The standard model with its inconsistencies

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frodo
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The standard model with its inconsistencies

Post by frodo »

Given that most people around here is contrary to the accepted standard model of MS, I think is good to know its details and discuss its inconsistencies.

I have found a video that explains the model quite good (good explanation, even if it explains a bad model)

The link



First problem I notice is that they assume three different pathways for breaking the BBB. One for activated lymphocytes, other for b-cells and other for Th17 cells. Each of these cell cross the BBB with different pathways. I find more easy to accept that the BBB is previously weakened and they cross it without any problem.

Other thing that is not explained is the NAWM presence before the BBB breakdown.

Maybe we could make here a list of the problems that this standard model presents?
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Re: The standard model with its inconsistencies

Post by Rogan »

Two problems with the standard model.

1. Hasn't found a root cause in 50 years.
2. The model's entire evidence base is off of inflicting healthy mice with EAE.

Mice are not humans and humans with "MS" don't get EAE.
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Re: The standard model with its inconsistencies

Post by Cece »

No auto-antigen has been identified in MS.
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NHE
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Re: The standard model with its inconsistencies

Post by NHE »

Rogan wrote:Two problems with the standard model.

1. Hasn't found a root cause in 50 years.
2. The model's entire evidence base is off of inflicting healthy mice with EAE.

Mice are not humans and humans with "MS" don't get EAE.
...and EAE mice, aka the SJL/J strain, are pretty messed up to begin with.

http://jaxmice.jax.org/strain/000686.html
SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene resulting in decreased levels of dysferlin protein in SJL/J mice and making this strain a good model for limb girdle muscular dystrophy 2B. SJL mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice. SJL are immunocompetent but have elevated levels of circulating T cells.
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Re: The standard model with its inconsistencies

Post by frodo »

To restart the thread, here is a model of NMO. They have found the target of the autoantibody and they know how the BBB opens. As you can see, there is only one breaching point and one only reason for it.

For me, the main problem with the current MS model is that requires three or four unexplained breaks in the BBB.

http://www.nature.com/nrn/journal/v16/n ... 98_F4.html
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Re: The standard model with its inconsistencies

Post by 1eye »

I prefer the model of injecting the mice with CSF from MS patients. It works, and the mice get real MS-type lesions.
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Re: The standard model with its inconsistencies

Post by Rogan »

Reading the history of the autoimmune model's shows that it was just flawed conjecture from the start.

Has anyone read Dr. Michael T. Kennedy's book "A Brief History of Disease, Science, and Medicine"…it's not brief but it's very interesting.

Most doctors that come up with breakthroughs are laughed at, stolen from, and ridiculed their entire lives. It's been happening for 100's of years.

Anyhow, he mentions the history of "Autoimmune Diseases". Started in 1943 Arnold Rich at Johns Hopkins Hospital lumped a bunch of "serum sickness" diseases together. These were severe reactions to animal serums and the sulfa drugs didn't clear it up. So at autopsy they detected a new unseen lesion before. They linked this to a disease called "peri-arteritis nodosa" Gruber (1925) who thought it was an allergic reaction. It's an inflammatory reaction surrounding small arteries and is widespread in organs including heart and kidneys.

Then Kennedy writes something I don't understand.

"In 1946 Rich described the history of hypersensititvity and distinguished between the tuberculin reaction and immunization against soluble antigens such as diphtheria. He described the cases of periarteritis seen with sulfa drug-induced serum sickness and then outlined a connection between immune reactions and a group of diseases including rheumatic fever, periarteritis nodosa, and lupus erythematosis." He also mentions Henoch-Schonlein purpura.

I am not a doctor but these diseases sound like rashes, allergic reactions not MS.

And then reading Lewis Thomas's great book "The Youngest Science" he gets it wrong also. He writes:

"I became convinced that multiple sclerosis was an autoimmune disease, caused by the presence within the brain of antibodies directed against a component of brain tissue itself. It was a new idea in the 1930s. Tomas Rivers, George Packer Berry, and Francis Schwentker had shown five years earlier at the Rockefeller Institute that monkeys developed brain lesions resembling multiple sclerosis after being injected repeatedly with extracts of monkey brain tissue; their observation had been an accidental one, made in the course of attempts to develop vaccines against various viruses known to cause brain disease."

These were all the most gifted esteemed doctors of the day. They were primarily infection disease wizards. They could cook up a serum from an animal and save people's lives. They saw all problems being infections. They were good at experimenting with animals and solving human disease.

What if they had MRI then? What if they had trained as an Interventional Radiologists. What would they say today? I hope they would be open minded enough to say bag the old model it was really just lumping and speculation.
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Re: The standard model with its inconsistencies

Post by 1eye »

I am heartened that some real success on human subjects has been achieved with, of all things, a Vitamin, and not one of the usual ones recommended by doctors. Especially now our Canada Food Guide is under review as being obsolete and inadequate. It is time people started to get serious about nutrition. We can't help the 50% of people who are by definition below average, and who are the prime prey of people who sell artificial non-food in stores and at junk/fast/"food" outlets. But we can, if we are smart about it, help ourselves.

The Standard Model, which is anything but self-consistent, has evolved in reaction to the frequent attacks on it that come from rational individuals, in large part in attempts to square it with the results of pseudo-scientific experimental "evidence". Many of the diseases once thought to be the result of similarly virulent pathogens, are now thought of as genetic breakdowns like cancers, often attended by attacks from specific viruses and bacteria, but not necessarily directly caused by them.

Fortunately the 'old guard' will eventually become silent, and more modern science will take its place.
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Re: The standard model with its inconsistencies

Post by CureOrBust »

1eye wrote:I am heartened that some real success on human subjects has been achieved with, of all things, a Vitamin, and not one of the usual ones recommended by doctors. Especially now our Canada Food Guide is under review as being obsolete and inadequate. It is time people started to get serious about nutrition. We can't help the 50% of people who are by definition below average, and who are the prime prey of people who sell artificial non-food in stores and at junk/fast/"food" outlets. But we can, if we are smart about it, help ourselves.
The levels of Biotin used are not fixing a nutritional deficiency.
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Re: The standard model with its inconsistencies

Post by 1eye »

The levels of Biotin used are not fixing a nutritional deficiency.
I would not be surprised if they are treating a condition triggered by a very deep nutritional problem, such as a wipeout of gut flora, or a combination of that with serious nutritional deficits such as those created by junk food consumption. The disease may surface long after the deficits have been forgotten.
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"I'm still here, how 'bout that? I may have lost my lunchbox, but I'm still here." John Cowan Hartford (December 30, 1937 – June 4, 2001)
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