Back up with me to the days before the surgery, ahead of the Day Three I wrote about in the last post.

You know about the anesthesiologist conversation from the first issue: the nerve blocking agent, the duration mapped against my basal rates, the postoperative bolus planned to cover the gap, the 30-minutes-or-90 plan for the procedure itself. You have probably had some version of that conversation. You probably had to start the questions to get the conversation going as well.

Here's the part I left out. We also worked through what the nursing team would have available for food afterward, and how that timing would line up with my normal insulin patterns. Pump in activity mode to slow done the insulin rate, my basal-bolus patterns laid against their standard recovery timeline, the sleep and wake-up patterns in the post-operative spaces.

Every one of those conversations started because I asked. Not because someone on the team brought it up. The medical team was wonderful, engaged, genuinely helpful once we got talking. But the focusing on these details was on me.

That's the thing about walking into an orthopedic setting with decades of T1D behind you. You know things the surgical team doesn't. And the medication interactions, the stuff I write in this newsletter, are exactly where your advocacy stops being optional. That knowledge is what keeps you safe when you can't keep yourself awake.

You know the calculation. A nurse offers you something for the pain, and before she finishes the sentence you're already running it: do I explain, will she understand, how long do I have. And underneath all of it, the one that actually matters. Somebody needs to know this before I'm under anesthesia.

The thing to carry out of this issue: while Tylenol is in your system, your CGM can read higher than your actual blood sugar.

Take a standard dose and your sensor can start reporting a number meaningfully above the truth, with the gap widening over the hour or two after you swallow it and lingering for hours after that. I have not found a study that pins down the size of that gap for someone with type 1 recovering from surgery, so I am not going to hand you a figure to quote at your care team. The direction is the part to hold onto, and the direction is always the same: high.

Think about what that means. Your CGM says you are running high. You correct. Your real blood sugar was already lower than the screen said, and now you have stacked insulin on top of a number that was never true.

That is the failure mode worth being scared of. A sensor can show a comfortable number while the person wearing it is genuinely low. The screen says fine. The body is not.

If you use a closed-loop system like Control-IQ or Loop, the algorithm sees that false high and increases your insulin automatically. No human decision required. Just silent, automated insulin delivery based on a number that isn't real.

Acetaminophen (Tylenol): The chemical structure fools your CGM sensor. The electrode can't tell the difference between Tylenol and glucose, so it reports both as sugar. Newer sensors (G6, G7) handle standard doses better, but IV acetaminophen in surgical settings still causes major misreadings.

NSAIDs (ibuprofen, naproxen): No CGM interference. These don't mess with your sensor. At high sustained doses they can lower blood sugar slightly through insulin-related pathways, but the kidney risks with T1D usually make this a conversation for your endo.

Opioids (tramadol, oxycodone, morphine): Different problem entirely. In one hospital study, 46.8% of T1D patients who got tramadol dropped to 70 mg/dL or below within five days[1]. Nearly half. Those were inpatients, where somebody was drawing a glucose every few hours and catching it. On a prescription at home, the catching part is yours. Opioids suppress your body's natural rescue response, the epinephrine surge and the glucagon release. When you're sedated you won't feel the shaking or the sweating. You won't wake to your CGM alarm.

Here's the twist that catches medical teams off guard: opioids typically raise blood sugar in people without diabetes, but lower it in people with diabetes. That inversion means providers don't expect what actually happens.

So "just take some Tylenol" is not a simple sentence when you wear a CGM. Your CGM number is not your blood sugar number while acetaminophen is in your system. Opioids don't only manage pain, they change how your body handles glucose. And your closed-loop pump has no idea you took anything at all.

Print it or take a photo. Ask both of them, not just one.

This checklist exists because of what went wrong for people who didn't have it. Use it.

When acetaminophen is in your system, your CGM is reporting a number that isn't yours, and a closed loop will act on it without asking you first.

So hand this checklist to one other person before your next procedure. Not to your surgeon. To whoever will be sitting in the room while you're asleep. They need to be able to say "he wears a CGM and he had IV Tylenol, please do a fingerstick" when you can't say anything at all.

If your surgery is already behind you, this week still has a job in it. Go read the label on whatever you took for pain last night. If acetaminophen is in there, the number your CGM showed you two hours later was not your number, and neither was the correction you gave for it. Tell the person who hands you that bottle what it does to your sensor, so somebody besides you is tracking it.

BTD Guide 1: Surveillance to Support is about turning diabetes data into understanding: when to trust your devices, when to double-check, how to read what the technology is actually telling you.

And tell them the story behind it. Has a medication ever made your CGM lie to you, and did you catch it in time or learn it the hard way? Say that one out loud to the person holding the checklist. A list somebody understands gets used. A list somebody was handed gets folded into a pocket.

Science works through iteration, meticulous perseverance, comparison, challenge, and identifying patterns across the spheres of science, so no single study is the whole answer. Findings come from other populations, animal models, or other tissues in the body, because living systems share enough molecules and machinery that these clues help us understand our own health. Individual papers are cited as keystones to stir thinking, and each one opens onto years of peer-reviewed work it was built on. Follow the citations when something is relevant to you: they open further readings you can bring to your care team. This is all part of being Better Together.

Next issue: why your blood sugar falls apart when your routine does, and the two anchors you can still rebuild.