A new concept and treatment options for MS

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby Leonard » Sun Jun 19, 2011 5:15 am

I think you are right, excessive insulin is part of story as is ccsvi (as a birth defect). It is this combination of mechanisms that has made MS a disease so difficult to unravel.

I also think that the excessive insulin secretion probably has a relationship with the MGmin-LDL cholesterol that grows on sugar, is very sticky and seals our veins. It is the connected nature of the metabolism, in this case liver and pancreas..

Metformin seems to be able to break down the ultrabad cholesterol and help the insulin to take the glucose into the cells. This medication is part of the equation too.

And I agree, as my own case clearly demonstrates, you do not need to be diabetic (yet) to have the high insulin.
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Postby lyndacarol » Fri Jun 24, 2011 5:12 pm

I think the following information fits perfectly with Leonard's ideas of metabolism and especially his mention of the liver. This thread seems to be an appropriate place to post it:

On Wednesday, June 22, 2011, one of the topics on the TV program, The Dr. Oz Show, was the four negative results of eating too much sugar (which I have consumed since childhood, along with too many other simple carbs which become glucose in the bloodstream): 1) high blood pressure, 2) high cholesterol, 3) liver disease, 4) insulin resistance. I found it very interesting (especially part three with the information by Dr. Vos on liver disease, insulin spikes, and insulin resistance – which I believe are fundamentally involved in MS) and thought you might too:

http://www.doctoroz.com/videos/1-food-y ... -lose-pt-1

http://www.doctoroz.com/videos/1-food-y ... -lose-pt-2

http://www.doctoroz.com/videos/1-food-y ... -lose-pt-3


I do take exception to Dr. Oz's explanation that it is sugar in the bloodstream that damages the blood vessels. I know that insulin is a very caustic substance; I think it is likely, or even more likely, that excess insulin is damaging the blood vessels.
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Postby tara97 » Sun Jun 26, 2011 9:41 pm

if you want to understand neurology and the liver research acute intermitant porphyria. it is hepatic. even if you dont believe as i do that porphyria causes MS you would still understand a great deal by knowing this illness.
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Postby Yodi » Tue Jun 28, 2011 5:11 am

http://www.bbc.co.uk/news/health-13887909


An extreme eight-week diet of 600 calories a day can reverse Type 2 diabetes in people newly diagnosed with the disease, says a Diabetologia study.

Newcastle University researchers found the low-calorie diet reduced fat levels in the pancreas and liver, which helped insulin production return to normal.

Seven out of 11 people studied were free of diabetes three months later, say findings published in the journal.

More research is needed to see whether the reversal is permanent, say experts.

Type 2 diabetes affects 2.5m people in the UK. It develops when not enough insulin is produced in the body or the insulin that is made by the body doesn't work properly.

When this happens, glucose - a type of sugar - builds up in the blood instead of being broken down into energy or fuel which the body needs.

The 11 participants in the study were all diagnosed with Type 2 diabetes within the previous four years.

They cut their food intake drastically for two months, eating only liquid diet drinks and non-starchy vegetables.

After one week of the diet, researchers found that the pre-breakfast blood sugar levels of all participants had returned to normal.

MRI scans of their pancreases also revealed that the fat levels in the organ had decreased from around 8% - an elevated level - to a more normal 6%.

Three months after the end of the diet, when participants had returned to eating normally and received advice on healthy eating and portion size, most no longer suffered from the condition.

Professor Roy Taylor, director of Newcastle Magnetic Resonance Centre at Newcastle University and lead study author, said he was not suggesting that people should follow the diet.

"This diet was only used to test the hypothesis that if people lose substantial weight they will lose their diabetes.

"Although this study involved people diagnosed with diabetes within the last four years, there is potential for people with longer-standing diabetes to turn things around too."
Susceptibility question
Dr Ee Lin Lim, also from Newcastle University's research team, said that although dietary factors were already known to have an impact on Type 2 diabetes, the research showed that the disease did not have to be a life sentence.

"It's easy to take a pill, but harder to change lifestyle for good. Asking people to shift weight does actually work," she said.

However, not everyone in the study managed to stay free of diabetes.

"It all depends on how much individuals are susceptible to diabetes. We need to find out why some people are more susceptible than others, then target these obese people. We can't know the reasons for that in this study," Dr Lim said.

Professor Edwin Gale, a diabetes expert from the University of Bristol, said the study did not reveal anything new.

