This Is MS Multiple Sclerosis Knowledge & Support Community

lyndacarol wrote:
Ignorance gives me license to imagine all kinds of possibilities. We've all heard that sunshine is good for us with MS. Why? Some scientists tie this with the general (and frequently cited!) observation of lower prevalence of MS with closer proximity to the equator (but with exceptions that are conveniently ignored). Sunshine is known to be absorbed by the skin, where eventually in the body it becomes Vitamin D. The assumption has been that it is Vitamin D that accounts for less MS. (Like many, I take Vitamin D supplements.) But sunshine has many components; could the mechanism be something else? Maybe the focus on D is incorrect. Is there evidence that Vitamin D is definitely the key ingredient?

I don't know much about sunshine, but I know it is a source of ultraviolet A and B (cause of sunburn) rays. I also know that ultraviolet rays are used to kill germs; they are even used in some water purification. If viruses or bacteria are involved in MS, maybe UVA or UVB rays affect them and thus the disease? Is THIS the mechanism at work? Maybe a dose of ultraviolet would be more useful than Vitamin D.

Possibly but evidence such as this study indicate it is vitamin D as the imunosuppressive element associated with sunshine.

I feel ignorance is no excuse for purposefully dismissing information so to promote a "pet theory" Lynda. I've posted this information before on the specific influences vitamin D has on the well identified elements the immune system employs in the disease of MS. Here it is again......

This is an excerpt from Vitamin D Supplementation in the Fight Against Multiple Sclerosis

1) Suppresses antibody production by B cells and the proliferation of T cells in the thymus.
2) Upregulates cytokines TGF-beta and IL-4. These proteins, which are produced by immune cells, act as suppressants of inflammatory T cells.
3) Inhibits production of pro-inflammatory cytokines such as IL-1, IL-2, TNF
and IFN gamma which also reduces inflamammatory reactions.
4) Interferes with T helper function and inhibits the passive transfer of cellular immunity by Th in vivo
5) Inhibits the production of NO (nitric oxide) by immune cells. NO has been identified as one of the most destructive products of the immune system and is an important factor in demyelination.
6) Inhibits the proliferation of activated and memory T cells. Such cells are
the main mediators of the inflammatory autoimmune reactions of MS.
7) Exerts immunomodulating effects in the CNS by inducing a profound
downregulation of antigen expression by both infiltrating and resident antigen-presenting
cells (e.g. macrophages).
8 ) Inhibits the actions of antigen presenting dendritic cells.

In summary, vitamin D hormone has numerous effects on the immune system and acts within the CNS. All of these effects have the combined result of significantly reducing inflammatory autoimmune reactions from occurring and they readily explain the impressive correlation between MS prevalence and vitamin D supply and why vitamin D hormone is so effective in suppressing a variety of animal autoimmune diseases including EAE (animal MS)

lyndacarol wrote: I've read (but can't recall the source--so my husband says I can't use this--see how well I listen?) that sunshine removes insulin from the body. (See? It all comes back to insulin for me!) Could this explain the situation with MS and the equator? Perhaps something in sunshine is removing excess insulin for those nearer to the equator.

If you could provide me with with a reputable source of this I would appreciate it. try Pubmed or Google for your search.

Cheers
Nick

lyndacarol wrote:
Ignorance gives me license to imagine all kinds of possibilities. We've all heard that sunshine is good for us with MS. Why? Some scientists tie this with the general (and frequently cited!) observation of lower prevalence of MS with closer proximity to the equator (but with exceptions that are conveniently ignored). Sunshine is known to be absorbed by the skin, where eventually in the body it becomes Vitamin D. The assumption has been that it is Vitamin D that accounts for less MS. (Like many, I take Vitamin D supplements.) But sunshine has many components; could the mechanism be something else? Maybe the focus on D is incorrect. Is there evidence that Vitamin D is definitely the key ingredient?

