This Is MS Multiple Sclerosis Community: Knowledge & Support

I thought IGF-1 was the "signaling factor" for insulin's cellular transmission and that it's different from insulin.... but I could be wrong.

Folks have tried to use IGF-1 to repair myelin before, but it's hard to get it past the BBB, so they used a virus as a transport mechanism in Lynda's study mentioned above. And the IGF-1 didn't do anything.

Here's a study from the Netherlands where they injected IGF into MSers..notice it states IGF is a growth factor that "should" provide signals to repair MS lesions....but it didn't.

Insulin-like growth factor (IGF)-1 is a growth factor that should provide the appropriate signals to promote repair of MS lesions, because it acts as a survival factor for cells of the oligodendrocyte lineage and stimulates myelin synthesis. In a pilot study on MS patients, no detectable remyelinating effects in the CNS were observed following subcutaneous administration of IGF-1. A number of reasons might explain a lack of beneficial effects: a) it is unlikely that subcutaneous administration of IGF-1 provides sufficient passage across the blood-brain-barrier and into the CNS, b) the biological actions of IGF-1 are tightly regulated by several insulin-like growth factor binding proteins (IGFBPs), which become upregulated in the demyelinated lesions and may prevent access of IGF-1 to its receptor, c) IGF-1 not only acts on oligodendrocytes, but also stimulates the proliferation of astrocytes, which form the glial scar that impedes repair processes.
link

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

That does not make it the same. Many people have warm milk to help them sleep, and others have warm milk in their coffee, but a coffee is very different to a glass of warm milk.

With diabetics injecting insulin every day, why are there studies on the effects of specific IGF-1? I think its because they are very different, and I have yet to read any scientific study saying they are in effect the same. I explicitly read effects for IGF-1, that are not suggested for "plain old" insulin. and I have also read how IGF-1 is different to the other IGF's (ie IGF-2, IGF-3 etc)

But IGF-1 will bind to components that insulin will not.

but all the studies treat IGF-1 very differently to insulin, and I have yet to read the exact same effects for insulin, that are seen with IGF-1. A pure and concentrated component of something is not the same as what it is derived from.

IGF isn't the same as insulin, the first promotes myelination the second (from what have read) does the opossite!

I do not mean to usurp a book recommendation from Sharon (Shayk); but I think The MS Solution: How I Solved the Puzzle of My Multiple Sclerosis by Kathryn R. Simpson, M.S. has important information for us--including about insulin, which is also a hormone. I import a post here from another forum because of this insulin connection:

"Sharon (Shayk) is absolutuly right when she said, Quote:
I've been reading more about thryoid issues lately and I do think it wouldn't hurt to ask your GP about it again. End quote.
This is something I intend to do after reading the book The MS Solution by Kathryn R. Simpson.

Overall, the book has good ideas, especially about checking hormone and vitamin/mineral levels. I take exception to her statement on IGF-1 on pages 141-142. Quote:
Growth hormone production is highest at puberty and declines progressively after age 21. Made in your pituitary, it stimulates bone and organ growth. It causes increased production and release of a substance called insulin-like growth factor 1 (IGF-1), which travels to target tissues such as bones, organs, and muscles to trigger growth and repair. It has also been shown to promote growth of myelin and nerves. End quote.


I prefer to believe the research reported in the recent Winter 08-09 issue of Momentum, publication of the NMSS (I am generally skeptical of this group and its projects), which addressed this idea with the following:

"The growth factor IGF-1 had shown some success in promoting myelin formation, so a Society-funded team led by Stephane Genoud, PhD (The Salk Institute, La Jolla, Calif.), injected it into mice with EAE. The injections actually WORSENED the disease. (Journal of Neuroimmunology 2005; 168:40-5) Such failures are important to pinpoint before they affect people with MS in clinical trials."

Here is the abstract of the work mentioned:

1: J Neuroimmunol. 2005 Nov;168(1-2):40-5. Epub 2005 Aug 24. Links
Targeted expression of IGF-1 in the central nervous system fails to protect mice from experimental autoimmune encephalomyelitis.Genoud S, Maricic I, Kumar V, Gage FH.
Laboratory of Genetics, The Salk Institute, 10010 N Torrey Pines Rd, La Jolla, CA 92037, USA.

Insulin-like growth factor 1 (IGF-1) has been identified as a critical molecule in the induction of myelination in the central nervous system (CNS). Systemic injection of IGF-1 has been shown to have a varied and transiently protective effect on the clinical course of experimental autoimmune encephalomyelitis (EAE). Since systemic IGF-1 can also modulate peripheral immune lymphocytes, we examined whether a sustained and local delivery of IGF-1 into the spinal cord would have any influence on the chronic course of EAE in C57/BL6 mice. The capability of adeno-associated virus (AAV) to be retrogradely transported efficiently from muscle to motor neurons of the spinal cord was used to overcome the difficulty routinely encountered when attempting chronic delivery of molecules into the CNS. We demonstrate that AAV-mediated delivery of IGF-1 in CNS did not have any beneficial effect on the clinical course of EAE. Injection of AAV-IGF1 after induction of the disease worsened the clinical symptoms. Furthermore, CNS expression of IGF-1 did not affect the pathogenic anti-MOG T cell response, as examined by proliferation and cytokine secretion. Thus, enhanced expression of IGF-1 in the CNS during inflammation does not have a significant effect on myelination. These data have important implications for the potential use of IGF-1 in the treatment of multiple sclerosis.

PMID: 16120466 [PubMed - indexed for MEDLINE

It's another one of those areas that deserves more examination!"

