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 mrhodes40 » Fri Feb 03, 2006 6:32 pm

well I ccame across this and wanted to share it. The idea that a high insulin level can be a problem for MSer that Lnda Carol put forth here and that she is so convinced is at issue ties in to DHEA :


Title: Mechanism of Mast Cell Activation
Author: Peters, SP
Year: 1995
Series Editor: Holgate, Busse and
Series Title: Blackwell Scientific Publications
Volume: Asthma and Rhinitis
Number of Pages: 221-230


--------------------------------------------------------------------------------
Title: Dehydroepiandrosterone (Dhea)--the "Mother Steroid". I. Immunologic Action
Author: Regelson, W.; Loria, R.; Kalimi, M.; (Date: May 31, 1994)
Journal: Ann N Y Acad Sci; V. 719; Pages: 553-63

Notes: Journal Article
Review
Review, Tutorial
Author Address: Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.


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Title: Case Report: Amelioration of Insulin Resistance in Diabetes with Dehydroepiandrosterone
Author: Buffington, C. K.; Pourmotabbed, G.; Kitabchi, A. E.; (Date: Nov, 1993)
Journal: Am J Med Sci; V. 306; Issue: 5; Pages: 320-4

Abstract: In hyperandrogenic females, the ratio of dehydroepiandrosterone (DHEA) to testosterone may be an important determinant of insulin sensitivity. This study involved changes in insulin sensitivity and glucose metabolism with therapeutic manipulation of DHEA (S)/testosterone in a female patient with non-insulin-dependent diabetes and hyperandrogenism. Therapeutic intervention included 1-month treatment with 0.25 mg dexamethasone at bedtime and 1-month dexamethasone + DHEA. Insulin sensitivity and glucose tolerance were assessed before and after each treatment regimen by examining: 1) fasting and oral glucose tolerance test glucose and insulin levels, 2) hypoglycemic response to intravenous insulin, and 3) erythrocyte insulin receptor binding. With dexamethasone alone, DHEAS, testosterone, and their ratio were reduced with a concomitant increase (30%) in oral glucose tolerance test insulin levels and a decrease (33%) in erythrocyte insulin binding. With DHEA + dexamethasone, the ratio of DHEAS/testosterone increased 16-fold along with a marked improvement in insulin sensitivity, as determined by a more than 30% reduction in fasting and oral glucose tolerance test insulin levels, a threefold stimulation of the rate of glucose disappearance with intravenous insulin, and a 30% increase in insulin binding. DHEA improved insulin sensitivity and reduced fasting and oral glucose tolerance test glucose levels and ameliorated the diabetic state. The ratio of DHEAS/testosterone is an important regulator of insulin sensitivity and glucose tolerance and that DHEA therapy may be beneficial in the treatment of certain forms of insulin resistance.
Notes: Journal Article
Author Address: Department of Medicine, University of Tennessee, Memphis.
I hope Sharon weighs in on this. I remember that DHEA is low in MS and adding apparently can be helpful, but don't have these studies at hand as it's not my area of interest. But perhaps the way to reduce insulin sensitivity is to think about that kind of approach. As usual talk that over with your doc (naturopath in this case... are you in the US?)
marie
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DHEA and Diabetes

Postby Shayk » Fri Feb 03, 2006 7:16 pm

Hi Marie--

I'll weigh in only very quickly tonight and perhaps more later in the week end. The quick "weigh in" is that DHEA is in clinical trials for diabetes here at what is now the Virginia Commonwealth University (VCU) Medical School. VCU also did one of the DHEA Phase I trials for MS.

I think there's lots of reasons for people with MS to consider at least obtaining physiologically normal levels of DHEA, if they've had their level checked and it is in fact low, which seems to be the case for people with MS.

Sharon
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Still on the insulin kick

Postby lyndacarol » Tue Feb 28, 2006 6:21 pm

I am hesitant to post my continued thoughts on the insulin angle due to the recent empassioned discussions of abx; I hope getting through the problem and finding consensus will forge stronger relationships and feeling of community at this website. But although I appear to be the lone believer in that hormone of insulin, the anonymity here and the assumed freedom to express ideas give me courage to post on.

