So I believe the graph that Holger showed is one that he “made” up to illustrate what he had heard. It might be a “leap” to suggest it is real data.
Same here. I was diagnosed T1 at 53, rapid onset, BG 809, DKA & close to death. No diabetes of either type in my family. I had no honeymoon phase & wasn’t LADA.
Could well be that the so called type 1 and type 2 have much in common and the slower onset with age is just an immune system with more experience.
Well, I grew up knowing Type 1 and then 18 years later I was introduced to Type 2(not the Insulin Resistance) Diabetes. Two different ages of onset and different treatments. Easily understood. These other Types(LADA and MODY), the young having Type 2 and the older People getting Type 1 and 1.5. It tends to boggle the mind.
I have explained the the original Type 1 and Type 2 to many People before but now most non-diabetics would probably melt into the floor, thinking that they shouldn’t have asked.
A Child and Adult Type 1 having different experinces, indeed.
You’re right. All the different names given through the years has been a Real mess.
So Melitta—you are not a Type 1.5 then. I totally missed the fast-onset of an Adult Type 1, somewhere along the line. I agree, you are correctly diagnosed. It doesn’t matter then at what age since this criteria has changed. Sorry, I got confused in this discussion. I thought you were dxd. a Type 1.5. Thanks for correcting my thoughts.
@BSC: You are right. It is a summary and visualization of what I have learned. To give it real scientific value we need epidemeologic data about the mean manifestation rate per 1000 people and age. It would be great to see the real likelihood for T1 manifestation in the general population which in my expectation should be very low (so the chart is exagerated to show the differences between the ages). Where can we start? Data of Finland for example? Should we involve our doctors to get this data? Would be a nice community efford. What do you think?
It’s not myth - it’s math. If more people survive to carry on the genetic predisposition, then more people can contract the disease. What can be debated is what factors cause those with genetics to manifest the disease; are those factors (environmental, diet, etc) on the increase.
I read the book. It does not touch on the mathematical fundamental - more humans carry the genes every year. When the world population becomes static, this will no longer hold true.
The error here is that Holger’s graph does not include ALL people with Type 1 autoimmune diabetes (and as Holger says it is not real data). Althought the existance of slow-onset Type 1 is well known, and has been documented via antibody testing for ~20 years, LADAs/slow onset T1/adult onset T1 are still included in the statistics for Type 2 diabetes, not in the stats for T1, even though that clearly is not appropriate. Since adult onset Type 1 diabetes accounts for two to three times the number of childhood cases (again, well documented in all the scientific literature that uses antibody testing, the gold standard for diagnosing Type 1a), it is not possible that the disease is “clearly occuring mostly before the age of 22.”
@Melitta: if ‘adult onset Type 1 diabetes accounts for two to three times the number of childhood cases’ as you have said then this would be suprising for me. If this is true there are good reasons to be alarmed about it. On the other hand I see the need for independent scientific data. There are high financial interest involved since the claim would lead to the conclusion that diabetics with T2 diagnosis should always be tested for antibodies - very big business with the growing number of people with T2. On the other hand it would be very helpful to get the real picture of T1 manifestation in the general population. Maybe the antibody test should be standard for 1 year. This would reveal how many cases of misdiagnosed T1 we have in one year. Would be very helpful to have an argument for the continuation of antibody testing.
Part of the problem with doing these sorts of studies is the whole gray nature of the issue. What would you measure, onset of antibodies? People have antibodies, but never get diabetes. What about onset? Can you measure that consistently? What does that mean? When you first need insulin? People go for years without needing insulin. It is complicated. It would be interesting to find a graph based on data, but I’ve not seen one, and I suspect as Melitta points out, it would misregister in a variety of ways the vast majority of adult onset, both LADA and particularly T2.
- When you said “Type 1 is diagnosed at all ages, always has been”, you
- meant Type 1(Child to Young Adult onset) and Type 1.5(Adult onset).
- Both autoimmune. These are not the same disease/condition because
- there are too many differences between them. That is why there is the .5
- or the a added. They cannot be clumped simply as Type 1, since they are
- totally different experiences or branches on the Diabetes tree.
- Back in 1958 young adults were considered Juvenile. Did they
- mention if these young adults developed Diabetes within days or
- months or did it take years for them to develop Diabetes? Why was
- Type 1a(.5) only discovered in 1980? Is it possible that Juvenile Diabetes
- mutated into autoimmune adult onset? What about Type 2? I thought they
- said it was only obese Adults who had Type 2. So where did these obese 4
- year olds with Type 2 come from? Did Type 2 Diabetes mutate also?
The “types” of diabetes have changed over time. Before the 80’s nobody talked about “Type 1” and “Type 2”: it was just “juvenile diabetes” and “adult onset diabetes”. In fact unless specifically specified as “juvenile diabetes” the assumption was that it wasn’t “juvenile diabetes”.
The terminology improved in the 80’s with the introduction of “Type 1” and “Type 2” and that was important. It recognized that T1’s can be diagnosed as adults. It recognized that T1’s live to adulthood. It recognized that T2 might happen in kids too. But still the terminology was incomplete - thus the invention of T1.5, LADA, T3, and other classifications.
