Thomas Reed Facebook ad: “Read this if you feel like you’re failing”

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The consultant at my diabetes clinic said something in our last appointment that I haven't been able to stop thinking about. She said: "Your numbers are the best I've seen from you in six years. What changed?" I said: "I found out where blood sugar actually goes." She looked at me. "Nobody had ever explained that to me," I said. "In six years. Nobody explained where it actually goes." There was a pause. "To be fair," she said quietly, "we don't explain it as well as we should." My name is Thomas. I'm 63. I worked as a secondary school science teacher for thirty-one years — retired three years ago — and I've had Type 2 diabetes for six. I tell you the science background because it matters for what comes next. When I was diagnosed at 57, I approached it the way I approached everything: I researched it properly. I read the studies. I understood the mechanism of insulin resistance. I knew what HbA1c represented. I knew what the target numbers were and why. And yet — despite thirty-one years of teaching human biology, despite understanding more about cellular physiology than most patients will ever know — there was a fundamental question I had never asked. When blood sugar rises after a meal, where is it supposed to go? I assumed the answer was something about the pancreas. About insulin shuttling it somewhere. About the liver. I was wrong. And the real answer changed everything. Here is the question your doctor has probably never asked you: When glucose leaves your bloodstream after a meal, where does it go? Most people assume the liver. Or that it gets "processed" somehow. Or that insulin just makes it disappear. The actual answer — from the landmark research of Ralph DeFronzo and colleagues, established definitively in 1981 and confirmed repeatedly since — is this: Approximately 80% of the glucose that leaves your bloodstream goes into your skeletal muscles. Your muscles. Not your liver. Not your pancreas. Not some metabolic processing centre. Your leg muscles. Your calf muscles. Your thigh muscles. The muscles you use when you walk, stand, and move. Your muscles are the single largest glucose-disposal system in your body, by an enormous margin. Eighty percent. The liver handles less than 10%. Adipose tissue handles less than 5%. Everything else combined is a rounding error. This is not obscure science. This is foundational physiology, documented for over forty years, taught in every endocrinology programme in the world. And it is almost never mentioned to patients. Now ask yourself the next question. What happens to blood sugar control when those muscles are not doing their job? I had Type 2 diabetes for six years. I knew about insulin resistance. I knew my cells weren't responding properly to insulin. I knew glucose was staying in my blood. What I did not know — what nobody had ever framed for me — was that the primary glucose disposal system in my body is not a hormonal one. It is a muscular one. And my muscles had been sitting idle for most of the day for years. I taught in a classroom. Then I retired and sat in an armchair. I walked the dog twice a day — twenty minutes each time. On a good week I did a bit of gardening. My muscles were absorbing approximately nothing. No wonder eighty percent of the glucose system wasn't working. I found this in a research paper — not from my consultant, not from my GP, not from the NHS Diabetes Prevention Programme I completed in 2020 — but from my own reading on a Tuesday afternoon when I was trying to understand why my HbA1c was still 68 after six years of doing everything correctly. And once I understood the 80%, everything else fell into place. Here is the complete picture that nobody had given me. Your skeletal muscles are designed to absorb glucose through two separate pathways. The first is insulin-dependent — insulin acts as a signal that opens transporter proteins called GLUT4 on the muscle cell surface. In Type 2 diabetes, this pathway is impaired. The GLUT4 transporters don't get the signal properly. They stay locked inside the cell. The 80% system fails. The second is contraction-dependent — when a muscle fibre contracts, it activates an entirely separate molecular pathway through a protein called AMPK, which moves GLUT4 to the cell surface without any insulin involvement. The muscle simply needs to work. Here is the thing that should have been told to me at diagnosis: The contraction pathway is completely intact in Type 2 diabetes. Insulin resistance does not affect it. The broken signalling cascade that makes your insulin-dependent pathway fail has no influence whatsoever on the contraction pathway. The second door, as I now think of it, works perfectly regardless of how resistant your cells have become to insulin. Which means: your 80% glucose disposal system is not broken. It is just switched off. Because your muscles are not contracting enough to activate it. The solution is not a new drug. It is not a stricter diet. It is not more willpower. It is getting your muscles to contract. For thirty-one years I told students that understanding the mechanism is the key to solving the problem. Diagnose the actual failure point, then address it specifically. For six years I had been managing my diabetes without understanding the actual failure point. My actual failure point: my 80% glucose disposal system was barely functioning because my muscles were barely contracting. The obvious answer: contract them more. The practical problem: I am 63 years old, with a back that had its opinions from decades of standing at whiteboards, two arthritic knees that my physiotherapist describes charitably as "not ideal," and a level of fatigue from six years of suboptimal blood sugar that makes sustained exercise feel less like a challenge and more like a punishment. And here — as the research paper explained with rather cruel precision — was the mechanism of that fatigue: When your muscles aren't absorbing glucose, your cells are starving for energy despite your blood being full of sugar. The exhaustion isn't imagined. It is a direct consequence of the 80% system failing. You feel depleted because your cells are not being fed. And because you feel depleted, you move less. And because you move less, your muscles contract less. And because your muscles contract less, the 80% system activates less. A circle I had been inside for six years without understanding its shape. I needed a way to activate the 80% system that didn't require