As stated earlier, I have no formal education in science; I admire those who do. I cannot understand this disease on the cellular level and can only look at the obvious and anecdotal and wonder "How can this be working? How can this be?" I know I am trying to make everything work with the insulin angle and this is not very scientific. It is like trying to stuff the foot of Cinderella's ugly stepsister into the glass slipper and make it fit smoothly. I'm trying to make every accepted fact about MS explainable by this idea of starting trigger, inflammation, insulin, resulting MS symptoms:

With credit and thanks to "beatms," I borrow his format.

1. Numerous causes--bacteria [C. pneumoniae, B. burgdorferi (cause of Lyme disease), maybe even the Texas A&M researcher, Dr. Luther Lindner's bacterium (posting on Antibiotics Forum by SMAYFIELD on Nov 07, 2004 concerning Dr. Lindner's research), et.al.]
viruses (EBV,HHV-6, et al.)
stress, trauma, surgery (maybe even breast implants!)
diet (high in pro-inflammatories) lead to...
2. Inflammation (severe chronic sinusitis, in my case) leads to...
3. Excess insulin production (hyperinsulinemia)--it seems to fit me so well, I just can't give up the idea! leads to...
4. Damage to blood vessels causing more inflammation and tingling
and/or
Burn-out of the pancreas' insulin-producing cells (type 2 diabetes)
and/or
Ultimately, calling in the immune system and damaging nerves


It seems we do not have a one-to-one relationship; it is not one specific bacterium that directly causes this one specific disease. Different treatments may be effective at interrupting the process at different points along the cascade in different people.

1. Antibiotics may be effective here at killing organisms. Or diet (I learned in grade school that germs are fed by glucose. Is that no longer accepted fact?). Or lifestyle.
2. Inflammation can be reduced by corticosteroids, tumeric (An article read since this post reported there are compounds in turmeric that increase insulin production--although my letter to the author did not result in the source for his statement, I have discontinued my turmeric supplement.), diet. Even minocycline, I recently read, is an old antibiotic that fights inflammation. Could this characteristic explain its reported action at improving MS? With name similarity, does doxycycline work in the same way? Bee venom also has anti-inflammatory components.
3. I have been taught that insulin production cannot be reduced directly, diet must be the approach here. [Though, according to the Physician's Desk Reference (PDR), pioglitazone reduces the amount of circulating insulin in the blood--could this account for the improvement Dr. Douglas Feinstein saw in studies at the University of Illinois at Chicago?]

Since it seems diet appears at several points, and I cannot dismiss The Gold Coast Cure experience reported by the author, I am trying her diet approach. I figure if the recommendation by some here is to try antibiotics for a year and see what happens, I can give the same trial period to diet. Doxycycline and most other antibiotics have been HARD on my system--stomach upset and intense diarrhea. Diet change should be easier for me to tolerate.

At the least, I have seen this benefit to my low-carb diet: Last year with a fasting blood glucose of 109, I was considered pre-diabetic; my latest blood tests included the result of 78 MG/DL, which is in normal range. I attribute this change and a reduction in bruising to diet. I will continue and hope to see some improvement in MS, too. If so, I will certainly post the news. This is my own study; N=1, me.

Can anyone tell me how to go about interesting a researcher to initiate a real, legitimate study? My Multiple Sclerosis Quarterly Report arrived last week; among the studies listed and enrolling participants was "'Study of Tongue Pressures'; Purpose: The purpose of this study is to examine tongue strength and endurance, how the tongue applies pressure during swallowing, and how the chin muscles react during swallowing in healthy volunteers and in patients with dysphagia (difficulty swallowing)."
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Postby Shayk » Tue Feb 28, 2006 9:29 pm

Hi Lynda Carol—

Here’s some rather random (and late at night) responses to some of the issues you raised.
I am hesitant to post my continued thoughts on the insulin angle due to the recent empassioned discussions of abx

I too am hesitant to continue to post any info about hormones given the abx focus/discussions, but, here’s the title of an abstract from the upcoming AAN meeting that may spur you along:
Fetuin-A Levels are Elevated in CSF of Patients with SPMS

Now, I have no scientific or medical background either. The text of the abstract states in part:
Altered levels of fetuin-A are associated with inflammation and several different functions have been described including the inhibition of insulin receptor activity…
It sounds to me like that’s relevant to your idea. They concluded:
Upregulation of fetuin-A levels in the CSF of SPMS is a novel finding and further investigation of its role may lead to a better understanding of the inflammatory response associated with disease progression.