- There have been many errors made in the writings of Medical Professionals.
The defining/treating/curing exists outside the writing and the terminology. Banting and Best made several major “errors” in their quest to extract insulin but they still did it.
I’ve lived through one major shift in diabetes classifications and seen many new “types” invented because the system still isn’t perfect. You don’t need to get worked up about how you are “defined” or “classified”. The classification is not who you are.
Haven’t read the book and I don’t know the specifics.
Based on the conversation so far though, Population Genetics 101 says that the probability for gene or set of genes to appear in a population depends on both survival/mortality rates and reproductive rate. So, 100 years ago and in some parts of the wold today, is and was type 1 diabetes a death sentence regardless of at what age or how you were diagnosed? If so, under those conditions, the only way type 1 diabetes could not impact the reproductive rate of its carriers is if it exclusively occured after the peak age for reproduction. Clearly, that was not and is not the case. You can get it at any age, including before and during peak reproduction. If you are dead, you can’t reproduce.
So, despite being diagnosed with type 1 diabetes, were type 1 diabetics of all ages having as much reproductive success back then as they are now? Independent of survival/mortality, does type 1 diabetes, once diagnosed, impact reproductive rate?
If I’m a 21 year old, at the peak of my reproductive age, and I have been diagnosed with type 1 diabetes, is my chance for reproductive success going to be less than a 21 year old who doesn’t have diabetes? I don’t think it’s a stretch to assume that things are a lot better for type 1 diabetics today, in that regard, than they were 100 years ago. Not only are type 1 diabetics surviving better today, they are thriving. Under those conditions, I don’t think it’s a stretch to assume that a higher prevalence of type 1 diabetics today may be due to increased survival and reproductive success for type 1 diabetics.
Of course, if there is an environmental component to type 1 diabetes like an effect from vitamin D, all genetic bets bets are off.
Thinking more about some of Holger and Melitta’s comments, I don’t think “self - limiting” is the strictly the case, but I don’t think that it’s a stretch to assume differential reproductive rates for type 1 diabetics today versus 100 years ago.
Also, without readng the book, could it be due to just more sophisticated diagnosis techniques? Is it just more likely that somebdy can be diagnosed with some level of type 1 diabetes today versus 100 years ago?
I do not think it is necessary to go back 100 years to conclude that the higher reproduction rate is responsible for the rising numbers. Even today 50% of the T1 population have great concerns about their reproduction: the women. Great effords and preparation is still necessary to have a healthy child. Based on my experience this situation has improved in the last 20 years but before that the decision was very often against pregnancy. Seen from this positive perspective of many more women considering pregnancy the current rise is remarkably low. To me this shows how unlikely it is that the child of a T1 will actually develop T1.
So you’re saying that given the higher prevalence of reproductive effort by type 1 diabetics today, that there should be a higher proportional increase among children than the 3% per year reported? Maybe, but it’s like Melitta says, you have to know the percentage increase across all age groups to really look at the effect of increased reproductive success by T1 diabetics on the prevalence of T1 diabetes.
I don’t know, is there any mention of data from identical twin studies?
I share your view that the data we have is insufficient. On the other hand we have the claim of a rising manifestation of T1 / T1.5. I am just arguing that the current rise is in fact a normalization. So many have decided against children in the past. Now with better treatment, education and efford we are able to overcome this. Of course this will lead to an increase since the genetic information will be passed to the next generation - although with a small likelihood. At least this how I try to make something positive out of it.
Sorry, but I think there is an increase in type 1 cases unrelated to survival or reproduction. There are too many like my son who are “the chosen one”, the only in their family on both sides to have this disease. So there are new mutations if the cause is genetic, or if it is an enviromental trigger then triggering is happening more often
Hi Tim:
Yes, I meant to say Juvenile. Type 1 and 2 have been engraved in my brain over the years. Auto default. Actually, our Family Dr. dxd. us with Sugar Diabetes not Juvenile Diabetes. We didn’t hear that phrase until sometime later although it did exist.
I wasn’t worked up about how I am classified. I already knew about the classifications. Except for the Adult Type 1(rapid onset). Melitta caught me off guard with that one. It all makes sense.
Thanks!
The feeling of being “the chosen one” is typical for type 1 diabetics. Even if one or two parents have type 1 the likelihood for the child to develop this condition is low. It might pass multiple generations before the little genetic predisposition finally meets all the circumstances to manifest T1. This might be caused by an environmental factor or a defect in vitamin D production. We do not know yet.
It is an interesting choice of words. The term “Chosen” has particular meaning to me as a Jew. In Jewish thought, the Jews are the “Chosen People,” not because God chose them, but because they accept the responsibility of the covenants (commandments) with God.
Perhaps, the same can be said about being diabetic. Truly being a “chosen one” involves accepting responsibility and adhering to that convenant. You don’t get to be a “chosen one” by not taking care of yourself.