Hi all! I’m new to the forum as a writer, but have been lurking for quite some time! I see that so many are on here and get more answers than with other forums, or even just doing their own research.
I was diagnosed Type 1 when I was 22. I’ve been diabetic for 5 years now. I always wondered what brought on my diagnosis, and always chalked it up to being extremely stressed right before: I was planning my wedding by myself, and finishing up my Associates Degree, then my mother had a stroke, and some close friends left my life. I’d say I was an emotional mess back then.
Anyway, as a child I was always super thin. I was 3 months premature, had two holes in my heart (that luckily healed on their own), but otherwise was fairly healthy.
One thing that has crossed my mind though is the herpes virus. When I was younger, I had chicken pox twice and shingles once. As an adult I got mono, and then an outbreak of fever blisters in my mouth a couple of times which I had to get medication for. I know that all are various forms of the Herpes virus. I have tried researching to see if Type 1 Diabetes is linked at all, but I can’t remember finding anything definitive.
Does anyone know if it is linked to T1D? Maybe I was always at risk for developing diabetes, or maybe it has nothing to do with it. I was just wondering if anyone has heard any correlation between the two? I understand that all infectons (mono, shingles, etc) are different types of the Herpes virus. I am hoping I don’t have any other form of the virus rear it’s ugly head in my lifetime!
Type 1 diabetes
“The exact cause of type 1 diabetes is unknown. In most people with type 1 diabetes, the body’s own immune system — which normally fights harmful bacteria and viruses — mistakenly destroys the insulin-producing (islet) cells in the pancreas. Genetics may play a role in this process, and exposure to certain environmental factors, such as viruses, may trigger the disease.”
Type 1 is certainly auto immune, although I’ve never heard a link to any specific virus or bacteria. I was diagnosed just before high school. The cold/flu season right before, I had three long bouts with strep right in a row. It was like it wouldn’t go away. Each time I got it, I would get so many shots of penicillin that they would tell me that if this one didn’t work they would have to try a different, longer acting antibiotic. That dose would kick it but it would soon return.
It has always been my opinion that that was my catalyst–that my body worked so hard to fight the strep that when it was finally gone my immune system sought another enemy and chose my pancreas.
Oh goodness! That’s such a crappy thing to go through, but I’ve wondered the same. All of my outbreaks of blisters and mono happened before I was diagnosed. I’d say my body had a lot going on prior to being diagnosed; I just never realized it all until afterwards.
The specific enterovirus which has some evidence linking it with onset of diabetes (especially in adults or older children) is Coxsackie B4 virus, but the science here is more recent. Incidentally, I got Coxsackie B4 about two years before my diagnosis (thanks nephews and nieces for the gift that keeps on giving!).
Then again, there are other studies (seeming to dominate Wiki’s crowd-sourced articles) which dispute any association between viral infection and Type 1. What is known is that developing T1 requires certain genetic sequences (certain haplotypes of the HLA sequence) and an environmental trigger. It’s quite possible that there are many different “types” of Type 1 dm, and that there are, consequently, different environmental triggers of Type 1 dm. It seems likely to me from my reading that viral infections can trigger onset of T1 in children and adults, but that there are also many cases where there doesn’t seem to be a link with infection.
As for herpes itself, I’ve not seen it linked with Type 1 in the literature. Given the prevalence of the “Type 1 genes” in the American population, and given the prevalence of herpes family viruses, if there was a strong association you’d think there would be a lot more cases of T1 in the US than there are… For the record, it’s likely that 100% of humans carry herpes simplex virus of some sort, and somewhere between 16 and 30% have had “active infections.” It’s so common in humans (as are the HLA autoimmune haplotypes) that I can’t imagine a strong association yielding a T1 rate of 0.4-1.0 % of the population.
If you want to know far more on the epidemiology and statistics of herpes simplex infections in humans than any human should ever know, then please read “The Straight Dope on Herpes Statistics.”
Thanks for posting some info about certain viruses! interesting to read! And good point about most people having the herpes virus. I was aware of that but I guess it’s true that a small percent has Type 1, so it would lessen the chances of it being a cause.
I have read that stress can “trigger” the auto-immune response. In my own case, I was 16 when I was diagnosed. I remember, I was in highschool and never home due to 3 extra-cirricular, after school activities plus working 20 hours a week at a part-time job, plus drivers education twice a week, plus piano lessons and practice, plus studying enough to maintain a straight A average. Who needs sleep … right? Well, it I have thought that my busy schedule potentially “triggered” the response to which I was already genetically predisposed.
I would also say that multiple illnesses on your part is essentially a stressor to the body.
Yes, autoimmune diseases and disorders are always, more or less, “triggered” by some kind of environmental event as far as we know. Viruses are very likely not the sole cause or triggering event for those susceptible to autoimmune disease. I also had a very high-stress period immediately prior to diagnosis (working on my dissertation with a baby on the way). Chemical exposure, acute stress, and viruses have all been associated with Type 1 onset.
We just don’t know enough about diabetes from a scientific standpoint to “prove conclusively” what triggers the disease in people, either at the population level or individually. We are starting to get an idea that some kinds of events can possibly trigger onset. And high-stress (and high school is about as high stress as many humans ever experience) environments are certainly one of those environmental events that are being investigated.
Regarding the “stress trigger” theory, it might also be a chicken/egg issue. My diagnosis came a few months after a few very stressful events, including my dad dying. I realized after the fact that the stress had caused lots of comfort carb consumption and my guess is that I overwhelmed my already failing pancreas. I think the T1 process had been going on for a long time, but the stress put me over the top.