I don't know much about sunshine, but I know it is a source of ultraviolet A and B (cause of sunburn) rays. I also know that ultraviolet rays are used to kill germs; they are even used in some water purification. If viruses or bacteria are involved in MS, maybe UVA or UVB rays affect them and thus the disease? Is THIS the mechanism at work? Maybe a dose of ultraviolet would be more useful than Vitamin D.

Possibly but evidence such as this study indicate it is vitamin D as the imunosuppressive element associated with sunshine.

I feel ignorance is no excuse for purposefully dismissing information so to promote a "pet theory" Lynda. I've posted this information before on the specific influences vitamin D has on the well identified elements the immune system employs in the disease of MS. Here it is again......

This is an excerpt from Vitamin D Supplementation in the Fight Against Multiple Sclerosis

1) Suppresses antibody production by B cells and the proliferation of T cells in the thymus.
2) Upregulates cytokines TGF-beta and IL-4. These proteins, which are produced by immune cells, act as suppressants of inflammatory T cells.
3) Inhibits production of pro-inflammatory cytokines such as IL-1, IL-2, TNF
and IFN gamma which also reduces inflamammatory reactions.
4) Interferes with T helper function and inhibits the passive transfer of cellular immunity by Th in vivo
5) Inhibits the production of NO (nitric oxide) by immune cells. NO has been identified as one of the most destructive products of the immune system and is an important factor in demyelination.
6) Inhibits the proliferation of activated and memory T cells. Such cells are
the main mediators of the inflammatory autoimmune reactions of MS.
7) Exerts immunomodulating effects in the CNS by inducing a profound
downregulation of antigen expression by both infiltrating and resident antigen-presenting
cells (e.g. macrophages).
8 ) Inhibits the actions of antigen presenting dendritic cells.

In summary, vitamin D hormone has numerous effects on the immune system and acts within the CNS. All of these effects have the combined result of significantly reducing inflammatory autoimmune reactions from occurring and they readily explain the impressive correlation between MS prevalence and vitamin D supply and why vitamin D hormone is so effective in suppressing a variety of animal autoimmune diseases including EAE (animal MS)

lyndacarol wrote: I've read (but can't recall the source--so my husband says I can't use this--see how well I listen?) that sunshine removes insulin from the body. (See? It all comes back to insulin for me!) Could this explain the situation with MS and the equator? Perhaps something in sunshine is removing excess insulin for those nearer to the equator.

If you could provide me with with a reputable source of this I would appreciate it. Try Pubmed or Google for your searches.

Cheers
Nick

Hey Jimbo

Thank you for the excellent references.

Cheers
Nick

First of all, I love this site for the chance it gives us to come together with ideas! Maybe this is one more example.

I found the U.S. Pharmacist article on vitamin D (link given by jimmylegs, June 9) especially interesting when the author, Yadhu Singh, Ph.D., of South Dakota State University, wrote:

Diabetes mellitus: The dependence of normal insulin secretion in pancreatic ß-cells on vitamin D has been known for many decades.

I need to learn more about this "dependence...that has been known for decades" and which I never heard of before!

Since I am unable to bring my insulin production down with diet, perhaps this vitamin D angle will help. I'm working harder on it! Since I believe hyperinsulinemia is involved in my MS, could this Vitamin D/insulin connection explain the lower prevalence of MS in populations living closer to the equator? (And the virtual non-existence among Eskimos who have, not only a low-carb diet, but one high in salmon and fish, which are dietary sources of vitamin D.)

According to the article, there seem to be many disorders linked to a vitamin D deficiency or insufficiency. With a spot about deficiency on our local news yesterday, the subject may be finally coming into its own!

lyndacarol wrote:...the virtual non-existence among Eskimos who have, not only a low-carb diet, but one high in salmon and fish, which are dietary sources of vitamin D.

