[AndreLaplume]

a shot to have the body remain uninflamed and the body regulate its own sugar levels than the shot for us to regulate it ourselves. Lets see if we hear more on this or if it mysteriously fades away. You would have thought such promising news would have made it into the major newscasts...never saw it mentioned except here!

Originally Posted by Just_Plain_John

No, I think you are mistaken. The pancreases keep trying to produce beta cells (insulin producers) but the nerve inflammation causes the new betas to be killed off. Once the inflammation is stopped with the capsaicin, the new betas get to work and make insulin, even in someone with D for a long time.

The trick will probably be getting the nerves to STAY uninflamed. I imagine that a shot for that nerve cluster is even harder than not bruising myself with a mealtime bolus... The technique of applying this medicine may take a little while, but the mechanism seems to be very promising.

If I remember right, this may also relate to multiple sclerosis - I'm not sure where I heard that part, though.

[Jak]

Andre, keep in mind that it is not just the inflammation that is a factor here. To quote: “These nerves secrete insufficient neuropeptides which sustain normal islet function, creating a vicious circle of progressive islet stress.”

Yes, they need to control the inflammation, but they also need to figure out how to either get those nerves producing the neuropeptides they lack, or somehow replace them (the neuropeptides) by another means.

Jak

[AndreLaplume]

I thought the study said the mice were cured by, in effect, destoying those nuero cells....

[Jak]

Originally Posted by AndreLaplume

I thought the study said the mice were cured by, in effect, destoying those nuero cells....

I've gone over this another time. I think what they're saying is that removing those nerve cells prevents diabetes, but does not cure it. I've edited the following information to make is more readable (I hope):

'“We...found that specific sensory neurons are critical for islet immune attack... These nerves secrete insufficient neuropeptides which sustain normal islet function, creating a vicious circle of progressive islet stress.”

Using diabetes-prone NOD mice...the research group learned how to treat the abnormality by supplying neuropeptides and even reversed established diabetes.

“The major discovery was that removal of sensory neurons expressing the receptor TRPV1 neurons in NOD mice prevented islet cell inflammation and diabetes in most animals...Disease protection occurred despite the fact that autoimmunity continues in the animals. This helped us to focus our studies on finding the new control circuit in the islets.”

Strikingly, injection of the neuropeptide substance P cleared islet inflammation in NOD mice within a day and independently normalized the elevated insulin resistance normally associated with the disease. The two effects synergized to reverse diabetes without severely toxic immunosuppression.'

From what I read it appears on the one hand they are talking about the removal of sensory nerves expressing the receptor TRPV1 neurons preventing inflammation and diabetes, while on the other hand they are talking about reversing (curing) established diabetes by adding neuropeptides. (I'm wondering, too, if the neuropeptides to which they refer are actually the capsaicin. Hmm.) Anyone else have any thoughts on this?

I guess I'll have to go do some research on TRPV1 receptor neurons and neuropeptides . . .

Jak

[erich]

After a quick scan of this thread I didn't see it mentioned about the mice being cured for four months.

Am I correct in assuming that due to life cycle that means 15-20 years for us?

Tahnks ,
Erich

[Harold]

Originally Posted by erich

After a quick scan of this thread I didn't see it mentioned about the mice being cured for four months.

Am I correct in assuming that due to life cycle that means 15-20 years for us?

Tahnks ,
Erich

Good point. Maybe they ran out of mice after curing all of them.

[Jak]

Originally Posted by erich

After a quick scan of this thread I didn't see it mentioned about the mice being cured for four months.

Am I correct in assuming that due to life cycle that means 15-20 years for us?

Tahnks ,
Erich

I dunno, Erich, but my first guess would be "no".

Jak

Originally Posted by erich

After a quick scan of this thread I didn't see it mentioned about the mice being cured for four months.

Am I correct in assuming that due to life cycle that means 15-20 years for us?

