The multivariable equation that is running with type 1 diabetes, celiac disease, and exocrine pancreatic insufficiency

I’ve written in the past about running with type 1 diabetes. I’ve tried running fasted, which works well in one sense because I have no extra insulin on board. I’ve modified my strategy further to run 2 or more hours after breakfast, so I have fuel but don’t have (much) IOB. But as I’ve extended my forays deeper into longer distance ultrarunning, and as I learned I have exocrine pancreatic insufficiency (EPI), running is getting a little more complicated.

For past thoughts on T1D running, here’s my post on running fasted and thinking about IOB. I also wrote more here last year about marathon and 50k ultramarathon training and how I use small doses of carbs to “correct” for dipping blood sugars. Last year, my body didn’t seem to need or want much additional fuel, so I didn’t force it. Part of that was likely a symptom of my undiscovered EPI. Now, however, that I am taking enzymes for pancreatic enzyme replacement therapy so I can digest what I eat, I have more energy (because my body is actually using what I eat), but I also get hungry and seem to need more fuel while running. But everything I eat needs enzymes to help me digest it, even things that I eat while ultrarunning.

So…it’s complicated to run with type 1 diabetes and micromanage insulin and carbs to manage blood glucose levels; and I’m limited in my fuel choices because I have celiac disease; and now I have to also carry, titrate, and dose enzymes for any fuel that I eat on the run as well.

Oh, and like insulin, the timing of enzymes matters. But there are no studies on enzyme digestion and how that changes during exercise, let along endurance activities like ultrarunning. So I am running in the dark, so to speak, trying to figure out things myself as I go along.

Here is more detail about what I’m doing and why I’m constantly running multivariable equations in my head while training for a 50k, 50 mile, and maybe even 100 mile run later this year:

First and foremost, managing blood sugar levels comes first.

I wear a CGM, so I can see how my blood sugar (BG) is changing during the run. I have a pump, so I can make any changes to insulin dosing. I also have an open source AID system (OpenAPS), so before running I set a higher target which tells the system not to give me as much insulin as it would otherwise. (It also does an awesome job with post-run insulin sensitivity changes! But that’s another post.) As I’ve previously written about, reducing insulin on board (IOB) when I know I’ll be running is the important first step, so I don’t have to start taking carbs and treating a low at the start of my run. Usually, my open source AID and I (by giving it a temporary target) do a good job getting me to my run start without much IOB, and ideally somewhere around 120-130 mg/dL.

From that level area, I can see rises and dips in BGs and dose accordingly. I carry easily dissolving small mint-like candies that are a few carbs (3-4g), or Airhead minis (8g of carbs), and with any dip below 120 or recurring drop that’s not coming up after 15 minutes since my last carb, I take more. These are pretty much straight sugar, and my body seems to do ok with absorbing carbs without enzymes, as long as there is no fat or protein involved.

However, with ultrarunning it’s generally considered to be ideal to proactively be consuming fuel to balance out the energy that you’re burning. Again, this is where I’m less experienced because for the last years, my body never wanted fuel and I did ok. However, now I seem to need fuel, so I’m working on figuring this out because food typically has some fat and protein, and I have to dose enzymes for it.

I carry a baggy with some single-enzyme (lipase) pills and some multi-enzyme (lipase for fat, amylase for carbs, and protease for protein) pills. I carry carefully measured single-serving snacks that I know the fat and protein quantity of. For each snack, I might need 1-2 enzyme pills of various sorts.

Timing matters: I can’t take enzymes and then snack slowly for 30 minutes. To eat slowly, I would need to take enzymes every 10-15 minutes to match the speed of eating so it will ultimately be there to help the food digest.

But, more carbs/food at once has an effect on how I feel while running and also to my BGs. I’ve tried to find things I love to eat running and can eat within 5 minutes – even while running 30 seconds and walking 60 seconds repeatedly – that are also less than 1-2 enzyme pills worth of fat and protein and aren’t too many carbs at once. These may be 15-20g carb snacks which means a bigger impact to my BG levels, and I may need to even do a small bolus (give insulin) for what I am eating. The challenge again is that food can hit BGs in about 15 minutes but it takes ~45 minutes for insulin activity to peak. And, during exercise, I’m more sensitive to insulin than I normally am. There’s no magical calculation to know how much “more” sensitive I am in the midst of a run, so I have to guess and thread the needle between not giving too much insulin that would cause a low BG but giving enough so I don’t spike above 180 mg/dL, which is what makes me feel icky while running.

Preferably, and very personally, I’d like to float up and down between 120-140 mg/dL or 130-150 mg/dL, which is higher than BGs usually hang out for me without exercise (remember: open source AID!), but is high enough that I have buffer against a low, so if I suddenly dip and I haven’t looked at my BGs in 15 minutes, I can usually still carb up and prevent an annoying low. (Lows matter even more on runs because they slow me down physically, which is usually not what I’m going for.)

It doesn’t always work that way. Sometimes I undershoot the insulin because I’ve miscalculated my effort running, and my BG drifts high and I have to decide whether or not to correct further. Other times, I overshoot (or have increased my run effort and didn’t take that into consideration) and cause BG to dip or dive toward low. Then I have to carb up but hopefully not so much that I cause a high.

My priority list therefore is: manage BGs, take in fuel, try not to over or undershoot on insulin for the fuel or overshoot carb corrections for drifting BGs, plus remember to take enzymes for the fuel and dose the right amount, plus stay on top of my electrolytes. Oh, and keep run-walking.

And along the way, I am also trying to document and learn whether the absorption of enzymes changes during different intensities or lengths of exercise; whether these over the counter enzymes are reliably measured enough for small snacks, and whether my personal ratios for fat and protein are any different during exercise the way my sensitivity to insulin changes during exercise.

It’s a lot of work. Plus, the pre-work that goes in to finding, measuring, and preparing foods that I think I want to eat during the run!

My current short list of single-serving snacks that I can tolerate while doing long runs includes: 8 gluten free peanut butter pretzel nuggets; 1 serving of chili cheese Fritos; 6 gluten free yogurt covered pretzels; and 1 gluten free stroopwaffle. Each of those is 15-20g of carb, 1-2 enzyme pills, and some of them have a bit of sodium. (I’m also fairly sensitive to sodium so I take electrolyte pills every 30-45 minutes while racing, but I’ve realized the extra fueling with a bit of sodium makes it so I don’t have to take the electrolyte pills every 30 minutes like I used to.)

When I build up to my longer (50 mile or maybe 100 mile ultras, if I get there!) runs, I’m also going to need additional “real food” options, as I doubt I will be able to or want to eat stroopwaffle and Fritos for as long as the run will take. This is just a theoretical list, but it includes tomato soup (sodium and warm liquid!), instant mashed potatoes (soft and not much chewing involved), grits and oatmeal (not together, but same reason as mashed potatoes). These all luckily also happen to be lower in fat and protein, which means easier to digest (in theory), and I am less likely to have better error margins against getting the enzyme dosing wrong given the small amounts of fat and protein.

What it comes down to is that running with type 1 diabetes is a giant constant personal science experiment. Celiac makes it more work, but also removes some of the variables by limiting what I can to eat: as at races I can’t eat out of any open bowl or package due to cross contamination concerns, and reading packages takes time, so it’s way safer to just eat what I bring myself. Having EPI on top of that means mastering the art of digesting food with pancreatic enzyme replacement therapy, which is its own special form of science experiment.

There’s a lot of variables, a lot of science, and a lot of learning going on every time I go for a run. Doesn’t it sound fun?!


(PS – If you’re someone with EPI who has some experience with endurance activity and changes to dosing enzymes..or find that it doesn’t change anything…please reach out! I’d love to chat and take my knowledge base from n=1 to n=2!)

Multivariable Equations: Running with Type 1 diabetes, celiac disease, and Exocrine Pancreatic Insufficiency

Findings from the world’s first RCT on open source AID (the CREATE trial) presented at #ADA2022

September 7, 2022 UPDATEI’m thrilled to share that the paper with the primary outcomes from the CREATE trial is now published. You can find it on the journal site here, or view an author copy here. You can also see a Twitter thread here, if you are interested in sharing the study with your networks.

Example citation:

Burnside, M; Lewis, D; Crocket, H; et al. Open-Source Automated Insulin Delivery in Type 1 Diabetes. N Engl J Med 2022;387:869-81. DOI:10.1056/NEJMoa2203913


(You can also see a previous Twitter thread here summarizing the study results, if you are interested in sharing the study with your networks.)

TLDR: The CREATE Trial was a multi-site, open-labeled, randomized, parallel-group, 24-week superiority trial evaluating the efficacy and safety of an open-source AID system using the OpenAPS algorithm in a modified version of AndroidAPS. Our study found that across children and adults, the percentage of time that the glucose level was in the target range of 3.9-10mmol/L [70-180mg/dL] was 14 percentage points higher among those who used the open-source AID system (95% confidence interval [CI], 9.2 to 18.8; P<0.001) compared to those who used sensor augmented pump therapy; a difference that corresponds to 3 hours 21 minutes more time spent in target range per day. The system did not contribute to any additional hypoglycemia. Glycemic improvements were evident within the first week and were maintained over the 24-week trial. This illustrates that all people with T1D, irrespective of their level of engagement with diabetes self-care and/or previous glycemic outcomes, stand to benefit from AID. This study concluded that open-source AID using the OpenAPS algorithm within a modified version of AndroidAPS, a widely used open-source AID solution, is efficacious and safe.

The backstory on this study

We developed the first open source AID in late 2014 and shared it with the world as OpenAPS in February 2015. It went from n=1 to (n=1)*2 and up from there. Over time, there were requests for data to help answer the question “how do you know it works (for anybody else)?”. This led to the first survey in the OpenAPS community (published here), followed by additional retrospective studies such as this one analyzing data donated by the community,  prospective studies, and even an in silico study of the algorithm. Thousands of users chose open source AID, first because there was no commercial AID, and later because open source AID such as the OpenAPS algorithm was more advanced or had interoperability features or other benefits such as quality of life improvements that they could not find in commercial AID (or because they were still restricted from being able to access or afford commercial AID options). The pile of evidence kept growing, and each study has shown safety and efficacy matching or surpassing commercial AID systems (such as in this study), yet still, there was always the “but there’s no RCT showing safety!” response.

After Martin de Bock saw me present about OpenAPS and open source AID at ADA Scientific Sessions in 2018, we literally spent an evening at the dinner table drawing the OpenAPS algorithm on a napkin at the table to illustrate how OpenAPS works in fine grained detail (as much as one can do on napkin drawings!) and dreamed up the idea of an RCT in New Zealand to study the open source AID system so many were using. We sought and were granted funding by New Zealand’s Health Research Council, published our protocol, and commenced the study.

This is my high level summary of the study and some significant aspects of it.

Study Design:

This study was a 24-week, multi-centre randomized controlled trial in children (7–15 years) and adults (16–70 years) with type 1 diabetes comparing open-source AID (using the OpenAPS algorithm within a version of AndroidAPS implemented in a smartphone with the DANA-i™ insulin pump and Dexcom G6® CGM), to sensor augmented pump therapy. The primary outcome was change in the percent of time in target sensor glucose range (3.9-10mmol/L [70-180mg/dL]) from run-in to the last two weeks of the randomized controlled trial.

  • This is a LONG study, designed to look for rare adverse events.
  • This study used the OpenAPS algorithm within a modified version of AndroidAPS, meaning the learning objectives were adapted for the purpose of the study. Participants spent at least 72 hours in “predictive low glucose suspend mode” (known as PLGM), which corrects for hypoglycemia but not hyperglycemia, before proceeding to the next stage of closed loop which also then corrected for hyperglycemia.
  • The full feature set of OpenAPS and AndroidAPS, including “supermicroboluses” (SMB) were able to be used by participants throughout the study.

Results:

Ninety-seven participants (48 children and 49 adults) were randomized.

Among adults, mean time in range (±SD) at study end was 74.5±11.9% using AID (Δ+ 9.6±11.8% from run-in; P<0.001) with 68% achieving a time in range of >70%.

Among children, mean time in range at study end was 67.5±11.5% (Δ+ 9.9±14.9% from run-in; P<0.001) with 50% achieving a time in range of >70%.

Mean time in range at study end for the control arm was 56.5±14.2% and 52.5±17.5% for adults and children respectively, with no improvement from run-in. No severe hypoglycemic or DKA events occurred in either arm. Two participants (one adult and one child) withdrew from AID due to frustrations with hardware issues.

