autoimmune

Being a raccoon and living with chronic disease

by Dana Lewis

Being a raccoon loading a dishwasher is a really useful analogy for figuring out: what you want to spend a lot of effort and precision on, where you can lower your effort and precision and still obtain reasonable outcomes, or where you can allow someone else to step in and help you when you don’t care how as long as the job gets done.

Huh? Raccoons?!

A few years ago Scott and I spotted a meme/joke going around that in every relationship there is a person who loads the dishwasher precisely (usually “stacks the dishwasher like a Scandinavian architect”) and one who loads the dishwasher like a “raccoon on meth” or a “rabid raccoon” or similar.

Our relationship and personality with dishwasher loading isn’t as opposite on the spectrum as that analogy suggests. However, Scott has a strong preference for how the dishwasher should be loaded, along with a high level of precision in achieving it. I have a high level of precision, but very low preference for how it gets done. Thus, we have evolved our strategy where I put things in and he re-arranges them. If I put things in with a high amount of effort and a high level of precision? He would rearrange them ANYWAY. So there is no point in me also spending high levels of effort to apply a first style of precision when that work gets undone. It is more efficient for me to put things in, and then he re-organizes as he sees fit.

Thus, I’ve embraced being the ‘raccoon’ that loads the dishwasher in this house. (Not quite as dramatic as some!)

A ChatGPT-created illustration of a cute raccoon happily loading the dishwasher, which looks fine but not precisely loaded.This came to mind because he went on a work trip, and I stuck things in the dishwasher for 2 days, and jokingly texted him to “come home and do the dishes that the raccoon left”. He came home well after dinner that night, and the next day texted when he opened the dishwasher for the first time that he “opened the raccoon cage for the first time”. (LOL).

Over the years, we’ve found other household tasks and chores where one of us has strong preferences about the way things should be done and the other person has less strong preferences. Similarly, there are some things that feel high-effort (and not worth it) for one of us but not the other. Over time, we’ve sorted tasks so things that feel high-effort can be done by the person for which it doesn’t feel high-effort, and depending on the preference level determines ‘how’ it gets done. But usually, the person who does it (because it’s low-effort) gets to apply their preferences, unless it’s a really weak preference and the preference of the non-doer doesn’t require additional effort.

Here are some examples of tasks and how our effort/preference works out. You can look at this and see that Scott ends up doing the dishwasher organization (after I load it like a raccoon) before starting the dishwasher and also has stronger preferences about laundry than I do. On the flip side, I seem to find it easier with routines for staying on top of household supply management including buying/re-ordering and acquiring and putting those away where we have them ready to go, because they’re not on a clear scheduled cadence. Ditto for managing the cats’ health via flea/tick medication schedules, scheduling and taking them to the vet, signing them up for cat camp when we travel, coordinating with the human involved in their beloved cat camp, etc. We end up doing a mix of overall work, split between the two of us.

A four-quadrant grid. Across the top it says "Effort" with low effort on the left and high effort on the right. Along the side it says "preference" with weak preference on the bottom and strong preference at the top. The implication is you can have a mix of preference and how much work certain chores are. Usually the person in the top left quadrant for a particular chore - representing easy or lower effort anad stronger preference - ends up doing that chore. For me that's household supply ordering; managing cat vet appts, etc. where due to Scott's much stronger preference his include the dishwasher, laundry, etc.
Could each of us do those tasks? Sure, and sometimes we do. But we don’t have to each do all of them, all the time, and we generally have a split list of who does which type of things as the primary doer.

Raccoons and burnout with chronic diseases

I have now lived with type 1 diabetes for almost 22 years. When I met Scott, I had been living with diabetes for 11 years. When he asked on one of our early dates what he could do to help, my answer was: “…nothing?” I’m an adult, and I’ve successfully managed my diabetes solo for decades.

Obviously, we ended up finding various ways for him to help, starting with iterating together on technological solutions for remote monitoring (DIYPS) to eventually closing the loop with an automated insulin delivery system (OpenAPS). But for the longest time, I still did all the physical tasks of ordering supplies, physically moving them around, opening them, managing them, etc. both at a 3-month-supply order level and also every 3 days with refilling reservoirs and changing pump sites and sensors.

Most of the time, these decades-long routines are literally routines and I do them without thought, the same way I put on my shoes before I leave the house. Yet when burnout is approaching – often from a combination of having five autoimmune diseases or having a lot of life going on while also juggling the ‘routine’ tasks that are voluminous – these can start to feel harder than they should.

Should, being the key word here.

Scott would offer to do something for me and I would say no, because I felt like I “should” do it because I normally can/am able to with minimal effort. However, the activation energy required (because of burnout or volume of other tasks) sometimes changes, and these minimal, low-effort tasks suddenly feel high-effort. Thus, it’s a good time to examine whether someone can – even in the short term and as a one-off – help.

It’s hard, though, to eradicate the “should”. I “should” be able to do X, I “should” be able to handle Y. But honestly? I should NOT have to deal with all the stuff and management of living with 5 autoimmune diseases and juggling them day in and day out. But I do have to deal with these and therefore do these things to stay in optimal health. “Should” is something that I catch myself thinking and now use that as a verbal flag to say “hey, just because I CAN do this usually doesn’t mean I HAVE to do it right now, and maybe it’s ok to take a break from always doing X and let Scott do X or help me with Y.”