Yep, the stress chicken and stress egg is hard to distinguish (unscramble?). I was working on my dissertation for a year prior to diagnosis, and although I didn’t gain weight, I was eating a ridiculous amount of “comfort carbs” and also getting far less exercise than normal. About six months before diagnosis, I started to have a lot of the “classic symptoms” along with regular, severe migraines. I got tested for all sorts of neurological issues, and was then prescribed reading glasses (since my eyesight had changed, which they chocked up to age). Migraines didn’t go away, and the afternoon fatigue (following a customary lunch of sandwich or burrito) got worse and worse, with accompanying unquenchable thirst and frequent urination. so, for what little it matters, here is my amateur medical forensic reconstruction of my own Type 1 presentation:
My parents kind of screwed me (unintentionally) by having the gall to be from families with severe, frequent, and persistent autoimmune disorders, including Type 1 diabetes (all adult onset LADA as far as we know).
I lived a relatively happy and healthy 38 years until my brother’s kiddos got Coxsackie B4 at school and shared it with the entire family during a beach vacation. I got a bad case of what I thought was the flu, but turned out to be CB4.
My immune system starts targeting my beta cells in Summer 2014.
My life gets way more stressful in Summer 2015 because some idiot signed me up for a PhD program in 2011 and the bill was finally coming due (in the form of delivering a dissertation) December 2015.
My regular exercise and eating routine goes to hell in a handbasket as I try desperately to write, work full time, and not get divorced in August 2015.
I defend in December 2015, by which time I’m experiencing almost daily visual migraines, my eyesight has changed, and I have to nap after lunch, can’t sleep at night, and am peeing twice an hour.
Several thousand dollars worth of MRIs and CATs later, I know I do not have a brain tumor, but I do now have a very expensive set of reading glasses.
May 2016, I have an annual physical and the blood work shows that my fasting BG is 187 mg/dL and my subsequent A1c is 7.5%. Previous year my fasting was 81 mg/dL and my A1c was 5.1%. (numbers estimated since I can’t actually remember, but…firmly non-diabetic May 2015, definitively diabetic in May 2016).
So, which came first? The genetics. Then most likely I got a viral infection that infected islet cells in addition to mucous membranes and other such nonsense. Then I got super stressed and was eating a ton of carbs, not sleeping, and being a crazy person. My pancreas more or less gave up the fight at that point (actually, not true… I apparently have a super-slow onset presentation of LADA and am limping along with a pretty good A1c right now).
I believe that once your body has started down the road of Type 1 - it is going there and there is nothing you can do to stop it. Different people will have their pancreas reduce/stop insulin production at different rates but at this point there is no turning it back.
In terms of the trigger “before” it happens, I still believe that if you are going to be Type 1 then you are going to be Type 1. If it wasn’t “this” trigger/virus/whatever then it would have been another one.
The question is unanswerable at the present state of the art. There are plenty of possibilities, but that’s all they are, no more.
What is known is that having one autoimmune condition places you at heightened risk for others, and they are often seen in clusters. So IF herpes can trigger an autoimmune reaction that can somehow morph into an a specific attack on beta cells, then in abstract theory it could be a link in the (indirect) chain. But all of this is angels on the head of a pin. There is exactly zero evidence that I am aware of, and as always, correlation is not causation.
I was also born three months premature (I’m legally blind as a result). I often wonder what effect being a preemie and spending months in the NICU had. I have a clear genetic predisposition, but I’ve read a lot about the “hygiene hypothesis” and it seems to me that those first few months were anything but normal as far as immune system development is concerned. I feel like my risk is an order of magnitude higher than others in my family, and it doesn’t take much of a “trigger” to cause my immune to start attacking something it shouldn’t. I mean, a lot of people in my family have allergies or an autoimmune condition, but I’m the only one that has multiples of each and who’s had a track record of steadily developing new ones from the time I was a toddler through to adulthood.
I have thought the same! It has to have some impact on a person for sure! My newest doctor is surprised that I don’t have any other major issues, like thyroid problems, etc. since a lot of Type 1’s have other diseases. I have asthma, eczema outbreaks at times, and herpes outbreaks, but nothing huge. Here’s to hoping it stays that way.
I’m on my phone, so can’t easily post the research I’ve been involved with as a volunteer subject over the past 25 yrs.
First, there are different types of Type 1 and they are likely triggered differently.
I was involved in research while living in the Netherlands & saw a graph where newly diagnosed Type 1 went nearly straight up at 1980 and the ages were older (28 yrs old was this profile.)
I was diagnosed in 1987 at age 28 and am nearly 100% Dutch ancestry. At the time they were looking for environmental factors, some are funny now like styrofoam containers. But around 1998 (from memory) they discovered that the Epstein-Barr virus (EBV) which is a herpes virus and causes mononucleosis had mutated. As someone else here noted, the Coxsackie virus is also being studied.
The current thinking is that there are people of Dutch and Scandinavian heritage who may never had Type 1 in their family (long documented history in my family and there never has been) who are now susceptible to Type 1. In the past seven or eight years whenever I hear of a newly diagnosed type 1, I asked if they have Dutch or Scandinavian Heritage and if they’ve been tested for Epstein-Barr. Hardly scientific, but three out of three are yes & yes.
Additional research in the Netherlands surrounds Multiple Sclerosis, Crohns, Ulcerative Colitis and their potential genetic similarities to this type of Type 1. For what it is worth, our son was born in the NL and though we have no previous history in our families, he developed UC at age 15 while in Australia. My best friend’s son (and our son’s friend) is of nearly 100% Dutch heritage and he developed UC at age 22 while in Australia. Just too many coincidences for me not to feel that this research is on the right track.
Again, the researchers are saying that this isn’t the only way Type 1 develops, but that it is likely for new cases in families with no prior history to have Epstein Barr be a new factor.