I felt these ideas needed to be with this forum--even if repeating the abstract, so I can find them again easily. I lose things so often! How do you folks keep track of things here?!!!

LC you probably have known this forever but you can filter the search by individual posts instead of topic and it's waaaay easier to find your own stuff. still a touch confusing when you start getting into the results but yea.

I am still trying to reduce my insulin level, so I found the episode of "60 Minutes" shown on Sunday, May 24, 2009, especially interesting because of this comment at the end of the segment on resveratrol: To view or read the entire segment see:http://www.cbsnews.com/stories/2009/01/25/60minutes/main4752082.shtml

The following article appeared in the September 2010 issue of the AARP Bulletin, although online it is attributed to the May issue.

http://www.aarp.org/health/conditions-t ... sease.html

This article does not mention Dennis J Selkoe (whose ideas were discussed on page 5 of this thread), but I think his ideas are fundamental to this new hypothesis that Alzheimer's disease is the result of clumps of amyloid beta protein called oligomers.

I continue to believe that excess insulin plays a key role in both MS and Alzheimer's. In Alzheimer's Disease, the Insulin Degrading Enzyme (IDE) is drawn first to the insulin (and used up in breaking down that hormone) and then is not available to break down the amyloid beta, allowing it to accumulate in the brain.

In MS, excess insulin is circulating in the bloodstream, causing damage to the blood vessels, even permeating the blood brain barrier, and triggering the immune system (including cholesterol deposits intended to repair the damage, but which may account for narrowing, i.e., stenosis).

I agree. I have hypoglycemia. I believe that cortisol drives down insulin and so in its exhaustion insulin might have its way. I hate insulin cuz it makes me so nervous and angry. insulin is a key that unlocks the cells so energy can enter. look up cortisol on wikipedia and then see all the things that that hormone is responsible for and in its absence would be disasterous. one thing is the prevention of the proliferation of T cells. another is that it moves sodium into the cells and potassium out. another is moving gastric acid into the stomach. what happens without the acid is too much bacteria and in my opinion too much vitamin K =highplatelets and too much folate also would disrupt B-12 there in the gut. it goes on and on but these hormones are the key YES!!

Although I posted the following information a few months ago to Leonard's thread, "I think I found it…," I feel that the information is also relevant to ideas in this thread:

I now think that "insulin resistance hypothesis" is more appropriate than "excess insulin hypothesis" as the starting point for MS.

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:



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



Has anyone seen this "American study?"

I have not seen the study they refer to. Interestingly, the Mayo Clinic recently noted on their site that glucosamine does not affect insulin resistance. The references are near the bottom of the page linked below.




NHE

NHE – a few more thoughts:

It is my understanding that "hyperinsulinemia (excess insulin)" is synonymous with "insulin resistance." The news-medical article stated "An American study has shown that glucosamine (often prescribed for joint problems) may cause insulin resistance."

Perhaps glucosamine does not raise blood glucose, just as the Mayo Clinic article does state (thank you so much, NHE, for that information), but affects only the pancreas and its insulin secretion.

Several years ago I read a Discover magazine article on artificial sweeteners; it was mentioned that artificial sweeteners increased insulin production in a mouse study. I suspect the same happens with humans. (Elsewhere, I have read that even a sweet sensation in the mouth causes the pancreas to secrete insulin.)

Although blood glucose is most commonly the trigger for insulin secretion, there may be MANY other reasons for the pancreas to pump out the hormone – the "sweetness" of artificial sweeteners, even infection of the pancreas by a virus or bacteria (even the inflammation of pancreatitis). I think the damaging culprit is insulin, not necessarily glucose.

Just sharing a few of my thoughts.

Hi Lynda,

.. and the insulin resistance is caused by the ligands that block the Vitamine D nuclear receptor.
The glucose transport will be inhibited.
And the poor cells will die (long term); or as a minimum the ion pump will not be charged (fast) enough (short term) giving typical symptoms..
The whole pallet of inflammatory diseases will need to be "re-engineered".
http://www.discoverymedicine.com/Shaopi ... infection/

The VDR dysfunction is the culprit of MS; of course the vascular narrowings in the neck cause the BBB to break creating the right conditions for MS to develop..
see this page (18) at
general-discussion-f1/topic15188-255.html

Leo

"Mike" might disagree that glucosamine does any harm to MSers.(SEE BELOW)

jackD

Lynda, could you please have a look at this: http://intelegen.com/nutrients/insulin_ ... weight.htm

and in particular at its recommendations:

A total approach to insulin resistance requires an understanding of its multifaceted aspects and the increased necessity for nutritional and lifestyle interventions. The use of diet, exercise, nutritional supplements and medications such as metformin are central not only to restoring metabolic balance, but for biological age reversal and life extension as well. The following program is recommended for optimal results.

1. Follow a low glycemic or BDK diet

2. Exercise regularly

3. Take 200-800 mcg of chromium and 50-150 mcg of vanadium daily

4. Take 500 mg of metformin two or three times per day or five to six capsules of VRP's GluControl.

What is your appreciation? does it resonate with things in your thread?

Leo

http://www.hardickchiropractic.com/inde ... order.html
Dr. Hans Michael Dosch, the study’s principal investigator and senior scientist at SickKids in Toronto, had previously concluded in a 1999 paper that there were surprising similarities between diabetes and multiple sclerosis, a central nervous system disease.

well, that's what the establishment might have liked... whow what prospect for study..

but the reality of course is that it is just the other way around: that multiple sclerosis is, just like diabetes, not a neurological disorder but a metabolic disease with some neurological "side" effects
(see for instance general-discussion-f1/topic15188.html ).