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.

Another will have insulin test

Postby lyndacarol » Sat Dec 02, 2006 4:49 pm

I have mentioned finding a college friend who got the MS diagnosis in 1991. She has just written me that I have convinced her "to have this checked" and will ask when she sees her primary care physician the end of January.

As you know, I will be VERY interested in her results and will let you know, too.
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"Diabetes breakthrough" article out of Canada

Postby lyndacarol » Sun Dec 17, 2006 10:08 am

I was alerted to this posting of Stavros' in the Low Dose Naltrexone forum:

Diabetes breakthrough

By National PostDecember 15, 2006

In a discovery that has stunned even those behind it, scientists at a Toronto hospital say they have proof the body's nervous system helps trigger diabetes, opening the door to a potential near-cure of the disease that affects millions of Canadians.

Diabetic mice became healthy virtually overnight after researchers injected a substance to counteract the effect of malfunctioning pain neurons in the pancreas.

"I couldn't believe it," said Dr. Michael Salter, a pain expert at the Hospital for Sick Children and one of the scientists. "Mice with diabetes suddenly didn't have diabetes any more."

The researchers caution they have yet to confirm their findings in people, but say they expect results from human studies within a year or so. Any treatment that may emerge to help at least some patients would likely be years away from hitting the market.

But the excitement of the team from Sick Kids, whose work is being published today in the journal Cell, is almost palpable.

"I've never seen anything like it," said Dr. Hans Michael Dosch, an immunologist at the hospital and a leader of the studies. "In my career, this is unique."

Their conclusions upset conventional wisdom that Type 1 diabetes, the most serious form of the illness that typically first appears in childhood, was solely caused by auto-immune responses -- the body's immune system turning on itself.

They also conclude that there are far more similarities than previously thought between Type 1 and Type 2 diabetes, and that nerves likely play a role in other chronic inflammatory conditions, such as asthma and Crohn's disease.

The "paradigm-changing" study opens "a novel, exciting door to address one of the diseases with large societal impact," said Dr. Christian Stohler, a leading U.S. pain specialist and dean of dentistry at the University of Maryland, who has reviewed the work.

"The treatment and diagnosis of neuropathic diseases is poised to take a dramatic leap forward because of the impressive research."

About two million Canadians suffer from diabetes, 10% of them with Type 1, contributing to 41,000 deaths a year.

Insulin replacement therapy is the only treatment of Type 1, and cannot prevent many of the side effects, from heart attacks to kidney failure.

In Type 1 diabetes, the pancreas does not produce enough insulin to shift glucose into the cells that need it. In Type 2 diabetes, the insulin that is produced is not used effectively -- something called insulin resistance -- also resulting in poor absorption of glucose.

The problems stem partly from inflammation -- and eventual death -- of insulin-producing islet cells in the pancreas.

Dr. Dosch had concluded in a 1999 paper that there were surprising similarities between diabetes and multiple sclerosis, a central nervous system disease. His interest was also piqued by the presence around the insulin-producing islets of an "enormous" number of nerves, pain neurons primarily used to signal the brain that tissue has been damaged.

Suspecting a link between the nerves and diabetes, he and Dr. Salter used an old experimental trick -- injecting capsaicin, the active ingredient in hot chili peppers, to kill the pancreatic sensory nerves in mice that had an equivalent of Type 1 diabetes.

"Then we had the biggest shock of our lives," Dr. Dosch said. Almost immediately, the islets began producing insulin normally "It was a shock ? really out of left field, because nothing in the literature was saying anything about this."

It turns out the nerves secrete neuropeptides that are instrumental in the proper functioning of the islets. Further study by the team, which also involved the University of Calgary and the Jackson Laboratory in Maine, found that the nerves in diabetic mice were releasing too little of the neuropeptides, resulting in a "vicious cycle" of stress on the islets.

So next they injected the neuropeptide "substance P" in the pancreases of diabetic mice, a demanding task given the tiny size of the rodent organs. The results were dramatic.

The islet inflammation cleared up and the diabetes was gone. Some have remained in that state for as long as four months, with just one injection.

They also discovered that their treatments curbed the insulin resistance that is the hallmark of Type 2 diabetes, and that insulin resistance is a major factor in Type 1 diabetes, suggesting the two illnesses are quite similar.