  • The pump used in the study initially had an issue with the battery, and there were lots of pumps that needed refurbishment at the start of the study.
  • Aside from these pump issues, and standard pump site/cannula issues throughout the study (that are not unique to AID), there were no adverse events reported related to the algorithm or automated insulin delivery.
  • Only two participants withdrew from AID, due to frustration with pump hardware.
  • No severe hypoglycemia or DKA events occurred in either study arm!
  • In fact, use of open source AID improved time in range without causing additional hypoglycemia, which has long been a concern of critics of open source (and all types of) AID.
  • Time spent in ‘level 1’ and ‘level 2’ hyperglycemia was significantly lower in the AID group as well compared to the control group.

In the primary analysis, the mean (±SD) percentage of time that the glucose level was in the target range (3.9 – 10mmol/L [70-180mg/dL]) increased from 61.2±12.3% during run-in to 71.2±12.1% during the final 2-weeks of the trial in the AID group and decreased from 57.7±14.3% to 54±16% in the control group, with a mean adjusted difference (AID minus control at end of study) of 14.0 percentage points (95% confidence interval [CI], 9.2 to 18.8; P<0.001). No age interaction was detected, which suggests that adults and children benefited from AID similarly.

  • The CREATE study found that across children and adults, the percentage of time that the glucose level was in the target range of 3.9-10mmol/L [70-180mg/dL] was 14.0 percentage points higher among those who used the open-source AID system compared to those who used sensor augmented pump therapy.
  • This difference reflects 3 hours 21 minutes more time spent in target range per day!
  • For children AID users, they spent 3 hours 1 minute more time in target range daily (95% CI, 1h 22m to 4h 41m).
  • For adult AID users, they spent 3 hours 41 minutes more time in target range daily (95% CI, 2h 4m to 5h 18m).
  • Glycemic improvements were evident within the first week and were maintained over the 24-week trial. Meaning: things got better quickly and stayed so through the entire 24-week time period of the trial!
  • AID was most effective at night.
Difference between control and AID arms overall, and during day and night separately, of TIR for overall, adults, and kids

One thing I think is worth making note of is that one criticism of previous studies with open source AID is regarding the self-selection effect. There is the theory that people do better with open source AID because of self-selection and self-motivation. However, the CREATE study recruited a diverse cohort of participants, and the study findings (as described above) match all previous reports of safety and efficacy outcomes from previous studies. The CREATE study also found that the greatest improvements in TIR were seen in participants with lowest TIR at baseline. This means one major finding of the CREATE study is that all people with T1D, irrespective of their level of engagement with diabetes self-care and/or previous glycemic outcomes, stand to benefit from AID.

This therefore means there should be NO gatekeeping by healthcare providers or the healthcare system to restrict AID technology from people with insulin-requiring diabetes, regardless of their outcomes or experiences with previous diabetes treatment modalities.

There is also no age effect observed in the trail, meaning that the results of the CREATE Trial demonstrated that open-source AID is safe and effective in children and adults with type 1 diabetes. If someone wants to use open source AID, they would likely benefit, regardless of age or past diabetes experiences. If they don’t want to use open source AID or commercial AID…they don’t have to! But the choice should 100% be theirs.

In summary:

  • The CREATE trial was the first RCT to look at open source AID, after years of interest in such a study to complement the dozens of other studies evaluating open source AID.
  • The conclusion of the CREATE trial is that open-source AID using the OpenAPS algorithm within a version of AndroidAPS, a widely used open-source AID solution, appears safe and effective.
  • The CREATE trial found that across children and adults, the percentage of time that the glucose level was in the target range of 3.9-10mmol/L [70-180mg/dL] was 14.0 percentage points higher among those who used the open-source AID system compared to those who used sensor augmented pump therapy; a difference that reflects 3 hours 21 minutes more time spent in target range per day.
  • The study recruited a diverse cohort, yet still produced glycemic outcomes consistent with existing open-source AID literature, and that compare favorably to commercially available AID systems. Therefore, the CREATE Trial indicates that a range of people with type 1 diabetes might benefit from open-source AID solutions.

Huge thanks to each and every participant and their families for their contributions to this study! And ditto, big thanks to the amazing, multidisciplinary CREATE study team for their work on this study.


September 7, 2022 UPDATE – I’m thrilled to share that the paper with the primary outcomes from the CREATE trial is now published. You can find it on the journal site here, or like all of the research I contribute to, access an author copy on my research paper.

Example citation:

Burnside, M; Lewis, D; Crocket, H; et al. Open-Source Automated Insulin Delivery in Type 1 Diabetes. N Engl J Med 2022;387:869-81. DOI:10.1056/NE/Moa2203913

Note that the continuation phase study results are slated to be presented this fall at another conference!

Findings from the RCT on open source AID, the CREATE Trial, presented at #ADA2022

An example of the challenges of (constantly) titrating pancreatic enzyme replacement therapy (PERT)

As someone new to EPI who is also new to figuring out how to optimally dose my pancreatic enzyme replacement therapy (PERT), I’m constantly balancing the cost of PERT from prescription enzymes against the cost of over the counter enzymes.

I’ve personally calculated that one pill of my current dose of PERT covers about 30-4o grams of fat, and 30 grams of protein.

Meals with more than 30 grams of protein get 2 PERT pills, but meals with more than 40 or so grams of fat could be covered by 1 PERT pill and some OTC lipase.

But not all meals come with nutrition information, which makes titrating PERT at every single meal a challenge.

And, now that I’ve realized I’m likely not sensitive to all FODMAPs after all (hooray, although I may still have some slight sensitivity to massive amounts of onion or garlic), I’ve been able to eat a lot more takeout food from restaurants, both enthralling my taste buds and challenging my brain trying to estimate how much fat and protein there is in what I am choosing to eat.

I’ve been keeping careful notes of what I’m eating along with my fat and protein estimates and the results following each meal. Then, if I want to repeat or alter a similar meal, I can use my data and results to guesstimate my next PERT dosing.

For example, we have a local taco place that has done a really good job to enable online ordering with gluten-free and celiac tags in the order, so you can order digitally without having to talk to humans at the store. A few weeks ago, I ordered 3 tacos and some queso dip. It was delicious. I estimated it was more than 30g of protein, so I took 2 PERT with it.

However, while I didn’t have post-meal immediate symptoms, my next-day results were slightly off, and I made a note that I probably needed a little more lipase the next time I had that quantity of tacos.

Yesterday, I ordered 3 tacos again but decided to try a small “street corn” appetizer instead of queso. Corn is less fat and protein than queso, but I figured there was still >30g of protein from tacos like from before, so I took 2 PERT. This time, due to my notes, I added a few lipase to cover additional fat.

I had no immediate post-meal symptoms and felt great! However, today indicated that I did not have enough enzymes, and I’m suspecting that it’s because I swapped one of my taco types. Last time, I had a shrimp taco, but this time I tried a lamb taco for my third taco type. Even with the reduced fat and protein going from queso to corn, the increase in fat and/or protein (likely the protein, given my extra lipase) from shrimp to lamb meant that my meal was not optimally dosed.A gif showing three tacos and queso plus 2 PERT got ok results, but next time I swapped queso for corn and added lipase and still got it wrong, likely due to increased fat and protein in lamb instead of shrimp in one of the tacos.

 

Next time, I need to pay closer attention to what kind of tacos I eat as well as whether I get queso or not. If I did the same meal (three tacos, one of which is lamb, and corn), I’d probably experiment with 3 PERT to cover the suspected increased protein that I was missing with the 2 PERT + extra lipase. If I went back to a shrimp taco and queso, I’d probably re-try 2 PERT + extra lipase again.

PERT dosing, like insulin dosing, involves a lot of experimentation and some art, and some science, to try to get it right (or better) every time.

(PS, if you didn’t see them, I have other posts about EPI at DIYPS.org/EPI)

A Do-It-Yourself Protocol for Over-The-Counter Enzymes for Suspected Exocrine Pancreatic Insufficiency (EPI) Before Gaining Access to Pancreatic Enzyme Replacement Therapy (PERT)

A humorous side note – the title of this blog, DIYPS, stands for “do-it-yourself pancreas system”, the name I gave my first automated insulin delivery (AID) system, back in 2013. An AID system doesn’t fully replicate all functions of the pancreas, so we evolved from describing it as an artificial pancreas system (APS) to automated insulin delivery (AID). But now that I have exocrine pancreatic insufficiency and am doing quite a bit of DIY around titration of enzymes….the name of this blog feels more appropriate than ever.

After I started writing about exocrine pancreatic insufficiency, I’ve gotten a lot of questions from friends and connections who think they might have EPI. (And they are likely not wrong – there are estimates that as many as 40% of people with type 1 diabetes have lowered elastase levels. Alone, that doesn’t indicate EPI, but if symptomatic and you’ve already ruled out celiac and gastroparesis, it should be (in my opinion) high on the list of things to test for. Ditto for other types of diabetes and anyone with celiac disease.) Some people, though, may have delays in getting doctor’s appointments, and/or clinicians who aren’t (yet) willing to order the elastase or other EPI-related tests without testing for other things first.

This post is for that group of folks, and anyone stumbling across this post who has seen their test results for their fecal elastase testing indicating they have “moderate pancreatic insufficiency” or “severe pancreatic insufficiency” and are wondering what they can do while they wait for their doctor’s appointment.

It’s also for people with EPI who are struggling to afford their pancreatic enzyme replacement therapy (PERT) or are limiting the number or size of meals they eat as a result of the cost of PERT.

A bit of background on why I did the math about OTC enzyme cost and why I had tested them myself

Due to the holidays in December 2021 I had a lag between getting my test results (over Christmas) and then confirming that my doctor would write a prescription for PERT, and then a delay in getting it filled by the pharmacy since they had to order it. One of the things I did during that time was read up a lot about PERT and also look to see if there were any other kinds of enzymes that would be useful to take if my doctor didn’t want to prescribe me PERT. I found out that PERT contains THREE types of enzymes, and together they’re known as pancrelipase. Pancrelipase contains lipase (helps digest fat), protease (helps digest protein), and amylase (helps digest starches and other complex carbohydrates). It’s typically made from ground up pig pancreas, which is one of the reasons that PERT costs so much. Amylase from non-pancreatic sources is not widely available for human consumption, but there are some other ways to make protease and lipase. And it turns out that these standalone enzyme versions, often produced by microbes, are available to buy over the counter.

While waiting for my test to be ordered, I went ahead and ordered a standalone lipase product that is over the counter (OTC). In part, that was because some of the reviews for lipase talked about having EPI and how they were only sensitive to lipase, and so this was a viable and cheaper alternative for them rather than taking PERT with all 3 enzymes, since they didn’t need that. Based on my experience with FODMAPs and trying an enzyme powder to target fructans (which did help me some), it seemed like trying small doses of lipase would help if I did have EPI, and likely wouldn’t hurt even if I did not have EPI.

And it helped. It didn’t reduce all my symptoms, but even minor doses (3000 units of lipase) made a noticeable difference in my symptoms and I got a sense for what meals were more fat and protein-laden than others.

As a result, when my test results came in and I was on the borderline for moderate EPI, I agreed with my HCP that since it likely wouldn’t hurt to take PERT (other than the cost), and it would be obvious if it helped, that I should try PERT.

So having done the tests with OTC (over the counter) lipase was helpful for deciding to take PERT and advocating for my prescription.

And it turns out, wow yes, I do have EPI and do definitely need PERT (more about my first two weeks on PERT here).

And as I wrote here, because I had the OTC lipase sitting around, even after I finally had access to PERT, I eventually titrated my dosing and calculated separate ratios for lipase:fat and protease:protein, so I can decide for every meal or snack whether I need one full PERT (all three enzymes), two PERT, a PERT plus some lipase (and how much), or just a standalone OTC lipase. The cost differs greatly between those options: one PERT might be $9 and a standalone lipase pill around $0.26. You can’t break apart a PERT (e.g. take only half), so adding a few lipase is a cost-effective approach if you don’t need more protease or amylase and the OTC lipase works for you.

Some of the reasons to explore over the counter enzymes with exocrine pancreatic insufficiency or a suspected case of EPI

One interesting thing about one of the main tests (fecal elastase) used to assess EPI is that it is NOT impacted by taking enzymes. Someone who is started on pancreatic enzyme replacement therapy (PERT) can still have an elastase test without stopping taking PERT. So if someone had an inconclusive result or was borderline and started taking PERT, but their doctor wanted to re-test again, the use of PERT would not affect the test. The same goes for other types of enzymes.

