Test demonstrates that type 1 diabetics produce low level insulin

New discovery in type 1 diabetes, an essay demonstrates that there is long -term insulin production, which could be key to reverse the disease.

Traditional doctrine argues that insulin production in people with type 1 diabetes ceases a year after diagnosis.However, new ultrasensitive blood trials have shown that many people with type 1 diabetes produce low level insulin for decades after diagnosis.

The data will be presented at the Congress of the European Association for the Study of Diabetes (EASD) 2014

The clinical consequences of low -level insulin production were previously unknown, but two studies presented at the EASD Congress of this week expand the previous data.

The first, directed by Professor Timothy McDonald of the Royal Devon and Exeter Hospital, shows that most patients with long -term type 1 diabetes continue to segregate insulin (as measured by peptide secretion C) and have peptideC detectable in urine and blood.

The second, led by Professor Denise Faustman of the Massachusetts General Hospital, demonstrates that extremely low peptide C levels seem to have clinical importance and can be useful to define groups of long -term diabetics that are the greatest risk of complications or poorMetabolic control

These data can support evidence for clinical trials that seek to invest type 1 diabetes, opening the clinical trial participation of recently diagnosed patients to the entire population of type 1.

Professors Faustman and McDonald will present their information at EASD 2014:

Denise Faustman, MD, PHD

Immunobiology Director, Massachusetts General Hospital;Associate Professor of Medicine, Harvard Medical School;and president of the BCG and Autoimmunity Working Group

Personally I am studying non -stop in all the publications I can about diabetes and with the C Peptide C is the second thing I have amazed.
The secret pancreas for each insulin molecule another of peptide C and that is so from fish to us.
That means that the c peptide is so important as the same insulin.
Maintenance studies of the insulin residual function show that 10% to 20% of diabetics maintain a minimum insulin production and that same proportion is that of diabetics that never develop long -term complications.
But the thing is more serious, in studies it is demonstrated that damage to microvascular, macrovascular kidney, retinopathy, etc. When managing peptide C, they reversed !!
The logical would be that the insulin we put also carried the same amount of peptide C especially because it is easier to manufacture by genetic engineering than the insulin itself.
The question:
Can you know why the demons are not administering to us ???????

How interesting everything you tell !!! ...

Totally agree with @roar !!

@Ernesto And then because type 2 diabetics that have a lot of peptide C in the blood usually have enough problems than type1 and faster?

@Sherpa41 The answer is a bit long but for what I have studied consistent and endorsed by hundreds of studies and publications.
I go in parts
DB2 have insulin resistance with what pancreas segregates huge amounts of insulin and peptide C, but not only of that but of the other co-scheduled product that is amiline.
Amiline is the thing that I have hallucinated most (the second the peptide c).
The excess of blood amiline produces that it is deposited mainly in: kidney, skin, nerves, gums and liver ...
Does it sound familiar?
Amiline when deposited forms a thing called amyloid substance that is one of the nightmares of anatomopathologists.
Amiloidosis is developed by primates and felines and "curiously" those who develop Alzheimer's are ... Yes, you have guessed it, primates and felines.
The function of the amiline is that in the postpandrium excess glycemia does not rise since it slows the absorption of the hydrates and gives the order to the pancreas of ceasing the production of glucagon with what insulin can work in full performance.
When the pancreas in the end already fails everything because the amyloid deposits are already there.
Ask the doubts that arise and will expand the information

I have a question, and he asked seriously, where do you get so much information?Are you a doctor?

Thank you very much for your comments.I missed these messages ... Owash!We miss you!

@tica I answer you.
I studied medicine but I decided not to exercise, and work as chemical, of many more things and in the last 10 years as a kind of advisor/commercial in biology and drinkable and wastewater treatments.
As for the information, the advantage that I have is that a text of medicine/biology for me does not represent any problem and in the faculty what we are told (only the good catheders) is that the important thing is not to know a fact, but to knowWhat book is and the Internet advantage is that I don't have to spend hours in the library taking moldy booklet dust.