Some of these “I should do it” tasks have actually become tasks that I’ve handed off long-term to Scott, because they’re super low effort for him but they’re mildly annoying for me because I have roughly 247 other tasks to deal with (no, I didn’t count them: that would make it 248).

For example, one time I asked him to open my shipment with 3 months worth of pump supplies, and unbox them so I could put them away. He also carried them into the room where we store supplies and put them where they belonged. Tiny, but huge! Only 246 tasks left on my list. Now, I order supplies, and he unboxes and puts them away and manages the inventory rotation: putting the oldest boxes on top (that I draw from first) and newer ones on bottom. This goes for pump supplies, CGM supplies, and anything else mail order like that.

A similar four quadrant chart with the same axes as the other graph, with effort on top (low left; high right) and execution preference (weak bottom, strong top). Similar to chores, we look at how our preferences and how much work it feels like, relative to each other, to decide if there are any tasks I can ask Scott to take on related to chronic disease management (like opening boxes and rotating stock of supplies being lower effort for him than me, due to my overall volume of tasks being higher)

This isn’t always as straightforward, but there are a lot of things I have been doing for 20+ years and thus find very low effort once the supplies are in my hand, like changing my pump site and CGM. So I do those. (If I was incapacitated, I have no doubt Scott could do those if needed.) But there’s other stuff that’s low effort and low preference like the opening of boxes and arranging of supplies that I don’t have to do and Scott is happy to take on to lower my task list of 247 things so that I only have about 240 things left to do for routine management.

Can I do them? Sure. Should I do them? Well, again, I can but that doesn’t mean I have to if there’s someone who is volunteering to help.

And sometimes that help is really useful in breaking down tasks that are USUALLY low effort – like changing a pump site – but become high effort for psychological reasons. Sometimes I’ll say out loud that I need to change my pump site, but I don’t want to. Some of that might be burnout, some of that is the mental energy it takes to figure out where to put the next pump site (and remembering the last couple of placements from previous sites, so I rotate them), combined with the physical activation energy to get up from wherever I am and go pull out the supplies to do it. In these cases, divide and conquer works! Scott often is more than happy to go and pull out a pump site and reservoir and place it where it’s convenient for me when I do get up to go do something else. For me, I often do pump site changes (putting a new one on, but I keep the old one on for a few extra hours in case the new one works) after my shower, so he’ll grab a pump site and reservoir and set it on the bathroom counter. Barrier removed. Then I don’t have to get up now and do it, but I also won’t forget to do it because it’s there in flow with my other tasks to do after my shower.

A gif showing a similar four quadrant graph (effort across top, execution preference along the side), showing a task going from the top left (low effort usually, strong preference for how it is done) moving to the right (high effort and still high preference), then showing it being split into two halves, one of which becomes a Scott task because it's lower effort sub-tasks and the remaining part is still high preference for me but has lowered the effort it takes.

There are a lot of chronic disease-related tasks like this that when I’m starting to feel burnout from the sheer number of tasks, I can look for (or sometimes Scott can spot) opportunities) to break a task into multiple steps and do them at different times, or to have someone do the task portions they can do, like getting out supplies. That then lowers the overall effort required to do that task, or lowers the activation energy depending on the task. A lot of these are simple-ish tasks, like opening something, getting something out and moving it across the house to a key action spot (like the bathroom counter for after a shower), or putting things away when they no longer need to be out. The latter is the raccoon-style approach. A lot of times I’ll have the activation energy to start and do a task, but not complete (like breaking down supply boxes for recycling). I’ll set them aside to do later, or Scott will spot this ‘raccoon’ stash of tasks and tackle it when he has time/energy, usually faster than me getting around to do it because he’s not burdened with 240 other tasks like that. (He does of course have a larger pile of tasks than without this, but the magnitude of his task list is a lot smaller, because 5 autoimmune diseases vs 0.)

Be a friend to your friend who needs to be a raccoon some of the time

I am VERY lucky to have met & fallen in love & married someone who is so incredibly able and willing to help. I recognize not everyone is in this situation. But there may be some ways our friends and family who don’t live with us can help, too. I had a really fantastic example of this lately where someone who isn’t Scott stepped up and made my raccoon-life instantly better before I even got to the stage of being a raccoon about it.

I have a bunch of things going on currently, and my doctor recommended that I have an MRI done. I haven’t had an MRI in years and the last one was pre-pandemic. Nowadays, I am still masking in any indoor spaces including healthcare appointments, and I plan to mask for my MRI. But my go-to n95 mask has metal in the nose bridge, which means I need to find a safe alternative for my upcoming MRI.

I was busy trying to schedule appointments and hadn’t gotten to the stage of figuring out what I would wear as an alternative for my MRI. But I mentioned to a friend that I was going to have an MRI and she asked what mask I was going to wear, because she knows that I mask for healthcare appointments. I told her I hadn’t figured it out yet but needed to eventually figure it out.