"We have known that starvation is a good cure for diabetes. If we introduced rationing tomorrow, then we could get rid of diabetes in this country.

"If you can catch people with diabetes in the early stages while beta cells are still functioning, then you can delay its onset for years, but you will get it sooner or later because it's in the system."

But Keith Frayn, professor of human metabolism at the University of Oxford, said the Newcastle study was important.

"People who lose large amounts of weight following surgery to alter their stomach size or the plumbing of their intestines often lose their diabetes and no longer need treatment.

"This study shows that a period of marked weight loss can produce the same reversal of Type 2 diabetes.

"It offers great hope for many people with diabetes, although it must be said that not everyone will find it possible to stick to the extremely low-calorie diet used in this study."

Dr Iain Frame, director of research at Diabetes UK, which funded the study, said the diet was not an easy fix.

"Such a drastic diet should only be undertaken under medical supervision. Despite being a very small trial, we look forward to future results particularly to see whether the reversal would remain in the long term."
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This is MS!

Postby Leonard » Mon Jul 11, 2011 2:14 am

This entire thread is built on the presumption that MS is a two stage disease.
This article confirms that idea: http://brain.oxfordjournals.org/content ... 0.abstract

The thread also suggests a link between diabetes and MS.
In this presentation, diabetes and MS are mentioned in one breadth (see slide 4).
http://excellence-in-rheumatology.org/s ... IAMOND.pdf

The presentation argues that the auto-immune hypothesis should be revisited:
from autoimmunity to an environmentally triggered immune disease.
The cause: the segmented filamentous bacteria (see slide 32).
The fact that MS is veno-centric support this view.
http://ccsvism.xoom.it/timeline_en.html see Thorben Fog

In this thread, we knew that MS was a metabolic disease and we were already down to the liver.
It is these segmented filamentous bacteria (SFB) from the bowel (gut/liver) that induce the immune system response in the brain.
http://en.wikipedia.org/wiki/Segmented_ ... s_bacteria
http://www.ncbi.nlm.nih.gov/pubmed/19833089

This chronic infection explains the bowel problems and coping strategies in people with multiple sclerosis.
http://cirrie.buffalo.edu/database/116358/
Apparently the chronic infection of the bowel by the SFB can be treated effectively by antibiotics. :D

In summary, I think it is this combination of vascular narrowings (possibly already from birth) and weakening of the tissue in the veins combined with the SFB that cause the MS. Things can be treated, by angioplasty and antibiotics. I would advice every one to ask his or her doctor about this. That is what I have done.
Last edited by Leonard on Mon Jul 11, 2011 3:04 am, edited 3 times in total.
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candida linked to type 2 diabetes

Postby fee001 » Mon Jul 11, 2011 2:40 am

Hi

Candida causes, sugar cravings and is linked to type 2 diabetes.

Google Candida, obesity, infertility, fatigue, rheumatoid Arthritus

CANDIDA is linked to many many conditions and that is why it should be public knowledge, doctors actively deny it due to its antibiotic link, this in my oppinion is a castrophic mistake as many have the condition, but are not aware of it. As I wasnt either and I probably had it for years, cant prove it though.

As for the restricted blow flow in the neck, mine was restored after Chiropractic Atlas adjustment.

Make up your own minds as to what is going on here.
I do my own research, and find my own answers Its good to talk
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Postby tara97 » Tue Jul 12, 2011 8:08 am

@ fee001 you still have to ask the question why am I so suseptable to bacteria while others are'nt so there must be a genetic factor because noone around me eating the same food living the same life is getting these infections. take the gastric ulcer for instance. they say that it is caused by an H-pylori infection but how would H-pylori thrive in the acidic environment of the stomach unless there were something impared about the secretion of gastric acid at one point. gastic acid is stimulated by cortisol this is why prednisone give one heart burn and acidic diarea btw.

I stongly believe that infections are a symptom not a cause. I have watched my tests and how sometimes my white blood cells are elevated. and one week later without any antibiotics there are not elevated. My unharnessed immune system is stopping these infections. it is not meant to stop infections with out cortisol to oversee this.

It is my belief that the waxing and waning motion we experience is from first prolonged supression of the immune system by the chronic elevations of cortisol to cortisol exhaustion and then the unharnessed immune response where cortisol is in too short of supply to keep things in check. the cause of the prolonged elevation of cortisol lies on an acute intermittent porphyria website. the neurological problems also lie there. cortisol drives down insulin but over time insulin resistance may occur also the excess nitrogen from the porphyrin may make for a bacteria rich environment. then when the body triess to recover it causes another acute porphyria attack which then hits the process all over again.