While pain scientists have been receptive to the research, immunologists have voiced skepticism at the idea of the nervous system playing such a major role in the disease. Editors of Cell put the Toronto researchers through vigorous review to prove the validity of their conclusions, though an editorial in the publication gives a positive review of the work.

"It will no doubt cause a great deal of consternation," said Dr. Salter about his paper.

The researchers are now setting out to confirm that the connection between sensory nerves and diabetes holds true in humans. If it does, they will see if their treatments have the same effects on people as they did on mice.

Nothing is for sure, but "there is a great deal of promise," Dr. Salter said.

© (c) CanWest MediaWorks Publications Inc.


<shortened url>

I am excited by the attention on the pancreas and mention of Dr. Hans Michael Dosch's 1999 paper which concluded, "there were surprising similarities between diabetes and multiple sclerosis...."

Since I think this news is appropriate to this thread, I am repeating the posting here, with much thanks to Stavros for the initial posting and with much thanks to another here who drew it to my attention.

I am excited by this research discovery, can you tell?
Last edited by lyndacarol on Sat Jan 30, 2010 4:15 pm, edited 3 times in total.
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Postby Chris55 » Mon Dec 18, 2006 8:26 am

I completely "stop" an incurable disease (intersistial cystitis) with nothing but supplements/diet changes. There is no real effective treatment and the cause is unknown. Some do suspect "autoimmunity". After all of my reading/research, I do not believe in autoimmunity diseases, i.e., the immune system attacks the body for no known reason. I believe it is a great "misc." diagnosis. JMO.

My episodes of IC seem to occur when I undergo a severe diet change. Since I refuse to live with this disabling disease, I tried everything I could get my hands on! The diet/supplements are like a miracle drug.

For those with MS, I believe diet is indeed critical. It's a matter of finding what is best for you.
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Astaxanthin-insulin connection?

Postby lyndacarol » Thu Dec 28, 2006 3:07 pm

The following is taken from a General Discussion posting on October 17, 2006, in which I responded to Minai concerning zeaxanthin:

"A friend with an MS diagnosis sent me info on a product she had used and thought it had improved her situation. Among many elements in the product description (most coming from the sea--seaweed) was astaxanthin. Is this the part that helped her?

Then on Sep 11, 2006, Reuters carried an article that a Japanese researcher, Dr. Kazuo Miyashita, from Hokkaido University found that rats and mice fed brown seaweed, also known as wakame, lost weight and expressed a protein that led to regulation of metabolism. The key compound was called fucoxanthin.

The article stated, "Miyashita and colleagues also found that fucoxanthin has 'strong' anti-diabetes effects by promoting the synthesis of DHA in the liver."


Now, I have no background in science; but it seems logical that the word similarities would indicate that these two are related to zeaxanthin. Is it possible that the improvements you observed are connected to the zeaxanthin, not the lutein at all?

For those who don't know me--I believe there is a connection between MS and excess insulin. A connection between MS and diabetes has been established. Maybe all these things are related through the pancreas.

By the way, if brown seaweed is the answer, I hope it comes in a capsule--I tried an Asian soup with wakame and it tasted AWFUL!"

_______
Next, the following on astaxanthin comes from page 10-11 in the book by Nicholas Perricone, M.D., 7 Secrets to Beauty, Health, and Longevity.

"Astaxanthin, The Multifunctional Antioxidant

Astaxanthin is a unique and multitalented antioxidant. It is also one of the reasons for wild salmon's status as a leading superstar in the realm of anti-aging foods. However, it is also important to take astaxanthin as a nutritional supplement to ensure optimum benefits.

Astaxanthin has the ability to protect the cell membrane from free radicals also known as reactive oxygen species, or ROS, including the most damaging of all, the singlet oxygen.
Carotenoids in general, and astaxanthin in particular, effectively absorb energy from free radicals and the singlet oxygen.