She instantly sprang into action. She looked up options for MRI-safe masks and asked a local friend who uses a CAN99 mask without wire whether the friend had a spare for me to try. She also ordered a sample pack of another n95 mask style that uses adhesive to stick to the face (and thus doesn’t have a metal nose bridge piece). She ordered these, collected the CAN99 from the local friend, and then told me when they’d be here, which was well over a week before I would need it for the MRI and offered to bring them by my house so I had them as soon as possible.

Meanwhile, I was gobsmacked with relief and appreciation because I would have been a hot mess of a raccoon trying to get around to sorting that out days or a week after she had sorted a variety of options for me to try. Instead, she predicted my raccoon-ness or otherwise was being a really amazing friend and stepping up to take something off my plate so I had one less thing to deal with.

Yay for helpers. In this case, she knew exactly what was needed. But a lot of times, we have friends or family who want to help but don’t know how to or aren’t equipped with the knowledge of what would be helpful. Thus, it’s useful – when you have energy – to think through how you could break apart tasks and what you could offer up or ask as a task for someone else to do that would lower the burden for you.

That might be virtual tasks or physical tasks:

  • It might be coming over and taking a bunch of supplies out of boxes (or medicine) and splitting them up and helping put them in piles or all the places those things need to go
  • It could be researching safe places for you to eat, if you have food allergies or restrictions or things like celiac
  • It could be helping divvy up food into individual portions or whatever re-sizing you need for whatever purpose
  • It could be researching and brainstorming and identifying some safe options for group activities, e.g. finding places with outdoor dining or cool places to walk and hike that suits everyone’s abilities and interests

Sometimes it’s the physical burden that it’s helpful to lift; sometimes it’s the mental energy burden that is helpful to lift; sometimes a temporary relief in all the things we feel like we have to do ourselves is more important than the task itself.

If you have a chronic disease, it’s ok to be a raccoon. There is no SHOULD.

Part of the reason I really like the raccoon analogy is because now instead of being annoyed at throwing things in the dishwasher, because whether I exert energy or not Scott is going to re-load it his way anyway, I put the dishes in without much precision and giggle about being a raccoon.

The same goes for chronic disease related-tasks. Even for tasks where Scott is not involved, but I’m starting to feel annoyed at something I need to do, I find ways to raccoon it a little bit. I change my pump site but leave the supplies on the counter because I don’t HAVE to put those away at the same moment. I usually do, but I don’t HAVE to. And so I raccoon it a bit and put the supplies away later, because it doesn’t hurt anyone or anything (including me) for those not to get put away at the same time. And that provides a little bit of comedic relief to me and lightens the task of changing my pump site.

It also helps me move away from the SHOULD weighing heavily in my brain. I should be able to get all my pump site stuff out, change it, and throw away and put away the supplies when done. It shouldn’t be hard. No one else has this challenge occasionally (or so my brain tells me).

But the burden isn’t about that task alone. It’s one task in the list of 247 things I’m doing every day to take care of myself. And sometimes, my list GROWS. January 18, my list was about 212 things I needed to do. Beginning January 19, my list jumped up to 230. Last week, it grew again. I have noticed this pattern that when my list of things to do grows, some of the existing “easy” tasks that I’ve done for 20 years suddenly feel hard. Because it is hard to split my energy across more tasks and more things to focus on; it takes time to adapt. And so being a raccoon for some of those tasks, for some of the time, provides a helpful steam-valve to output some of the challenges I’m juggling of dealing with all the tasks, because those tasks 100% don’t have to be done in the same way as I might do during “calm” static times where my task list hasn’t expanded suddenly.

And it doesn’t matter what anyone else does or what they care about. Thus, remove the should. You should be able to do this, sure – if you weren’t juggling 246 other things. But you do have 246 things and that blows apart the “should”.

Free yourself of the “should” wherever possible, and be a raccoon wherever it helps.

What It Feels Like To Take Thyroid Medication

by Dana Lewis

I’ve been taking thyroid medication for a few months now. It surprised me how quickly I saw some symptom resolution. As I wrote previously, I started taking thyroid medication and planned to get more lab work at the 8 week mark.

The theory is that thyroid medication influences the production of new thyroid hormones but not the stored thyroid hormones; thus, since it takes around 6 weeks for you to replace your stores of thyroid hormones, you usually get blood work no sooner than 6 weeks after making a change to thyroid medication.

I had noted, though, that some of my symptoms included changes in my heart rate (HR). This was both my overnight resting HR and how my HR felt during the day. I had hypothesized:

Given I have a clear impact to my heart rate, I’m hypothesizing that I might see changes to the trend in my heart rate data sooner than 6 weeks – 2 months, so that’ll be interesting to track!

This turned out to be an accurate prediction!

My provider had suggested starting me on a low dose of “antithyroid” medication. Guidelines typically suggest 10-20mg per day, with plans to titrate (adjust) the dose based on how things are going. However, in my case, I have subclinical hyperthyroidism – not actual hyperthyroidism – which means my thyroid levels themselves (T3 and T4) were in range. What was out of range for me was my thyroid stimulating hormone (TSH), which was below range, and my thyroid antibodies, all of which were above range. (If you want to read about my decision making and my situation with Graves’ disease with eye symptoms and subclinical hyperthyroidism, read my previous post for more details.)

I ended up being prescribed a 5mg dose. Thinking about it, given my T3 and T4 were well within range, that made sense. I started taking it in early August.