Tahnks ,
Erich

I couldn't find anything specific in regards to a four-month cure in mice being equivalent to 15-20 years in humans, but according to the following, it would be a mistake to make such an assumption based on the life cycle of mice as compared to the human life cycle:

"The phenotypic differences mentioned above between mice and humans due to telomerase deficiency are a perfect example. As proven time and time again in other biomedical fields, what occurs in the aging process of other mammals may not be representative of human biology (reviewed in Davenport, 2003). Therefore, if we base our understanding of human aging on model organisms, even mammals, we must be careful about extrapolating findings into humans. One of the reasons why the mechanisms responsible for human aging remain largely a mystery is the lack of appropriate models where scientists can test their hypotheses and the controversy relating to the interpretation of findings in those organisms."

[erich]

Today in The Washington Post there was this article that gum disease may be linked to more serious health problems, in this case pancreatic cancer.
washingtonpost.com

Seems inflammation is a much bigger villain than anyone expected.

Erich J. Knight

This Hot Pepper story in the National Review of Medicine I thinks spells out the work in a little more detail:

NRM: Canadian team cracks type I diabetes code

[Cjohnson202]

Once again, I volunteer myself for testing....lol

[Emmasmommy]

HI all im new here but My Daughter attends the clinic at the hospital for sick children (the place "discovered" this) I have been asking many questions about what it is they found. From what they have told me this may not be a cure for everyone. But this maybe a cure for some from what they have found not all diabeties is directly linked to the nervous system but the ones that are this is very promissing. I hope and pray that this is just the start of some great things to come. My son is curently part of a world wide study that is looking for a "triger" being related to mile protien being given to infants through formula. They are using "high risk" Kids (my 4 month old tested positive for the gene) and they are giving half the kids milk based and the other half milk free for the first 6 months of life. This is a 10 year study and hopefully it eaither can pervent or give us more information about what causes this for the kids that are not nervus system related. Just my 2 cents

[Jak]

Originally Posted by erich

This Hot Pepper story in the National Review of Medicine I thinks spells out the work in a little more detail:

NRM: Canadian team cracks type I diabetes code

Thanks, Erich. This article explains it much better than any of the others I've read. Unfortunately perhaps, it explains in more detail why it may not be a cure of all of us. However, as mentioned, it "opens up an entirely new field of investigations in type l and possibly type ll diabetes, as well as tissue selective autoimmunity in general." Here's hoping something good comes from this -- hopefully soon.

Jak

Originally Posted by Emmasmommy

HI all im new here but My Daughter attends the clinic at the hospital for sick children (the place "discovered" this) I have been asking many questions about what it is they found. From what they have told me this may not be a cure for everyone. But this maybe a cure for some from what they have found not all diabeties is directly linked to the nervous system but the ones that are this is very promissing. I hope and pray that this is just the start of some great things to come.

Hi Mom. What you say about any eventual cure evolving from this research maybe not being a cure for everyone with type 1 backs up the information from the link Erich provided. Too bad for some, but hopefully it will lead to a cure for at least some of us.

How old was your daughter when she was diagnosed?

Jak

Originally Posted by Jak

How old was your daughter when she was diagnosed?

Jak

Just checked another post. Fourteen months it is.

Jak, also from Canada (Saskatchewan)

[Emmasmommy]

My daughter was 14 months when she was dx

[LiveNormal]

Originally Posted by Jak

Thanks, Erich. This article explains it much better than any of the others I've read. Unfortunately perhaps, it explains in more detail why it may not be a cure of all of us. However, as mentioned, it "opens up an entirely new field of investigations in type l and possibly type ll diabetes, as well as tissue selective autoimmunity in general." Here's hoping something good comes from this -- hopefully soon.

Jak

Hi Jak, do you mind pasting the original text of this report in this thread? I tried to connect to it but to no avail...

I was diagnosed 7years back in 2000. Back then, we tried oral medicine for 6 months before proceeding to using 30/70 mixtard. My current Endo told me I am not type 1. In his opinion, no type1 can survive 6 months without insulin.

[erich]

National Review of Medicine
JANUARY 15, 2007 VOLUME 4 NO. 1

ADVANCES in MEDICINE

Canadian team cracks type I diabetes code

Targeting defective neurons could lead to a cure for types I and II

By William D Donaldson



Canadian researchers may well have just cracked the root cause of type I diabetes, opening up new avenues of treatment, prevention and potential cure for this baffling disease. What's more, the findings could have major implications for the more prevalent type II diabetes — maybe even other autoimmune pathologies as well.

