Insulin--Could This Be the Key?

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

Postby viper498 » Sun Jul 09, 2006 4:33 pm


I was just browsing through PubMed and found this research abstract. It has to do with insulin and AD and MS, and immediately thought of you. Unless you have already seen this one, i think you will find it interesting.

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nice one

Postby jimmylegs » Sun Jul 09, 2006 5:10 pm

great find v!
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Important abstract!

Postby lyndacarol » Mon Jul 10, 2006 3:33 pm

Viper, thank you, thank you--for thinking of me immediately, for finding and posting the abstract from PubMed. I had not seen it until you posted it. I think this work in Washington state is very important!
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Postby viper498 » Mon Jul 10, 2006 6:00 pm

LyndaCarol, no problem at all. I think its a good connection to your insulin theory. I'll be interested to see what more pops up in the future about insulin.

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Re: Vitamin D/ insulin connection?

Postby NHE » Wed Jul 12, 2006 1:57 am

lyndacarol wrote:Yes, NHE, I think the fish oil is important on both ends of insulin!

(By the way, are prostaglandins and eicosanoids the same thing?)

No. Well sort of. Eicosanoids are a broader cartegory which include prostaglandins, leukotrienes, and thromboxanes. So, it could be said that prostaglandins are eicosanoids, but not all ecosanoids are prostaglandins. :wink: Of potential interest are Prostaglandin E2 (PGE2) and Leukotriene B4 (LTB4) both of which are promoted by consumption of omega-6 fatty acids and both of which are known to promote inflammation and are decreased by consuming omega-3 fatty acids. The preceeding discussion is from George Jelinek's book Taking Control of Multiple Sclerosis.

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Postby LisaBee » Wed Jul 12, 2006 4:02 pm

Here's one (or two) for you, lyndacarol, and maybe Shayk will like them too for the hormone connections.

I had posted on the LDN (low dose naltrexone) forum about a pancreatic cancer case report using LDN as an experimental treatment in one patient, as an example of how LDN papers get published for other diseases, but not, it seems for MS (although plenty of MSers are taking LDN). It got me thinking about whether LDN has anything to do with insulin, and has anyone looked at that, and well, here are two studies on naltrexone and hyperinsulinemia. There are more, but these are most recent.

What this has to do with MS, and people who are not postmenopausal or who don't have polycystic ovary syndrome I don't yet know, but it's interesting, mainly because naltrexone seemed to only impact people's clinical response if they were hyperinsulinemic by normalizing it. It would be an interesting and short term study to neasure gonadotrophins in MS vs normal subjects taking LDN, and see what happens. It might be educational. It might show changes only in some patients with MS, and not others. Then the next question, would such changes correspond with improvement related to MS? The possibilities are out there, and researchers are looking at the effects of naltrexone on a variety of conditions. Why not publish something on MS???? - Lisa

Curr Pharm Des. 2006;12(8):1001-12. Related Articles, Links

Role of opioid antagonists in the treatment of women with glucoregulation abnormalities.

Guido M, Romualdi D, Lanzone A.

Department of Obstetrics and Gynaecology, Universita Cattolica del Sacro Cuore, Roma, Italy.

Beta-endorphin were detected in the endocrine pancreas and seem able to influence insulin and glucagon release. Hence, endogenous opioids could have a role in glucoregulation and in the pathogenesis of obesity beyond the previously detected effects on appetite. Metabolic abnormalities, such as hyperinsulinemia, insulin-resistance and obesity, are common features of polycystic ovary syndrome (PCOS), and seem to have a pathogenetic role in this disorder. A link between opioids and PCOS-related hyperinsulinism is suggested by the finding of altered central opioid tone and elevated beta-endorphins levels, directly correlated with body weight, in these patients. Furthermore, naloxone and naltrexone significantly reduce the insulin response to glucose load only in hyperinsulinemic PCOS patients. This effect is obtained chiefly through an improvement of insulin clearance. Naltrexone is also able to ameliorate the abnormal gonadotrophins secretion and to improve the ovarian responsiveness in obese PCOS women undergoing ovulation induction with exogenous GnRH. Such effects are believed to be obtained through an amelioration of hyperinsulinemia. Gonadal steroids modulate the opioid system both centrally and in peripheral districts. Nevertheless, the decline of ovarian function does not abolish the opioidergic control of glucoregulation. Post-menopausal period is characterised by a high prevalence of hyperinsulinemia and insulin-resistance. In particular, an association between hyperinsulinemia and increased opioid activity was found in postmenopausal women showing a central body fat distribution. Both naloxone and naltrexone ameliorate the metabolic imbalance also when it appears in the climacteric period, and mainly by increasing insulin clearance. The benefits of naltrexone may represent in the future a useful tool for the treatment of women with hyperinsulinism in the clinical practice.