What it felt like to start taking antithyroid medication for the first time:

For context, my primary most bothersome symptoms were eye symptoms (eyelid swelling, sometimes getting a red patchy dry area outside the outer corner of my eye, eye pressure that made me not want to wear my contacts); increased resting overnight HR and higher HR during periods of rest during the day; and possibly mood and energy impacts.

  • Within a week (!) of starting the antithyroid medication, my overnight HR began lowering. This can be influenced by other factors like exercise etc., but it was also accompanied by fewer days with higher heart rate while I was sitting and relaxing! I definitely felt a noticeable improvement within a week of my heart rate-related symptoms. 
  • My eyelid swelling went away toward the end of the first week. Then after 3 or so days, it came back again for a few days, then went away for 12 days. It came back for several days, went away for another 6 days. Came back, then…nothing! I went weeks without eyelid swelling and none of the other eye-related symptoms that typically ebbed and flowed alongside the eyelid swelling. HOORAY!
  • It’s unclear how much my mood and energy were directly effected by the wonky thyroid antibody levels compared to being a correlation with the symptoms themselves. (I was also resuming ultramarathon training during this time period, following the recovery of my broken toe.) However, I definitely was feeling more energetic and less grumpy, as noticed by my husband as well.

What is interesting to me is that my symptoms were changed within a week. They often talk in the medical literature about not knowing exactly how the thyroid medication works. In my case, it’s worth noting again for context that I had subclinical hyperthyroidism (in range T3 and T4 but below range TSH) and Graves’ disease (several thyroid antibodies well above range) with correlated eye symptoms. The theory is that the eye symptoms are influenced by the thyroid antibody levels, not the thyroid levels (T3 and T4) themselves. So although the thyroid medication influences the production of new thyroid hormones and it takes 6 weeks to replace your store of thyroid hormones; my working hypothesis is that the symptoms driven by TSH and thyroid antibodies are influenced by the production of those (rather than the stores) and that is why I see a change to my symptoms within a week or so of starting thyroid medication.

I went for repeat lab work at 8 weeks, and I was pretty confident that I would have improved antibody and TSH levels. I wasn’t sure if my T3 and T4 would drop below range or not. The lab work came back in and… I was right! TSH was back to normal range (HOORAY), T3 and T4 were slightly lower than the previous numbers but still nicely in the middle of the range. Yay! However, my TSI (thyroid stimulating immunoglobulin) was still well above range, and slightly higher than last time. Boo, that was disappointing, because there are some studies (example) showing that out of range TSI can be a predictor for those with Graves’ disease for the need to continue antithyroid medication in the future.

Animated gif showing changes to various thyroid labs two days and 8 weeks after annual lab work. T3 and T4 remain in range, TSH returns from below to in range, TSI remains above range; TRAb, TgAB, and TPO were above range but not re-tested at 8 weeks.

As I wrote in my last post:

I am managing my expectations that managing my thyroid antibody and hormone levels will be an ongoing thing that I get to do along with managing insulin and blood sugars and managing pancreatic enzymes. We’ll see!

The TSI was a pointer that although I had reduced all of my symptoms (hooray) and my T3 and T4 were within range, I would probably need ongoing medication to keep things in range.

However, as a result of the lab work, my provider suggested dropping down to 2.5mg dose, to see if that would manage my thyroid successfully without pushing me over to hypothyroidism (low T3 and T4) levels, which can be a risk of taking too much antithyroid medication. He suggested switching to 2.5mg, and repeating lab work in 3 months or if I felt unwell.

I agreed that it was worth trying, but I was a little nervous about reducing my dose, because my T3 and T4 were still well within the middle of normal. And, I had an upcoming very long ultramarathon. Given that with the start of thyroid medication I saw symptoms change within a week, and I was two weeks out from my ultra, I decided to wait until after the ultramarathon so I could more easily monitor and assess any symptoms separately from the taper and ultra experience.

Recovery from my ultramarathon was going surprisingly well, enough so that I felt ready to switch the medication levels pretty soon after my ultra. I started taking the 2.5mg dose (by cutting the 5mg dose in half, as I had some remaining and it was easier than ordering a changed prescription to 2.5mg).

I carefully watched and saw some slight changes to my HR within the first week. But, I was also recovering from an ultramarathon, and that can also influence HR. Again, I was looking at both the overnight resting HR and noting any periods of time during the day where I was resting when my HR was high (for me). I had two days where it did feel high during the day, but the following days I didn’t observe it again, so I chalked that up to maybe being related to ultramarathon recovery.

But a little over a week and my right eye started feeling gunky. I had just been to the eye doctor for my annual exam and all was well and my eye didn’t look red or irritated. I didn’t think much of it. But a few days after that, I had rubbed my right eyelid and realized it felt poofy. I felt my left eyelid in comparison, and the right was definitely swollen in comparison. Looking in the mirror, I could see the swollen eyelid pushing down the corner of my right eye. Just like it had done before I started thyroid medications. Ugh. So eye symptoms were back. A few days later, I also woke up feeling like my eyes hurt and they needed lubrication (eye drops) as soon as I opened my eyes. That, too, had been a hallmark of my eye symptoms from last October onward.