You also wrote:
It seems we do not have a one-to-one relationship; it is not one specific bacterium that directly causes this one specific disease. Different treatments may be effective at interrupting the process at different points along the cascade in different people.

I totally agree. You also asked:
Even minocycline, I recently read, is an old antibiotic that fights inflammation. Could this characteristic explain its reported action at improving MS?

The anti-inflammatory activity may be part of its reported action at improving MS but I think another one may be its neuroprotective properties. Here are just a couple of abstracts on that: Strategies to promote neural repair and regeneration after spinal cord injury
A number of medications such as erythropoietin and minocycline have demonstrated neuroprotective properties in animal models of spinal cord injury
.
Antioxidant properties of minocycline
Minocycline is neuroprotective in animal models of a number of acute CNS injuries and neurodegenerative diseases.

I don’t know if the abx in the Wheldon/Stratton protocol possess similar neuroprotective properties or not.

I think it’s great you’re pursuing the diet and your ideas. Good luck with both of them.

Sharon
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Stuffing that glass slipper again?

Postby lyndacarol » Wed Mar 08, 2006 5:09 pm

Having learned that ovulation is an inflammatory event and having read the article on this website's first page, "Oral Contraceptives May Cut Multiple Sclerosis Risk" (now archived), I wonder if this can be happening because contraceptives stop ovulation.

This seems to fit into the "glass slipper" of (1) something causing (2) inflammation, which leads to (3) excess insulin production, which leads to (4) "autoimmunity"--MS. It seems perfectly logical to me, but then, I am unencumbered by scientific knowledge!
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Postby Shayk » Wed Mar 08, 2006 6:36 pm

Hi Lynda Carol

I too am unencumbered by scientific knowledge. :lol: It allows me to speculate about all sorts of things about MS.

I don't buy into the "auto-immune" theory of MS, so I won't comment on your "glass slipper" idea.

I've done some reading about hormones and MS though and there does seem to be some correlation between levels of hormones (ratios) and MRI activity. Correlation Between Sex Hormones and MRI Lesions in MS
RESULTS: Patients with high estradiol and low progesterone levels had a significantly greater number of Gd enhancing lesions than those with low levels of both these hormones. Patients with a high estrogen to progesterone ratio had a significantly greater number of active MRI lesions than those with a low ratio. CONCLUSION: Estradiol and progesterone may influence disease activity in MS. If further studies confirm these results, it may be possible to develop therapy by altering levels of these hormones.


I can attest to the idea that high levels of estradiol and low progesterone may influence the number of lesions. :) When I first had my hormone levels tested I had some estradiol but no progesterone. 8O I also had a boatload of lesions.

I personally think both estrogen and progesterone may contribute to neuroprotection and that may be why oral contraceptives cut MS risk. Here's a sample of some of that literature. First up, in another thread Ian posted info about mitochondrial dysfunction and axonal loss. Mitchondria play a central role in estrogen-induced neuroprotection
Indeed, the parental estrogens and novel analogs stabilize mitochondria under Ca(2+) loading otherwise sufficient to collapse membrane potential. The cytoprotective and mitoprotective potencies for 14 of these analogs are significantly correlated, suggesting that these compounds prevent cell death in large measure by maintaining functionally intact mitochondria. This therapeutic strategy is germane not only to sudden mitochondrial failure in acute circumstances, such as during a stroke or myocardial infarction, but also to gradual mitochondrial dysfunction associated with chronic degenerative disorders such as AD, PD and HD.

I happen to think personally that there is a significant neurodegenerative element in the MS disease process. That's why the emphasis there.

Another, Both estrogen and progesterone attenuate edema formation following diffuse traumatic brain injury in rats
we demonstrate in both male and ovariectomized female rats that a single physiological dose of either hormone at 30 min after diffuse traumatic brain injury reduces both blood brain barrier permeability and edema formation.

