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Stopping Type 1 Diabetes From Birth

There are separate antibodies for the insulin molecule, beta cells, and other cells.

So one could theoretically produce enough insulin just fine with healthy beta cells, but as soon as they are released, WHAM, gone.

So, "riddle me this.?"
Why isn't my immune system attacking the insulin I've been injecting on a daily basis for the last 42 years..?? Logically my Lantus & Novorapid is a "foreign body" created in a lab & doing it's job. (A little too well sometimes!)

Now I'm pretty amazed at some of the developments regarding research with diabetes. But what I'm seeing regarding a "cure", is little more than "Disney magic" creating footmen out of mice in a lab.. At "midnight" the news just disappears... ;)
 
I've asked that exact question on my blog, several times, and despite scouring sci hub have found no answers, so please, if you know the answer, or know someone who does, then please, enlighten me. I'm serious, I'm here to learn, and have no pretense of anything but ignorance about how insulin specific antibodies exist but only attack endogenous insulin molecules rather than synthetic, exogenous insulin. Does humalog evade IA2 antibodies? If so, how? If the researchers think that pre-training babies to tolerate the insulin molecule can help avoid type 1 diabetes, then they must have the answers to this riddle. It is indeed a riddle that I've heard basically zero about. I believe I even asked the researchers involved in powdered insulin and they don't know.

However, I'm fairly certain that I know about this topic than the vast majority of diabetics on this website, despite my inability to answer this question. The very existence of insulin-specific antibodies must mean the auto-immunity is reacting to a molecule shape it considers foreign. Therein lies the answer, I believe. Junk / damaged insulin is being produced by damaged beta cells that are infected by enteroviruses which are present in perhaps 99% of the human population.
 
I've asked that exact question on my blog, several times, and despite scouring sci hub have found no answers, so please, if you know the answer, or know someone who does, then please, enlighten me. I'm serious, I'm here to learn, and have no pretense of anything but ignorance about how insulin specific antibodies exist but only attack endogenous insulin molecules rather than synthetic, exogenous insulin. Does humalog evade IA2 antibodies? If so, how? If the researchers think that pre-training babies to tolerate the insulin molecule can help avoid type 1 diabetes, then they must have the answers to this riddle. It is indeed a riddle that I've heard basically zero about. I believe I even asked the researchers involved in powdered insulin and they don't know.

However, I'm fairly certain that I know about this topic than the vast majority of diabetics on this website, despite my inability to answer this question. The very existence of insulin-specific antibodies must mean the auto-immunity is reacting to a molecule shape it considers foreign. Therein lies the answer, I believe. Junk / damaged insulin is being produced by damaged beta cells that are infected by enteroviruses which are present in perhaps 99% of the human population.

Dude? It's a conundrum.. I phoned round labs in the 1980's regarding putting myself up for "stem cell research?" This was before the Internet for me, reading stuff in new scientist? They thought I was an "animal rights activist."? & got "stone walled."
Don't underestimate the experiences of diabetics here, (of any type.) they embrace & work with the current tech & knowledge provided whatever personal circumstances financially or otherwise..
We all wish an end to the same issue.

Personally? I may not have tested as a "risk" back in the day before diagnosis 43 to 50 years back...who knows..

We eat animals but not babies. I don't feel apparently healthy kids should be put through this sort of experiment. On an ethical level...

"'Give me a child until he is 7 and I will show you the man." comes to mind on this particular topic..
 
Until we know 100% for sure what the actual cause, or causes of type 1 diabetes is / are, I think most people's intuition (mine included) are probably incorrect.

Humility is a good thing to have, in moderation of course. There are plenty of topics I lack knowledge in, or have incorrect assumptions or understanding in, surely, since I'm just a lay person who happens to have read a lot about it. I am dismayed though, after leaving this site for a few years and coming back to interact with Dan Darkes and I still see incorrect information (e.g. type 1s produce zero insulin) being passed off as gospel truth. I find it odd how such false memes persist. The facts are out there, even posted in the news section of this site, but it's obvious that people either don't read it or just ignore it. For instance, recent study results prove that both BCG and verapamil have measurable improvements for type 1 diabetics. And nobody's really talking about it here. I wonder why that is.

Back on topic, I worry about giving type 1 to my future kids, if I have any, so this is important to me. I want to give them the best chance of having a normal life. Hopefully they'll inherit more of my wife's resilience to this disease and that combined with a low-carb diet from the day they are weaned off milk will train their little guts to not be sugar addicted.
 
For instance, recent study results prove that both BCG and verapamil have measurable improvements for type 1 diabetics. And nobody's really talking about it here. I wonder why that is.
The BCG trial was discussed on this forum. As was pointed out in the discussions at the time, the BCG sample size was very small: https://blogs.diabetes.org.uk/?p=10671

It's probably worth noting that 9/10 people with diabetes, so at least that proportion on this forum, have type 2.
Type 1 discussions have, understandably, much less visibility.
 
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There are separate antibodies for the insulin molecule, beta cells, and other cells.