Ernesto said:

The excess of blood amiline produces that it is deposited mainly in: kidney, skin, nerves, gums and liver ...
Amiline when deposited forms a thing called amyloid substance that is one of the nightmares of anatomopathologists.
When the pancreas at the end already does not care because the amyloid deposits are already there ...
Ask for the doubts that arise and will expand the information

I am glad that someone with the ability to translate the medical magazines can explain them, I hope you are a lot here and you can give us the original version of many news and not the one that gives us a journalist without an idea of ​​medicine.And so a boat soon ...

1-Is there no treatment to clean amiline deposits or something that slows its formation?

2- What is the cause that convinces you most to explain the appearance of the DM1?Is it also the theory that relates it to amiline deposits around beta cells?

3-When do you think a cure or treatment will come out that replaces the torture of continuous insulin injection?

@Sherpa41 I will answer you in parts ... and prepare because the answers will not like you.
The amyloid substance is described by the great virchow around 1870 and gives it that name for its resemblance to the microscope with the starch, it is described in relation to associated diseases in that time to old age.
It is associated with diabetes 2 (evidently in that time the 1 did not survive) to renal failure, Alzheimer's, etc.
As was associated, it was not clear if it was the cause or effect.
Towards the 50s an amyloid precursor is identified but it is not known where there is even the function it has, what is known is that in which they develop problems there is more quantity and in which no, there is less.
Once you have located the source of the amyloid substance you can start doing something.
In the 80s it is identified that it is the pancreas that segregates it and more specifically the Beta cells.
The problem that arises with amiline when it is in large quantities in blood is that it is added in deposits that damage the cells.
Like all proteins, amiline has a primary structure that is the list in order of the amino acids that form it, a secondary structure that is the first folding that occurs, a tertiary structure that is the three -dimensional structure and according to the protein that is aQuaternaria that is how these proteins are grouped to form a larger structure.
The hormones have a part that is the "active" and other parts that are the support for that "key" to act or that is properly transported or that the organism degraded it or not ... as the case is.
The research immediately takes a very logical path, can we vary the primary structure without touching the active zone so that it folds otherwise in its secondary structure?
The answer was immediately and it is yes !!!
In the early 90s, Pramlintida acetate of Commercial Name Symlin that is not added in amyloid substance and also makes the aggregates are also dissolved.
When the pancreas administer it, it segregates the minimum with what lowers the production of your own amiline in favor of which we inject.
In the DB2 as we also inject it before eating causes a sensation of "full stomach" before there really is food in the stomach with which the hunger decreases that is one of the problems of the 2.
The other effect of amiline is that postpandrial glycemia does not rise so much and then maintains in the period between meals.
Postpandrial glycemia peaks are more important to avoid long -term damage than high glycosilada .... Do you find it strong?To my much.
The LDL cholesterol (the nightmare of endocrine visits) rises due to the oxidative stress of postpandial hyperglycemia.The above is strong this comes out of the scale.
I include links where you see that the Symlin is not a novelty and I have lowered a file where the medicine patent application for Europe of the Year of the Year ¡¡1993 !!!!
Link
The thing is so clear that in this Mexican page of 1995 it is said directly:
In other words, the DM is characterized by a deficiency of both I (insulin) and amiline.
Why are Symlin not being managed both to the DB1 and the DB2?
I don't understand it, I sincerely escape me, it leaves me speechless.
Laboratory evil?Fully discarded since your interest is that they prescribe it and sell it.
INEptitude of the Spanish Medicine Agency?It is possible, this is an organism in which there are people who are not worth it for boat.
Government blockage not to spend money by adding costs to treatment?I think it is as much as possible although I do not believe that the most minimal cost/benefit analysis resists, but since it does not existNo public statistics of the number of diabetics in Spain or possessed of the cost of the movemos moventos in the pure specification.
In the field of rumors and leaks I have read that the cost of diabetes and associated processes ranges between 8% and 12% of total social security welfare spending, so anything that involves spending more today to lower thatLong -term ratio is an investment that offers no doubt.
Finally I put a couple of links so that you report if you feel like it not only for what I write and I have tried to be with a more or less "normal" language
Link
Link