Estrogen and progesterone as neuroprotective agents in the treatment of acute brain injuries
the steroids are now showing considerable promise as neuroprotective and neuroregenerative agents in stroke and traumatic brain injuries. Collectively, these two hormones have been reported to reduce the consequences of the injury cascade by enhancing anti-oxidant mechanisms, reducing excitotoxicity: altering glutamate receptor activity, reducing immune inflammation, providing neurotrophic support, stimulating axonal remyelinization and enhancing synaptogenesis and dendritic arborization.[/i] Estrogen has often been tried as a prophylactic treatment in females for ischemic brain injury, while progesterone has, thus far, been given as a post-injury treatment for both male and female subjects with acute, ischemic and traumatic injuries of the brain and spinal cord.

I emphasized progesterone because I do like to include the men whenever possible. They have hormones too. :wink:

The upshot I guess is that my focus is on neuroprotection and not necessarily the inflammation.

Take care and definitely keep thinking about possibilities Lynda Carol. I tend not to focus on inflammation because it too may be protective and I don't think they've figured that out yet (what's good/what's bad inflammation.)

Sharon
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Postby Arron » Wed Mar 08, 2006 7:15 pm

Just wanted to call out an excellent post, Sharon. As always, well researched and well thought out. We all appreciate your time and thinking.
Disclaimer: Any information you find on this site should not be considered medical advice. All decisions should be made with the consent of your doctor, otherwise you are at your own risk.
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Postby Shayk » Thu Mar 09, 2006 6:28 am

A very sincere thank you for comments Arron. :)

--sharon
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pointers re: endocrine role in ms?

Postby jimmylegs » Thu Mar 23, 2006 8:44 am

hi i just recently got onto the non-autoimmune idea.

while i've been looking at diet from the get-go, now i'm looking at how diet influences our body's hormone balance which can in turn affect ms. (3rd trimester studies).

i think it was wikipedia where i read that our body builds progesterone (elevated in late pregnancy) from cholesterol (i for one have not been ingesting cholesterol for about 15 years so that's something for me to look into - my diet lacked cholesterol and along with that, vitamins D and B12).

i have also had high TNF evidenced by onset of skin problems since... puberty! - whoa, that light just went on for the first time, have i had progesterone problems all along? - and TNF is apparently reduced in late pregnancy too. i also have typically had a bunch of problems, which in mindblowing hindsight all point to a hormone imbalance... wow i feel so very, very dumb!

so anyway, now i'm taking my temp daily to see if i get any changes associated with my body making progesterone after monthly ovulation. i guess you don't ovulate when your diet's crap, so maybe i had an underlying problem with low progesterone which i made worse by eating so poorly that perhaps i didn't even ovulate/secrete progesterone at all?

is this making any sense?? sorry i don't have a good list of references yet but i will work on that.

anyway it's starting to look as though by trying to figure out how to improve my MS problems by seeing how my diet could help my progesterone levels, that i have potentially uncovered a crazy underlying hormone situation that explains pretty much every health problem i've had since puberty. i need to do tons more research - any pointers would be appreciated :D

anyone else see benefit in starting a forum section on endocrinology?

ttfn :D
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Insulin is a hormone

Postby lyndacarol » Thu Mar 23, 2006 1:33 pm

jimmylegs,
Let me respond to your post with my limited understanding. I count on others here to jump in with corrections and additions.

I still think changes in insulin levels occur during pregnancy and affect MS.

I believe there are two sources for cholesterol--your diet and your own body. If you don't take in enough cholesterol in your diet, your body makes (in the liver, I think) up the difference. Despite the drug company ads, zero cholesterol is not desirable--we need cholesterol for certain body processes!

I don't understand how progesterone might figure in it all. But keep looking and keep questioning!

I have read (sorry, I don't have the source) that ovulation is an inflammatory event; this fits in the inflammation/insulin line-up for me. I have also read (again, no source) that the Basal Body Temperature, that is, temp taken first thing in the morning, before you get out of bed, should be about 97.6 (much below that indicates excess insulin in the body)--mine has been as low as 96.3 and is never up to 97.6.