Let's not forget that such a diet is also quite high in omega-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Omega-3 oils such as EPA lead to the production of series 3 prostaglandins which are cell signaling molecules. The series 3 prostaglandins prevent platelets from sticking together, improve blood flow, and reduce inflammation.

In contrast, saturated fats which are rich in arachidonic acid lead to the production of series 2 prostaglandins. This class of prostaglandins promote platelet stickiness which plays a role in heart disease and strokes. Moreover, arachidonic acid promotes the production of inflammatory leukotrienes while omega-3s, such as EPA, promote the production of less inflammatory leukotrienes.

I realize that the above description is oversimplified. For a more detailed discussion of fat metabolism, I would recommend taking a look at Fats That Heal, Fats That Kill by Udo Erasmus. Another book with some good info in it is The Encyclopedia of Healing Foods by Michael Murray.

NHE

Hi LyndaCarol
You wrote some posts back:

Since I am unable to bring my insulin production down with diet,

You might want to check out alpha lipoic acid. It's been studied for MS.

Alpha Lipoic Acid Inhibits Insulin Secretion

CONCLUSIONS/INTERPRETATION: This study is the first to demonstrate that alpha-LA directly affects beta cell function. The chronic effects of alpha-LA include AMPK activation and reductions in insulin secretion and content, and cell growth.

Take care

Sharon

I GREATLY appreciate the info on Alpha-Lipoic acid and insulin secretion,. Inhibiting secretion is exacly what I want to do! I have tried alpha-LA for MONTHS, with no observable changes. I don't understand it.

Keep thinking of me.

Lyndacarol, could you perhaps adjust the dosage and see if ALA has an impact? I know that some people on this site are taking much higher dosages than the RDA

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

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

And, ljm, I was using triple the suggested dosage--no effect.

For my convenience, I post this here.

As a child, I enjoyed hearing the Hindu fable of "The Blind Men and the Elephant." Each of the six men with his hands on a different part of the same elephant had a different perception of the animal. Perhaps we are each a blind man with a part of the whole puzzle. We just need to put them together.

With credit and thanks to jimmylegs, I repeat her link to a Vitamin D article:

http://www.uspharmacist.com/index.asp?s ... 8_1352.htm

"Vitamin D Part 1: Are We Getting Enough?" by Yadhu N. Singh, PhD

At the end of Part 1, I found this particularly interesting:

Table 2: Cells with Cytosolic or
Nuclear and/or Membrane-Bound
Vitamin D Receptors 1-3

Activated T-Cells; Liver Cells
Aortic Endothelial Cells; Muscles Cells
Chrondocytes; Neurons
Circulating Monocytes; Osteoblasts
Colon Enterocytes; Ovarian Cells
Distal Renal Tubules; Parathyroid Cells
Endocrine Cells, Stomach; Prostate Cells
Epidermal Cells; Pituitary Cells
Islets Cells, Pancreas; Placenta Cells
Intestinal Cells; Skin Fibroblasts
Keratinocytes, Skin; Transformed B-Cells

Then:

http://www.uspharmacist.com/index.asp?s ... 8_1396.htm

"Vitamin D Part 2: Low Status and Chronic Diseases"

In the section on Diabetes Mellitus was the sentence posted earlier:

"The dependence of normal insulin secretion in pancreatic ß-cells on vitamin D has been known for many decades."


Thanks to Nick, I found more interesting material by Reinhold Vieth, PhD:

http://www.direct-ms.org/pdf/VitDVieth/ ... R%2061.pdf

The Pharmacology of Vitamin D, Including Fortification Strategies

"Multiple sclerosis is more prevalent in populations having lower levels of vitamin D nutrition or ultraviolet exposure (26; 30-32), and it has been proposed that vitamin D intake, ranging from 1,300 to 3,800 units per day, helps prevent the disease (32).

Lyndacarol,

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.

<shortened url>

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!

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.

Brock

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. 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.

NHE

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. maurizioguido@libero.it

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]