This also causes electrolyte imbalences as cortisol moves sodium into the cell and potassium out and eventually this will cause an intercellular magnesium deficiency and callcium load in the cell cause the sense of nervousness, tremors and eventually muscles will freeze in the contracted possition.

Before when we had our first attack our adrenals and organs could handle the hit and restore homeostasis. the more we are hit, the harder it was to rebalence and we wax and wane and deteriorate as these imbalences worsen.
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Postby lyndacarol » Mon Jul 18, 2011 6:05 pm

I have long believed in an "excess insulin hypothesis." This evolved into a "metabolic hypothesis" because hyperinsulinemia (or insulin resistance) is considered part of metabolic syndrome. Now I have discovered another branch and I encourage those people who think along similar lines to google "skeletal muscle insulin resistance." There has been LOTS of research in this area and LOTS of papers written (I am still reading through these.).

And under "treatment for skeletal muscle insulin resistance" I admit I find it hard to explain this report: http://diabetes.diabetesjournals.org/co ... 7.abstract If skeletal muscle insulin resistance is part of MS, how can heat (known to aggravate MS temporarily) be a positive and reduce SM insulin resistance? Or might this partly explain the lower prevalence of MS near the equator (where temperatures are warmer)?

Nevertheless, I think Leonard et al. will find this information interesting.
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Postby fee001 » Mon Jul 18, 2011 9:44 pm

Tara97

Get checked for Candida which causes leaky gut and numerous other problems, it can invade your whole system and have many affects..

Fiona
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Postby Cece » Wed Jul 20, 2011 8:07 am

www.neurology.org/content/45/12/2261.abstract
Effects of unbalanced diets on cerebral glucose metabolism in the adult rat
http://www.neurology.org/cgi/content...act/45/12/2261

Quote:
From the Departments of Neurology (Drs. Al-Mudallal and Harik) and Neurological Surgery (Dr. Lust), Case Western Reserve University School of Medicine, Cleveland, OH; and the Neurology Service (Dr. Levin), VA Medical Center, and Department of Neurosciences, New Jersey School of Medicine and Dentistry, Newark, NJ.
Supported in part by USPHS grants HL 35617 and AM 30066 and by the Research Service of the Department of Veterans Administration.
Received December 6, 1994. Accepted in final form March 28, 1995.
Address correspondence and reprint requests to Dr. Sami I. Harik, Department of Neurology, University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 500, Little Rock, AR 72205.

We measured regional cerebral metabolic rates for glucose and selected cerebral metabolites in rats fed one of the following diets for 6 to 7 weeks1) regular laboratory chow; (2) high-fat, carbohydrate-free ketogenic diet deriving 10% of its caloric value from proteins and 90% from fat; and (3) high-carbohydrate diet deriving 10% of its caloric value from proteins, 78% from carbohydrates, and 12% from fat. In preliminary experiments, we found that moderate ketosis could not be achieved by diets deriving less than about 90% of their caloric value from fat. Rats maintained on the ketogenic diet had moderately elevated blood beta-hydroxybutyrate (0.4 mM) and acetoacetate (0.2 mM), and a five- to 10-fold increase in their cerebral beta-hydroxybutyrate level. Cerebral levels of glucose, glycogen, lactate, and citrate were similar in all groups. 2-Deoxyglucose studies showed that the ketogenic diet did not significantly alter regional brain glucose utilization. However, rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization and increased cerebral concentrations of glucose 6-phosphate. These findings indicate that long-term moderate ketonemia does not significantly alter brain glucose phosphorylation. However, even marginal protein dietary deficiency, when coupled with a carbohydrate-rich diet, depresses cerebral glucose utilization to a degree often seen in metabolic encephalopathies. Our results support the clinical contention that protein dietary deficiency coupled with increased carbohydrate intake can lead to CNS dysfunction.

eat your protein....
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Postby Cece » Wed Jul 20, 2011 8:08 am

I pulled that article from this thread, on a social anxiety forum, lots of interesting research posted there.