A good diet can't hurt. Especially an anti-inflammatory one--avoiding anything that might raise insulin by raising the blood sugar! Unfortunately, that's all the good stuff I LOVE to eat--cookies, cakes, bread, etc.--all the sweet stuff! But I have been good about diet since the beginning of March; but no improvement in MS yet!
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progesterone, insulin, diet, abstracts

Postby jimmylegs » Fri Mar 24, 2006 6:51 am

hi there thanks for your info :)

i know you are correct about the body making some of its own cholesterol but what i don't know is whether our bodies make enough for everything when you don't include dietary cholesterol for over a decade.

i don't imagine good diet will help in only a few weeks - it took me a decade of bad habits to get into this situation - but i can tell you i've been eating pretty well and supplementing heavily with methyl b12 and a huge array of other things since the beginning of feb, and i stopped doing things that strip vitamins eg alcohol intake. i have noticed improvement (even though i still do have a coffee in the morning :twisted: hehehe) but couldn't tell you if that's just regular old recovery from an attack.

i just looked at diabetes + progesterone and in female patients their progesterone is lower than health controls during the luteal phase of the cycle. for what little that's worth :?

then i searched on insulin and ms and found two interesting abstracts so far (see below). one hypothesizes positive impact of an alternating calorie intake pattern on a variety of diseases. the other notes that there is a high importance on IGF-1 in remyelination (IGF-1 being produced by the liver, dependent upon good nutrition - wikipedia)

i think whatever goes wrong whether insulin, progesterone, immune system, or something else, that treating your body well seems to be the answer. so i'm focused on diet, exercise, and since sadly i can't stop that pesky time/aging thing, i'm thinking about supplementing with some natural estrogen/progesterone ratio something-or-other (definitely needs more research!) when/if i find that my levels are out of whack.

that's all for now, take care,

di


Med Hypotheses. 2006 Mar 8;
The effect on health of alternate day calorie restriction: Eating less and more than needed on alternate days prolongs life.
Johnson JB, Laub DR, John S.

Department of Surgery, Louisiana State University Medical Center, 2547A Lyon Street, 2nd Floor, San Francisco, CA 94123, United States.

Restricting caloric intake to 60-70% of normal adult weight maintenance requirement prolongs lifespan 30-50% and confers near perfect health across a broad range of species. Every other day feeding produces similar effects in rodents, and profound beneficial physiologic changes have been demonstrated in the absence of weight loss in ob/ob mice. Since May 2003 we have experimented with alternate day calorie restriction, one day consuming 20-50% of estimated daily caloric requirement and the next day ad lib eating, and have observed health benefits starting in as little as two weeks, in insulin resistance, asthma, seasonal allergies, infectious diseases of viral, bacterial and fungal origin (viral URI, recurrent bacterial tonsillitis, chronic sinusitis, periodontal disease), autoimmune disorder (rheumatoid arthritis), osteoarthritis, symptoms due to CNS inflammatory lesions (Tourette's, Meniere's) cardiac arrhythmias (PVCs, atrial fibrillation), menopause related hot flashes. We hypothesize that other many conditions would be delayed, prevented or improved, including Alzheimer's, Parkinson's, multiple sclerosis, brain injury due to thrombotic stroke atherosclerosis, NIDDM, congestive heart failure. Our hypothesis is supported by an article from 1957 in the Spanish medical literature which due to a translation error has been construed by several authors to be the only existing example of calorie restriction with good nutrition. We contend for reasons cited that there was no reduction in calories overall, but that the subjects were eating, on alternate days, either 900 calories or 2300 calories, averaging 1600, and that body weight was maintained. Thus they consumed either 56% or 144% of daily caloric requirement. The subjects were in a residence for old people, and all were in perfect health and over 65. Over three years, there were 6 deaths among 60 study subjects and 13 deaths among 60 ad lib-fed controls, non-significant difference. Study subjects were in hospital 123 days, controls 219, highly significant difference. We believe widespread use of this pattern of eating could impact influenza epidemics and other communicable diseases by improving resistance to infection. In addition to the health effects, this pattern of eating has proven to be a good method of weight control, and we are continuing to study the process in conjunction with the NIH.
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Encouragement

Postby lyndacarol » Sat Mar 25, 2006 9:55 am

I have found further encouragement for my inflammation/insulin campaign. Indeed, it is encouragement for each one of us at this site!

In looking through archived articles at acceleratedcure.org I was searching "pioglitazone" because I know researchers found a woman with MS who had improvement for 3 years on the drug and are now doing further study.

