This Is MS Multiple Sclerosis Community: Knowledge & Support

1. Another local friend with MS had her fasting insulin level tested--it was in the moderately high range with 12.6.

2. In my attempt to gather further information about an MS-insulin connection, I received the following from an associate professor of biology: "The possibility that insulin might be involved in the etiology of MS is not new. There are citations dating back to the early 1950's on this topic."

Now I am trying to get my hands on some of these citations. Any suggestions?

hey LC i ran
insulin "multiple sclerosis"
at pubmed and there are hits from 2006 back to 1953. 10 pages of hits. the 1953 one didn't have an abstract and the thing says "article in undetermined language" (?!) but i think other refs will be useful
ttfn!

On July 10 Viper posted a link here to a PubMed abstract, "Insulin resistance, inflammation, and cognition in Alzheimer's Disease: Lessons for multiple sclerosis."

I got hold of the entire paper and heartily agree with this sentence from the Introduction: "Until recently, very little attention has been devoted to the relationship between MS and systemic insulin abnormalities such as diabetes and insulin resistance; however, emerging evidence suggests that this relationship deserves exploration."

There is much info in this paper--some we know already, such as "...brief corticosteroid therapy, an established treatment for relapsing-remitting MS, elevates plasma glucose and insulin levels and impairs memory.[10] These effects are reversed when corticosteroids are discontinued;...Collectively, these observations point to insulin abnormalities as a potential intervening factor in MS"

Section 2.3 MS, corticosteroids, and insulin resistance has more info than I can copy here. If interested, perhaps you can get a copy of this article in the Journal of the Neurological Sciences from your neurologist.

The quest to lower my insulin production continues, and to that end, I googled "pancreas" and found lots to read. In the Wikipedia material I found:

"Possible causes of hypoglycemia include:

* Oral hypoglycemic agents (e.g., any of the sulfonylureas, or similar drugs, which increase insulin release from beta cells in response to a particular blood glucose level).
* External insulin (usually injected subcutaneously).
* Ingestion of low-carbohydrate sugar substitutes (animal studies show these can trigger insulin release according to a report in Discover magazine August 2005, p18)." Here is a link to the entire article for those who care to read it:

http://www.discover.com/issues/aug-05/d ... weeteners/

I found the info on sugar substitutes particularly interesting (especially since Splenda affects me negatively); I have seen several articles claiming they are not good for MSers--perhaps because "they trigger insulin release"?

Now I have obtained the issue through the library and find it very good! You may find this info about sugar substitutes interesting, too: "There is only one sweet receptor ,...But unlike any other receptor in the body, it has more than one region that can be activated by different molecules. 'It's like having a gun with two triggers,' DuBois says."....

"Cyclamate is 45 times as sweet as sugar, aspartame and saccharin are 180 and 300 times as sweet, respectively, and sucralose [Splenda] is 600 times sweeter. But the next generation of aspartame, known as neotame, is 13,000 times as sweet as sugar, and other compounds have been isolated that are 100,000 times as sweet."....

"Sucralose, for instance, fits more snugly in the receptor than sucrose, partly because its chlorine atoms carry a stronger charge than the oxygen atoms they replaced. Neotame, which was recently approved by the FDA, locks in so tightly it keeps the receptor firing like a machine gun."

And, yes, "animal studies suggest that artificial sweeteners can also trigger the release of insulin--"

I realize that people find information that supports their beliefs--this is probable one more example. But everything seems to fit so well for me!

oo

There is an article on this forum about researchers not being able to distinguish diabetes and MS in a culture dish.

I have no idea how one determines if MS is in the dish, but someone answered the thread and said it is true. If a person wants to eliminate insulin resistance, eat no carbs or low carbs and a lot of insulin won't be released unless too much protein is consumed.

Lots of low carbers have found this out and many no longer need their insulin if they were diabetic before low carbing.

I have been on a low carb diet for years and have not seen any improvement of my MS due to this diet even though my sugar levels are always within the norm according to my blood tests.

People can believe anything that they want. As for myself, I admit to being totally ignorant as to the cause of MS and I have no faith that anyone else knows the cause either.

gwa

oo

Although some believe they know the cause of their MS, I do not (I only look for possibilities.); I only throw my ideas out there and welcome kind comments and suggestions from all. I don't take offense easily and I appreciate your thoughts, Lyon. I, too, see this site as a place to exchange ideas, to share frustrations, and perhaps to contribute to progress in this awful disease.

Concerning type 1 diabetes--we have heard that there is often a connection with MS, as you describe, Lyon (I was surprised by the low prevalence of type 1 in MSers.). You would be interested in this passage from the paper, "Insulin resistance, inflammation, and cognition in Alzheimer's Disease: Lessons for multiple sclerosis," (found only with the help of Viper and referenced above):

"In this review, we also asked how insulin abnormalities may relate to understanding and treating MS. MS increases the risk for type 1 diabetes mellitus; however, the low prevalence of type 1 diabetes in MS (~1-3%), limits the potential influence of this particular insulin abnormality to a small proportion of MS patients. In contrast, type 2 diabetes is common in the general population, and therefore, it is likely that many older MS patients are at risk for type 2 diabetes. This raises three questions for future studies. First, what is the prevalence of type 2 diabetes among patients with MS, expecially, older MS patients? Second, are there factors in MS, such as limited physical exercise, that may increase the risk for insulin resistance and type 2 diabetes? Third, does the co-occurrence of MS and insulin resistance or type 2 diabetes modify the extent or pattern of cognitive deficits observed in MS alone? In addition to the potential risk for developing type 2 diabetes, relapsing-remitting MS patients frequently are treated with intravenous corticosteroids, which induce reversible insulin resistance, hyperinsulinemia, and memory impairment. Future studies are needed to characterize the long-term effects of chronic exposure to methylprednisolone on cognition."

gwa--you may be interested in the passage above as well, since you follow a low carb diet and wrote: "If a person wants to eliminate insulin resistance, eat no carbs or low carbs and a lot of insulin won't be released unless too much protein is consumed. "

I also follow low carb, have a normal blood sugar level, but have high insulin levels (If tested, I'll bet your insulin would be high, too.). I think my pancreas simply malfunctions and secretes too much all the time (not just in response to high glucose.)