Astaxanthin provides powerful protection to the lipid bi-layer that surrounds our cells as well as the mitochondria and the nucleus within the cells. This dual function of protection is unique to astaxanthin and one of the reasons it plays such an important role in the protection of cells. Because astaxanthin can penetrate different portions of the cell, it protects all organs and systems throughout the body. This broad-based protection is the foundation for the multifunctional benefits that have become associated with astaxanthin and its anti-aging properties. The health areas that have been studied include:

> Cardiovascular: Recent studies have indicated the tendency of astaxanthin to reduce blood pressure. The antihypertensive mechanism may in part be explained by the tendency of astaxanthin to increase blood flow. It is hypothesized by the researchers that this results from blood vessel relaxation and dilation. Also, in one of the studies, a 50% drop in the incidence of stroke was noted in the astaxanthin-treated group.
> Type 2 diabetes: A preliminary study indicates that astaxanthin supplementation may improve control of type 2 diabetes and inhibit progressive kidney damage. This study also supports the findings of an earlier study that indicates that astaxanthin may preserve pancreatic function as well as insulin sensitivity.

Other benefits include:

>Improved skin elasticity and reduced appearance of fine lines
>Eye fatigue (asthenopia) reduction
>Improved muscle endurance and recovery following vigorous exercise
>Reduced gastric inflammation and dyspepsia


It is important to note that all of these studies were performed using the AstaREAL brand of natural astaxanthin, which is produced from the microalgae Haematococcus pluvialis, a natural carotenoid pigment and biological antioxidant believed to be the world's richest source of astaxanthin, in fully enclosed and protected biosystems either in Sweden or on the Island of Maui in Hawaii. As with so many nutritional supplements, it is critical to know that you are getting the highest-quality, most vigorously tested -- for both safety and efficacy -- formula possible. AstaREAL is a trademark of Fuji Chemical Industry."




Now, as the resident "insulin proponent", I wonder if some of some of the effects of salmon-eating on MS could be due to, not only omega-3s and Vitamin D, but to the fact that "astaxanthin may preserve pancreatic function as well as insulin sensitivity."

More food for thought!
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Pioglitazone and Neuroprotection in SCI

Postby Shayk » Sat Dec 30, 2006 7:51 pm

Lynda Carol

I noticed “pioglitazone” mentioned in a couple of threads but I thought I’d stick this info in the insulin thread since pioglitazone is used to treat diabetes (I think). Anyway, in this abstract about spinal cord injury in rats, “pioglitazone” showed some potential neuroprotective properties.

Thiazolidinedione Class of PPAR{gamma} Agonists Prevent Neuronal Damage, Motor Dysfunction, Myelin loss, Neuropathic Pain and Inflammation Following Spinal Cord Injury in Adult Rats.
Both pioglitazone and rosiglitazone……significantly decreased the lesion size (by 57 to 68%, p<0.05), motor neuron loss (by 3 to 10 fold, p<0.05), myelin loss (by 66 to 75%, p<0.05), astrogliosis (by 46 to 61%, p<0.05) and microglial activation (by 59 to 78%, p<0.05) after SCI.

Pioglitazone also significantly enhanced the post-SCI induction of neuroprotective heat-shock proteins and anti-oxidant enzymes.


So, let’s hope the Phase II Clinical trial of pioglitazone for MS shows positive results. It seems like it has the potential to impact the MS disease process in several ways (at least in adult rats with SCI).

SCI might be relevant in MS, per the “inside-out” model described in this abstract.
the rather unexpected similarity between spinal cord injury (SCI) and MS where axonal injury, oligodendrocyte apoptosis and demyelination are all present. In SCI, transection of axons leads to delayed oligodendrocyte apoptosis with secondary demyelination…..

This implies that axonal injury could trigger demyelination. In this instance, lesions develop from the axon (inside) to the myelin (outside) (Inside-Out model).


It would be really nice if pioglitazone is therapeutic and neuroprotective. 8)

Sharon
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Pioglitazone, diabetes, insulin,...and neuroprotection

Postby lyndacarol » Sun Dec 31, 2006 9:20 am

Thank you, Sharon. Yes, pioglitazone is used in diabetes. And yes, I think your posting was absolutely appropriate to the insulin thread!

I agree wholeheartedly with your last sentence!!! It would be really nice!!!
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First observations in pathogenesis of MS

Postby lyndacarol » Sat Jan 06, 2007 1:51 pm

First Lyon posted this link in October:

http://www.nationalmssociety.org/Brochu ... yofMS1.asp

It mentioned that almost 80 years ago scientists found most damage around the blood vessels in MS.