The cause of the DB1 that convinces me the most.
As I have answered before, in the 1 the amiline problem does not exist since it does not occur and that is one of the problems of the DB1
There is a clear association between a series of genes related to immunity and the development of the disease that for what I have seen can reach up to 20% of total probability.
But .... I have seen studies that convince me of association between the development of the DB1 and the enterovirus.
Enterovirus is the well -known summer intestinal flu and this has logic since it is from the family of the flu virus and has the ugly habit of coating with a cover taken from ours cells to escape detection by the immune system, but thatIt can raise a problem since if our immunity discovers that within that cover is the "enemy" can put it on the list of things to attack and ... shit!I also have that cover.
What follows you already know ... debut, scare, insulin, etc.
I read that there is a study and a budget to develop a vaccine for the Enterovirus and protect the population of the DB1.
Now comes anger:
The cost was calculated at 7,000 million euros and in Europe there is at this time budget to carry it forward.
How does your body stay?I personally the day I saw it made a review of insults and blasphemies as not for my time of the Navy.
If you want, I look for the link and put it even if I will take a valium before.

This amiline analog ... Isn't it that they don't give it to type1 because we would have to click 2 times before each meal, with all the increase in material and complications and gain that that would imply?

Since according to the links you have put, you cannot prick along with insulin, they only recommend it to people who do not get good control or who want to have superfect control.I do not know, but if they tell me that I have to prick something else, that apart from insulin-dependent I am amilino-dependent ... I prefer to shoot myself.The only thing I want is to be independent of all of one p*, that I have been chained to insulin and glucometer injections.

Then that the cause can be an Enterovirus that camouflages and confuses the system with beta cells, then reverse that situation would be very difficult, although there are many studies on re-educating the immune system to correct that.And you have not answered me when you think a cure or treatment can come out of insulin injections.Do you think that viacyte type encapsulated cells will work in the near future or do you believe more in another type of system?

If the Beta of the pancreas produces three things and the three evolution considers them as important that all mammals have them chemically almost equal, do you consider that the treatment only with one of them is correct?
I don't see it that way
The C peptide can be placed in the same dose that you put the fast, slow, pump or whatever insulin.
Amiline cannot be mixed since the dose is very small and is on demand when it is eaten.
I guess you spent honeymoon ... Place those two missing products is something like returning to the honeymoon and remove the nightmare of long -term damage.
The problem according to it is that once you have destroyed the population of beta cells although the immune system ceases the attack there is no much to do except to prolong the honeymoon.
Immunosuppression treatments have been tested on the debut and nothing has been achieved

