From Gut Hormones to Global Headlines: The Complex Reality of Ozempic
- Najma Hussein
- Jul 31
- 5 min read
It All Started With a Gut Feeling
Long before Ozempic became a hot topic, scientists were already chasing a curious idea: that the gut was more than just a digestive organ; it was hormonal.
In 1902, British physiologists William Bayliss and Ernest Starling discovered secretin, the first hormone ever identified, proving that the gut could send chemical signals to other organs without nerve input. Just three years later, Starling coined the term “hormone” itself
By the 1970s, researchers had isolated a new class of hormones called incretins; gut-derived signals that boosted insulin release after eating. One of these was GLP-1, short for glucagon-like peptide-1. But there was a problem: native GLP-1 was destroyed within minutes in the body.
That led to a decades-long search to make a synthetic version, a molecule that could mimic GLP-1’s powerful effects but stick around long enough to be useful. The result was semaglutide, a lab-designed GLP-1 receptor agonist made resistant to degradation and long-acting enough for once-weekly injections.
In 2017, semaglutide was approved for type 2 diabetes. In 2021, it became a weight-loss drug under the name Wegovy. And today, it’s rewriting the script on how we treat and talk about obesity, metabolism, and more.
Is This Really Just a Weight-Loss Drug?
Ozempic, the brand name for semaglutide, exploded into public consciousness seemingly overnight. Touted as a miracle for weight loss and hailed for its promise in diabetes and heart health, it’s now the subject of global fascination, celebrity endorsements, and even black-market demand.
But what does this drug actually do inside the body? And what does its rapid rise say about society’s evolving relationship with health, weight, and medicine?
Let’s break down the biology.
It Starts in the Brain: How Semaglutide Rewires Hunger and Reward
Semaglutide works by mimicking GLP-1, a hormone that helps regulate blood sugar and appetite. It binds to receptors in key brain regions that control food intake, like the hypothalamus and the brainstem and flips the biological switches that tell us we're full.
Here's how it pulls that off:
In the arcuate nucleus of the hypothalamus, semaglutide boosts POMC/CART neurones (which suppress appetite) and blocks NPY/AgRP neurons (which drive hunger), tipping the brain toward satiety.
It reduces cravings by dampening dopamine release in the ventral tegmental area (VTA) and nucleus accumbens; meaning high-calorie foods lose their appeal.
It even enhances vagal signaling from the gut to the brain, amplifying fullness signals during meals.
The result? People eat less and not because they’re forcing themselves to, but because they genuinely don’t feel like it.
This isn’t just behaviour modification but rather a full-body recalibration.
More Than Just Weight Loss?
Semaglutide’s reach goes far beyond appetite suppression. It orchestrates metabolic improvements across multiple organs:
In the pancreas, it boosts glucose-dependent insulin release and protects insulin-producing β-cells.
In the liver, it reduces gluconeogenesis by downregulating PEPCK and G6Pase ; enzymes responsible for sugar production.
In adipose tissue, it promotes the browning of white fat, increasing thermogenesis and energy expenditure.
It enhances heart health by reducing inflammation, lowering blood pressure, and improving endothelial function.
The SELECT and SUSTAIN clinical trials have already shown reductions in heart attacks, strokes, and kidney complications; even in non-diabetics.
And yet, for all its life-saving potential, it’s not semaglutide’s biology that’s capturing the world’s attention...
Ozempic Goes Viral: When a Lifesaving Drug Becomes a Lifestyle Trend
Once confined to endocrinology clinics, semaglutide is now a household name. TikTok testimonials, influencer shoutouts, and celebrity before-and-after photos have transformed it into a cultural symbol; one that’s both celebrated and controversial.
Its social ascent however comes with consequences:
Off-label demand has skyrocketed, creating shortages for diabetics who depend on it for blood sugar control.
Illicit sales and counterfeit versions have emerged, putting consumers at risk.
It’s been co-opted by some fitness communities and biohackers, sometimes stacked with stimulants to accelerate weight loss.
And beneath the glamour lies a more complicated truth: some users are reporting side effects like nausea, muscle loss, or the now-infamous "Ozempic Face"; a term for facial gauntness linked to rapid weight loss.
The Ethics of Access: Who Gets to Have Ozempic?
As the drug becomes more popular, so do the ethical questions surrounding it:
Should someone struggling with obesity but not diabetes have equal access?
