This Is MS Multiple Sclerosis Knowledge & Support Community

Lisa--

I definitely like them, not sure if it's because of the hormone connection or the naltrexone connection though. I've mostly viewed LDN through the "glutamate toxicity" lense so I find the abstracts fascinating.

With regard to the issue of insulin and diabetes, there's this abstract Effects of DHEA Replacement on Insulin Sensitivity and Lipids in Hypoadrenal Women

Animal studies have shown that DHEA administration prevents diabetes.

In conclusion, replacement therapy with 50 mg of DHEA for 12 weeks significantly increased insulin sensitivity in hypoadrenal women, thereby suggesting that DHEA replacement could have a potential impact in preventing type 2 diabetes.

Unfortunately, absent any medical or scientific background, I don't even know the difference between "insulin sensitivity" and "hyperinsulinemia" so I definitely hope Lynda Carol weighs in on this.

A couple of comments on DHEA. (1) That abstract suggests it may prevent type 2 diabetes. There were 2 successful Phase I Clinical Trials of DHEA for MS. DHEA is low in people with MS. (2) The topic of "hypoadrenals" and/or something's wrong with the adrenal glands in people with MS is a huge question of mine.

The mere fact that DHEA is low in people with MS (it's produced in the adrenal glands) and that a higher percentage of women than men with MS had low testosterone levels (most testosterone in women comes from the adrenals) are two of the things that really make me wonder even more about any relationship between adrenal functioning and MS. Of course, cortisol (the stress hormone) comes from the adrenals as well and it produces "glutamate toxicity". I think DHEA is the natural antagonist of cortisol.

Take care all--I do think there's probably a connection between "hyperinsulinemia" and hormones but it's definitely beyond my comprehension.

Sharon

Hot off the presses...

MS linked with Type 1 Diabetes

also, given inflammatory bowel disease has been linked with MS, this might be salient to this discussion:

Patients with refractory Crohn's disease or ulcerative colitis respond to dehydroepiandrosterone: a pilot study.

First of all, Sharon, I apologize that I am so slow to answer with definitions.

As a nonscientist, I have been trying to come up with definitions of hyperinsulinemia and insulin sensitivity that are simple, but accurate. I will do my best to explain my understanding; I invite those health professionals here to jump in with their preferred definitions. And, by all means, correct any misinformation I have, please.

According to the Mayo Clinic website, "hyperinsulinemia means you have too much insulin in your blood."

As for insulin sensitivity, I think it is necessary to understand the ideal role of insulin and the aberrations of Insulin resistance (see Wikipedia at http://en.wikipedia.org/wiki/Insulin_resistance ) and Metabolic syndrome at http://mayoclinic.com/health/metabolic% ... me/DS00522 (I think these two are one and the same thing).

In the case of MS, I think the cells are 'in'sensitive to insulin, causing the pancreas to secrete greater amounts of insulin in an effort to prompt the cells to take in the accompanying glucose. I think this excess insulin in the blood stream is causing initial damage that leads to MS diagnosis--even causiing damage to the blood vessels themselves which we sense as "tingling" (paresthesia), even irritating the bladder into spasm and incontinence, and other "MS" symptoms.

I am still trying (unsuccessfully so far) to reboot my pancreas back to normal secretion; as I have said before, diet hasn't done it for me (even after adding 1/4 teaspoon of cinnamon to my morning tea since reading "Cinnamon Extracts Boost Insulin Sensitivity" at http://www.ars.usda.gov/is/AR/archive/j ... 0.htm?pf=1 ); neither has Vitamin D (see Dr. Yadhu Singh's article in US Pharmacist referenced earlier here--I appreciate info from jimmylegs that connected me to D!). But I persist with both and remain confident this is the right track!

That is the beauty of this site--we can each search and share and try to help each other in our individual searches and respect the choice of each. And, most of all, be supportive of one another.

lyndacarol wrote:I am still trying (unsuccessfully so far) to reboot my pancreas back to normal secretion; as I have said before, diet hasn't done it for me

Not that i would ever support an overdose on any vitamin, but I read the following, and thought of you. Being the resident Insulin info junkie, its probably not news to you.

One Symtom/Risk factor of overdose on Biotin, is "Reduced / slowed insulin release". Biotin would clearly have some effect on insulin. I found this at:
http://www.acu-cell.com/bx2.html

Thank you, Cure, for thinking of me! This is JUST the way I imagine this site will work--the info you supplied was news to me! Although I have this obsession with insulin, I readily admit that there is LOTS I don't know! I appreciate anything you can offer to educate me further!

I must look into this connection of Biotin and insulin! If anything, I seem to qualify for a deficiency--unusual, temporary hair loss about a year ago, brittle nails, loss of appetite (for YEARS now), and other symptoms to smaller degree. It is not in the B Complex I take each day; I wonder if there is a blood test for Biotin that I can request of my internist.

you can get b-complex with biotin and inositol etc, i haven't seen a complex without em in a long time. they can test for biotin lc:

<shortened url>

I have MS and just like many others, I have hypoglycemia attacks. Just the opposite of diabetes mellitus. Go figure.....

hey lc have we seen this one before? insulin mentioned wrt rls.