As for the solution by mother cells
I have read many times news and even recommendations to governments by committees of experts of the type:
It is not worth implementing new pharmacists that suppose a cost since according to experts in the 15 -year "order" there will be transplants of mother cells or something similar.
The problem is that this error is based on the difference between mathematical and common language.
When we say "order" we mean that the decimal comma moves a single position ahead and behind, that is, order 15 comprises from 1.5 to 150.
It means that the experts who say this what they really say is that they do not expect it before 1.5 years but I would miss them to take more than 150 years.
This is not an evil but a way to calculate, this summer I had to make an opinion about a water that was damaging an installation and in the analysis that I did in person, the sodium value gave me 1300 and met with another expert with another expertAnd because of the effects we saw with our own eyes we knew that we were in rank above 1,000 and below 5,000.However, the property had another analysis with an unconfessable economical interest that said there were 100, so without confirming my analysis we knew that 100 was out of rank and therefore it was wrong.
So for that it is for dealing with these issues as ranges, to limit a fork between 1.5 and 150 years
In addition, in all predictions, a "breakup" is implied, that is, the appearance of a genius or an unexpected discovery (as a Japanese team intended to have found and that in the end the "alleged discoverer" is committed suicide) and unfortunately this cannot be boughtWith money, however bulky the check we cannot make a Mozart, an Einstein or a Darwin appear.
In addition, as all things in science we are counting that nature is not unpleasant in the sleeve that will make everything impossible.
Anyway, growing mother cells that said, in a bar, it seems sucking I assure you that it is a nightmare.
I have cultivated bacteria and it was already very difficult, cultivating human tissue in a laboratory is available to a few and already reprogramming mother cells gets out of the scales.
The problem is that today it can be done and has been done but how many people would be missing for how long to treat a single DB1 patient?
I answer you with an estimate, of the order of 10 specialists from the upper level in a laboratory of the highest technology for a year ... and you know what that means, that there is no number of technicians and pay does not work for them to appearGeniuses as I said before.
For me, the solution comes to deepen chemistry, investigate whether there is any enzyme or hormone but not discovered, put in production and release existing products and direct efforts in the implementation of automatic pumps and continuous analyzers to automate everything and be ableLife in which only something similar to a pump with computer handle had to be placed with an MCG.
It is much cheaper to develop software.
For me personally if I put 3 more injections a day with meals and that insulin carries peptide C I accept it in order to stay on an endless honeymoon.

Ernesto said:
The peptide C can be placed in the same dose that you put on the fast, slow, pump or whatever insulin.
Amiline cannot be mixed since the dose is very small and is on demand when it is eaten.

The C Peptide I suppose it would be good to put it although I think I remember some study and did not find long -term improvement.Do you know any study that shows that in human patients something improves?

You because you just have been clicking you but those of us who have 20 we have the areas to the limit of punctures.If the control were incredibly better yet, but that does not seem either.

And never pass the honeymoon.And I think that although the amiline improves postprandial control, insulin injections will continue to be far from the control provided by beta cells and continue long -term damage.

Ernesto said:
The problem as I see it is that once you have destroyed the population of beta cells although the immune system ceases the attack there is not much to do except to prolong the honeymoon.
Immunosuppression treatments have been tested on the debut and nothing has been achieved

It seems that with only one year of diabetic you are already as pessimistic as those who carry 50. I will only tell you that my cousin DM1 was injected with beta cells in the 90s and ceased to be completely diabetics.That if it takes immunosuppressants because the same year they transplanted a kidney.I believe that one day not too distant they would get that, but without immunosuppression.

Repeated

If there are studies that show improvement even in the short term, the problem is that when the effect on healthy people has been studied, no effect is observed since its action mechanism is not usual but also acts by activating DNA areas and once theCellulas have the dose that makes them start up even though you increase the dose does not increase the effect, it would be something like that once you give the room light button, no matter how much you press the bulb the bulb does not illuminate more

Sherpa, explain to us about the beta cells that put your cousin.Was type 1?And is it no diabetic anymore ???

Beta transplant cells?

Regina said:
Sherpa, explain to us about the beta cells that put your cousin.Was type 1?And it is no longer diabetic ???

Yes, it was type 1 and for 20 years it is no longer click.She passed since she was very small to twenty and so many being diabetic, it was the only type1 she knew.That is why when I debuted (precisely 20 years ago) I went to talk to her to explain how he had the disease, and told me that it went very badly, that it was an atypical case with constant income, they put a pacemaker,Then he began to need dialysis and since he was very young, he was transplanted a kidney right away and incidentally, as he took immunosuppressants, they also put beta cells (I think that in the liver), he stopped being diabetic just when I began to be.

And I don't have contact with her anymore, but through other relatives I know that it is fine and I heard that they inject more beta cells years ago.Oh and his parents had a lot of pasta, although I know that their kidney transpaltent and the first beta cell injection were made by the public.