Is it right that wealthier individuals can pay out-of-pocket for weight loss while low-income diabetics go without.
If semaglutide is life-changing, should insurance providers cover it, and if so, for whom?
Health systems like the NHS are already facing difficult decisions about who should be prioritised; diabetics, heart patients, or those seeking weight management.
Meanwhile, U.S. lawmakers are investigating the high cost of GLP-1 drugs, suggesting pricing reforms may be on the horizon.
Why We Need to Talk About Dependency?
Semaglutide isn’t a cure. Its effects vanish when the drug stops; with studies showing up to 67% of weight regained within a year.
This has led some doctors to warn off a growing pattern: “Ozempic withdrawal,” a cluster of symptoms including intense hunger, anxiety, and rapid rebound weight gain.
For some, semaglutide may become a lifelong medication. That raises questions not just about cost and access but about how we understand chronic diseases like obesity.
Final words: Where Does This Leave Us?
Semaglutide is more than a trend. It’s the product of decades of scientific work, a tool with the power to reshape not just individual metabolisms, but public health itself.
But it’s also a mirror; reflecting society’s struggles with beauty, body image, inequality, and medical ethics.
We’ve learned how this drug works. Now, the harder question is what kind of world we want to build around it.
One where weight loss is a status symbol?
Or one where metabolic health is treated as a universal right?
The answer, like semaglutide itself, won’t come in a single dose.
References:
Chiappini, S., Vickers-Smith, R., Harris, D., Papanti Pelletier, G. D., Corkery, J. M., Guirguis, A., Martinotti, G., Sensi, S. L., & Schifano, F. (2023). Is There a Risk for Semaglutide Misuse? Focus on the Food and Drug Administration’s FDA Adverse Events Reporting System (FAERS) Pharmacovigilance Dataset. Pharmaceuticals, 16(7), 994. https://doi.org/10.3390/ph16070994 (Accessed on: 03/07/2025)
Drucker, D. J., Habener, J. F., & Holst, J. J. (2017). Discovery, characterization, and clinical development of the glucagon-like peptides. Journal of Clinical Investigation, 127(12), 4217–4227. https://doi.org/10.1172/jci97233 (Accessed on: 03/07/2025)
Friedrichsen, M., Breitschaft, A., Tadayon, S., Wizert, A., & Skovgaard, D. (2021). The effect of semaglutide 2.4 mg once weekly on energy intake, appetite, control of eating, and gastric emptying in adults with obesity. Diabetes, Obesity and Metabolism, 23(3), 754–762. https://doi.org/10.1111/dom.14280 (Accessed on: 02/07/2025)
Kommu, S., Whitfield, P., & Affiliations. (2025). Semaglutide Continuing Education Activity FDA-Approved Indications. (Accessed on: 01/07/2025)
Pandey, A., Ye, Y., Wells, C. R., Singer, B. H., & Galvani, A. P. (2024). Estimating the lives that could be saved by expanded access to weight-loss drugs. Proceedings of the National Academy of Sciences, 121(43). https://doi.org/10.1073/pnas.2412872121 (Accessed on: 02/07/2025)
Papakonstantinou, I., Tsioufis, K., & Katsi, V. (2024). Spotlight on the Mechanism of Action of Semaglutide. Current Issues in Molecular Biology, 46(12), 14514–14541. https://doi.org/10.3390/cimb46120872 (Accessed on: 03/07/2025)
Price, K. (2024). “Beyond weight loss”: what is the future of semaglutide? pharmaceutical-journal.com/article/feature/beyond-weight-loss-what-is-the-future-of-semaglutide (Accessed on: 03/07/2025)
Tamayo-Trujillo, R., Ruiz-Pozo, V. A., Cadena-Ullauri, S., Guevara-Ramírez, P., Paz-Cruz, E., Zambrano-Villacres, R., Simancas-Racines, D., & Zambrano, A. K. (2024). Molecular mechanisms of semaglutide and liraglutide as a therapeutic option for obesity. Frontiers in Nutrition, 11. https://doi.org/10.3389/fnut.2024.1398059 (Accessed on: 02/07/2025)
Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., Wharton, S., Yokote, K., Zeuthen, N., & Kushner, R. F. (2021). Once-Weekly Semaglutide in Adults with Overweight or Obesity. New England Journal of Medicine, 384(11), 989–1002. https://doi.org/10.1056/nejmoa2032183 (Accessed on: 02/07/2025)
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