Nutritional Influences on Illness

by Melvyn R. Werbach, MD

Restless Legs Syndrome

This syndrome is marked by an unpleasant crawling or aching sensation in the lower legs, between the knee and the ankle, often accompanied by restlessness in other parts of the body, especially in the flexor muscles of the arms and legs. The discomfort appears only at rest and elicits an irresistible need to move the limbs. It generally appears in the evening and early night and may be associated with severe insomnia.1

While, as usual, most of the research is preliminary, the results of studies
investigating the effects of nutrients on restless legs syndrome (RLS) suggest that it has several causes, and that patient-specific dietary changes, nutrient repletion and nutrient pharmacotherapy are often effective treatments.

Dietary Factors

Based on afternoon glucose tolerance testing, many patients with RLS,
particularly if they also have spontaneous leg cramps, appear to have
hyperinsulinism causing functional "hypoglycemia" during testing, in fact,
occasional patients may have an attack of muscle cramps concomitantly with their lowest level of plasma glucose. In an open trial, a group of 350 patients with this type of glucose tolerance curve were placed on a sugar-free, high protein diet along with frequent nibbling and at least one night feeding. The vast majority experienced a prompt remission or, at least, a striking reduction in symptoms.2

Caffeine has been shown to increase subjects' proneness to develop symptoms at lower levels of blood glucose.3 It is therefore no surprise that a xanthine-free diet (no coffee, tea, cola beverages, cocoa) has been reported to be another effective dietary measure - sometimes following a short period of caffeine withdrawal.1

Vitamins

RLS may also be an early neurologic manifestation of folate deficiency, the most common of all the vitamin deficiencies. Often the deficiency is not due to a poor diet, but to a genetic factor causing a folate dependency. While not all RLS patients complain of uncomfortable sensations, folate-deficient patients always suffer from them.4 Since high doses of folic acid (5-30 mg daily) appear to be needed to normalize folate nutriture and induce a recovery, baseline lab testing and follow-up along with medical supervision is advisable.

Vitamin E supplementation has been reported to be effective in several case reports. For example, in a group of 9 patients, 7 had complete relief following supplementation, one had almost 75% relief and one had 50% relief.5 About 300 IU daily appears to be effective, although it may take up to three months for the full benefit to become apparent.6

Minerals

Iron deficiency, which is known to cause akathisia (restlessness) may
theoretically cause restless legs syndrome by reducing dopaminergic and opiate neurotransmission.7 Indeed, in one study, 25% of a group of RLS patients had a low serum iron, while 24% of a group of patients with iron-deficiency anemia had RLs.8 Iron-deficient patients respond well to supplementation. Two months after 15 such patients had begun to take ferrous sulphate 200 mg. 3 times daily, the patients whose serum ferritins were lowest initially improved the most.9

Magnesium deficiency, which is known to increase neuromuscular excitability, can also cause the syndrome.10 Once again, repletion should be effective.

Other Nutrients

The primary role of the neurotransmitter serotonin in the central nervous
system is said to be the modulation and facilitation of skeletal muscle
function.11 If serotonin regulation plays a role in RLS, supplementation with L- tryptophan, serotonin's nutritional precursor, could therefore be of value. While tryptophan supplement needs to be studied further, it did appear to be effective in the treatment of two RLS patients even though they had failed to respond to numerous medications.12

Summary

Evaluate your patient for functional "hypoglycemia," and deficiencies of folic acid, iron or magnesium, and treat as indicated. If these specific
abnormalities are not found, consider trials of vitamin E and L-tryptophan.

Doctor Werbach cautions that the nutritional treatment of illness should be
supervised by physicians or practitioners whose training prepares then to
recognize serious illness and to integrate nutritional interventions safely
into the treatment plan.

Next Month: Nutritional Treatments for Autism

References

1. Lutz EG. Restless legs, anxiety and caffeinism. J Clin Psychiatry 39:693-8, 1978.

2. Roberts HJ, Spontaneous leg cramps and "restless legs" due to diabetogenic
(functional) hyperinsulinism: A basis for rational therapy. J Med Assoc 60
(5):29-31, 1973.

3. Kerr D, Sherwin RS, Pavalkis F, et al. Effect of caffeine on the recognition of and responses to hypoglycemia in humans. Ann Intern Med 119:799-804, 1993.

4. Boutez MI et al. Neuropsychological correlates of folic acid deficiency:
facts and hypotheses, in MI Botez, EH Reynolds, Eds. Folic Acid in Neurology, Psychiatry, and Internal Medicine. New York, Raven Press, 1979

5. Ayres S, Mihan R. ÒRestless legsÓ syndrome: response to vitamin E. J Appl Nutr 25:8-15, 1973.

6. Ayres S, Mihan R. Leg cramps and Òrestless legÓ syndrome responsive to vitamin E. Calif Med 111:87-91, 1969.

7. Pall HS, Williams AC, Fonseca A, et al. Restless legs syndrome. Neurology 37: 1436, 1987.

8. Ekborn KA. Restless legs syndrome. Neurology 10:868-73, 1960.

9. O'Keeffe ST, Gavin K, Lavan JN. Iron status and restless leg syndrome in the elderly. Age Ageing 23(3):200-3, 1994.

10. Popoviciu L, Asgian B, Delast-Popoviciu D, et al. Clinical, EEG,
electromyographic and polysomnographic studies in restless legs syndrome caused by magnesium deficiency. Rom J Neurol Psychiatry 31(1):55-61, 1993.

11. Jacobs BL. Serotonin and behavior; emphasis on motor control. S Clin
Psychiatry 52: 12 (suppl);17-23, 1991.

12. Sandyk R. L-tryptophan in the treatment of restless legs syndrome. Letter. Am J Psychiatry 143(4):554-5,1986.

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