The astonishing results — though only seen in mice so far — seem to have overturned the longstanding assumption that type I diabetes is caused by a defect in immune cells. The cells that are actually responsible for the pathogenesis of the disease are sensory nerve cells in the pancreas called TRPV1 neurons, researchers from the Toronto Hospital for Sick Children and the University of Calgary reported in the journal

on December 15. With that understanding, they succeeded in reversing the disease without any serious immunosuppressive side effects.

A NERVOUS BREAKDOWN
It's well known that diabetes involves a progressive failure of the insulin-producing º cells in the pancreatic islets of Langerhans. The stress and death of these cells attracts autoantigens that in turn draw in lymphocytes, which attack the remaining º cells. But those same autoantigens are also present elsewhere in the body, and despite decades of research, it remained unclear why such a severe autoimmune reaction occurred only in the pancreas — until now.

"We started to look at nervous system elements that seemed to play a role in type I diabetes and found that specific sensory neurons are critical for islet immune attack in the pancreas," Dr Hans Michael Dosch, the study's principal investigator and senior scientist at the Toronto Hospital for Sick Children, explained in a release.

What's more, the nerves' own function is dependent on local insulin levels: in the absence of sufficient insulin, they produce less of the neuropeptide known as substance P. Lack of substance P, the researchers hypothesised, in turn harms º cell function, further reducing insulin production.

To test their theory, the team destroyed TRPV1 neurons by injecting capsaicin into the pancreas of non-obese diabetic (NOD) mice — the mainstay model of diabetes research. Capsaicin (present in hot peppers) is known to specifically target the neurons, leaving the surrounding tissue untouched.

At 20 weeks' age, more than 70% of the islets were completely free of infiltration by lymphocytes — a hugely significant reduction in autoimmune inflammation. Capsaicin treatment delayed the onset of diabetes and reduced its final incidence by about 80%.

FROM MICE TO MEN
Eliminating the sensory neurons in a mouse model certainly seemed to prevent diabetes, but its applicability to human treatment might be questionable, the researchers knew. After all, destroying neurons in newborn children on the off chance that they might otherwise develop type I diabetes is likely to raise some eyebrows.

"We are now working hard to extend our studies to patients, where many have sensory nerve abnormalities, but we don't yet know if these abnormalities start early in life and if they contribute to disease development," said Dr Dosch. Starting in the next few months, he hopes to look for sensory abnormalities in children born to families at high-risk of type I diabetes, and to follow them in order to identify a connection to disease onset.

In the meantime, there's another even more promising avenue to explore. The researchers also discovered that injecting substance P, the neuropeptide whose production is impaired in faulty pancreatic sensory neurons, produced equally startling results. Injected into the pancreatic artery of diabetic mice, it caused the disease to simply disappear in more than half of them, for periods ranging from two weeks to two months. Insulin resistance fell and blood glucose levels were normalized. Even in the mice whose diabetes remained, metabolic control improved and the weight loss typical in diabetic NOD mice was avoided.

BEYOND TYPE I
Buoyed by their findings, the researchers extended their study to type II diabetes, a much more prevalent form of the disease where insulin resistance is even more pronounced. They compared mice of the B6 strain, a model of type II diabetes, with and without expression of TRPV1. Sure enough, the latter group showed much better glucose response after glucose challenge, suggesting that TRPV1 may play a role in type II disease as well.

And that's just the start of it. The mutant gene that causes the TRPV1 defect in the NOD mouse is located on a stretch of DNA called the Idd4 diabetes risk locus. There's reason to believe that risk loci associated with other autoimmune diseases overlap with this snippet, raising the possibility that TRPV1 might play a role in more than just diabetes.

Collaborator Dr Pere Santamaria of the University of Calgary said the implications could be monumental. "This discovery opens up an entirely new field of investigations in type I and possibly type II diabetes, as well as tissue selective autoimmunity in general. We have created a better understanding of both type I and type II diabetes, with new therapeutic targets and approaches derived for both diseases."

[LiveNormal]

Thank you so much, Erich ...