I’ve realized that the following groups of people might want to investigate various OTC enzyme options:

  • Someone who has been diagnosed with EPI, but has done careful testing with meals of various sizes (low fat & high protein, high fat & low protein, etc.) to determine that they really only need lipase, may benefit from cheaper lipase-only OTC options.
  • Someone who has a test result for EPI but doesn’t yet have an appointment with their doctor or a prescription for PERT could start taking some OTC enzymes for quicker symptom relief, even if they ultimately want to use PERT for all their enzyme needs once they get their prescription filled.
  • Someone diagnosed with EPI who cannot afford the ideal dose of PERT that they need for their meals and snacks, may want to calculate the out of pocket costs for OTC lipase (not covered by insurance) vs the cost of PERT with or without insurance.
  • Someone who can’t get tested for EPI, but suspects they have EPI, might want to also explore OTC lipase and/or OTC multiple enzyme products.

However, not everyone with EPI will want OTC enzymes. Some people may have great insurance coverage, so their PERT costs them less than $9 a pill. OTC enzymes are not covered by insurance, but I’d still do the math and assess what your standard cost is per pill, because it may surprise you how cheap add-on OTC lipase is vs. your insurance deductible or copay to take additional PERT for larger meals. The other reason some people may not want to take OTC enzymes is the pill burden: OTC doses tend to be smaller, so you usually need to take more pills to cover the same meal as a single, larger PERT.

Picking what enzymes (in general, or specific brands) work for you

I often see a variety of OTC enzyme products recommended in peer groups on social media for EPI. There are no studies that I can find assessing the efficacy of these OTC brands (meaning, how good they are). I would be very cautious when trying different single or multiple enzyme products and keep a careful log of your symptoms from before enzymes as well as symptoms at every meal that you take enzymes, and your bathroom results afterward. This can help you assess OTC enzymes as well as PERT if you get access to it. By having a good log of your symptoms, you can tell if you’re taking enough enzymes (OTC or PERT) or if you’re developing new symptoms (which could be a side effect of whatever brand/type you are taking).

There are multiple brands and sizes of PERT, too, and it’s possible that a filler product or how the PERT is made by one brand doesn’t work well for you. If that’s the case, you can try another brand of PERT.

The same goes for OTC enzymes: it is very possible some types of pills may be made with ingredients that could bother you and cause symptoms themselves. You should definitely be very cautious if you go this route and explore small doses and ensure no side effects (no new symptoms) before increasing any doses.

When I search for lipase, it’s easy to find standalone lipase (here is an example, as an Amazon affiliate link). When I search for protease, it’s more common to find products that are multiple enzymes (e.g. lipase AND protease AND other random things that are “good for digestion”). Personally, I’m very wary of anything OTC that’s described as “digestive enzymes” and prefer to stick to products that only have the ingredients I’m looking for.

A pro-con list for over the counter (OTC) enzymes for EPI. Pros include: lower cost overall and per pill; that you can take smaller quantities of individual enzymes; and you can buy them without a prescription. Cons include: it's not covered by insurance so cost is out of pocket; you have to take more pills with smaller amounts of enzymes; it's not regulatory approved so othere are no studies on efficacy; and providers may not be able to advise for titration.
In diabetes, we often say “your diabetes may vary” (YDMV), indicating that different people can have different experiences.

In EPI, it’s no different – “your digestion may vary” and it’s important to test and record and find what works for you, and to find a balance of reducing or eliminating symptoms with enzymes in a cost-effective way that you can afford.

(PS, if you didn’t see them, I have other posts about EPI at DIYPS.org/EPI)

Cost calculations of Pancreatic Enzyme Replacement Therapy (PERT) for Exocrine Pancreatic Insufficiency (EPI) and alternative over the counter enzyme products

I previously wrote about my experience figuring out that I have exocrine pancreatic insufficiency (known as EPI or PEI), and also a little bit about starting on pancreatic enzyme replacement therapy (PERT). I talked briefly about the method I was using to figure out the right amount of PERT for me, but I realize that there’s a lot more detail I could provide about how to titrate enzymes in general, and not just PERT.

Some background first, though. When I write about PERT (pancreatic enzyme replacement therapy), I am talking about the FDA-approved class of drugs (called “pancrelipase”) that contain THREE types of enzymes, which the FDA calls “pancreatic enzyme products” or PEPs. Pancrelipase contains lipase (helps digest fat), protease (helps digest protein), and amylase (helps digest starches and other complex carbohydrates). As of 2010, all pancrelipase products that are marketed for EPI must be FDA approved.

Any time I refer (here or in other blog posts) to other enzyme products (either single enzyme or multi-enzyme), I’m referring to over the counter products that are not FDA approved.

Why does FDA approval matter for PEPs? FDA approval is essentially a rubber stamp saying you can trust the FDA to have validated that the companies making these products are making them as they describe them, meaning if they say they have 25,000 units of lipase, they actually have 25,000 units of lipase in them. (And protease and amylase). FDA-approved PEPs used in PERT are made from ground up pig pancreas (really), which is why they’re expensive. There is no generic PEP or PERT. (FDA also has a nice page here explaining the importance of understanding what is and is not an approved PEP/PERT product, and it also explains the brands that are currently approved and the differences between them.) This matters because when you talk about the cost people will probably suggest a “generic” of PERT, but there isn’t one.

However, there are non-FDA-approved over the counter enzyme products. They do exist, but because they have not been vetted by the FDA, I (and you!) should be wary about trusting them when they say they contain X units of lipase or any other enzyme product. Additionally, there are no studies (that I can find) comparing the efficacy between over the counter enzymes (single or multi-enzyme products) and FDA-approved PERT. (If you have found such a study, please leave a comment!)

So does that mean you can’t take them? No, I’m not saying that. What I am saying is you should only try other products with enzymes if you are willing to carefully test and vet FOR YOURSELF whether they work FOR YOU or not. (P.S. – did I mention I’m not a doctor? This is not medical advice; for medical advice, talk with your doctor. Although, doctors may not be aware of the over the counter enzyme options either, and this post might be worth sharing with them as well).

Three goals for optimally titrating enzymes for exocrine pancreatic insufficiency

I have three goals for getting my PERT dose titrated well.

  • First, get enough enzymes (through PERT) to reduce all symptoms.
  • Second, test and assess my lipase:fat and protease:protein ratios so I can figure out how to optimally dose enzymes for new meals of different amounts of fat and protein.
  • Third, optimize for reducing cost with enzymes, through a combination of supplementing PERT with standalone lipase and/or using lipase for fat-only snacks.

Here’s an example of how you might consider vetting over the counter enzyme products, and using them to supplement your FDA-approved (and hopefully insurance-covered) PERT:

As I mentioned earlier, I titrated and found out that my current dose of PERT covers about 30-40 grams of fat and 30 grams of protein. Some individuals only need support in digesting fat (e.g., need only lipase), but I have found that my body also needs support in digesting protein. (However, I don’t appear to need much amylase for carbohydrates.) Therefore I am tracking what amount of fat and protein I am eating with every meal. A 25,000 (lipase) dose of my PERT also contains enough protease to cover 30 grams of protein. Sometimes, I eat higher (>30-40g) fat meals that mean I need more lipase. So I would need two pills of the current dose of PERT, because 25,000 only covers ~30-40g of fat (FOR ME).

But – what if there was another way to get additional lipase without needing a full second pill of PERT, if I don’t need the additional support for more protein for this meal?

Enter over the counter enzyme options. In this example, a single enzyme option for lipase. Here is an example (Amazon affiliate link) to a standalone, single enzyme lipase product that is available as an over the counter product.

I personally have experimented with using standalone over the counter lipase to supplement my PERT dose, for the reason described above (needing more lipase but not necessarily needing more protease or amylase). The reason I would choose standalone lipase has to do with cost.

PERT, being ground up pig pancreas, is expensive. There is no generic for PERT! However, there have been methods to develop lipase from microbes as well as other sources beyond animals. Thus, it is possible to have a standalone source of lipase that is a lot cheaper than PERT. How much cheaper? Well, the bottle linked above when I calculated this was $23.50 for 90 pills. One pill each contains roughly 3,150 units of lipase (again, caveat from above about trusting the amount in over the counter products). That means each pill ($23.50/90 pills) is $0.26 USD, and each 1,000 units of lipase is roughly $0.08.

This math is then helpful to compare the cost of PERT. Depending on the size of prescription PERT, you might see a prescription anywhere from 3,000 to 25,000 to 36,000 units (depending on the brand, they have different amounts, but they are all measured based on units of lipase). Using GoodRx, you can generally compare retail prices of medications, such as this search for 24,000 PERT of one brand (90 capsules) or this search for 25,000 PERT of a different brand (also 90 capsules). Both of them are in the ballpark (for 90 capsules each) of $700-900, so let’s use $800 for 90 capsules for simple math. The per-pill price is $8.89 ($800/90 pills). The per-1,000 unit of lipase cost depends on whether you are using the 24,000 PERT ($8.89/24) or 25,000 PERT ($8.89/25) option, but those are roughly $0.37 and $0.36 per 1000 units of lipase.

So if you were to consume a meal that was ~10g of fat above your current PERT dose, and you didn’t need additional protein support, it would be cheaper to add on additional lipase (at $0.08 per 1000 units of lipase) as a standalone enzyme product instead of an additional PERT (which is, per our estimates, ~$0.36 per 1000 units of lipase). You don’t get to break apart a PERT (It can’t be cut in half, for example), so the per-pill cost is the better comparison. Adding a 3000-ish unit lipase onto your meal to cover an additional 10g of fat costs $0.26, and a second PERT is $8.89.

Therefore, a meal that needs 28,000 lipase is cheaper as 1 PERT and 1 extra standalone lipase rather than 2 PERT.

This of course assumes you have tested the standalone lipase and found that it works for you. I personally have done so and found that standalone lipase of the brand I chose works for this purpose (there are many brands and sizes: again, test what works for you), so I can titrate my meals as PERT+lipase, or even take 1-2 lipase (depending on the fat content) for a snack that’s mainly fat. However, again, a caveat that I personally am sensitive to protein and am tracking everything that I’m eating, so I know my personal math very well. Typical PERT dosing and recommendations is to take “2 or more” for meals or “1-2 for snacks”, but that completely ignores how much fat and protein is in the meals, and might be significantly undertreatment or overtreatment for you.

Why does undertreatment matter? Well, you get symptoms. Those are no fun.

Why does overtreatment matter? Well, you can get constipation. (I haven’t had it, but it also doesn’t sound like fun). At the extreme end of the scale, there is also a risk of fibrosing colonopathy if you take more than certain units per kg of body weight for a long time. (If you’re concerned about this issue and haven’t discussed it with your doctor, do so – they should be able to tell you where the risk threshold is based on your personal body weight if you don’t want to calculate it yourself).
A gif showing a square moving along a spectrum from "too little" to "too much enzyme". Too little enzyme and you have symptoms, not enough and you reduce but don't eliminate symptoms. Enough enzymes and you eliminate symptoms. Too much risks constipation.

My approach was making sure my meals were covered first with prescription PERT, then evaluating additional standalone products that I could use to supplement or replace PERT depending on what I was eating, so I could prioritize reducing symptoms and then for improving the cost required to achieve that.

There are other standalone enzyme products, including products containing multiple enzymes. If you join one of the Facebook groups for EPI, you’ll see people recommencing various names of enzymes for over the counter products. But again, you really should test things and see if they work for you. Read all the ingredients on any product you’re taking. A lot of times you can search for lipase and you’ll get a multiple-enzyme product. And that product may have additional ingredients or fillers that don’t sit well with you. You may even find that one brand of prescription PERT might not work for you, whereas another one does.

My suggestions include:

  • Carefully test any product, whether it’s PERT or over the counter enzymes. Keep a good log of your post-meal symptoms and next-day symptoms (e.g. bathroom results) and try different meals with different amounts of fat and protein.
  • If you have symptoms regularly with a certain amount of enzymes, it could be either that this particular brand (over the counter or even prescription PERT) does not work well for you, OR that you are not taking enough enzymes to cover your needs.
  • If in doubt, talk with your doctor. They may/not have opinions on over the counter products, especially if they haven’t had other patients reporting back what is working for them or not, since there are no studies on those particular brands (and of course, they’re not FDA approved). But with approved PERT, they should be able to give you some more input on how to increase your dose or change your prescription to adjust. Having the data on how much fat and protein you’re eating and what results you’ve been getting could help you (and them) get to a more optimal dose more quickly.