So one could theoretically produce enough insulin just fine with healthy beta cells, but as soon as they are released, WHAM, gone.

Recent news reports, shared right here on DCOUK, suggest it's damaged or "junk" insulin molecules and beta cells that are attacked by the immune system, so the disease itself isn't an auto-immune malfunction per se, but a perfectly valid immune response to damaged cells which it considers foreign, perhaps creating damaged insulin from an enterovirus (CVB-1). This is confirmed by the fact that all type 1s have some endogenous insulin production and thus functional, mature beta cells, throughout their lives (via both cp tests and autopsies proving it).

I sometimes wonder if any large percentage of those who post in this forum read the news section here, no offense. This data is well-known, and has been for years. Auto-Insulin-antibodies are not news, they've been known for decades now.

Interesting....

I will confirm I don't visit the news section often, if at all......

so its being suggested that the immune response is happening due to damaged insulin molecules as well as damaged beta cells...?

so I should really be changing my response to reflect the immune systems dislike of both the cells and the insulin from said cells....;)...

my understanding has been increased today, thanks....

so, something else, like a virus has caused this damage? what is stopping this virus from damaging all the beta cells in the lifetime of a diabetic...?
 
I expect a virus has something to do with some cases of type1. But I am not convinced there is a single process responsible for the immune cells starting to attack the bete cells.
 
Coxsackie Virus B is one possible cause amongst many:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2570378/

Certain viruses might promote autoimmunity.

A significant number of viruses have been associated with type 1 diabetes, including enteroviruses such as Coxsackievirus B (CVB) (4), but also rotavirus (5,6), mumps virus (7), and cytomegalovirus (8). Rubella virus has been suggested to cause type 1 diabetes, but so far only congenital rubella syndrome has conclusively been associated with the disease (911). The prime viral candidates for causing type 1 diabetes in humans are enteroviruses. Enterovirus infections are more frequent in siblings developing type 1 diabetes compared with nondiabetic siblings, and enterovirus antibodies are elevated in pregnant mothers whose children later develop type 1 diabetes (12). Interestingly, studies in the Finnish population demonstrated that appearance of autoantibodies in genetically susceptible children paralleled the seasonal pattern of enterovirus infections (13). More specifically, a temporal association has been observed between the appearance of the first autoantibodies and signs of enterovirus infection both among siblings of affected children and among children with increased HLA-conferred diabetes susceptibility (14).

CVB4 is the most common enteroviral strain found in pre-diabetic and diabetic individuals. CVB RNA has been detected in blood from patients at the onset or during the course of type 1 diabetes (15,16). Furthermore, cellular immune responses to CVB antigens were found to be enhanced in type 1 diabetic patients after the onset of the disease (17). One CVB4 strain was isolated from the pancreas of a deceased diabetic child, passaged through murine β-cells, and found to induce diabetes after inoculation in mice (18). Recently, Dotta et al. (19) also detected CVB4 in pancreatic tissue specimens from three of six type 1 diabetic patients. Elshebani et al. (20) recently found that enterovirus isolates obtained from newly diagnosed type 1 diabetic patients could infect and induce destruction of human islet cells in vitro.

Recently, Oikarinen et al. (21) have isolated enteroviruses from intestinal biopsy samples in 75% of type 1 diabetes cases versus 10% of control patients, possibly reflecting persistent enterovirus infection of gut mucosa in type 1 diabetic patients. In sum, isolation of enteroviral antigens from diabetic individuals, particularly after recent onset, is becoming a fairly reproducible finding, supporting a role for these viruses in disease development. However, it is still unclear whether this phenomenon is indeed a common etiology for the majority of patients diagnosed with type 1 diabetes, or whether it can be found only in a particular subpopulation of individuals with perhaps higher genetic susceptibility to infection.

(In other words, they don't know whether these infections are causal factors or consequences of type 1. I suspect the former)

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It's interesting they mention Finnish children getting type 1 often, who have similar diets and environment to Russian ones across the border, because I've read independently that they have a much higher risk (nearly SIX times) of type 1 diabetes despite that. And one possible cause is the over-use of anti-biotics in western countries compared to Russia where its use is much rarer and restricted (apparently, I'm not an expert on this).

I do think antibiotics could be implicated here somewhat, as per several studies on the subject (they alter the mix of gut microbes and reduce biodiversity which is necessary for fight off viral infections):

https://www.sciencedaily.com/releases/2016/08/160822124927.htm

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One thing seems clear: try to avoid giving antibiotics to your babes, if you can. And even avoid taking them yourselves because germs are shared amongst family members (even from your skin! There's a theory out there about type 2 diabetes being transmitted by touch for this reason. And enteroviruses for type 1 babies probably come from the mother, certainly some source at the home. I would check for this type of infection in all family members and pets too).

And you don't need to take antiobiotics for the full course, and can stop taking them when you feel better. General broad-spectrum antibiotics create antibiotic-resistant germs and destroy your healthy gut germs in the process (resulting in "gut dysbiosis") which is crucial to avoid auto-immunity. It kills the good and the bad germs indiscriminately. You don't want this.
 
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