The short version
What I'm working with
Type 1 diabetes since 2018
My immune system destroyed the cells that make insulin. I dose it myself, every hour of every day, with help from a DIY closed loop.
Underactive thyroid treated
Years of quietly elevated thyroid values dragged on energy, recovery and glucose control. Since late 2025 it's finally dialled in.
Glandular fever 2014, resolved
Epstein-Barr virus cost me months of training and taught me the first big lesson: you can't out-train a body that's fighting something.
Condition 01
Type 1 diabetes
In plain terms
Your body runs on glucose, and insulin is the key that lets glucose into your cells. In Type 1 diabetes, the immune system destroys the cells that produce insulin, so the key is simply gone. It has nothing to do with lifestyle or sugar intake, and it doesn't go away.
The job it leaves you with: measure glucose constantly and supply exactly the right amount of insulin at exactly the right time, forever. Too little and glucose climbs, sapping performance and damaging the body over years. Too much and it crashes, which in the short term is the dangerous one.
What it means on the start line
Sprinting and Type 1 interact in a way most people don't expect. Short, maximal efforts flood the body with adrenaline, which tells the liver to dump glucose, so a 100 m race can send my glucose up, not down. The bill arrives later: in the hours after intense work, muscles restock their fuel and glucose can drop hard, sometimes in the middle of the night.
So every session is planned twice: once as training, once as a glucose problem. Where is my level before the start? How much insulin is still active? What did the last session do to tonight's numbers? Racing at the sharp end means solving that in real time, on the grid, with a heart rate of 180.
What my own data shows
I was diagnosed in October 2018, rushed to hospital in ketoacidosis with a blood glucose of 35.6 mmol/L (roughly six times a normal fasting value) and an HbA1c of 118 mmol/mol. That's the "before" picture.
Today the picture is live: the cards below are my actual current numbers, straight from my CGM, updated automatically. This year my average glucose has run around 8.8 mmol/L with a variability (CV) of 38%, just above the <36% stability target I'm chasing. The consensus time-in-range target is above 70% and I'm not there yet. It's on the data page, uncensored, because that's the point of this site.
The closed loop that keeps me racing
Since 2023 I run a DIY closed loop, three pieces of technology in a conversation that never stops:
A FreeStyle Libre sensor on my arm measures glucose continuously, around the clock.
An Android app reads the sensor every minute and streams the values onward.
An open-source algorithm predicts where glucose is heading and adjusts insulin delivery.
My own platform stores every reading next to training, sleep and labs, and looks for patterns.
Go deeper: the physiology, if you want it
The autoimmune part. Type 1 is confirmed by antibodies (in my case GAD antibodies) that mark the immune system's attack on the insulin-producing beta cells of the pancreas. Once enough beta cells are gone, insulin production effectively stops. Ketoacidosis, how I was diagnosed, is what happens without insulin: cells can't use glucose, the body burns fat uncontrolled, and acidic ketones build up in the blood. It's a medical emergency.
Why sprints raise glucose. Maximal efforts trigger catecholamines (adrenaline, noradrenaline), which drive the liver to release glucose faster than muscles take it up: a stress response built for fight-or-flight. In a non-diabetic body, a puff of insulin mops this up minutes later. My insulin comes from an algorithm and a depot under the skin, which is far slower, so short intense work reliably spikes me, while long steady work drops me.
Why the lows come later. After intense training, muscles refill their glycogen stores for up to 24-48 hours and insulin sensitivity rises; the same dose suddenly works much harder. That's why the riskiest moment isn't the race; it's the night after.
What the loop can and can't do. AndroidAPS predicts glucose from recent readings, insulin on board and carbs, then modulates delivery. It's brilliant at the slow game: overnight, between meals. But a 12-second all-out effort moves faster than any subcutaneous insulin can. Around racing, the algorithm assists; the athlete still has to think.
Condition 02
The thyroid that ran slow
In plain terms
The thyroid is the body's metabolic thermostat: it sets how fast every cell burns energy. Mine ran slow (hypothyroidism) for years. The frustrating part: the symptoms are vague enough to blame on anything. Tired? Train less. Recovering badly? Sleep more. Meanwhile the actual dial being turned down was hormonal, and no amount of discipline fixes that.
What it means for a sprinter
A slow thyroid is like training with the parking brake half on: flat energy, slower recovery between sessions, and (the part that took me years to see) worse glucose control, because low thyroid hormone also blunts how well insulin works. Stacked on top of Type 1, it quietly made everything harder while looking like "just fatigue".
What my own data shows
My TSH (the pituitary's "work harder" signal to the thyroid, which rises when the thyroid underdelivers) was elevated from 2014 all the way to mid-2025, peaking at 9.44 in September 2025 (labs typically want it roughly between 0.4 and 4). Over that same stretch my HbA1c crept up to 44-47 mmol/mol despite honest effort.
Once my levothyroxine dose was properly dialled in, TSH dropped to 1.55 by late May 2026, and energy, recovery and glucose predictability turned a corner I could feel within weeks. The lesson I keep repeating: don't manage conditions in isolation. The full write-up is in the journal.
Go deeper: the thyroid-glucose connection
The axis. The pituitary releases TSH to tell the thyroid to produce T4, which the body converts into T3, the hormone that actually sets cellular metabolic rate. When the thyroid underdelivers, TSH climbs as the pituitary shouts louder. That's why a high TSH means an underactive thyroid.
Why it drags on glucose. Thyroid hormone influences how much glucose the gut absorbs, how the liver stores and releases it, and how sensitive muscle is to insulin. Run low, and insulin becomes less effective while glucose handling slows. For someone dosing insulin manually, that means stubborn, unexplained variability that's easy to misattribute to carbs or training stress.
Why "in range" wasn't enough. For years my TSH sat in the technically-acceptable zone before finally spiking out of it. Treated properly, it now sits around 1.5, and the difference between "acceptable" and "optimal" turned out to be the difference between surviving training and absorbing it.
The 2014 detour
Glandular fever, the first teacher
Before any of the above, Epstein-Barr virus (mononucleosis) sidelined me for months in 2014 with the kind of fatigue you can't push through, because pushing through makes it worse. For a teenager who believed effort fixed everything, that was a formative defeat.
It's also where this whole approach started: recovery is not the absence of training, it's a biological process you can watch, measure and respect. Ten years later, that's literally what the data page does every night.
Why share this
Because someone is searching for this at 2 a.m.
When I was diagnosed, I wanted one thing: proof that someone with this condition was still training flat out, and an honest account of how. Not inspiration: information. This site is me paying that forward: the plain-language version, the sprint-specific version, and the actual numbers.