(PS, if you didn’t see them, I have other posts about EPI at DIYPS.org/EPI)

What you should know about starting on Pancreatic Enzyme Replacement Therapy (PERT)

It’s been about two weeks since I started on pancreatic enzyme replacement therapy (PERT) and it’s been really interesting to experience the difference it is making for me.

For context (and you can read more here), I have moderate exocrine pancreatic insufficiency (EPI or PEI), but I have very obvious symptoms following anything I eat for a few hours, as well as next-day bathroom habits. My clinician didn’t think trying PERT would be a problem even though my elastase levels were only borderline low, and it didn’t hurt. It definitely helped in multiple ways.

Here’s what the experience has been like starting on PERT, what I like about it, what I found challenging, what it’s like to scientifically titrate your dosing of PERT, and a handful of random other thoughts.

Here is what I like about Pancreatic Enzyme Replacement Therapy (PERT)

With undiagnosed EPI, for the last almost two years, I would eat food with dread. And not a lot of food (averaging 2 meals a day), because I had to severely limit the kinds of things I was eating to try to reduce my symptoms (with mixed success). With my first few doses of PERT, I ate relatively small, careful and low-FODMAP meals so I could better assess whether PERT was working.

And wow, was it working.

With the first few small (and low-FODMAP, to reduce variables that I was testing) meals, I had an immediate improvement. I didn’t realize until I took PERT how sick I felt every time I ate anything, even when I didn’t have obvious post-meal symptoms of gas, stabbing abdominal pain, or next-day bathroom habits. With PERT, I felt…nothing? Which is apparently how I used to feel after I would eat. There was no sick feeling, no bloating within an hour, and no discomfort for hours. There was no gas after I ate or overnight. In the morning, I didn’t have steatorrhea.

I got braver and experimented with a few bigger meals. In some cases, I still felt not-sick after I ate, but did develop some gas. However, it was significantly reduced.

From tracking the cumulative fat and protein levels in everything I ate, I was able to see that things less than 50 grams of fat and protein (combined) worked exceptionally well with the level of PERT I had started on. PERT has different dosing options, and I had started on a relatively moderate dose. I saw that some of my 70-ish gram meals were fine, but the ones in the 90s definitely needed more PERT.

Even when I could tell I needed more PERT, though, it wasn’t a complete failure. Even for meals with 90+ grams of fat+protein, I had a reduction in feeling sick, way less gas, and improved bathroom habits, even if they weren’t as ideal as what happened when I ate <50g of fat and protein meals.

As I discussed in my previous post, I had felt like a boiling frog where I didn’t really feel good every day, but there was usually nothing obviously wrong (no broken bone, no stabbing pain every day). So it was hard to know what was wrong. Now, taking PERT, I can see a clear difference on the days when the dosing is well-titrated to what I’m eating (no symptoms after I eat, plus I feel a lot better!) compared to when the dosing isn’t optimal (reduced symptoms but still there, sometimes will still feel sick or abdominal discomfort).

I also now have back the lab results of the bloodwork I asked my gastroenterologist to run on fat-soluble vitamins (A, D, E) and iron, to make sure I didn’t have any deficiencies that need addressing. Thankfully, I didn’t – which is probably influenced by the fact that I am absorbing some of what I eat without PERT, but is also likely due to the fact that I take two multivitamins daily plus additional vitamin D supplements. I can imagine that I would have much lower levels without the supplementation, so I’m glad I had built the habit in the last two years of making sure I was taking my vitamins. (Which I wasn’t doing before two years ago consistently, and intuitively was worried about getting the right nutrients given the changes I was making to what I was eating, so that was a good habit to have built up!)

As a pleasant result of taking PERT, I’m also seeing improvements in symptoms that I did not think were correlated with EPI.

For example, in October I developed severely dry eyes, which I’ve never had before. I’ve been using lubricating eye drops several times a day and gel drops at night ever since. After about a week of PERT, I realized that I was waking up in the morning and my first thought wasn’t about putting drops in my eyes because they weren’t painfully dry. And then on days following when my PERT dosing wasn’t optimal (as evidenced by post-meal gas or abdominal discomfort, etc), my eyes are more dry than they are on the other days.

Another thing I’ve noticed is the skin on my face improving. In the last year, I started having more acne breakouts and changes to my skin tone. This, like the eye dryness, has started to noticeably improve in the last week or so (with no other changes to routine or the weather: it’s still winter here!).

What I find challenging about Pancreatic Enzyme Replacement Therapy (PERT)

There’s not a lot of guidance to patients regarding PERT titration (changing dosing levels as needed). My GI doc wrote a script for one size and said we could size up if it wasn’t working. That was it.

Thankfully, I have 19 years of experience with titrating insulin dosing for everything I’m eating, and I have an inclination to use spreadsheets to track things, so I began to take PERT and write down the relevant details of what I was eating (date, timing, what it was, how much fat and protein it had, what PERT dose I took), the result (any post-meal symptoms including timing) and whether it caused steatorrhea or other bathroom-related changes. From this, I was able to very quickly group meals into “wow that worked awesome”, “hmm, this reduced symptoms but it wasn’t perfect”, and “wow that needed more PERT”. For me, those roughly ended up being <50 grams combined of fat and protein (“wow that worked awesome”), around 70 grams (“hmm, this reduced symptoms but it wasn’t perfect on every front”), and more than 90 grams (“wow that needed more PERT”).

Interestingly, a lot of the medical literature I read about PERT indicates that most people are not taking enough. Given my analysis of my own data, that’s currently true. (Personally I’m currently trying to collect more data in each category before I discuss dosing with my clinician, to figure out what dosing or prescription I might need).

I’m only two weeks in, so I can’t yet give solid advice to anyone else taking PERT, but I imagine in the future I would likely feel more confident saying the following to someone else starting on PERT:

  • If you can, write down the date, timing, what you eat, and the nutrients (e.g. fat, protein, and carb) of what you’re eating, and track what symptoms you have when following a meal. Also make sure to note how many and what dose of PERT you took.
  • See if you can group the data between which meals turned out well, which could be improved, and what didn’t work. That may help you discuss with your doctor what level of enzyme you need for what type of meal.

Anecdotally in the EPI communities, people discuss taking 3-4 of the largest dose PERT for meals, vs 1-2 for their snacks. It seems to be very, very individual about what people need. Some people (like me with moderate EPI) have symptoms, others can have severe insufficiency (severe EPI) but have fewer symptoms. As a result, we may need more or less PERT, depending on how our bodies are generating symptoms.

One frustration I have about GI-related conditions, whether that’s those that result in people using the low FODMAP diet or EPI resulting in the need for PERT – and even in the diabetes community where insulin is needed – is that there’s very much a perception of individual blame in the day-to-day operations. If you have symptoms, you probably did something wrong. You ate a high FODMAP thing, or you ‘stacked’ FODMAPs…or for EPI, you didn’t take enough PERT or you ate the wrong thing. In diabetes, you didn’t take enough insulin, or you did it at the wrong time, or you forgot, or you ate too much, or you ate the wrong thing…. There is SO much blame and shame going around, and it’s frustrating to see (and experience).

Having tracked my data for two weeks now, I can see very clear cause and effect in the data: when I feel great, my PERT dosing has been well-matched to what I was eating. When I have some symptoms, the PERT dosing was not-optimal, and sometimes as a result I have a lot of symptoms and don’t feel well. It’s a very clear cause and effect relationship between having sufficient enzymes or not having enough enzymes. I am working to not feel guilty, e.g. I did something ‘wrong’ by choosing the wrong sized meal to go with the PERT dosing, and instead frame it as data that I’m collecting to inform the future prescription I need of PERT.

(My point here is that I don’t like the blame/shame that goes around, and yet, I still feel it, too. I’m trying to remove myself from those patterns of thinking, because it’s not at all helpful.)

It’s helpful instead for me to think “Wow, that was not enough PERT this time! Next time I should take 2 of this dose, or supplement my single PERT with standalone lipase” rather than feel shame or guilt because I ate a “big” meal. This is in part why I’m trying to stay away from thinking and using words like “big” or “small” meal, because the size is so arbitrary, depending on whether you’re looking at volume of food on a plate, thinking about calories, carbohydrates (to take insulin for it), or the fat and protein amounts (to dose PERT for it).

Also, everyone with EPI is likely VERY different from one another, and so my cutoffs of 70 or 90g of fat+protein may be numerically more or less than what someone else needs. (Those who take PERT will also notice I am very careful to not specify what PERT dose my one pill is, because everyone’s needs are different, and I don’t want anyone to accidentally anchor on my dose numbers, because what I need may not be what everyone else needs.)

And I can imagine some folks without EPI reading this with their own perceptions of fat and protein levels thinking judgmental thoughts about the numerical amounts of what I’m eating at different times.

Having to track fat and protein makes me grumpy, for a few reasons. In part, because it’s “one more thing” to track (in addition to general carbohydrate estimates to be able to dose insulin or inform my automated insulin delivery system about what I’m eating). In part, because I set up a spreadsheet to learn from what I’m doing, so I need to count it, input it into my spreadsheet, and then analyze the data later. I know I won’t always need to do this, and eventually I’ll learn intuitively what dosing I need for different types of meals.

But, I now have to remember to get out my PERT, take it “with the first bite” (which I interpret as swallow the PERT and then immediately try to put a bite of food in my mouth so I match the timing of the food with the PERT), then write down the timing of when I took my PERT and input the fat and protein and details of the meal into my spreadsheet…and then remember to also enter carbohydrates into my automated insulin delivery system (which I don’t have to do, but I get better outcomes with a meal announcement so I want to do so. When I’m not working on PERT titration, it doesn’t feel like a burden.).

Although I am grumbling about the titration learning curve and process of figuring out my dosing and what I am eating, I know it’s like any learning curve: I will figure it out soon, and the routine of taking PERT will become as easy as remembering to enter carbs or take insulin for what I’m eating.

And as a short-term benefit and reward of learning to dose PERT for what I’m eating, I feel so much better. Immediately, after every meal, as well as the next day, and I also feel better overall while improving other ‘symptoms’ that I didn’t realize were correlated with my EPI. Hooray!

What it’s like to start on Pancreatic Enzyme Replacement Therapy (PERT)

What You Should Know About Exocrine Pancreatic Insufficiency (EPI) or Pancreatic Exocrine Insufficiency (PEI)

I have a new part-time job as a pancreas, but this time, I don’t have any robot parts I can make to help.

This is a joke, because I have had type 1 diabetes for 19+ years and 7 years ago I helped make the world’s first open-source artificial pancreas, also known as an automated insulin delivery system, that we jokingly call my “robot parts” and takes care of 90+% of the work of living with type 1 diabetes. PS if you’re looking for more information, there’s a book for that, or a free 3 minute animated video explaining automated insulin delivery. 

The TL;DR of this post is that I have discovered I have a mild or moderate exocrine pancreatic insufficiency, known as EPI (or PEI, pancreatic exocrine insufficiency, depending on which order and acronym you like). There’s a treatment called pancreatic enzyme replacement therapy (PERT) which I have been trying.

It took a long time for me to get diagnosed (almost 2 years), so this post walks through my history and testing process with my gastroenterologist (GI doctor) and the importance of knowing your own body and advocating for yourself when something is wrong or not quite right.

Background

About six years after I was diagnosed with type 1 diabetes, I was doing a summer internship in Washington, D.C. (away from home) and started getting chest tightness and frequent abdominal pain. Sometimes it felt like my abdominal muscles were “knitting” into each other. Because I had type 1 diabetes, I had heard at one point that about 10% of people with type 1 also develop celiac disease. So, thankfully, it was as simple as calling my endocrinologist and scheduling testing, and getting an endoscopy and biopsy to confirm I had celiac disease. It took about 2 months, and the timing was mostly that long due to getting back to Alabama after my internship and the testing schedule of the hospital. This is relevant detail, because I later read that it takes an average of 7 years for most people to get diagnosed with celiac disease. That has been floating around in my brain now for over a decade, this awareness that GI stuff is notoriously hard to diagnose when you’re not lucky enough to have a clear idea, like I did, of an associated condition.