The plan had been to wait until 3 months after this medication change to repeat labs. I’m going to try to wait until the 6-8 week mark again, so we can see what the 2.5mg does to my T3 and T4 levels alongside my TSH. But, my prediction for this next round of lab work is that T3 and T4 will go up (maybe back to the higher end but likely still within range; although the possibility to fully go above range), and that my TSH will have dropped back down below range, because the symptom pattern I am starting to have mimics the symptom pattern I had for months prior to starting the 5mg thyroid medication.

Why only wait 6-8 weeks, when my provider suggested 3 months?

These symptoms are bothersome. The eyelid swelling thankfully subsided somewhat after 4 days (after the point where it got noticeable enough for my husband to also see it compressing my outer corner of my eye, which means anyone would be able to visibly see it), but I’m watching it to see if it returns with a cyclical pattern the way it went away previously, expecting it to likely return to constant every day eye swelling. Since it influences my vision slightly (because the eyelid is pushed down by the swelling), that impacts my quality of life enough to take action sooner. If it gets really bad, I might discuss with my provider and get labs even sooner, but I’m going to try to tough it out to 6-8 weeks to get a full picture of data of how the 2.5mg impacted all of my levels and also see what pattern of symptoms return when, because it will be interesting to compare the symptom levels at 5mg (essentially all gone within 1-2 weeks) and at 2.5mg compared to my original, pre-thyroid medication symptom levels and patterns.

But depending on those labs, I predict that I will return to taking the 5mg dose, and hopefully my symptoms will go away completely and stay away. Then it’ll be a future decision on if/when to try titrating down again; possibly guided by the TSI level, since the TSI was still above range when we had switched me to 2.5mg (despite the change in TSH back to range).

The good news is, though, that in future I should be able to use the 1-2 weeks of symptom data to determine whether a change in dose is working for me or not, instead of having to wait a full 6-8 weeks, because my symptoms seem to be driven by the TSH and antibody levels, rather than out of range T3 and T4 levels (because they were and are still in the middle of the goal range).

I also discussed this with my eye doctor. You’ll note from my previous post that I was very concerned about the eye impacts and symptoms, so I had asked my eye doctor if she’s still comfortable treating me (she is), and we talked about what things would cause me to get a referral to a specialist. So far my symptoms don’t seem on track for that; it would be my eyes protruding from the socket and having pressure that would possibly need surgery. Disappointingly, she confirmed that there’s really no treatment for the symptoms since they’re caused by the antibody levels. There’s no anti-swelling stuff to put on my eyelid to help. Instead, the goal is to manage the antibody levels so they don’t cause the symptoms. (Which is everything I’m talking about doing above, including likely returning to the 5mg dose given that my eye symptoms resumed on the 2.5mg dose).

—

In summary, I think it is worth noting for anyone with Graves’ disease (whether or not they have subclinical or actual hyperthyroidism) that it is possible to see symptom changes within a week or two of starting or changing your thyroid medication. I can’t find anything in the literature tracking symptom resolution on anything shorter than a 6 week time period, but maybe in the future someone will design a study to capture some of the real-world data and/or run a prospective study to capture this data and see how prevalent this is for symptoms to resolve on a much shorter time frame, for those of us whose symptoms are driven not by thyroid levels themselves (T3 and T4) but for the TSH and TSI and other thyroid antibodies (TPO etc).

If you do start thyroid medication, it’s worth logging your symptoms as soon as  possible, ideally before you start your medication, or if it’s too late for that, start logging them afterward. You can then use that as a comparison in the future for if you reduce, increase, or are directed to stop taking your medication, so you can see changes in the length of time it takes to develop or reduce symptoms and whether the patterns of symptoms change over time.

What it feels like to take thyroid medication

Stigma and the impact on people with chronic illnesses

by Dana Lewis

I have a new thing, and I didn’t want to talk about it. In part, because of stigma. Mostly, because of stigma.

Stigma has played a huge role in how I have responded to my own chronic autoimmune diseases for almost 20 years, in fact. I’m incredibly disappointed that not much has changed in all this time.

When I was diagnosed with type 1 diabetes almost 20 years ago, I was very aware of the stigma against people with any type of diabetes. I grew up in Alabama. People with diabetes were perceived by society to be lazy, out of control of their own behaviors, and any complications or outcomes were their own fault.

It wasn’t – and isn’t – their fault. The tools and technologies (not much technology then) did not give people a chance at good or great outcomes. The tools and technologies failed people. Yet, people and their behaviors were and often still are blamed, shamed, and treated poorly in society and in medicine and the healthcare system.

The first day I was diagnosed and sent from my primary care doctor’s office to the pediatric endocrinologist, I was scared. Diabetes in society was presented to me as amputations and kidney disease and other not so great things. I didn’t know anyone with type 1 diabetes. And when the pediatric endo came into the room for the first time and said, “Don’t worry. We can get you an insulin pump, it’ll be great!” my reaction was: absolutely not. An insulin pump will be a visible label that I have diabetes. Instead of a chance of being blamed, shamed, and treated badly – I will almost certainly be labeled, blamed, shamed, and treated badly. No, thanks.

And so I didn’t get on a pump (at first). It wasn’t until I realized that a pump would give me freedom, to sleep in and not have to wake up and eat a pre-allotted amount and take insulin, that I decided the personal freedom was worth the labeling, dirty looks, blame, shame, and negative treatment.

