The Poke and the Plunge: Starting My GLP-1 Journey

Tracking my weight, metabolism, and what it means to finally ask for help

My father was a diabetic. Diagnosed the same year of my birth, 1957 — as though we arrived in the world together, he and his disease, just in time to greet me. And so for all seventeen years I lived under his roof, I watched him inject himself with insulin. Every morning. The ritual was so unremarkable in our household that I absorbed it the way children absorb everything essential: without comment, without drama, as simply the way things were. A father, a needle, a small ceremony of survival before breakfast.

It normalized something in me — a willingness, or at least an acceptance, that care sometimes requires puncture. That bodies sometimes need intervention from the outside in. I carried that normalized self-administered care into my long life after he passed. Vitamins, supplements, the occasional prescription. I've been a reasonably conscientious steward of this aging vehicle.

And yet. I had never injected myself with anything.

So this morning, holding a small syringe loaded with 0.2 milligrams of compounded semaglutide, I felt something I hadn't expected: genuine apprehension. The poke and plunge of a hypodermic needle — even a tiny subcutaneous one, a barely-there pinch into belly fat — felt like a threshold. Not a dramatic one. But a real one.

I am sixty nine years old. I come from a family that struggled with blood sugar, with weight, with the cascading health consequences that trail both. I have struggled with my own weight most of my adult life. And today I decided to try something that didn't exist when my father was alive — something that, had it existed, might have changed his life considerably.

I have decided for the next four months I would keep a journal about this effort to reduce weight using this “wonder” drug that is cementing itself into American culture.  I wish my daily thoughts remain honest enough.  You can follow the journal here,  Joe’s Grand Reduction Scheme - 2026.  And obviously if you want to share stories about you and your health/weight journey, I’m all ears.  TMI or not, I think we can use some frankness when it comes to aging and health.

Where This Drug Came From

The story of GLP-1 drugs is one of those science narratives that unfolds over decades, through unexpected doors, and ends up somewhere nobody originally intended to go.

GLP-1 stands for glucagon-like peptide-1. It's not a pharmaceutical invention — it's a hormone your body already makes, released from the lining of your small intestine when you eat. Its job, in the original biological version, is elegant: it tells the pancreas to produce insulin, tells the liver to ease up on dumping glucose into the bloodstream, slows how quickly food empties from the stomach, and — crucially — sends signals to the brain's appetite centers that say you're done, you've had enough. It is, in other words, a chemical coordinator of satiety.

The problem with your own GLP-1 is that it breaks down almost immediately — within minutes of being released. So researchers knew what it did but couldn't figure out how to make it last long enough to be therapeutically useful.

The unlikely breakthrough came from a Gila monster.

In the 1980s and early 90s, a scientist named John Eng was studying the venom of the Gila monster lizard and discovered a compound — exendin-4 — that closely mimicked human GLP-1 but was far more resistant to breakdown. It stuck around. By 2005, a synthetic version of that lizard peptide reached the market as exenatide (Byetta), the first GLP-1 receptor agonist approved for type 2 diabetes. It required twice-daily injections and was a modest step, but the door was open.

Danish pharmaceutical company Novo Nordisk then spent years engineering semaglutide — a molecule that binds to albumin in the blood, which dramatically extends its half-life. The result was a drug you only needed once a week. Ozempic, semaglutide at doses aimed at diabetes management, was approved in 2017. And then something happened in the clinical trials that nobody had exactly planned on: people were losing substantial amounts of weight. Not a few pounds. Meaningful, life-altering amounts.

Wegovy — the same semaglutide molecule at higher doses, explicitly indicated for chronic weight management — was approved in 2021, and the conversation shifted. This wasn't just a diabetes drug anymore. This was something that appeared to address the neurological architecture of hunger itself.

The Current Landscape

The GLP-1 family has now expanded into a small ecosystem of options, each with its own profile:

Semaglutide (Ozempic for diabetes, Wegovy for weight) remains the flagship. Weekly injection, now also available in an oral form (Rybelsus, though absorption is trickier). It's the molecule with the longest track record in weight management trials — showing average losses of 15% or more of body weight over 68 weeks in the major studies.

Tirzepatide (Mounjaro for diabetes, Zepbound for weight) is Eli Lilly's answer, approved in 2022 and 2023 respectively. It's a dual agonist — it activates both GLP-1 receptors and GIP receptors (another gut hormone), and the early data suggests it may be even more effective for weight loss, with some trials showing averages approaching 20-22% body weight reduction. It's the new heavy hitter and the one generating the most buzz in clinical circles right now.

And then there are the compounded versions — pharmacy-made formulations that became widely available during the Ozempic and Wegovy shortages of 2022-2024. These are not FDA-approved branded products; they're made to order by licensed compounding pharmacies, and they've been controversial (the FDA has tried to restrict them as the shortage eased) but they remain accessible and significantly more affordable for people without insurance coverage or the means to pay $1,000+ a month for the brand-name versions.

What I'm Actually Doing

I'm working with NOOM — specifically their GLP-1 program, which builds in a behavioral coaching component alongside the medication. And I find that pairing meaningful, because the drug is not magic. It changes the neurological context in which you make food choices. But it doesn't make the choices for you.

Their approach is a slow, microdose titration — beginning well below the standard starting doses. This week’s injection: 0.2 milligrams of compounded semaglutide. For reference, the standard Wegovy starting dose is 0.25 mg per week, so I'm beginning slightly below even that modest starting point. The theory of the slow build is straightforward: the GI side effects that drive many people off these drugs — nausea, vomiting, digestive disruption — are largely dose-dependent. Ease in slowly, and your body has time to adapt before the full therapeutic dose arrives.

My formulation includes something worth noting: Glycine. This is an amino acid — the simplest one, structurally — and in this context it functions primarily as a stabilizer and buffer in the compound solution. Glycine has its own modest biological story (it plays roles in collagen synthesis, sleep regulation, and may have mild anti-inflammatory properties), but in a compounded semaglutide formulation, it's largely there to maintain the stability of the active molecule and ease the injection experience. It's not the headliner. But I find it interesting that even the supporting cast in these compounds has its own history and biology.

Why I'm Writing About This

I turned sixty nine this year. I've been watching the conversation around GLP-1 drugs with a mixture of cautious interest and the particular skepticism that comes from having watched too many diet revolutions promise everything and deliver less. The grapefruit diet. Low-fat. Atkins. Keto. The long parade of systems and programs and philosophies, each with its true believers and its disappointing attrition rate.

But this one feels different — not because the marketing says so, but because the mechanism is different. We're not talking about restricting what you eat through willpower or clever point-counting. We're talking about intervening in the hormonal conversation your gut has with your brain about hunger. That's a different conversation entirely.

I am also aware that I am writing about this as an older adult, for an audience of older adults and their companions. And the research on GLP-1 drugs in people over sixty-five is still thinner than I'd like. What works in a 45-year-old may work differently in a body that has been navigating metabolism, muscle loss, and insulin sensitivity for seven decades. I want to document what I actually experience — not what the trials suggest I should experience.

My father managed his diabetes with insulin for decades, and he did it with quiet matter-of-factness. I don't know if that pragmatism was passed to me genetically or environmentally, but I felt something of it this morning as I pinched a fold of belly, pressed the small needle in, and pushed the plunger.

It barely hurt at all.

Whether it helps — that story is still ahead of us.