From the introduction of the pubmed article was the sentence, "There are still times in modern medicine when a single patient can enlighten our understanding of a disease or disease process, and can serve as an impetus for further discovery."

I have always been concerned that my suspicion began with just 5 people with high insulin levels, but now I am encouraged again to hear only A SINGLE ONE can make the difference! Now I just have to decide where to take it next--any suggestions out there?

This may not be the definitive answer, but just one to be checked out. Let me encourage you with your own suspicions to pursue whatever seems right for you. I heard a phrase the other day that applies to us here--"unity in our diversity." We have unity in seeking the answer to MS; but we are diverse in what we bring to that search--our backgrounds, our experiences, our abilities, our theories.

I appreciate this forum and chance to express and hear all kinds of ideas; I see many potential benefits coming from this "brainstorming."
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Fasting serum insulin test results

Postby lyndacarol » Sat Apr 22, 2006 3:24 pm

For you who wrote that you would be "following up" by asking your physician to order a "fasting serum insulin test," you want the results:

For this test, the desirable normal result should be below 10 (My understanding now, 1-16-10, is that optimal range is 4 to 7 UU/ML.). Mine was 12. I am interested in your outcome; I hope you will be willing to share the information with me.

Excess insulin production eventually burns out those insulin-producing beta cells in the pancreas, resulting in type-1 diabetes. Could this explain the common occurrence of diabetes with MS, if hyperinsulinemia (excess insulin) is involved with MS?
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Postby Nick » Tue Apr 25, 2006 9:28 am

lc

Your hypothesis is interesting. Please continue in your postings as this kind of intellectual intercourse is one of my cherished reasons for frequenting these types of forums.

I quite like your focus on MS & type 1 diabetes. I am, however, a believer in the autoimmune disease process for both MS and type I diabetes. I believe their similarities result from certain common denominators, notably European heritage, genetic predisposition, causal food proteins and a deficiency in protective elements.

lyndacarol wrote:Excess insulin production eventually burns out those insulin-producing beta cells in the pancreas, resulting in type-1 diabetes. Could this explain the common occurrence of diabetes with MS, if hyperinsulinemia (excess insulin) is involved with MS?


I think this would be the lay description for type 2 rather than type 1 diabetes. It has been well documented that in type 1 diabetes, the GAD protein in the pancreas is targeted and assailed by the immune system resulting in impaired islets and consequent insulin production impairment.

[Excerpt]The process of molecular mimicry is deceivingly simple but entails a lot of understanding of the workings of the immune system. Basically molecular mimicry means that part of a molecule of a given protein closely resembles a part of another totally different protein. Proteins are made up of strings of amino acids and in molecular mimicry one series amino acids(eg~10) in one protein is very similar to a string of ten amino acids in another protein. Given that there are 20 different amino acids it is a rather rare occurrence to find such mimicking arrangements but many examples have been demonstrated.

The main types of proteins which came into play in autoimmune disease are:

1. self proteins which are part of the human body. An example of this would be myelin basic protein which is the most common protein in myelin and the GAD protein of the pancreas;

2. proteins of infectious agents such as viruses and bacteria;

3. food proteins. For example over 400 different proteins occur in cow's milk and most have over 150 amino acids.

To understand how molecular mimicry works in the induction of autoimmunity one must understand the basic mechanisms of an immune response to a foreign invader in the body. The immune system recognizes a part of the protein portion of the invader. It does this with T cells which have receptors which bind to short segments(~10 amino acids) of a foreign protein. A macrophage will engulf a foreign invader (e.g. a bacteria or food particle) and break it down into fragments.

A special molecule in the macrophage then carries a protein fragment(peptide) to the surface of the cell and "presents" it to the millions of circulating T cells. A T cell which has a matching receptor locks onto the presented protein fragment. The T cell then becomes activated and stimulates other portions of the immune system to begin an immune response against all proteins which contain a similar looking amino acid string. The details of what constitutes a similar looking string are beyond this summary but suffice to say it has been found that a variety of similar, yet somewhat different strings, can be recognized by the same T cell.

Thus, it is easy to understand how molecular mimicry can trigger an autoimmune reaction. If the protein fragment from a foreign invader which is presented to the T cell closely resembles part of a self protein then the activated immune system will not only attack all foreign invaders which have the same string of amino acids but will also attack a very similar string in a self protein. It has been shown that parts of proteins in various foods and infectious agents resemble parts of various self proteins. Sometimes a three way mimicry occurs with a protein fragment from a food closely resembling that of an infectious agent which in turn closely resembles part of a self protein.