So, with type 1 diabetes and celiac disease, I use automated insulin delivery to get great outcomes for my diabetes and a 100% very careful gluten-free diet to manage my celiac disease, and have not had any GI problems ever since I went gluten-free.

Until January/February 2020, when I took an antibiotic (necessary for an infection I had) and started to get very minor GI side effects on day 5 of the 7-day antibiotic course. Because this antibiotic came with a huge warning about C. diff, and I really didn’t want C. diff, I discontinued the antibiotic. My infection healed successfully, but the disruption to my GI system continued. It wasn’t C. diff and didn’t match any of the C. diff symptoms, but I really lost my appetite for a month and didn’t want to eat, so I lost 10 pounds in February 2020. On the one hand, I could afford to lose the weight, but it wasn’t healthy because all I could bring myself to eat was one yogurt a day. I eventually decided to try eating some pecans to add fiber to my diet, and that fiber and change in diet helped me get back to eating more in March 2020, although I generally was eating pecans and dried cranberries (to increase my fiber intake) for breakfast and wasn’t hungry until late afternoon or early evening for another meal. So, since my body didn’t seem to want anything else, I essentially was eating two meals a day. My GI symptoms were better: not back to how they were before February 2020, but seemed manageable.

However, in July 2020, one night I woke up with incredibly painful stabbing abdominal pain and thought I would need to go to the ER. Thankfully, it resolved enough within minutes for me to go back to sleep, but that was scary. I decided to schedule an appointment with my gastroenterologist. I took in a record of my symptoms and timing and explained what was most worrisome to me (sudden stabbing pains after I ate or overnight, not seemingly associated with one particular type of food; changes in bathroom habits, like steatorrhea, but not as severe as diarrhea). He made a list of suspected things and we began testing: we checked for C. diff (nope), parasites (nope), bloodwork for inflammation (nope, so no Crohn’s or IBS or IBD), my celiac markers to make sure I wasn’t being accidentally glutened (nope: 100% gluten-free as proven by the blood work), H. pylori (nope), and did a CT scan to check for structural abnormalities (all good, again no signs of inflammation or any obvious issues).

Because all of this happened during the global COVID-19 pandemic, I was cautious about scheduling any in-person tests such as the CT scan or the last test on my list, a colonoscopy and endoscopy. I have a double family history of colon cancer, so although it was extremely unlikely, given everything else on the list was coming back as negative, it needed to be done. I waited until I was fully vaccinated (e.g. 2 weeks after 2 shots completed) to have my colonoscopy and endoscopy scheduled. The endoscopy was to check for celiac-related damage in my small intestine since I hadn’t had an endoscopy since my diagnosis with celiac over a decade ago. Thankfully, there’s no damage from celiac (I wasn’t expecting there to be any damage, but is a nice confirmation of my 100% very careful gluten free diet!), and the colonoscopy also came back clear.

Which was good, but also bad, because…SOMETHING was causing all of my symptoms and we still didn’t know what that was. The last thing on my doctor’s list was potentially small intestine bacterial overgrowth (SIBO), but the testing is notoriously non-specific, and he left it up to me as to whether I decided to treat it or not. Having run out of things to test, I decided to do a two-week course of an antibiotic to target the bacteria. It helped for about two weeks, and then my symptoms came back with a vengeance. However, I had realized in spring 2021 (after about 9 months of feeling bad) that sometimes the stabbing abdominal pain happened when I ate things with obvious onion or garlic ingredients, so January-July 2021 I had avoided onion and garlic and saw a tiny bit of improvement (but nowhere near my old normal). Because of my research on onion and garlic intolerances, and then additional research looking into GI things, I realized that the low FODMAP diet which is typically prescribed for IBS/IBD (which I don’t have) could be something I could try without a lot of risk: if it helped, that would be an improvement, regardless of whatever I actually had.

So in August 2021, as noted in this blog post, I began the low FODMAP diet first starting with a careful elimination phase followed by testing and adding foods back into my diet. It helped, but over time I’ve realized that I still get symptoms (such as extreme quantities of gas, abdominal discomfort and distention, changed bathroom habits) even when I’m eating low FODMAP. It’s possible low FODMAP itself helped by avoiding certain types of food, but it’s also possible that it was helping because I was being so careful about the portions and timing of when I was eating, to avoid “stacking” FODMAPs.

One other thing I had tried, as I realized my onion and garlic intolerance was likely tied to being “fructans”, and that I had discovered I was sensitive to fructans in other foods, was an enzyme powder called Fodzyme. (I have no affiliation with this company, FYI). The powder works to target the FODMAPs in food to help neutralize them so they don’t cause symptoms. It worked for me on the foods I had experimented with, and it allowed me to eat food that had onion powder or garlic powder listed as a minor ingredient (I started small and cautious and am working my way up in testing other foods and different quantities). I longingly wished that there were other enzymes I could take to help improve digestion, because Fodzyme seemed to not only reduce the symptoms I had after I ate, but also seemed to improve my digestion overall (e.g. improved stool formation). I did some research but “digestive enzymes” are generally looked down upon and there’s no good medical research, so I chalked it up to snake oil and didn’t do anything about it.

Until, oddly enough, in November 2021 I noticed a friend’s social media post talking about their dog being diagnosed with exocrine pancreatic insufficiency (EPI). It made me go look up EPI in humans to see if it was a thing, because their experience sounded a lot like mine. Turns out, EPI is a thing, and it’s very common in humans who have cystic fibrosis; pancreas-related surgeries or pancreatic cancer; and there is also a known correlation with people with type 1 diabetes or with celiac disease.

Oh hey, that’s me (celiac and type 1 diabetes).

I did more research and found that various studies estimate 40% of people with type 1 diabetes have low levels of pancreatic elastase, which is a proxy for determining if you have insufficient enzymes being produced by your pancreas to help you digest your food. The causal mechanism is unclear, so they don’t know whether it’s just a ‘complication’ and side effect of diabetes and the pancreas no longer producing insulin, or if there is something else going on.

Given the ties to diabetes and celiac, I reached out to my GI doctor again in December 2021 and asked if I should get my pancreatic elastase levels tested to check for exocrine pancreatic insufficiency (EPI), given that my symptoms matching the textbook definition and my risk factors of diabetes and celiac. He said sure, sent in the lab request, and I got the lab work done. My results are on the borderline of ‘moderate’ insufficiency, and given my very obvious and long-standing symptoms, and given my GI doc said there would be no harm from trying, I start taking pancreatic enzyme replacement therapy (called PERT). Basically, this means I swallow a pill that contains enzymes with the first bite of food that I eat, and the enzymes help me better digest the food I am eating.

And guess what? For me, it works and definitely has helped reduce symptoms after I’m eating and with next-day bathroom habits. So I consider myself to have mild or moderate exocrine pancreatic insufficiency (EPI).

(Also, while I was waiting on my test results to come back, I found that there is a lipase-only version of digestive enzymes available to purchase online, so I got some lipase and began taking it. It involves some titration to figure out how much I needed, but I saw some improvement already from low doses of lipase, so that also led me to want to try PERT, which contains all 3 types of enzymes your pancreas normally naturally produces, even though my elastase levels were on the borderline of ‘moderate’ insufficiency. Not everyone with lower levels of elastase has insufficiency in enzymes, but my symptoms and response to lipase and PERT point to the fact that I personally do have some insufficiency.)

More about my experiences with exocrine pancreatic insufficiency

Unfortunately, there is no cure for exocrine pancreatic insufficiency. Like Type 1 diabetes, it requires lifelong treatment. So, I will be taking insulin and now PERT likely for the rest of my life. Lazy pancreas! (Also, it’s possible I will need to increase my PERT dose over time if my insufficiency increases.)

Why treat EPI? Well, beyond managing very annoying symptoms that impact quality of life, if left untreated it’s associated with increased mortality (e.g. dying earlier than you would otherwise) due to malnutrition (because you’re not properly absorbing the nutrients in the food you’re eating) and bone density problems.

Oddly enough, there seem to be two versions of the name (and therefore two acronyms) for the same thing: EPI and PEI, meaning exocrine pancreatic insufficiency or pancreatic exocrine insufficiency. I haven’t found a good explanation for why there are two names and if there are any differences. Luckily, my research into the medical literature shows they both pop up in search results pretty consistently, so it’s not like you end up missing a big body of literature if you use one search term or the other.

Interestingly, I learned 90% of people with cystic fibrosis may need PERT, and thankfully my friend with CF didn’t mind me reaching out to ask her if she had ever taken PERT or had any tips to give me from her knowledge of the CF community. That was nice that it turns out I do know some other people with EPI/PEI, even though they don’t usually talk about it because it seems to go hand in hand with CF. Some of the best resources of basic information about EPI/PEI are written either by CF foundations or by pancreatic cancer-related organizations, because those are the two biggest associated conditions that also link to EPI/PEI. There are also other conditions like diabetes and celiac with strong correlations, but these communities don’t seem to talk about it or have resources focused on it. (As with low FODMAP resources where everything is written for IBS/IBD, you can extrapolate and ignore everything that’s IBS/IBD specific. Don’t be afraid to read EPI/PEI information from communities that aren’t your primary community!)

Sadly, like so many GI conditions (remember in the intro I referenced 7 years average diagnosis time with celiac), it seems ridiculously hard to get to a diagnosis of EPI. I essentially self-diagnosed myself (and confirmed the diagnosis in partnership with my GI doc who agreed to run the tests). I am still very surprised that it never came up on his list of possible conditions despite having symptoms that are textbook EPI and having diabetes and celiac, which are known correlations. Apparently, this is common: I read one study that says even people with super high-risk factors (e.g. pancreas surgery, pancreatic cancer) aren’t necessarily screened, either! So it’s not just me falling through the cracks, and this is something the gastroenterology world needs to be better about. It’s also common for patients to bring this up to their doctors vs their doctors suggesting it as a potential diagnosis – this study found 24% of people brought up EPI, like I did, to their doctors.

Also, unfortunately, I had a few people (including family members) suggest to me in the last two years that my symptoms are psychosomatic, or stress-related. They’re clearly, as proven by lab work, not psychosomatic or stress-related but are a result of my exocrine pancreatic functions failing. Please, don’t ever suggest someone dealing with GI issues is experiencing symptoms due to stress – this is the kind of comment you should keep to yourself. (The last time someone mentioned this to me was months ago, and it still bothers me to think about it.)

Advocate for yourself

One of the very important things I learned early on when living with type 1 diabetes was the importance of knowing my own body, and advocating for myself. This unfortunately was a hard lesson learned, because I had general practice (GP or primary care / PCP) doctors who would refuse to treat me because I had diabetes because they were concerned about prescribing something that would mess up my blood sugars. They’d completely ignore the point that whatever infection I had would cause MORE disruption to my blood sugars by having me be sick and suffer longer, than I would have disruption to my blood sugar levels from a prescription. Sigh. So for the last almost two decades, I have had to go into every health encounter prepared to advocate for myself and make sure I get the medical expertise for whatever I’m there for, and not the less experienced take on diabetes (assuming I wasn’t there for diabetes, which I usually wasn’t).

This has translated into how I approached finding solutions for my GI symptoms. Per my history described above, I had increasing but minor GI symptoms from February-July 2020. Having new, stabbing pains in my abdomen led me to the gastroenterologist for a long list of testing for various things, but I had to continue to push for the next round of testing and schedule and manage everything to proceed through the list we had discussed at my appointment. Later, after we ran through the list, I had to try things like low FODMAP for myself, and then do additional research and identify the test for EPI as a likely next step to try.

I felt a little like the ‘boiling frog’ analogy, where my symptoms gradually worsened over time, but they weren’t startling bad (except for the points in time when I had stabbing abdominal pain). Or the two times, almost one year apart (Oct 2020 and Dec 2021) where I had what I considered bad “flares” of something where I got really hot and feeling really ill all of a sudden, but it wasn’t COVID-19 and it wasn’t anything specific causing it, there were no obvious food triggers, and the only thing I could do was lay down for 2-3 hours and rest before I started to feel better. Those were probably correlated with “overdoing it” with physical activity, but I’ve also run a marathon and a 50k ultramarathon in the last year and didn’t have problems on those days, so there’s not a certain threshold of activity that appears to cause that. Thankfully, that has only happened two times.