Now from msnews.bostoncure.org I read a posting on January 3, 2007, by skedlo, which stated:
Below is a link to an abstract linking immune response to worsening of atherosclerosis. This might not seem like it would be important compared to MS. But, in Dr. Le Gacs papers, listed on the site, he goes into specific detail about vascular events causing lesions in the capillaries (implicating BBB breakdown initially) being the first observed events in the pathogenesis of MS -- not demyelination, which comes later. This may have serious implications to further understanding how MS begins, and ways to stop, minimize damage or a faster track to diagnosis of MS. http://www.nature.com/modpathol/journal ... 0791a.html


The common implication of blood vessels or vascular system intrigues me--of course, you know I think excess circulating insulin is causing initial damage and then the immune system steps in.

More food for thought.
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Postby Lyon » Sat Jan 06, 2007 2:34 pm

Hi Lynda,
Thanks for the reading material!
Bob
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Need help in finding Dr. Legac's papers

Postby lyndacarol » Sat Jan 06, 2007 3:14 pm

My, Lyon, you are fast! In the short time I took to look for the Legac papers referred to in skedlo's posting you are here!!!

I am interested in finding the actual abstracts or articles reporting his "specific detail about vascular events causing lesions in the capillaries...being the first observed events in the pathogenesis of MS...."

I have searched at the nature site, tried google--no luck. I would like to find it directly, can anyone help me? I believe his name is Paul LeGac, M.D. in France.
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Re: Need help in finding Dr. Legac's papers

Postby Lyon » Sat Jan 06, 2007 3:34 pm

lyndacarol wrote:I have searched at the nature site, tried google--no luck. I would like to find it directly, can anyone help me? I believe his name is Eric Legac, M.D. in France.
So far the best results seem to be shown by typing "Legac vascular" into the search engines. But like me, you are probably going to bump into sites which want money for the information. I'm too cheap to spend money before I know for sure that it's the paper I want.

My wife's trying to talk me into a movie tonight so I'm not going to have time to do an exhaustive search but my interest is up. I got the idea from one of the initial summaries I viewed that Legac seemed to be saying that parasites seem to mediate this effect. It was just a quick peek, I'm probably jumping the gun.

If you've got the time, do as I do, become a stalker. Find out where he works, get his email address and write and ask him to send you the paper. It's worked every time so far.

Bob
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Postby jimmylegs » Sat Jan 06, 2007 4:31 pm

plus the correspondence contact is from UBC which is sooo cooool! i love vancouver. you should go visit him personally LC :)
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Stalkress on the loose

Postby Lyon » Sat Jan 06, 2007 9:18 pm

Gosh jimmy, there have been claims in the past that you are a stalker but I gave you the benefit of the doubt........at this point I have to wonder how you instantly knew this guy's GPS coordinants and brand of cologne he wears? :lol:
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the united states of whatever

Postby jimmylegs » Sat Jan 06, 2007 11:36 pm

well best friends i guess! hahaha whatever!
legs
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Postby Lyon » Sun Jan 07, 2007 2:25 pm

That's good. You know I'm kidding you.
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sherlocklegs

Postby jimmylegs » Sun Jan 07, 2007 3:22 pm

just to clear up the mystery, when you read the abstract posted above

http://www.nature.com/modpathol/journal/v16/n5/full/3880791a.html

it says this:

Mod Pathol 2003;16(5):460–470

Granzyme B in Atherosclerosis and Transplant Vascular Disease: Association with Cell Death and Atherosclerotic Disease Severity
Jonathan C Choy B.Sc.1, Paul C McDonald Ph.D.1, Agripina C Suarez B.Sc.1, Vivian H Y Hung1, Janet E Wilson B.Sc., M.T.1, Bruce M McManus M.D., Ph.D.1 and David J Granville Ph.D.1

1The iCAPTUR4E Centre/UBC McDonald Research Laboratories, Department of Pathology and Laboratory Medicine, St. Paul's Hospital/Providence Health Care–University of British Columbia, Vancouver, British Columbia, Canada

Correspondence: David J. Granville, Ph.D., The iCAPTUR4E Centre/UBC McDonald Research Laboratories, Room 292, Burrard Building, St. Paul's Hospital, Vancouver, British Columbia, V6Z 1Y6 Canada. fax: (604) 806-8351; e-mail: dgranville@mrl.ubc.ca

Accepted 13 February 2003.
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