And I regret it. I regret how stigma shaped my reaction to possible tools and technology that would aid me. I’ve strived ever since to not let that factor into my choices.

But last week, I realized stigma was still playing a role. I have a new thing, and I rationalized my choice not to blog about it because it’s a well-known thing, and as a newbie, surely I didn’t have anything to add to the public discourse about this thing. Information is available about this new thing, and I wouldn’t be adding anything new. What did I have to say that hasn’t been said before about this common topic?

But after a few days, I realized my decision to not blog about my experience was also driven by stigma and fear of how I’ll be treated when I share publicly that I have YetAnotherThing on my list of things I’m managing. It’s an autoimmune thing, again. It’s not “my fault”. It’s not at all in my control.

Because my immune system is too strong for my body to handle, I have not one, not two, but now three autoimmune things. (And 4 things total, but exocrine pancreatic insufficiency is possibly not an autoimmune thing so I leave it off the list even though it’s on my overall list of things I’m managing.)

Like people with physical or visible disabilities, having a chronic disease and talking about it publicly gives people the feeling that they can publicly shame and blame me “for my own good”. Or hypothesize on what I’ve “done wrong” to get to this point. Or to “suggest” things I can do to better manage. Often, these things are scientifically wrong. (Note: this is why ‘cinnamon’ is a joke for people with type 1 diabetes. There is no cure or treatment for type 1 diabetes other than taking insulin for the rest of our lives. Cinnamon does not cure diabetes, yet it and other things are presented to people with diabetes as “alternative” methods that would in fact, kill me if I relied upon those and stopped taking insulin.)

I dislike this. I dislike the fact that being open about what I’m dealing with, in order to possibly help other people also dealing with the same thing or identifying gaps in the healthcare system, invites judgment and all of this commentary. Let me be clear: I do not invite that. Ever. Not now, not in the future. Not about diabetes, not about celiac, not about exocrine pancreatic insufficiency, and not about my new thing. I’ve noticed more and more other advocates writing in their tweet threads or their blog posts “This is not soliciting advice or suggestions”, because so often we ARE bombarded with “advice” or “suggestions” that are unsolicited, and like I mentioned above, possibly dangerous if not outright deadly.

I don’t have answers. I can’t fix the stigma in society. The best I can do is perhaps write about it and talk about it and help shine a light on the fact that it 100% does impact people. It prevents other people from seeking healthcare when they need it. It prevents people from sharing and processing their feelings, or reaching out for help when they need it. It causes harm. And we all need to do better as a society.

So I am sighing a lot, and writing this blog post first so I can process my feelings that are blocking me from writing the next blog post. The one with scientific information and citations as well as an articulation of my experience and situation, in hopes that one day someone on page 18 of a search engine will find it when they need it. It’s not for everyone.

But as always, I think that if it eventually helps one person, then it’ll be worth it. It’ll be worth the stigmatizing response that some people will have now and in the future when they realize I am someone living with multiple autoimmune diseases. I hope. It’s always my hope. I’ve had this tagline on my email ever since I first had email, and I still believe it’s true today which is why I wrote this blog post and am now turning to writing the next one:

“Doing something for someone else is more important than anything you would do for yourself.”

Graves’ Disease, Subclinical Hyperthyroidism, and Everything I Have Learned About It (So Far)

by Dana Lewis

TLDR: I have newly diagnosed Graves’ Disease, I have associated eye stuff (called “Graves’ orbitopathy” or “Graves’ ophthalmopathy” or “thyroid eye disease”), subclinical hyperthyroidism, and a new learning curve. Below is what I’ve learned so far and what I’m still exploring.

As a person with type 1 diabetes (T1D) – which is an autoimmune disease – I am screened yearly for various high-risk related conditions. For example, celiac disease and thyroid issues, because those are fairly common in people with type 1 diabetes. I already have celiac disease (developed ~6 years after I developed T1D), but we have continued to screen every year in my annual blood work for thyroid markers, usually by screening T4 and TSH. Occasionally, T3 and/or TPO antibodies are also screened.

I remember vividly the chortle that my prior endocrinologist made after we diagnosed my celiac disease in college, probably in response to my comment about being frustrated of having “another” thing to deal with in addition to T1D. He chortled and said something like “once you have one (autoimmune thing), you’re likely to have two. Once you have two, you’ll be likely to have three.”

I didn’t like it at the time, and I don’t like it now. However, he’s not wrong. When your immune system has a little extra kick in it and you develop one autoimmune disease, the rates of having another autoimmune thing are increased. Thus, the typical yearly screening in T1D for celiac & thyroid.

I went 6 years between T1D and celiac, then almost 12-13 years to discover I now have exocrine pancreatic insufficiency (EPI). That’s not necessarily an autoimmune thing but may be a side effect of long-term T1D. Regardless, I was still thankful for the long period of time between T1D and celiac, then T1D+celiac and EPI. I was assuming that something else was coming eventually, but that I’d likely have a few years before the shoe dropped.

Nope.

I wasn’t terribly surprised when I scheduled my annual endocrinology appointment and did my annual blood work to find that one of my thyroid values was off. Specifically, my TSH (thyroid stimulating hormone) was low / below normal range. However, my T4 was smack dab in the middle of normal range. I got my blood work back Tuesday and waited for my virtual appointment on Friday to discuss in detail with my endocrinologist.