In Celiac disease part of the gliadin molecule (found in various grains such as wheat and rye), part of adenovirus 12 and part of a gut protein all closely resemble each other and the result of such mimicry is an immune attack on the gut when food containing gliadin protein is eaten. A similar three way mimicry occurs between a cell wall protein in grains and legumes, part of the Epstein Barr virus and part of the collagen in joints. This leads to rheumatoid arthritis in genetically susceptible people. For type 1 diabetes parts of milk proteins and viral proteins mimic proteins in the insulin-producing beta cells of the pancreas.

For MS it has been established that numerous viruses and bacteria have amino acid strings which mimic parts of proteins in the myelin proteins of the central nervous system. Undoubtedly food proteins also contain such mimicking protein fragments and thus two and three way mimicry is a ready explanation for why the immune system attacks myelin and causes MS.


Below is my post of April 18.

Nick's foreword

I believe the following information is very important for a variety of reasons.

Cheers
Nick
--------------

In Children with Autoimmune Disease, Response Starts Early

Newswise - Children with neurological autoimmune diseases develop immune reactions to other targets in their bodies and in food early in their disease, according to research that will be presented at the American Academy of Neurology 58th Annual Meeting in San Diego, Calif., April 1 - 8, 2006.

T cells are the body's regulators of the immune response. Increased T cell proliferation is a characteristic of autoimmune disease, in which the immune system attacks body tissues.
However, it wasn't known whether this increased proliferation occurred early, or as a result of chronic autoimmunity, said lead researcher Brenda Banwell, MD, from the Department of Pediatric Neurology at the Hospital for Sick Children in Ontario, Canada.


The researchers studied 166 children: 63 with an autoimmune demyelinating syndrome (either multiple sclerosis or an isolated event of central nervous system autoimmunity), 43 with type I diabetes (also an autoimmune disease), 31 with a non-autoimmune neurological condition, and 30 healthy controls. They examined blood samples for T cell proliferation in response to exposure to a variety of antigens (targets), including myelin protein from nerve cells, proteins in the pancreas, and proteins in milk.

As expected, more children with central nervous system autoimmunity had T cell proliferation after exposure to myelin than control children (50 percent versus 10 percent). About a quarter of these children also showed a response to proinsulin, a T-cell target in type I diabetes. Over sixty percent also responded to a protein in milk. Ninety percent of the children with type I diabetes responded to pancreatic antigens as expected, but almost as many (79 percent) responded to myelin, and 90 percent responded to milk protein.

Even at the onset of their disease, children with autoimmune diseases harbor T cells that will react against proteins within their tissues, Banwell said. The responses seen against milk proteins raise the possibility that substances in food may be associated with autoimmunity.

This study was supported by The Wadsworth Foundation.
The American Academy of Neurology, an association of more than 19,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer disease, epilepsy, multiple sclerosis, Parkinson disease, and stroke.

For more information about the American Academy of Neurology, visit http://www.aan.com.
Editor's Note: Dr. Banwell will present this research during a scientific platform session at 1:30 Thursday, April 6 in room 6AB of the San Diego Convention Center.

----------------

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This booklet emphasizes the high risk for contracting MS of first-degree relatives of persons with MS. It discusses the causal factors of MS with special emphasis on vitamin D deficiency as a primary cause. Finally it demonstrates that adequate vitamin D can likely prevent MS in most cases and provides a recommended supplementation regime.

Booklet # 3 Multiple Sclerosis: The Alberta Disadvantage
This booklet demonstrates that the province of Alberta, the home of DIRECT-MS, has by far the highest rates of MS in the world: Prevalence 340/1000,000; Incidence 20/100,000.
Data and arguments are provided to support the argument that the main reason for the MS Epidemic is that all the main causal factors are present in Alberta, with low vitamin D supply being especially problematic.

Presentations

We have found that a Voiced PowerPoint presentation (‘Webcast’) is an effective way to communicate the science and the recommendations for nutritional strategies for controlling MS and preventing it in the first place.

