Maybe I’m just slow, but you’re saying that if you have T1 or T2, and your children get covid, they have a high risk of developing T1 or T2.
@Jan I’ve read several articles of late that have indicated there’s a correlation of having had Covid and then developing T1/T2 despite whether there is a family history. I have NOT reviewed the reports themselves. As with most medical studies, I’m suspicious whether there is a relationship or it’s just perceived based on a statistical analysis and then including an “it this then that” conclusion that may or may not actually exist.
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Significantly increased, not high, but otherwise correct.
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I think there is only one isn’t there? I couldn’t determine whether there was any peer review (but I haven’t read it all through yet; I have other more interesting things to do, such as watching paint dry.) It’s not a medical study, it’s a statistical review; no research involved. As such it suggests topics for future medical research but doesn’t prove or disprove anything. (As I said, I haven’t checked all the way through - statistics like this can be used to disprove a prior hypothesis but there doesn’t seem to be a hypothesis to disprove.)
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So what is the current thinking on how you develop T1? I was diagnosed after having a really, really bad influenza virus at age 22. Not right after, but I lost so much weight I stopped menstruation, and that’s what led me to the Dr. I always assumed it was from an over reactive immune system to the virus. 🤷
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The last I heard it’s one or a combination of:
- Environmental
- Bodies response to illness (viral infections)
- It’s not hereditary (it doesn’t run in the family)…although often times multiple people in the family line have, or have had it.
- It is genetic (it lives in your genes)…The presence of certain genes appears in many (but not all) T1D patients.
That’s what I’ve read and I think are the current consensus but they just don’t know for sure…
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I think this table showing the significant differences of Type 1 incidence rates between countries proves the genetic/ancestry correlation. https://www.diabetes.org.uk/about_us/news_landing_page/uk-has-worlds-5th-highest-rate-of-type-1-diabetes-in-children/list-of-countries-by-incidence-of-type-1-diabetes-ages-0-to-14
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There is a strong genetic component (something like 70% of it is genetic) BUT also you have to have a trigger of some sort, and the fact that incidence is rising a few percent every year is a clear indication that some environmental factor (whether a virus or different lifestyle habits, etc.) is setting it off.
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Which would be a lovely bit of research, because once they understand the trigger they can usually design a way to interrupt the trigger from working. I would hope someone is putting significant money for research on this, since it is so much simpler to prevent than figure out a way to turn off someone’s immune response once they have it.
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Assuming that was about environmental factors affecting autoimmune diabetes then there does seem to be a lot of money going into it:
Elsewhere you gave a reference to one item of the Coxsackie B research. The point I gleaned from that paper is that there is strong evidence that infections from that virus can remain inside the cells; so the virus chemical sticks around, perhaps being replicated sporadically by the cells normal reproduction machinery but it is not “expressed” in that there are no symptoms. This is like chickenpox and shingles - both variations on herpes (a symptom, like COVID) caused by the varicella virus. The virus remains embedded in cells after childhood infections then manifests in later life, perhaps when the cell reproduction machinery gets prompted to reproduce the virus DNA.
From @Chris’s Finnish reference (repeated above):
We have recently observed that CVB1 was linked to the initiation of the autoimmune process leading to type 1 diabetes in Finnish children. Viral persistency in the pancreas is currently considered as one possible mechanism.
That’s an abstract of the abstract 
, the rest of the paper (including the rest of the abstract 
is everything a good scientific paper should be. Incomprehensible.
All the same, it suggests to me that T1D responses might be sort-of like shingles or, in my case herpes opthalmicus - something that just suddenly happened to me out-of-the-blue but almost certainly reflects some previous infection. Something that doesn’t simply depend on our immune system but also depends on environmental factors which may include stuff from many, many years ago.
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This is back to the original question of the thread (wow CDC ceetainly did NOT help you there did they?!) which I think I can help clarify.
There are two issues at play with medical diagnoses and COVID vaccinations that tend to get confused:
First category: people with normal immune systems but with medical problems or risk factors that mean they’re more likely to get seriously ill if they get COVID. These people were prioritized when vaccines first became available to get in the front of the line. Things like being elderly, lung disease, etc. Diabetes (all types at least the way it was usually interpreted) IS in this category. However the two shot series, and booster 6 months later (when available for your age bracket) are considered enough because most people with diabetes alone have a normal functioning immune system so the vaccine works normally for them.
Second category: immune compromised people. This would mean you have a deficient immune system, either due to a syndrome like Digeorge or due to a treatment you receive like chemo or immune suppressants after an organ transplant or for an auto-immume disease, such as rheumatoid arthritis or Crohns. These people do not mount a very good antibody response to vaccines, so their PRIMARY vaccine series (not a booster) is supposed to include a third dose about 2 months out. Diabetes is NOT in this category.
It gets confusing because people with immunosuppressive medical conditions/treatments were also in category #1 (because COVID is more likely to make them seriously sick) AND type 1 diabetes is an autoimmune disease like many of the ones in category 2 (although not one that is treated with immunosupression).
So, to use Liam as an example, since his diabetes would put him at risk of getting more sick from a COVID infection, he would have been able to get the vaccine before others back in early 2021 (if he’d been old enough) because doses were scarce and he would benefit more (category 1). But now that doses are NOT scarce, his healthy immune system means that his recent 2 shot series should generate strong protection similar to other kids, so he doesn’t have to get more doses than others.
Omicron is unfortunately crazy infectious, and vaccines protect us partially but not 100%, but at this time there’s no evidence I know of that a 3 shot PRIMARY series (three shots spaced close together instead of 2) protects those of us with normal immune function, including type 1 kiddos against it better. If it had to be so infectious, thank goodness infection for vaccinated folks is rarely severe. And I’m glad the younger kiddos first shots were so recent!
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Excellent summary; thanks.