Since I’m me, I was curious about the interplay between normal thyroid levels (T4, and I suspected my T3 was likely still in range) but a low TSH value. What did that mean? General consensus seems to define this as “subclinical hyperthyroidism”. It’s not always treated, unless you are older (>65), have osteoporosis or heart disease, or TSH levels are <0.1.

I’m <65, don’t (as far as I know) have osteoporosis or heart disease, and my TSH levels are between 0.1 and 0.4, which is the low end of the normal range. So general treatment guidelines (see this example from the AAFP) suggest treatment isn’t necessarily warranted.

However…there’s more information that factors into the decision making. First, I had my last annual eye exam in October. All was well. Yet in November, I developed really gritty, dry eyes and went in for an appointment. I was diagnosed with dry eyes (gee, thanks!) and recommended to use gel drops at night before bed and regular eye drops during the day as needed. I did end up needing eye drops several times every day.

Then at the end of December or early January, we realized I had exocrine pancreatic insufficiency (EPI). I had been wondering if my dry eyes was related to the lack of digestion and absorption of nutrients, which also influences how my body uses the water content from food. It did seem to get a little better in the following months, because while I still needed the eye gel at night, I eventually moved to several days a week where I didn’t seem to need the eye drops during the day – yay!

However, in February and early March, I started to physically notice a shift in my resting overnight heart rate (HR). My Pebble 2+ HR watch and my Oura ring, both of which measure HR and heart rate variability (HRV), confirmed that both metrics were getting worse. I had a slowly increasing overnight HR and associated decrease in HRV. I am used to fluctuations, because the intensity of my ultrarunning can also influence HR the next day as a signal for whether my body has recovered yet or not. But instead of a day or two of increased numbers, I had an increasing trend line over several weeks, and it started to physically become bothersome. I actually raised the idea of getting my thyroid blood work done early this year, and was about to request the lab work, when after ~6 weeks or so the trend seemed to reverse and things (HR-wise) went back to “normal” for me.

Then I broke my toe in July and the same thing happened, but I chalked it up to sleep disruption from the pain and recovering from the fracture. My HR was continuing to rise even as the pain subsided and my toe was clearly healing. And looking back at my HR data, I can see it actually started to rise at the beginning of July, about two weeks before I broke my toe, so it’s not solely influenced by my broken toe.

As a result of these HR increases (that are noticeable and bothersome because I’m also not sleeping well at night and I physically feel the higher HR during the day), and the ongoing dry/gritty eyes, I suspected that the cause of my “subclinical hyperthyroidism” was Graves’ disease.

I’ve seen estimates that ~30% of people with Graves’ disease have what is called “Graves’ orbitopathy” (and other estimates suggest 20-50%, like this one), so the combination of my ongoing eye symptoms and the low TSH suggested that further lab work assessing various thyroid antibody levels would be able to confirm whether Graves’ disease was the likely source of the subclinical hyperthyroidism.

Therefore, I wasn’t surprised during my virtual visit that my endocrinologist ordered additional labs (repeat of T4 and TSH; adding in T3, TPO antibodies, and TSI (Thyroid Stimulating Immunoglobulin), Thyrotropin Receptor Ab, and Thyroglobulin Ab). Treatment plan, if any, would be based on these results.

I managed to get in that (Friday) afternoon for the repeat lab work, and my results started trickling in by the time I woke up Saturday morning. First, T3, T4, TPO, and TSH came back. T4 was still normal; as I expected, T3 was also normal. TPO antibodies were high, as expected, TSH was still low, as I expected. Saturday night, Thyroglobulin Ab came back high, as expected. Monday, TSI came back high, as expected. Tuesday, my last test result of Thyrotropin Receptor Ab came back, also high as expected.

The summary was: all antibodies high; TSH low; T3/T4 normal.

My endocrinologist messages me Tuesday afternoon confirming mild Graves’ disease with subclinical hyperthyroidism.

The challenge is that I have normal T3/T4 levels. If those were high, we’d treat based on those levels and use those levels coming back into normal range and any change in antibody levels to assess that things were going well.

But the guidelines for subclinical hyperthyroidism don’t really indicate treatment (except on an individual level based on age, other conditions, or undetectable TSH <0.1, as I mentioned).

However, from what I’ve read, the “eye stuff” seems to be driven not by thyroid levels but by the presence of the increased thyroid antibodies. Treatment would possibly bring down the thyroid antibody levels, which might help with the eye disease progression. But not a guarantee. So my doctor left it up to me to decide whether to treat it or not.

Given the ongoing presence of active eye disease (I haven’t been able to wear my contacts for two weeks right now due to swelling/pain in the eyes, plus itching and redness), and the bothersome heart rate feeling, I have decided to try antithyroid medication. I’ll be on a relatively low dose of an “antithyroid” drug, again with the goal of trying to reduce my antibody levels.