me to run a physics classroom on two arthritic knees. The same paper introduced me to NMES. Neuromuscular Electrical Stimulation. Fifty years of clinical use. Hospital rehabilitation, stroke recovery, athletic training. The technology sends electrical pulses to motor nerves, causing muscles to contract — involuntarily, repeatedly, forcefully. Real contractions. Not a sensation. Not a massage. Actual muscle fibres firing, AMPK activating, GLUT4 transporters moving to the cell surface. The 80% system activating from a chair. A 2023 meta-analysis of nine controlled trials confirmed that NMES significantly reduced fasting blood glucose in Type 2 diabetes patients. Other research showed that electrical stimulation preferentially recruits the type II muscle fibres — the most glucose-hungry fibres, the ones that burn through blood sugar fastest — that normal walking typically doesn't reach. I found FootPulse — a foot-based NMES device — through the research trail. The feet connect through nerve pathways to the calf muscles, one of the largest and most metabolically active muscle groups in the lower body. Fifteen minutes. Sitting down. £70. I had a science teacher's scepticism. I also had a science teacher's respect for mechanism. The mechanism was sound. I ordered it. I am a data person. I tracked everything. Before first use: fasting glucose 9.6 mmol/L. Thirty minutes after first 15-minute session: 8.2 mmol/L. A 1.4-point reduction. I wrote it down and told myself not to draw conclusions from a single data point. Evening two. Before: 9.1. After: 7.8. Another 1.3-point reduction. By the end of week one I had a pattern — not a single fluke measurement but a consistent directional shift in fasting readings. 9.1. 8.7. 8.4. 8.1. Numbers I had not seen without medication adjustment in two years. Week two brought something I had not anticipated. The fatigue — the specific, particular, bone-level exhaustion of six years of insufficient cellular energy — was measurably different. I was reaching the end of the afternoon and still being able to think. I marked papers after dinner for the first time in years. I went to bed when I chose to, not when my body overruled me. This makes mechanistic sense, which I found satisfying. When the 80% system is working — when glucose is being properly absorbed throughout the day — the energy starvation that drives the fatigue eases. Cells are being fed. The afternoon shutdown becomes less severe. Week three, I slept through the night on four consecutive days. The 3am waking — which I had assumed was simply a feature of being 63 — largely stopped. Blood glucose instability causes nocturnal cortisol release. Cortisol is an arousal hormone. Stable blood sugar, stable sleep. I had been treating the symptom for years without knowing the cause. Week seven, I weighed myself on a Monday morning. Down six pounds. Without changing my diet. Without medication adjustment. Because insulin levels were lower — a consequence of the 80% system doing its job, of blood sugar dropping, of the pancreas no longer needing to overproduce — and because chronically elevated insulin is the primary mechanism of fat-storage lock in this condition. Lower insulin means the lock releases. Six months later. HbA1c: down from 68 to 51. Seventeen points. The largest single reduction in six years. My consultant asked what had changed. I explained the 80% figure, the contraction pathway, the GLUT4 dual-pool mechanism. She listened properly — the kind of listening that doesn't happen in ten- minute NHS appointments. "The science is sound," she said. "I think we underestimate how much the muscle disposal system matters compared to the insulin pathway." She asked me to send her the papers. I sent her four. Fasting glucose: averaging 6.7–7.2. Down from 9+. Energy: I finished writing a book chapter last month — something I had been putting off for two years because I couldn't sustain focus. Finished in three weeks. Weight: down eleven pounds. Feet: warmer. The persistent cold that I had accepted as neuropathy is less marked. The calf pump activation from regular FootPulse sessions improves circulation to the extremities. I notice it. I shared what I had found with the online communities where people managing Type 2 gather to share what their appointments don't tell them. A 57-year-old woman who had been cycling through diet programmes for four years: "Eight weeks in. First time my fasting readings have been consistently under 8. I now understand why the diets weren't working — I was addressing the wrong system." A 66-year-old man with peripheral neuropathy who couldn't walk comfortably: "The feet first. Then the glucose numbers. Then the energy. In that order, over about six weeks. The tingling at night is less. The numbers are better. I hadn't expected both." A 52-year-old who had just increased her Metformin dose again and was desperately looking for something additional: "My GP is looking at reducing the dose at my next review. I wasn't expecting that conversation for at least another year." Here is what I want you to take from everything I have written. Your muscles are supposed to handle 80% of your blood sugar. That is not a statistic I invented. It is forty years of established physiology. If your muscles are not absorbing glucose properly — because they're not contracting, because they're sitting idle for most of the day, because the contraction pathway that bypasses insulin has barely been activated — then 80% of your glucose disposal system is failing. No diet addresses this directly. No medication currently on the market targets skeletal muscle glucose uptake through the contraction pathway. The NHS Diabetes Prevention Programme doesn't explain it. Most GP appointments don't mention it. It is the biggest gap in diabetes self-management and the most overlooked opportunity for people who are doing everything else right and still not getting the results they deserve. FootPulse costs £70. Ninety-day money-back guarantee. Track your fasting glucose readings. Give the 80% system a chance to work. If it doesn't — return it. You have lost nothing but fifteen minutes a day and a piece of information you now have regardless. If it does — and six years of not knowing followed by six months of finally understanding tells me the mechanism is real — you will know, perhaps for the first time, what it feels like when the system that is supposed to handle most of your blood sugar is actually doing its job. Eighty percent. All this time, it was the muscles.

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