The first presentation is Prospects for Vitamin D Nutrition. The discussion is narrated by Reinhold Vieth of the departments of Pathology and Laboratory Medicine, Mount Sinai Hospital and Laboratory Medicine and Pathobiology, University of Toronto.

Dr. Vieth addresses the topics of:
Vitamin D and Human Evolution
Clinical relevance of higher vitamin D intakes
Toxicology of Vitamin D

The second webcast is entitled Preventing Multiple Sclerosis and is the second in a series of web casts regarding nutrition and Multiple Sclerosis. The focus of the Prevention presentation is how MS can be easily, safely and inexpensively prevented by focusing on protective factors. This is a must see for those people with MS who have children.

Our first webcast, Nutritional Strategies for Controlling Multiple Sclerosis, addresses similar issues. It presents the probable causes of MS and how to effectively control those elements. A review of the protective factors and how to incorporate them into your lifestyle is also covered.
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Musings on MS as I sat in the sunshine

Postby lyndacarol » Sun May 07, 2006 12:52 pm

I consider myself quite average and so figure there are some like me out there, who let their minds run wild. MS colors every aspect of my life and I think about it most of the time. As I sat in the sunshine today, I thought about it again. I share my thoughts with you; maybe you have had the same or can add real information to these musings.

Since I didn't know the appropriate spot for posting, I chose this one on insulin (since you know sooner or later it will be involved!).

Ignorance gives me license to imagine all kinds of possibilities. We've all heard that sunshine is good for us with MS. Why? (According to Kathryn R. Simpson on page 148 of her book, The MS Solution, "Some think that melatonin, not vitamin D, may be the answer to why people at higher latitudes are more prone to MS.") 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 the hormone Vitamin D. The assumption has been that it is Vitamin D that accounts for less MS. (Like many, I take Vitamin D supplements--even took 8000IU per day for over a year, but with no improvement in MS so I no longer believe in the vitamin D/MS connection.) But sunshine has many components; could the mechanism be something else? I think so; I'm working on a new angle to sunshine/equator. 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.

Edited again 3/24/10 -- UV radiation is being considered by some as a possible explanation for a geographic distribution which is the lower prevalence of MS near the equator. Scorpion posted this article: http://www.physorg.com/news188487865.html

I am convinced that Vitamin D is NOT the mechanism responsible for this; nor is melatonin; nor UV radiation either. I DO now think that the photoperiod IS the mechanism because it reduces glucocorticoids. See link below on bear study.


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!) My latest idea centers on glucose--glucocorticoids, to be precise. Could this explain the situation with MS and the equator? Perhaps something in sunshine is removing excess insulin for those nearer to the equator.

Edited 1/30/10: With my belief in the insulin hypothesis, I am convinced that the geographic distribution of MS can be explained by the longer days found nearer the equator. The following paper:

http://www.bearbiology.com/fileadmin/tpl/Downloads/URSUS/Vol_16_2/Owen_Czekala_Vol_16_2_.pdf
seems to offer an explanation through the circadian rhythm and production of glucocorticoids, not the vitamin D that sunshine offers. Melatonin may play a role as Kathryn R. Simpson mentioned in her book. I believe it is simply this factor of more hours of daylight (longer days) that accounts for the lower prevalence of MS as one approaches the equator. (According to the paper on the bears study, this results in lower levels of glucocorticoids. In my opinion, this leads to a lower glucose level, followed by a lower insulin level.)


Edited again, 2/5/10 -- After rereading the bear study numerous times, and believing in the insulin angle, I have incorporated the idea of photoperiod (the length of the day) resetting the circadian clock which reduces glucocorticoids produced in the body.

To augment the photoperiod to which I am exposed (and thus reduce glucocorticoids and resulting blood sugar level and ultimately the insulin level), I have ordered a lightbox through www.sunbox.com and will use this for 20-30 minutes each morning. I will report any changes here after a reasonable trial.


I admit that the heat element of sunshine turns me into a bit of "a noodle" (I like that description, Harry.) and many of you probably think I have been in the sun too long today! You may be right. Please shed more "light" (I love puns, even if they are supposed to be low forms of humor.) on my ramblings.
Last edited by lyndacarol on Wed Mar 24, 2010 7:00 pm, edited 5 times in total.
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