This is why I ended up deciding to write this blog post after all: I have not been able to find any clear treatment guidelines for subclinical hyperthyroidism and Graves’ disease with active eye symptoms (from Graves’ orbitopathy). The literature does suggest that treatment to reduce thyroid antibodies even with in-range T3 and T4, targeting a return to normal TSH levels, may be helpful in reducing Graves’ orbitopathy symptoms. This isn’t well known/established enough to have been documented in treatment guidelines, but does seem to occur in many people who are treated.

So hopefully, anyone else with low TSH and high antibodies suggesting Graves’ disease but normal T3 and T4 levels that suggests subclinical hyperthyroidism and also has other symptoms (whether that’s heart rate or other common hyperthyroid symptoms like increased sweating, shaking, heart palpitations, heat intolerance, sleep disturbances) that are bothersome, now have an example of what I chose, given my situation as described above.

I also thought sharing my question list at different stages for my endocrinologist would be helpful. After I saw that I had low TSH and in range T4, and suspected this meant I had subclinical hyperthyroidism from Graves’ disease, given my eye symptoms, the questions I asked my endocrinologist were:

  • What additional lab work did we need to confirm subclinical hyperthyroidism and Graves’ disease as the cause? What additional information or lab work would give us a treatment plan?As expected, he repeated TSH and T4, added T3 and TPO and the other antibody tests described above: TGAb, TRab, TSI. This would confirm subclinical hyperthyroidism and Graves’ as the likely source.

     

  • Do I need treatment, since the guidelines generally don’t suggest treatment with normal T3/T4 and TSH between .1 and .4?Initially he suggested treatment would be an option, and after the repeat and expanded lab work, left it up to my decision. Given my symptoms that are actively bothering me, I’m choosing to try low-dose antithyroid medication.
  • For hyperthyroidism treatment, beta blockers seem to be part of treatment guidelines for managing symptoms in the short-term, since it takes ~6 weeks for antithyroid medication to show up in lab results. Were beta blockers warranted in my case?My endo typically doesn’t like to prescribe beta blockers unless there are extreme symptoms. He gave an example of someone with a T4 (I think) around 10 and extreme visible shaking. He left it up to me, but his opinion was the side effects, such as lethargy, would outweigh the benefits for mild symptoms, so it is better to treat the root cause. I agreed and did not ask for a beta blocker prescription.
  • I also asked if a DEXA scan was warranted to check my bone density.I haven’t had one in over a decade, and celiac and EPI and now Graves’ puts me at possible higher risk of bone density issues. And, since the presence of osteoporosis changes the treatment recommendation for subclinical hyperthyroidism, we agreed it was worth doing. I have it scheduled in a few weeks. My last one over a decade ago was normal.
  • Finally, I asked about my eye care, now that I have a known eye thing (Graves’ orbitopathy). Do I need to get referred to an ophthalmologist, or can I continue to see my existing optometrist for annual eye care (including diabetes eye exam) and contact fittings?My endocrinologist suggested that my optometrist can continue to manage my eye care, unless something changes significantly. Ophthalmologists, based on his response and my research, seem to handle severe eye disease treatments that aren’t likely warranted for me. I’ll probably need supportive eye care (e.g. gel drops, regular eye drops) for now. However, I’m planning to send a note to my eye doctor and flag that I want to talk about Graves’ eye things and a plan for monitoring severity and progression over time, and check whether she’s comfortable supporting me or if she prefers to refer me to someone else. 


After my repeat labs came back, my endocrinologist messaged me to confirm things and ask if I wanted him to send in the prescription as previously discussed. This exchanged answered the additional questions I had at this time:

  • What is the treatment timeline? How soon might I see results?He suggested repeat labs at the 2 month mark. Ideally, we’d see reduced antibody levels and my hope is that my eye symptoms will have also improved and/or I won’t have any additional weeks without being able to wear contacts.

    Given I have a clear impact to my heart rate, I’m hypothesizing that I might see changes to the trend in my heart rate data sooner than 6 weeks – 2 months, so that’ll be interesting to track!

     

  • Side effects?Common side effects with antithyroid drugs are rash/allergic type response, headache, or agranulocytosis. He told me to discontinue and contact the office if I had any of those symptoms.

    He didn’t go into detail, but I’ve read about agranulocytosis and it seems like if you have a fever and strong sore throat, you need to discontinue and probably will have blood work ordered to make sure your white blood cell counts are ok. Don’t google too much on this one as it sounds scary, but it’s also rare – less than 2% of people seem to have this.

     

  • The only question he didn’t answer was whether it makes a difference in efficacy to take the antithyroid drugs at night or in the morning.Probably, the answer is it doesn’t matter, and whatever time you can take it consistently is best. However, I want to optimize and get the best results from taking this, so I’m bummed that there doesn’t seem to be any evidence (let me know if you’ve found anything in medical literature) suggesting how to optimize timing of it. 

So that’s where I am today.

I now have type 1 diabetes, celiac disease, exocrine pancreatic insufficiency, and Graves’ disease (contributing to subclinical hyperthyroidism). It’s possible that we can fix the subclinical hyperthyroidism, and that I won’t need to be on antithyroid medication long-term. However, the data for those of us with Graves’ orbitopathy isn’t super optimistic compared to those without Graves’ eye disease; so I am managing my expectations that managing my thyroid antibody and hormone levels will be an ongoing thing that I get to do along with managing insulin and blood sugars and managing pancreatic enzymes. We’ll see!