If only researchers would study the questions posed above, perhaps my suspicions could be removed! In the meantime, I appreciate your tolerance of my unconventional ideas. At least it gives me some satisfaction to express them; as a nonscientist, I feel helpless to make meaningful contributions, but I want to do SOMETHING!

I came across this tid-bit (and it is small) but this page appears to imply that b3 has some effect on insulin/glucose also. Read the third paragraph under "side effects and warnings"
http://www.mayoclinic.com/health/niacin/NS_patient-niacin

I just posted the following on the Tysabri forum and, although the discussion concerned Tysabri and Diabetes, I think the information is more appropriately located here. So here it is!

The online McGraw-Hill entry defines Metabolic Syndrome: "Starting in the 1960s and 1970s, researchers began to document a clustering of the elements of cardiovascular risk in certain patients. It wasn't until 1988 that a unifying cause--insulin resistance--was proposed and the term syndrome X applied. After several name changes over the past two decades, including the term diabesity used in lay publications, the name became metabolic syndrome."

At the labtestsonline site is "What is Insulin Resistance? Insulin resistance is a decreased ability to use insulin to transport glucose into the body's cells where it is needed for energy production. The pancreas tries to compensate for the cells' glucose deprivation by producing more insulin. The net result is elevated levels of insulin and C-Peptide in the blood along with normal or elevated glucose levels. Glucose, insulin, and C-Peptide levels may help your doctor diagnose this condition."

I think excess insulin may even lower glucose levels too low in some people to hypoglycemia.

Might that line from paragraph three, "...decreased ability to use insulin to transport glucose into the body's cells where it is needed for energy production," account for the fatigue associated with MS?

I try to understand the ideas around this disease, but I am NO scientist. Most of it is over my head. I keep thinking that maybe part of MS has as simple a discovery waiting as ulcers, Barry Marshall, and H. pylori(It did take 20 years for him to receive a Nobel Prize--just last year!) This hope was reinforced when I read on page 61 in The Language of God by Francis Collins about "Occam's Razor, a misspelled attribution to the fourteenth-century English logician and monk William of Ockham. This principle suggests that the simplest explanation for any given problem is usually best."

Then Lyon posted a link for the NMSS brochure, "The History of MS," on October 30. ( http://www.nationalmssociety.org/Brochu ... yofMS1.asp ) These thoughts came to me as I read it:

"Doctors of the time assumed the same disease rarely struck the same person twice because a disease “used up” the materials in the body it needed to live, much the way crops use up soil nutrients and die unless they are rotated."

Coming from a simple background, having lived on a farm as a child, I found the crop analogy comfortable. Perhaps this is the source of my simple-thinking.

Again according to the brochure: "At this time [first half of the twentieth century], scientists suspected that some form of toxin or poison caused MS. Because most MS damage occurs around blood vessels, it seemed reasonable that a toxin circulating in the bloodstream leaked out into the brain, even though no researcher could find a trace of it."

"Most damage...around blood vessels"--If scientists have known this for almost a hundred years, isn't it logical to start looking there again? (I feel ashamed that I did not know this before! This is MY disease--I should know the details of it! I have used the telephone-wire-and-insulation analogy too often!) How did researchers get away from looking at the circulation to all this complex "autoimmune" stuff? There certainly haven't been the big discoveries in that thinking that I would have expected if on the right track. Couldn't excess insulin "circulating in the bloodstream" start the cascade? I still think MS belongs under the jurisdiction of endocrinology and not neurology!

oo

Lyndacarol,

You've brought up some good points in this post and this is a good discussion you all have going here, very, very interesting.

Lyon, I read about the link of type II diabetes and Alzheimer's. My Mom had both, so naturally, I'm very careful to watch my risk factors for developing either of these. I don't even like to take IVSM, because it creates havoc with my blood sugar and they have to give me insulin shots when I'm in the hospital having the infusions.

_________________
Take care, Ewizabeth Previously Avonex, Rebif & Copaxone RRMS ~Tysabri, 31 infusions, ended 9/09. Starting Copaxone 12/09, waiting for Cladribine to be approved in 2010.

Thank you for your work to post the latest article, Lyon.

Some time ago I posted about Dennis J. Selkoe at Harvard who believes that an Insulin Degrading Enzyme (IDE) is involved with Alzheimer's. As well as insulin, the enzyme breaks down amyloid-beta (which is believed to accumulate in the brain as plaques which cause Alzheimer's), but the IDE is preferentially drawn to insulin. Excess insulin would occupy all the IDE, it seems to me, and almost guarantee Alzheimer's.

Mild Cognitive Impairment has been documented in MS; has anyone recorded how often full-blown Alzheimer's occurs in MS patients?

Recently (Oct 11) there was a Reuters article concerning work at the University of Chicago on this enzyme and how it may lead to new diabetes and Alzheimer's drugs. Given my belief in insulin's involvement with MS, maybe those same drugs would help us MSers.

I will find and post a link to the Reuters article for those interested.

Here is the article, "Pac Man enzyme key to new diabetes, Alzheimer drugs":

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