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ceapaire t1_j7b6huj wrote

Type one is genetic, and requires some sort of trigger (thought to be usually a virus, though as far as I'm aware they've not been able to pinpoint anything). Odds are that most people with the genetic predisposition will get it triggered at some point in their lives, so COVID may have been the trigger for a lot of people. But it won't be statistically any more than normal, since they'd likely be exposed to something that triggers it anyways.

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Cleistheknees t1_j7c6xg2 wrote

Hey, just a heads up, basically everything you said here is wrong. Please avoid making authoritative claims like this if you aren’t educated on the topic, especially in subs like this. It’s how misinformation spreads.

> Type one is genetic

The ambiguous association patterns of genes like HLA and CTA4 basically proves that this statement cannot be conclusively true.

> and requires some sort of trigger (thought to be usually a virus, though as far as I’m aware they’ve not been able to pinpoint anything).

Again, sometimes. There are genotypes which are autosomal dominant for immune destruction of beta cells, like GCK-MODY. Further, there are no documented environmental triggers for T1D, so, again, stating this conclusively is wrong.

> Odds are that most people with the genetic predisposition will get it triggered at some point in their lives

There is no evidence to support this, at all, and quite a bit against it. The penetration of genes implicated in T1D is low. The concordance rate in monozygotic twins is low. 90% of people with T1D have no known relatives with the disease. Etc.

> so COVID may have been the trigger for a lot of people. But it won’t be statistically any more than normal, since they’d likely be exposed to something that triggers it anyways.

What? This makes zero sense.

Source: doctorate in evolutionary biology, and 25+ years with T1D, but only the former matters here

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ceapaire t1_j7cex77 wrote

I was repeating what I was told by Dr.s in a research study I was in for T1D.

>There is no evidence to support this, at all, and quite a bit against it. The penetration of genes implicated in T1D is low. The concordance rate in monozygotic twins is low. 90% of people with T1D have no known relatives with the disease. Etc.

They also provided me with This study that says there's likely a genetic component since identical twins as well as non-identical if one has multiple of the antibodies. And it at least held enough weight for TrialNet to expand their testing for twins to lifetime instead of cutting it off at 18, as they do with any other relatives.

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Cleistheknees t1_j7cgenh wrote

To reiterate, if you’re saying “X is Y”, and it’s only true 30% of the time, then the statement is incorrect.

> They also provided me with This study that says there’s likely a genetic component since identical twins as well as non-identical if one has multiple of the antibodies.

There is most certainly a genetic component to autoimmune type 1 diabetes. That much is beyond question. However, you did say quite a bit more than “there’s a genetic component”.

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