PMID: 16533167 [PubMed - in process]

Fertil Steril. 2004 Apr;81(4):1047-54. Related Articles, Links

Use of naltrexone in postmenopausal women with exaggerated insulin secretion: a pilot study.

Cucinelli F, Soranna L, Perri C, Barini A, Cento RM, Mancuso S, Lanzone A.

Department of Obstetrics and Gynecology, Catholic University of Sacred Heart, Rome, Italy.

OBJECTIVE: To determine the effect of naltrexone (an opiate receptor blocker) on insulin metabolism in postmenopausal women with different insulinemic patterns. DESIGN: Randomized placebo-controlled study. SETTING: Academic research environment. PATIENT(S): Forty-one healthy normoinsulinemic or hyperinsulinemic postmenopausal women. INTERVENTION(S): Oral glucose tolerance test (OGTT) before and after 5 weeks of the opioid antagonist (naltrexone, 50 mg/d orally) or the placebo administration; euglycemic-hyperinsulinemic glucose clamp. MAIN OUTCOME MEASURE(S): Glucose, insulin, and C-peptide plasma levels assessed in fasting condition and during the OGTT. Insulin sensitivity was calculated as total body glucose utilization. RESULT(S): Naltrexone reduced fasting and stimulated insulin response to the glucose load while inducing a significant improvement of the hepatic extraction, only in the hyperinsulinemic patients. No differences were found in the C-peptide pancreatic secretion and in the peripheral insulin sensitivity. No net change in the glycoinsulinemic metabolism was observed in normoinsulinemic patients or in placebo-controlled normoinsulinemic and hyperinsulinemic subjects. CONCLUSION(S): Similar to that reported in premenopausal women, endogenous opioid peptides are involved in the modulation of glycoinsulinemic metabolism in postmenopause. Through a prevalent action on liver insulin metabolism, without any clear improvement of insulin resistance and pancreatic beta-cell function, the chronic administration of naltrexone appears to reduce the hyperinsulinemia in those women with an exaggerated insulin response to the OGTT.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 15066462 [PubMed - indexed for MEDLINE]
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Postby Shayk » Wed Jul 12, 2006 7:06 pm


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. :wink: (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. :lol:

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Postby Arron » Wed Jul 12, 2006 10:06 pm

Hot off the presses...

MS linked with Type 1 Diabetes
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Postby Arron » Wed Jul 12, 2006 10:11 pm

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.
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Definitions of hyperinsulinemia...

Postby lyndacarol » Sat Aug 12, 2006 5:33 am

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 ) and Metabolic syndrome at ... 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 ... 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.
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Re: Definitions of hyperinsulinemia...

Postby CureOrBust » Sat Aug 12, 2006 5:37 pm

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:
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Insulin info always appreciated!

Postby lyndacarol » Sat Aug 12, 2006 6:57 pm

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.
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biotin test: check

Postby jimmylegs » Sun Aug 13, 2006 4:53 am

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:

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Postby carolew » Sun Aug 13, 2006 5:27 pm

I have MS and just like many others, I have hypoglycemia attacks. Just the opposite of diabetes mellitus. Go figure..... :?:
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Postby jimmylegs » Mon Aug 14, 2006 2:11 am

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


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


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


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


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.
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