Other than those scenarios, it wasn’t like breaking my ankle where there was a clear “everything was fine and now something is broken”, but it was more like “I have had not-good-digestion and various increasing GI symptoms that don’t fit any clear problem or diagnosis on our shortlist of the 5 likely things it might be. It’s not excruciating but it is increasingly impacting my quality of life, and twisting myself into a pretzel with an evolving pattern of dietary modifications is not solving it”. It took me continuing to advocate for myself and not accepting suffering for the rest of my life (hopefully!) with these symptoms to get to an answer, which for me, so far, seems to be moderate exocrine pancreatic insufficiency.

What it’s like to start taking pancreatic enzyme replacement therapy (PERT)

PERT is typically measured by the units/amount of lipase it contains, even though it contains all 3 types of enzymes. (Some of the Medicare documents in different states actually are really helpful for comparing the size of dosing across the different brands of PERT. That also helped me look up the various brands in my insurance plan to see whether there would be a price difference between two of the most common brands.) Depending on symptoms and your level of insufficiency, like insulin, it requires some titration to figure out the right doses. I’ve been attempting to track generally the amount of fat that I’m eating to try to get a sense of my “ratio” of fat to lipase needed, although the research shows there is likely not a linear correlation between grams of fat and units of lipase needed. Another way to think about it is at what level of grams of fat in your meal do you need more than your current dose. For example, one pill of PERT at my current dose seems to work up to around 70 or so grams of fat per meal, as long as it doesn’t have more than 50% protein. Meals containing much more fat (120 g or so) definitely require more, as do meals with either a higher quantity of protein or a closer ratio of 1:1 fat to protein.

Different people have different needs with regard to whether they need enzyme support “just” for fat, or also for protein and carbs. I appear to at least need some support for carbs as well as protein, but am still establishing at what levels I need which dosing of which enzymes.

Personally, I am tracking to see whether my symptoms are reduced or eliminated in the hours following my meals (gas, abdominal discomfort, a sick feeling after eating) as well as the next day (bloating/abdominal distension, bathroom habits such as reduced steatorrhea), and overall whether I have any more of those really bad “flares”. My initial tests of taking PERT show improvements after my meals (I don’t feel sick after I eat anymore!) and often the next day.

After the first few days of trying food that was low FODMAP but giving me minor symptoms before PERT, I’ve also felt confident enough to try meals that I’ve avoided eating for over a year, such as a gluten free burger from one of our nearby local favorites! Even though it’s been well over a year since I’ve had it last, I immediately could tell a difference in how I felt eating it, due to taking PERT with it. There was no wave of fatigue before I was halfway through the burger, and no gas or feeling sick to my stomach after eating. I had clearly forgotten what it was like to not feel miserable after eating and to actually enjoy eating food! So far, PERT has been exceeding my expectations (although those were rather low).

It makes it slightly less annoying, then, to think about the price of PERT. Roughly, one month of PERT at the dosage I’m currently on costs the same as 3 vials of insulin in the US (in the ballpark of $800). Like insulin, PERT is necessary and worthwhile (and thankfully I do have health insurance).

Pancreases are great when they work…and expensive to replace!

A play on the spiderman meme of two spiderman's pointing at each other, indicating similar things. Labeled "exocrine pancreatic functions" and "endocrine pancreatic functions", indicating both of mine are not working as they should be.

TLDR: I have a new thing, exocrine pancreatic insufficiency, to deal with. Thankfully, there’s a treatment (PERT) that I can use to reduce symptoms and hopefully limit the potential impacts on morbidity long term. If you have diabetes or celiac and you have unexplained GI symptoms over time, you might want to do some research into EPI and discuss it with your gastroenterologist.

Also…for any endocrinologist reading this…or any other healthcare providers…if you have patients with diabetes and suspected GI issues, please consider EPI as a possible diagnosis once you’ve ruled out celiac disease and other likely suspects. Given the high rates of lowered elastase in all types of diabetes, it’s worth screening for EPI in patients with otherwise-unexplained steatorrhea or similar symptoms.

Looking back at work and accomplishments in 2021

I decided to do a look back at the last year’s worth of work, in part because it was a(nother) weird year in the world and also because, if you’re interested in my work, unless you read every single Tweet, there may have been a few things you missed that are of interest!

In general, I set goals every year that stretch across personal and professional efforts. This includes a daily physical activity streak that coincides with my walking and running lots of miles this year in pursuit of my second marathon and first (50k) ultramarathon. It’s good for my mental and physical health, which is why I post almost daily updates to help keep myself accountable. I also set goals like “do something creative” which could be personal (last year, knitting a new niece a purple baby blanket ticked the box on this goal!) or professional. This year, it was primarily professional creativity that accomplished this goal (more on that below).

Here’s some specifics about goals I accomplished:

RUNNING

  • My initial goal was training ‘consistently and better’ than I did for my first marathon, with 400 miles as my stretch goal if I was successfully training for the marathon. (Otherwise, 200 miles for the year would be the goal without a marathon.) My biggest-ever running year in 2013 with my first marathon was 356 miles, so that was a good big goal for me. I achieved it in June!
  • I completed my second marathon in July, and PR’d by over half an hour.
  • I completed my first-ever ultramarathon, a 50k!
  • I re-set my mileage goal after achieving 400 miles..to 500..600…etc. I ultimately achieved the biggest-ever mileage goal I’ve ever hit and think I ever will hit: I ran 1,000 miles in a single year!
  • I wrote lots of details about my methods of running (primarily, run/walking) and running with diabetes here. If you’re looking for someone to cheer you on as you set a goal for daily activity, like walking, or learning to run, or returning to running…DM or @ me on Twitter (@DanaMLewis). I love to cheer people on as they work toward their activity goals! It helps keep me inspired, too, to keep aiming at my own goals.

CREATIVITY

  • My efforts to be creative were primarily on the professional side this year. The “Convening The Center” project ended up having 2 out of 3 of my things that I categorized as being creative. The first was the design of the digital activities and the experience of CTC overall (more about that here). The second were the items in the physical “kit” we mailed out to participants: we brainstormed and created custom playing cards and physical custom keychains. They were really fun to make, especially in partnership with our excellent project artist, Rebeka Ryvola, who did the actual design work!
  • My third “creative” endeavor was a presentation, but it was unlike the presentations I usually give. I was tasked to create a presentation that was “visually engaging” and would not involve showing my face in the presentation. I’ve linked to the video below in the presentation section, but it was a lot of work to think about how to create a visually and auditory focused presentation and try to make it engaging, and I’m proud of how it turned out!

RESEARCH AND PUBLICATIONS

  • This is where the bulk of my professional work sits right now. I continue to be a PI on the CREATE trial, the world’s first randomized control trial assessing open-source automated insulin delivery technology, including the algorithm Scott and I dreamed up and that I have been using every day for the past 7 years. The first data from the trial itself is forthcoming in 2022. 
  • Convening The Center also was a grant-funded project that we turned into research with a publication that we submitted, assessing more of what patients “do”, which is typically not assessed by researchers and those looking at patient engagement in research or innovation. Hopefully, the publication of the research article we just submitted will become a 2022 milestone! In the meantime, you can read our report from the project here (https://bit.ly/305iQ1W ), as this grant-funded project is now completed.
  • Goal-wise, I aim to generate a few publications every year. I do not work for any organization and I am not an academic. However, I come from a communications background and see the benefit of reaching different audiences where they are, which is why I write blog posts for the patient community and also seek to disseminate knowledge to the research and clinical communities through traditional peer-reviewed literature. You can see past years’ research articulated on my research page (DIYPS.org/research), but here’s a highlight of some of the 2021 publications:
  • Also, although I’m not a traditional academic researcher, I also participate in the peer review process and frequently get asked to peer-review submitted articles to a variety of journals. I skimmed my email and it looks like I completed (at least) 13 peer reviews, most of which included also reviewing subsequent revisions of those submitted articles. So it looks like my rate of peer reviewing (currently) is matching my rate of publishing. I typically get asked to review articles related to open-source or DIY diabetes technology (OpenAPS, AndroidAPS, Loop, Nightscout, and other efforts), citizen science in healthcare, patient-led research or patient engagement in research, digital health, and diabetes data science. If you’re submitting articles on that topic, you’re welcome to recommend me as a potential reviewer.

PRESENTATIONS

  • I continued to give a lot of virtual presentations this year, such as at conferences like the “Insulin100” celebration conference (you can see the copy I recorded of my conference presentation here). I keynoted at the European Patients Forum Congress as well as at ADA’s Precision Diabetes Medicine 2021; an invited talk ADA Scientific Sessions (session coverage here); the 2021 Federal Wearables Summit: (video here); and the BIH Clinician Scientist Symposium (video here), to name a few (but not all).
  • Additionally, as I mentioned, one of the presentations I’m most proud of was created for the Fall 2021 #DData Exchange event:

OTHER STUFF

I did quite a few other small projects that don’t fit neatly into the above categories.

One final thing I’m excited to share is that also in 2021, Amazon came out with a beta program for producing hardcover/hardback books, alongside the ability to print paperback books on demand (and of course Kindle). So, you can now buy a copy of my book about Automated Insulin Delivery: How artificial pancreas “closed loop” systems can aid you in living with diabetes in paperback, hardback, or on Kindle. (You can also, still, read it 100% for free online via your phone or desktop at ArtificialPancreasBook.com, or download a PDF for free to read on your device of choice. Thousands of people have downloaded the PDF!)

Now available in hardcover, the book about Automated Insulin Delivery by Dana M. Lewis

How to deal with wildfire smoke and air quality issues during COVID-19

2020. What a year. We’ve been social distancing since late February and being very careful in terms of minimizing interactions even with family, for months. We haven’t traveled, we haven’t gone out to eat, and we basically only go out to get exercise (with a mask when it’s on hiking trails/around anyone) or Scott goes to the grocery store (n95 masked). We’ve been working on CoEpi (see CoEpi.org – an open source exposure notification app based on symptom reports) and staying on top of the scientific literature around COVID-19, regarding NPIs like distancing and masking; at-home diagnostics like temperature and pulse oximetry monitoring, prophylactics and treatments like zinc, quercetine, and even MMR vaccines; and the impact of ventilation and air quality on COVID-19 transmission and susceptibility.

And we live in Washington, so the focus on air quality got very real very quickly during this year’s wildfire season, where we had wildfires across the state of Washington, then got pummeled for over a week with hazardous levels of wildfire smoke coming up from Oregon and California to cover our existing smoke layer. But, one of our DIY air quality hacks for COVID-19 gave us a head start on air quality improvements for smoke-laden air, which I’ll describe below.

Here are various things we’ve gotten and have been using in our personal attempts to thwart COVID-19:

  • Finger pulse oximeter.
    • Just about any cheap pulse oximeter you can find is fine. The goal is to get an idea of your normal baseline oxygen rates. If you dip low, that might be a reason to go to urgent care or the ER or at least talk to your doctor about it. For me, I am typically 98-99% (mine doesn’t read higher than 99%), and my personal plan would be to talk to a healthcare provider if I was sick and started dropping below 94%.
  • Thermometer
    • Use any thermometer that you’ll actually use. I have previously used a no-touch thermometer that could read foreheads but found it varied widely and inconsistently, so I went back to an under the tongue thermometer and took my temperature for several months at different times to figure out my baselines. If sick or you have a suspected exposure, it’s good to be checking at different times of the day (people often have lower temps in the morning than in the evening, so knowing your daily differences may help you evaluate if you’re elevated for you or not).
    • Note: women with menstrual cycles may have changes related to this; such as lower baseline temps at the start of the cycle and having a temperature upswing around or after the mid-point in their cycle. But not all do. Also, certain medications or birth controls can impact basal temperatures, so be aware of that.
  • Originally, n95 masks with outlet valves.
    • Note: n95 masks with valves cannot be used by medical professionals, because the valves make them less effective for protecting others. (So don’t freak out at people who had a box of valved n95 masks from previous wildfire smoke seasons, as we did. Ahem.) 
    • We had a box we bought after previous years’ wildfire smoke, and they work well for us (in low-risk non-medical settings) for repeated use. They’re Scott’s go-to choice. If you’re in a setting where the outlet valve matters (indoors in a doctor’s/medical setting, or on a plane), you can easily pop a surgical/procedure mask over the valve to block the valve to protect others from your exhaust, while still getting good n95-level protection for yourself.
    • They were out of stock since February, but given the focus on n95 without valves for medical PPE, there have been a few boxes of n95 masks with outlet valves showing up online at silly prices ($7 per mask or so). But, kn95’s are a cheaper per mask option that are generally more available – see below.
    • (June 2021 note – they are back to reasonable prices, in the $1-2 range per mask on Amazon, and available again.)
  • kn95 masks.
    • kn95 masks are a different standard than US-rated n95; but they both block 95% of tiny (0.3 micron) particles. For non-medical usage, we consider them equivalent. But like n95, the fit is key.
    • We originally bought these kn95s, but the ear loops were quite big on me. (See below for options if this is the case on any you get.) They aren’t as hardy as the n95s with valves (above); the straps have broken off, tearing the mask, after about 4-5 long wears. That’s still worth it for them being $2-3 each (depending on how many you buy at a time) for me, but I’d always pack a spare mask (of any kind) just in case.
      • Option one to adjust ear loops: I loop them over my ponytail, making them head loops. This has been my favorite kn95 option because I get a great fit and a tight seal with this method.
      • Option two to adjust ear loops: tie knots in the ear loops
      • Option three to adjust ear loops: use things like this to tighten the ear loops
    • We also got a set of these kn95s. They don’t fit quite as well in terms of a tight face fit, but these actually work as ear loops (as designed), and I was able to wear this inside the house on the worst day of air quality.
  • Box fan with a filter to reduce COVID-19 particles in the air:
    • We read this story about using an existing AC air furnace filter on a box fan to help reduce the number of COVID-19 particles in the air. We already had a box fan, so we took one of our spare 20×20 filters and popped it on. I’m allergic to dust, cats (which we just got), trees, grass, etc, so I knew it would also help with regular allergens. There are different levels of filter – all the way up to HEPA filters – but we had MERV 12 so that’s what we used.
  • Phone/object UV sanitizer
    • We got a PhoneSoap Pro (in lavender, but there are other colors). Phones are germy, and being able to pop the phone in (plus keys or any other objects like credit cards or insurance cards that might have been handled by another human) to disinfect has been nice to have.
    • The Pro is done sanitizing in 5 minutes, vs the regular one takes 10 minutes. It’s not quite 2x the price as the non-pro, but I’ve found it to be worthwhile because otherwise, I would be impatient to get my phone back out. I usually pop my phone in it when I get home from my walk, and by the time I’m done washing my hands and all the steps of getting home, the phone is about or already done being sanitized.
  • Bonus (but not as useful to everyone as the above, and pricey): Oura ring
    • Scott and I also both got Oura rings. They are pricey, but every morning when we wake up we can see our lowest resting heart rate (RHR), heart rate variability (HRV), temperature deviations, and respiratory rate (RR). There have been studies showing that HRV, RHR, overnight temperature, and RR changes happen early in COVID-19 and other infections, which can give an early warning sign that you might be getting sick with something. That can be a good early warning sign (before you get to the point of being symptomatic and highly infectious) that you need to mask up and work from home/social distance/not interact with other people if you can help it. I find the data soothing, as I am used to using a lot of diabetes data on a daily and real-time basis (see also: invented an open source artificial pancreas). Due to price and level of interest in self-tracking data, this may not be a great tool for everyone.
    • Note this doesn’t tell you your temperature in real time, or present absolute values, but it’s helpful to see, and get warnings about, any concerning trends in your body temperature data. I’ve seen several anecdotal reports of this being used for early detection of COVID-19 infection and various types of relapses experienced by long-haulers.

And here are some things we’ve added to battle air quality during wildfire smoke season:

  • We were already running a box fan with a filter (see above for more details) for COVID-19 and allergen reduction; so we kept running it on high speed for smoke reduction.
    • Basic steps: get box fan, get a filter, and duct tape or strap it on. Doesn’t have to be cute, but it will help.
    • I run this on high speed during the day in my bedroom, and then on low speed overnight or sleep with earplugs in.
  • We already had a small air purifier for allergens, which we also kept running on high. This one hangs out in our guest bedroom/my office.
  • We caved and got a new, bigger air purifier, since we expect future years to be equally and unfortunately as smoky. This is the new air purifier we got. (Scott chose the 280i version that claims to cover 279 sq. ft.). It’s expensive, but given how miserable I was even inside the house with decent air quality thanks to my box fan and filter, little purifier, and our A/C filtered air… I consider it to be worth the investment.
    • We plugged it in and validated that with our A/C-filtered air combined with my little air purifier and the box fan with filter running on high, we already had ‘good’ air quality (but not excellent). We also stuck it out in the hallway to see what the hallway air quality was running – around 125 ug/m^3 – yikes. Turns out that was almost as high as the outside air, which is I’ve had to wear a kn95 mask even to walk hallway laps, and why my eyes are irritated. example air quality difference between hallway and our kitchen. hallway is much higher.
  • Check your other filters while you’re on air quality monitoring alert. We found our A/C intake duct vent had not had the air filter changed since we moved in over a year ago… and turns out it’s a non-standard size and had a hand-cut stuffed in there, so we ordered a correctly sized one for the vent, and taped a different one over the outside in the interim.
  • The other thing to fight the smoke is having n95 with valves or kn95 masks to wear when we have to go outside, or if it gets particularly bad inside. Our previous strategy was to have several on hand for wildfire season, and we’ll continue to do this. (See above in the COVID-19 section for descriptions in more detail about different kinds of masks we’ve tried.)
  • 2022 update: I got a mini personal air purifier to try for travel (to help reduce risk of COVID-19 in addition to all other precautions like staying masked on planes and indoor spaces), but it also turned out to be beneficial inside during the worst of our 2022 wildfire smoke season. I had a slightly scratchy throat even with two box fans and two different air purifiers inside; but keeping this individual one plugged in and pointed at my face overnight eliminated me waking up with a scratchy throat. That’s great for wildfire smoke, and also shows that there is some efficacy to this fan for it’s intended purpose, which is improving air around my face during travel in inside spaces for COVID-19 and other disease prevention.

Wildfires, their smoke, and COVID-19 combined is a bit of a mess for our health. Stay inside when you can, wear masks when you’re around other people outside your household that you have to share air with, wash your hands, and good luck.

Poster and presentation content from @DanaMLewis at #ADA2020 and #DData20

In previous years (see 2019 and 2018), I mentioned sharing content from ADA Scientific Sessions (this year it’s #ADA2020) with those not physically present at the conference. This year, NO ONE is present at the event, and we’re all virtual! Even more reason to share content from the conference. :)

I contributed to and co-authored two different posters at Scientific Sessions this year:

  • “Multi-Timescale Interactions of Glucose and Insulin in Type 1 Diabetes Reveal Benefits of Hybrid Closed Loop Systems“ (poster 99-LB) along with Azure Grant and Lance Kriegsfeld, PhD.
  • “Do-It-Yourself Artificial Pancreas Systems for Type 1 Diabetes Reduce Hyperglycemia Without Increasing Hypoglycemia” (poster 988-P in category 12-D Clinical Therapeutics/New Technology—Insulin Delivery Systems), alongside Jennifer Zabinsky, MD MEng, Haley Howell, MSHI, Alireza Ghezavati, MD, Andrew Nguyen, PhD, and Jenise Wong, MD PhD.

And, while not a poster at ADA, I also presented the “AID-IRL” study funded by DiabetesMine at #DData20, held in conjunction with Scientific Sessions. A summary of the study is also included in this post.

First up, the biological rhythms poster, “Multi-Timescale Interactions of Glucose and Insulin in Type 1 Diabetes Reveal Benefits of Hybrid Closed Loop Systems” (poster 99-LB). (Twitter thread summary of this poster here.)

Building off our work as detailed last year, Azure, Lance, and I have been exploring the biological rhythms in individuals living with type 1 diabetes. Why? It’s not been done before, and we now have the capabilities thanks to technology (pumps, CGM, and closed loops) to better understand how glucose and insulin dynamics may be similar or different than those without diabetes.

Background:

Mejean et al., 1988Blood glucose and insulin exhibit coupled biological rhythms at multiple timescales, including hours (ultradian, UR) and the day (circadian, CR) in individuals without diabetes. The presence and stability of these rhythms are associated with healthy glucose control in individuals without diabetes. (See right, adapted from Mejean et al., 1988).

However, biological rhythms in longitudinal (e.g., months to years) data sets of glucose and insulin outputs have not been mapped in a wide population of people with Type 1 Diabetes (PWT1D). It is not known how glucose and insulin rhythms compare between T1D and non-T1D individuals. It is also unknown if rhythms in T1D are affected by type of therapy, such as Sensor Augmented Pump (SAP) vs. Hybrid Closed Loop (HCL). As HCL systems permit feedback from a CGM to automatically adjust insulin delivery, we hypothesized that rhythmicity and glycemia would exhibit improvements in HCL users compared to SAP users. We describe longitudinal temporal structure in glucose and insulin delivery rate of individuals with T1D using SAP or HCL systems in comparison to glucose levels from a subset of individuals without diabetes.

Data collection and analysis:

We assessed stability and amplitude of normalized continuous glucose and insulin rate oscillations using the continuous wavelet transformation and wavelet coherence. Data came from 16 non-T1D individuals (CGM only, >2 weeks per individual) from the Quantified Self CGM dataset and 200 (n = 100 HCL, n = 100 SAP; >3 months per individual) individuals from the Tidepool Big Data Donation Project. Morlet wavelets were used for all analyses. Data were analyzed and plotted using Matlab 2020a and Python 3 in conjunction with in-house code for wavelet decomposition modified from the “Jlab” toolbox, from code developed by Dr. Tanya Leise (Leise 2013), and from the Wavelet Coherence toolkit by Dr. Xu Cui. Linear regression was used to generate correlations, and paired t-tests were used to compare AUC for wavelet and wavelet coherences by group (df=100). Stats used 1 point per individual per day.

Wavelets Assess Glucose and Insulin Rhythms and Interactions

Wavelet Coherence flow for glucose and insulin

Morlet wavelets (A) estimate rhythmic strength in glucose or insulin data at each minute in time (a combination of signal amplitude and oscillation stability) by assessing the fit of a wavelet stretched in window and in the x and y dimensions to a signal (B). The output (C) is a matrix of wavelet power, periodicity, and time (days). Transform of example HCL data illustrate the presence of predominantly circadian power in glucose, and predominantly 1-6 h ultradian power in insulin. Color map indicates wavelet power (synonymous with Y axis height). Wavelet coherence (D) enables assessment of rhythmic interactions between glucose and insulin; here, glucose and insulin rhythms are highly correlated at the 3-6 (ultradian) and 24 (circadian) hour timescales.

Results:

Hybrid Closed Loop Systems Reduce Hyperglycemia

Glucose distribution of SAP, HCL, and nonT1D
  • A) Proportional counts* of glucose distributions of all individuals with T1D using SAP (n=100) and HCL (n=100) systems. SAP system users exhibit a broader, right shifted distribution in comparison to individuals using HCL systems, indicating greater hyperglycemia (>7.8 mmol/L). Hypoglycemic events (<4mmol/L) comprised <5% of all data points for either T1D dataset.
  • B) Proportional counts* of non-T1D glucose distributions. Although limited in number, our dataset from people without diabetes exhibits a tighter blood glucose distribution, with the vast majority of values falling in euglycemic range (n=16 non-T1D individuals).
  • C) Median distributions for each dataset.
  • *Counts are scaled such that each individual contributes the same proportion of total data per bin.

HCL Improves Correlation of Glucose-Insulin Level & Rhythm

Glucose and Insulin rhythms in SAP and HCL

SAP users exhibit uncorrelated glucose and insulin levels (A) (r2 =3.3*10-5; p=0.341) and uncorrelated URs of glucose and insulin (B) (r2 =1.17*10-3; p=0.165). Glucose and its rhythms take a wide spectrum of values for each of the standard doses of insulin rates provided by the pump, leading to the striped appearance (B). By contrast, Hybrid Closed Loop users exhibit correlated glucose and insulin levels (C) (r2 =0.02; p=7.63*10-16), and correlated ultradian rhythms of glucose and insulin (D) (r2 =-0.13; p=5.22*10-38). Overlays (E,F).

