Insulin by the bed. Sweetarts by the couch (and everywhere). Meds moved to the office desk. Eye drops by the kitchen chair. My sweetheart helped me stage the whole house like a field hospital, because two short flights of stairs were about to become the hardest thing I did all day, and anything I might need had to already be wherever I landed.

That's how I prepared for this surgery. The way I've learned to prepare for anything with T1D: control every variable I can before I can't control any of them.

Then the diet. I stopped eating by schedule and started eating by glucose meter. Level and stable? Eat. Not there yet? Wait. High-protein, high-fiber foods meant I wasn't chasing the constant "keep eating" signal, and honestly my stress-killed appetite helped for once. My body's under high stress. That's going to be a theme through this whole recovery, so the meter decides when and what I eat now.

But the conversations made the real difference. I sat with my anesthesiologist and talked through the nerve blocking agent, how it works between the nodes of Ranvier, shutting down sodium channels along the neuron. We mapped the duration against my basal rates, planned a postoperative bolus, talked through my pump's activity mode. The surgical team said 30 minutes in a perfect world, 90 if they found surprises. I planned for both.

The nurses, the anesthesia team, the surgeon: every single person was genuinely helpful and engaged. So here's what I'd tell you. Have those conversations before you're on the table. What you learn there carries forward into everything that comes after.

It helps that I understand these molecules from the inside. I studied insulin at the molecular level during my master's research in structural molecular biology. When the anesthesiologist talked through sodium channel blockade, I could follow the mechanism. When I planned my basal rate adjustments, I was thinking about how insulin assembles from inactive oligomers into its active form, and how stress hormones change that process. That's what the training adds to doing this since 1990: you stop being a patient receiving instructions and start being a collaborator in your own care.

Your insulin isn't broken. Your body just declared war on it.

I want to hand you this number with its limits already attached, because the limits matter. It isn't an Achilles study. It's shoulders. In people with diabetes who had a rotator cuff repaired, the ones whose A1c climbed during months 3-6 after surgery re-tore at 51.1%. The ones who held it steady or brought it down: 14.3%[1].

Different tendon. I have not come across that same study on the Achilles, and you deserve to know what the evidence actually covers. But look at what got measured. Not shoulder anatomy. Blood sugar, during the months a repair is remodeling. That's the same blood and the same repair cells your leg is using, in the same window.

That's not a small difference. That's the difference between healing once and doing this all over again.

When your body sustains a major injury or goes through surgery, it floods your bloodstream with stress hormones: cortisol, epinephrine, glucagon. Your body isn't being difficult. It's doing exactly what evolution designed it to do, which is mobilize energy for survival.

In someone without T1D, the pancreas compensates by releasing extra insulin to counterbalance this hormone surge. In us, that compensation doesn't exist. Our carefully calibrated pump settings and ratios face a hormonal assault they were never designed for.

What each hormone does:

Cortisol blocks glucose from entering your muscles. It tells your liver to manufacture new glucose from protein. It breaks down muscle tissue to feed that glucose factory.

Epinephrine dumps stored glycogen into your bloodstream. It triggers fat breakdown, flooding free fatty acids that make insulin resistance worse.

Glucagon cranks liver glucose output to maximum. Normally insulin suppresses this after meals, but in T1D that brake is weak.

Patients with blood glucose above 200 mg/dL at surgery face significantly higher infection and mortality rates. But the old "tight control" target of 80-110 mg/dL was abandoned because it caused dangerous lows in stressed patients. Blood sugar swings wildly as stress hormones fluctuate.

Current evidence supports 120-150 mg/dL as the recovery sweet spot: low enough to protect healing tissue, high enough to avoid dangerous lows when hormone levels shift unpredictably. In normal times I’d much prefer to have the glucose in the tight range and still have the goal during recovery.

That range is calibrated for healing, not for perfection. You have permission to aim for good enough to heal.

This one's hard to hear, but you need to know it.

The clearest measurement we have comes from rats. Researchers cut and repaired Achilles tendons in diabetic and non-diabetic animals, then pulled them until they failed. At week 4, the diabetic tendons had about the strength the non-diabetic ones had at week 2. A two-week lag. At week 6 they gave out around 28 Newtons of force instead of around 41[2].

Animal data, and worth naming as such. But it's the same tendon and the same repair, and it points the same direction as everything else here.

Standard rehab timelines weren't built with you in mind. Whether yours should run longer is a conversation to have out loud with your surgeon.

Surgery isn't a one-day event for your blood sugar. It reshapes your metabolic reality for months, and each stretch breaks your settings a different way.

Days 1-7, the acute stress phase. You need more insulin. Your CGM graph isn't telling you that you failed. It's showing you exactly what cortisol and epinephrine do to a body without a working pancreas.

Weeks 2-8 and beyond, the immobility phase. You need different insulin, not just more of it. Your ratios were built for a body that walks around.

Months 3-6, the remodeling phase. This is the stretch that decides whether the repair survives, and it's the one you're most likely to relax during. By then you feel better. You're moving more. Life starts to feel normal. Your tendon is still actively rebuilding itself, and that shoulder study wasn't about the operation. It was about what happened in these months.

Your orthopedic surgeon may not have any of this in front of them. Orthopedic training doesn't cover diabetic tendon healing in depth, which means raising it falls to you.

Bring this to your pre-op appointment. Say it out loud, even if it feels like you're overstepping:

"My tendon may heal slower because of diabetes, so I want to talk about whether my immobilization and rehab timeline should run longer than standard. And I read that in people with diabetes who had a rotator cuff repair, the ones whose A1c rose during months 3 to 6 re-tore at about 51%, and the ones who held it steady were closer to 14%. I know that's a different tendon than mine. I still want a recovery-specific plan with my endocrinologist for that window[1]."

If you're already post-surgery, the ask changes: have your endo help you build a recovery-mode pump profile with 10-20% higher basal rates and stronger correction factors.

Your insulin isn't failing you. Your settings were calibrated for a body that walks around, and that body is temporarily unavailable.

So this week, tell one person in your house which phase you're in and what it's costing you. Not the numbers. The phase. "I'm in the part where my insulin barely works and it isn't my fault" is a sentence that changes how someone reads your bad afternoon.

BTD Guide 1: Surveillance to Support is where we build the skill of reading your data as a story instead of a scoreboard. Your CGM after surgery isn't grading you. It's reporting.

Then let them talk. Ask what they saw from where they were standing: did your care team account for your diabetes on their own, or did they watch you bring it up every single time? You already know your answer. Hearing theirs is how the two of you stop carrying that part separately.

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 the chicken dinner you ate to heal is still in your numbers eight hours later, and the bolus that catches it.