because of a mitochondrial energy failure caused by poor gut functioning (e.g. due to failure of large intestine vitamin production and absoption)? Is this triggering (by mistake) the lectin/innate immunity mechanism to kill the cell?
- Does our body make smart use of the lectins produced by nature that leak through the gut (now it is the small intestine), or does the liver also make its own lectins (as suggested on Wikipedia)?
- Are the membranes of neuronal cells in MS patients more vulnerable to the combination of carbohydrates/cytokines and/or lectins, or is the problem just the supply side / higher exposure to lectins from a "broken" gut?
- Is the calcification of veins at older age and the corresponding insulin resistance the result of lectin caused lysis?
- Has the liver a crucial gatekeeper role (to filter out and/or process lectins) as suggested by the case of the Kaukasian women with MS who got a new liver and recovered from MS?
- Is the innate immune system closely related to the lectin mechanism? (the lectin mechanism is one of mechanisms of the innate immune sytem as suggested by wikipedia with lectins produced by the liver, but this may be wrong and lectins may be plant based)
- Are cancer control and T2DM/MS "auto" immunity by the innate immune system the same, i.e. is the binding of killer lectins to control cancer the same thing as easy binding of killer lectins to neurons?
- And what is the role of carbohydrates and possibly other things (cytokines?) to influence lectin binding and how can that be influenced e.g. by low fat/no sugar diet (re: the double hit in inflammatory response)? And what is the role of other food that may disrupt the digestive tract (e.g. modern wheat)?
I don't exclude here the possibility that ultimately a new concept will prevail that embraces both autoimmunity and reactivity or that the understanding of things becomes so fluid that autoimmunity and reactivity loose their meaning...
Another candidate for the "small diffusable protein"
Posted: Fri Oct 18, 2013 2:15 am
by Leonard
Is this protoxin another candidate for the "small diffusable protein" in Gay's paper (see above postings)?
noted the 33 kD protoxin, fascinating...
I suppose this protoxin could also be a candidate for the mysterious 35kDa antigen in Gay's paper...
is it the sole mechanism or an additional one to the lectins?
are these toxic for the oligodendrocytes precursor cells (OPCs)?
is this the mechanism breaking down our myelin?
the treatment of Clostridium Difficile by Fecal Microbiota Transplantation (re: FMT, Borody) is common place these days and carried out around the world.
do the good results of Borody for patients with MS find an explanation here?