HCL Results in Greater Coherence than SAP

Non-T1D individuals have highly coherent glucose and insulin at the circadian and ultradian timescales (see Mejean et al., 1988, Kern et al., 1996, Simon and Brandenberger 2002, Brandenberger et al., 1987), but these relationships had not previously been assessed long-term in T1D.

coherence between glucose and insulin in HCL and SAP, and glucose swings between SAP, HCL, and non-T1DA) Circadian (blue) and 3-6 hour ultradian (maroon) coherence of glucose and insulin in HCL (solid) and SAP (dotted) users. Transparent shading indicates standard deviation. Although both HCL and SAP individuals have lower coherence than would be expected in a non-T1D individual,  HCL CR and UR coherence are significantly greater than SAP CR and UR coherence (paired t-test p= 1.51*10-7 t=-5.77 and p= 5.01*10-14 t=-9.19, respectively). This brings HCL users’ glucose and insulin closer to the canonical non-T1D phenotype than SAP users’.

B) Additionally, the amplitude of HCL users’ glucose CRs and URs (solid) is closer (smaller) to that of non-T1D (dashed) individuals than are SAP glucose rhythms (dotted). SAP CR and UR amplitude is significantly higher than that of HCL or non-T1D (T-test,1,98, p= 47*10-17 and p= 5.95*10-20, respectively), but HCL CR amplitude is not significantly different from non-T1D CR amplitude (p=0.61).

Together, HCL users are more similar than SAP users to the canonical Non-T1D phenotype in A) rhythmic interaction between glucose and insulin and B) glucose rhythmic amplitude.

Conclusions and Future Directions

T1D and non-T1D individuals exhibit different relative stabilities of within-a-day rhythms and daily rhythms in blood glucose, and T1D glucose and insulin delivery rhythmic patterns differ by insulin delivery system.

Hybrid Closed Looping is Associated With:

  • Lower incidence of hyperglycemia
  • Greater correlation between glucose level and insulin delivery rate
  • Greater correlation between ultradian glucose and ultradian insulin delivery rhythms
  • Greater degree of circadian and ultradian coherence between glucose and insulin delivery rate than in SAP system use
  • Lower amplitude swings at the circadian and ultradian timescale

These preliminary results suggest that HCL recapitulates non-diabetes glucose-insulin dynamics to a greater degree than SAP. However, pump model, bolusing data, looping algorithms and insulin type likely all affect rhythmic structure and will need to be further differentiated. Future work will determine if stability of rhythmic structure is associated with greater time in range, which will help determine if bolstering of within-a-day and daily rhythmic structure is truly beneficial to PWT1D.
Acknowledgements:

Thanks to all of the individuals who donated their data as part of the Tidepool Big Data Donation Project, as well as the OpenAPS Data Commons, from which data is also being used in other areas of this study. This study is supported by JDRF (1-SRA-2019-821-S-B).

(You can download a full PDF copy of the poster here.)

Next is “Do-It-Yourself Artificial Pancreas Systems for Type 1 Diabetes Reduce Hyperglycemia Without Increasing Hypoglycemia” (poster 988-P in category 12-D Clinical Therapeutics/New Technology—Insulin Delivery Systems), which I co-authored alongside Jennifer Zabinsky, MD MEng, Haley Howell, MSHI, Alireza Ghezavati, MD, Andrew Nguyen, PhD, and Jenise Wong, MD PhD. There is a Twitter thread summarizing this poster here.

This was a retrospective double cohort study that evaluated data from the OpenAPS Data Commons (data ranged from 2017-2019) and compared it to conventional sensor-augmented pump (SAP) therapy from the Tidepool Big Data Donation Project.

Methods:

  • From the OpenAPS Data Commons, one month of CGM data (with more than 70% of the month spent using CGM), as long as they were >1 year of living with T1D, was used. People could be using any type of DIYAPS (OpenAPS, Loop, or AndroidAPS) and there were no age restrictions.
  • A random age-matched sample from the Tidepool Big Data Donation Project of people with type 1 diabetes with SAP was selected.
  • The primary outcome assessed was percent of CGM data <70 mg/dL.
  • The secondary outcomes assessed were # of hypoglycemic events per month (15 minutes or more <70 mg/dL); percent of time in range (70-180mg/dL); percent of time above range (>180mg/dL), mean CGM values, and coefficient of variation.
Methods_DIYAPSvsSAP_ADA2020_DanaMLewis

Demographics:

  • From Table 1, this shows the age of participants was not statistically different between the DIYAPS and SAP cohorts. Similarly, the age at T1D diagnosis or time since T1D diagnosis did not differ.
  • Table 2 shows the additional characteristics of the DIYAPS cohort, which included data shared by a parent/caregiver for their child with T1D. DIYAPS use was an average of 7 months, at the time of the month of CGM used for the study. The self-reported HbA1c in DIYAPS was 6.4%.
Demographics_DIYAPSvsSAP_ADA2020_DanaMLewis DIYAPS_Characteristics_DIYAPSvsSAP_ADA2020_DanaMLewis

Results:

  • Figure 1 shows the comparison in outcomes based on CGM data between the two groups. Asterisks (*) indicate statistical significance.
  • There was no statistically significant difference in % of CGM values below 70mg/dL between the groups in this data set sampled.
  • DIYAPS users had higher percent in target range and lower percent in hyperglycemic range, compared to the SAP users.
  • Table 3 shows the secondary outcomes.
  • There was no statistically significant difference in the average number of hypoglycemic events per month between the 2 groups.
  • The mean CGM glucose value was lower for the DIYAPS group, but the coefficient of variation did not differ between groups.
CGM_Comparison_DIYAPSvsSAP_ADA2020_DanaMLewis SecondaryOutcomes_DIYAPSvsSAP_ADA2020_DanaMLewis

Conclusions:

    • Users of DIYAPS (from this month of sampled data) had a comparable amount of hypoglycemia to those using SAP.
    • Mean CGM glucose and frequency of hyperglycemia were lower in the DIYAPS group.
    • Percent of CGM values in target range (70-180mg/dL) was significantly greater for DIYAPS users.
    • This shows a benefit in DIYAPS in reducing hyperglycemia without compromising a low occurrence of hypoglycemia. 
Conclusions_DIYAPSvsSAP_ADA2020_DanaMLewis

(You can download a PDF of the e-poster here.)

Finally, my presentation at this year’s D-Data conference (#DData20). The study I presented, called AID-IRL, was funded by Diabetes Mine. You can see a Twitter thread summarizing my AID-IRL presentation here.

AID-IRL-Aim-Methods_DanaMLewis

I did semi-structured phone interviews with 7 users of commercial AID systems in the last few months. The study was funded by DiabetesMine – both for my time in conducting the study, as well as funding for study participants. Study participants received $50 for their participation. I sought a mix of longer-time and newer AID users, using a mix of systems. Control-IQ (4) and 670G (2) users were interviewed; as well as (1) a CamAPS FX user since it was approved in the UK during the time of the study.

Based on the interviews, I coded their feedback for each of the different themes of the study depending on whether they saw improvements (or did not have issues); had no changes but were satisfied, or neutral experiences; or saw negative impact/experience. For each participant, I reviewed their experience and what they were happy with or frustrated by.

Here are some of the details for each participant.

AID-IRL-Participant1-DanaMLewisAID-IRL-Participant1-cont_DanaMLewis1 – A parent of a child using Control-IQ (off-label), with 30% increase in TIR with no increased hypoglycemia. They spend less time correcting than before; less time thinking about diabetes; and “get solid uninterrupted sleep for the first time since diagnosis”. They wish they had remote bolusing, more system information available in remote monitoring on phones. They miss using the system during the 2 hour CGM warmup, and found the system dealt well with growth spurt hormones but not as well with underestimated meals.

AID-IRL-Participant2-DanaMLewis AID-IRL-Participant2-cont-DanaMLewis2 – An adult male with T1D who previously used DIYAPS saw 5-10% decrease in TIR (but it’s on par with other participants’ TIR) with Control-IQ, and is very pleased by the all-in-one convenience of his commercial system.He misses autosensitivity (a short-term learning feature of how insulin needs may very from base settings) from DIYAPS and has stopped eating breakfast, since he found it couldn’t manage that well. He is doing more manual corrections than he was before.

AID-IRL-Participant5-DanaMLewis AID-IRL-Participant5-cont_DanaMLewis5 – An adult female with LADA started, stopped, and started using Control-IQ, getting the same TIR that she had before on Basal-IQ. It took artificially inflating settings to achieve these similar results. She likes peace of mind to sleep while the system prevents hypoglycemia. She is frustrated by ‘too high’ target; not having low prevention if she disables Control-IQ; and how much she had to inflate settings to achieve her outcomes. It’s hard to know how much insulin the system gives each hour (she still produces some of own insulin).

AID-IRL-Participant7-DanaMLewis AID-IRL-Participant7-cont-DanaMLewis7 – An adult female with T1D who frequently has to take steroids for other reasons, causing increased BGs. With Control-IQ, she sees 70% increase in TIR overall and increased TIR overnight, and found it does a ‘decent job keeping up’ with steroid-induced highs. She also wants to run ‘tighter’ and have an adjustable target, and does not ever run in sleep mode so that she can always get the bolus corrections that are more likely to bring her closer to target.

AID-IRL-Participant3-DanaMLewis AID-IRL-Participant3-cont-DanaMLewis3 – An adult male with T1D using 670G for 3 years didn’t observe any changes to A1c or TIR, but is pleased with his outcomes, especially with the ability to handle his activity levels by using the higher activity target.  He is frustrated by the CGM and is woken up 1-2x a week to calibrate overnight. He wishes he could still have low glucose suspend even if he’s kicked out of automode due to calibration issues. He also commented on post-meal highs and more manual interventions.

AID-IRL-Participant6-DanaMLewis AID-IRL-Participant6-contDanaMLewis6 – Another adult male user with 670G was originally diagnosed with T2 (now considered T1) with a very high total daily insulin use that was able to decrease significantly when switching to AID. He’s happy with increased TIR and less hypo, plus decreased TDD. Due to #COVID19, he did virtually training but would have preferred in-person. He has 4-5 alerts/day and is woken up every other night due to BG alarms or calibration. He does not like the time it takes to charge CGM transmitter, in addition to sensor warmup.

AID-IRL-Participant4-DanaMLewis AID-IRL-Participant4-contDanaMLewis4 – The last participant is an adult male with T1 who previously used DIYAPS but was able to test-drive the CamAPS FX. He saw no TIR change to DIYAPS (which pleased him) and thought the learning curve was easy – but he had to learn the system and let it learn him. He experienced ‘too much’ hypoglycemia (~7% <70mg/dL, 2x his previous), and found it challenging to not have visibility of IOB. He also found the in-app CGM alarms annoying. He noted the system may work better for people with regular routines.

You can see a summary of the participants’ experiences via this chart. Overall, most cited increased or same TIR. Some individuals saw reduced hypos, but a few saw increases. Post-meal highs were commonly mentioned.

AID-IRL-UniversalThemes2-DanaMLewis AID-IRL-UniversalThemes-DanaMLewis

Those newer to CGM have a noticeable learning curve and were more likely to comment on number of alarms and system alerts they saw. The 670G users were more likely to describe connection/troubleshooting issues and CGM calibration issues, both of which impacted sleep.

This view highlights those who more recently adopted AID systems. One noted their learning experience was ‘eased’ by “lurking” in the DIY community, and previously participating in an AID study. One felt the learning curve was high. Another struggled with CGM.

AID-IRL-NewAIDUsers-DanaMLewis

Both previous DIYAPS users who were using commercial AID systems referenced the convenience factor of commercial systems. One DIYAPS saw decreased TIR, and has also altered his behaviors accordingly, while the other saw no change to TIR but had increased hypo’s.

AID-IRL-PreviousDIYUsers-DanaMLewis

Companies building AID systems for PWDs should consider that the onboarding and learning curve may vary for individuals, especially those newer to CGM. Many want better displays of IOB and the ability to adjust targets. Remote bolusing and remote monitoring is highly desired by all, regardless of age. Post-prandial was frequently mentioned as the weak point in glycemic control of commercial AID systems. Even with ‘ideal’ TIR, many commercial users still are doing frequent manual corrections outside of mealtimes. This is an area of improvement for commercial AID to further reduce the burden of managing diabetes.

AID-IRL-FeedbackForCompanies-DanaMLewis

Note – all studies have their limitations. This was a small deep-dive study that is not necessarily representative, due to the design and small sample size. Timing of system availability influenced the ability to have new/longer time users.

AID-IRL-Limitations-DanaMLewis

Thank you to all of the participants of the study for sharing their feedback about their experiences with AID-IRL!

(You can download a PDF of my slides from the AID-IRL study here.)

Have questions about any of my posters or presentations? You can always reach me via email at Dana@OpenAPS.org.