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iayork t1_j79ik7f wrote

Probably not.

In 2017 there was a flurry of media reports claiming that infection with the pandemic H1N1 virus ("H1N1pdm09") might cause diabetes. These were all based on an unpublished presentation, not a paper and not peer-reviewed, from a Norwegian group.

The group subsequently published a more complete study, which was inconclusive:

>Overall, we could not demonstrate a clear association between clinically reported pandemic influenza infection and incident type 1 diabetes.

--Pandemic influenza and subsequent risk of type 1 diabetes: a nationwide cohort study

To help explain what "inconclusive" means, similar studies were able to conclusively link a 1 in 20,000 risk of narcolepsy to a specific vaccine. So presumably if there's any risk it's lower than 1 in 20,000; more likely it’s zero.

As far as I know, no subsequent studies have found any link.

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jerden t1_j7a5ek5 wrote

Replying to [deleted] (#1,727,278)

Having a "generally poor lifestyle" has nothing to do with developing Type 1 diabetes. You're likely thinking of Type 2. In Type 1 diabetes, usually when you are relatively young, your pancreas ceases making any insulin. Lifestyle has nothing to do with it. In Type 2, your pancreas doesn’t make enough insulin, and the insulin it is making doesn’t always work as it should (can be related to an unhealthy lifestyle).

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Tephnos t1_j7avffy wrote

Replying to iayork (#1,726,334)

> To help explain what "inconclusive" means, similar studies were able to conclusively link a 1 in 20,000 risk of narcolepsy to a specific vaccine. So presumably if there's any risk it's lower than 1 in 20,000.

Can you elaborate on why then more recent research has shown that it seems H1N1 was causing narcolepsy itself? Countries that did not use that specific vaccine were seeing surges of narcolepsy incidents as well. Is this not a case of awareness bias, or whatever it is called? How can we be sure it was purely the vaccine?

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iayork t1_j7b61qk wrote

Replying to andre3kthegiant (#1,728,586)

“The article”? There are literally hundreds of them. This is a very well known phenomenon.

Unsurprisingly, the virus infection is much more likely to cause narcolepsy than was the vaccine, so vaccination against H1N1 protects against narcolepsy overall. But since this only happened with a single vaccine, it was replaced by the other vaccines.

For anti-vax loons reading this, I’ll point out that the hysterical anti-vax voices didn’t find this out, it was discovered very rapidly by the usual surveillance that public health groups routinely conduct. Vaccine-associated effects are routinely detected even when they only occur at a 1 in 20,000 incidence (or much lower, as we saw with the J&J COVID vaccine, where adverse effects were rapidly identified at the 1 in 200,000 level). And even though the vaccine overall was protective and beneficial, when these very rare events were detected the vaccine was immediately pulled from use.

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ceapaire t1_j7b6huj wrote

Replying to iayork (#1,726,334)

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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iayork t1_j7b7m06 wrote

Replying to Tephnos (#1,728,233)

Post-vaccination monitoring is active and aggressive (especially in the Scandinavian countries where the link was made). Unfortunately viral surveillance, while a part of normal public health, is underfunded and understaffed, but hey, what could go wrong?

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bionic_human t1_j7bg75a wrote

Replying to iayork (#1,726,334)

Given that the autoantibody response starts months or years prior to the development of clinical symptoms, it’s plausible that SARS-CoV2 infection accelerated the presentation of symptoms among people who were already autoantibody-positive yet asymptomatic. That would account for the initial spike in diagnoses, which appeared to correlate due to the myopic nature of the initial studies, but once that initial wave came through, later studies would be expected to find no overall increase in incidence.

🤷‍♂️

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Lyrle t1_j7biu6p wrote

Replying to Tephnos (#1,728,233)

In genetically susceptible humans, one of the proteins in H1N1 triggers an autoimmune attack by T cells against specific brain cells, and those brain cells dying causes narcolepsy.

Most flu vaccines by happenstance never included that protein. The vaccine that caused narcolepsy in susceptible people included the triggering protein.

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jerden t1_j7blvfc wrote

Replying to sweet-banana-tea (#1,728,823)

I mean, sure. Any chronic condition can and usually does impact the way a human lives their life. But the commenter was drawing a link between a "generally poor lifestyle" (I'm assuming they mean in terms of poor activity levels and food choices) and being diagnosed with Type 1 diabetes, where there is absolutely no link between the two.

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jerden t1_j7bpvqo wrote

Replying to pspahn (#1,727,417)

Most likely the opposite in the vast majority of cases, as Type 1 diabetes requires constant attention to insulin requirements and carbohydrate intake to maintain blood sugar, leading them to be far more aware of their health and diet to survive. However, that's not what the commenter was asking. The commenter was trying to draw a link to a poor lifestyle and the development of Type 1, to which there is absolutely no link. Most people are diagnosed as children.

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bunkSauce t1_j7bycwe wrote

H1N1 affected like what, 15% of the population? And maybe 15% ish of the population were adolescents?

So 2.25% of the population were potentially kids affected with H1N1?

And 1% of the US has diabetes type 1?

So... the number of diabetic youth who may have been exposed to H1N1 is like 0.0225%?

I highly doubt, just from those numbers alone, that an association between H1N1, youth, and diabetes... would have any tangible, noticeable, or measureable effect in a truly controlled study. Literally even a 10% increase could be written off as an effect of many different factors other than H1N1.

Anyways. The idea of an association between H1N1 and diabetes has already been disproven. Don't fall down any anti vacc rabbitholes, this appears adjacent to that stuff.

Edit: reduced percent of population with diabetes, to refine from type 1 and 2, to just type 1.

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Cleistheknees t1_j7c6xg2 wrote

Replying to ceapaire (#1,728,658)

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

Replying to Cleistheknees (#1,730,356)

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

Replying to ceapaire (#1,730,711)

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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GiverOfUseless t1_j7crm69 wrote

Replying to iayork (#1,726,334)

What I have heard from one of my teachers is that Covid “caused” an increase in type 1 diabetes as normally it is revealed through a virus that causes stress to the immune system so then type 1 diabetes “appears” because it was going to eventually it just activated it early

Based on this I do believe that H1N1 would cause an “increase” in type 1 diabetes as it revealed it

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bionic_human t1_j7fg4kq wrote

Replying to open_reading_frame (#1,733,507)

I would expect it to occur with any virus that causes metabolic disruption. I haven’t seen any statistical analysis on timing of new diagnoses, but many T1s report getting diagnosed around holidays, during which virus transmission (even asymptomatic) naturally spikes.

I’d imagine to even begin to get a feel for it, you’d need a huge sample size and accurate medical record coding to mine for. KP and other large health systems would be the most likely to have the necessary data, but someone would have to see enough value in the research/potential results to actually fund the analysis, even if you had access to the data.

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