The brain glucose metabolism link with dopamine <shortened url>

omega 3s contribute to the production of ketone bodies which are an alternate source of energy for the brain when glucose is limited, as it may be in CCSVI.
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Postby fee001 » Wed Jul 20, 2011 9:10 am

TARA97

You may have a problem getting tested for Candida, as Doctors deny its existance due to it having an antibiotic link, although it can be caused by poor diet or stress. It does exist though

I have posted details on candidiasis on here, take a look at symptoms and if it fits. then ask to be tested.

Fiona
I do my own research, and find my own answers Its good to talk
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Postby MegansMom » Wed Jul 20, 2011 12:43 pm

No matter what the fuels are if the "transit time" ( meaning the time it takes oxygenated/ glucose rich blood to get into the brain, be used up and exit) is delayed the cells starve. If they starve long enough they get injured, and if that continues the cells die.
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My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-
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Postby lyndacarol » Sat Jul 23, 2011 12:44 pm

In keeping with Leonard's thoughts, and in refining my ideas on the MS process, I now think that "insulin resistance hypothesis" is more appropriate than "excess insulin hypothesis" as the starting point.

The following article describes insulin resistance, and the list of symptoms even includes hemochromatosis, which others on this website have long suspected of being involved in their MS diagnosis:

http://www.news-medical.net/health/What ... tance.aspx

In the following article, the Yale researcher describes his hypothesis for insulin resistance:

"Our hypothesis was that the metabolic syndrome is really a problem with how we store energy from food," Shulman explained. "The idea is that insulin resistance in muscle changes the pattern of energy storage."

After providing the study's subjects with two meals high in carbohydrates, Shulman and his colleagues turned to magnetic resonance spectroscopy to measure the production of liver and muscle triglyceride, the storage form of fat, and of glycogen, the storage form of carbohydrates. "What we found is that (insulin) sensitive individuals took the energy from carbohydrate in the meals and stored it away as glycogen in both liver and muscle," said Shulman.

In the insulin resistant subjects, the energy obtained from their carbohydrates rich meals was rerouted to liver triglyceride production, elevating triglycerides in the blood by as much as 60 percent and lowering HDL cholesterol (the good cholesterol) by 20 percent. "In contrast to the young, lean, insulin-sensitive subjects, who stored most of their ingested energy as liver and muscle glycogen, the young, lean, insulin-resistant subjects had a marked defect in muscle glycogen synthesis and diverted much more of their ingested carbohydrate into liver fat production," Shulman and his colleagues reported.

"What we see," he noted, "is alterations in patterns of energy storage. An additional key point is that the insulin resistance, in these young, lean, insulin resistant individuals, was if MS independent of abdominal obesity and circulating plasma adipocytokines, suggesting that these abnormalities develop later in the development of the metabolic syndrome."

The new findings promise to help untangle the early molecular events of a syndrome at the root of one of the world's most significant health issues. "Knowing how insulin resistance alters energy storage before it leads to more serious problems can help those susceptible prevent the onset of the metabolic syndrome," Shulman said.

Another key observation was that skeletal muscle insulin resistance precedes the development of insulin resistance in liver cells, and that fat production in the liver is increased. "These findings also have important implications for understanding the pathogenesis of nonalcoholic fatty liver disease, one of the most prevalent liver diseases in both adults and children Shulman said.

http://www.news-medical.net/news/2007/07/17/27656.aspx

This focus on energy storage is reminiscent of Dr. Terry Wahls' ideas on mitochondria. Dr. Shulman's comment that insulin resistance alters energy storage before leading to more serious problems suggests to me that insulin resistance may be the culprit leading to MS. Apparently, skeletal muscle insulin resistance is the first step toward general insulin resistance (and then MS? Nonalcoholic fatty liver disease? Other "autoimmune diseases?").

I find hope in the article's conclusion that exercise can counter skeletal muscle insulin resistance, I need to find time for more exercise!

If insulin resistance is implicated in MS, then the causes of insulin resistance will be important to us too:

Since I have suspected that glucosamine, a sugar-based supplement, and all artificial sweeteners stimulated the pancreas to produce insulin, I found the article's sentence especially interesting:

http://www.news-medical.net/health/Caus ... tance.aspx

An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance.


Has anyone seen this "American study?"
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Postby tara97 » Mon Jul 25, 2011 1:35 pm

your right linda. I agree with the excess insulin. my theory goes with yours because cortisol drives down insulin so the question is does low cortisol equal high insulin. i am telling you porphyria with secondary adrenal insuficiency and from there it is infinite. porphyria causes an instable energy metabolism. imagine if heme sythesis were disrupted what would that do to everything.
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