The Insanity Loop: Why We Keep Treating Type 2 Diabetes Backwards
- Healing_ Passion
- 6 days ago
- 5 min read
In September 2025, Diabetologia published a comprehensive review titled “Pharmacological therapies for type 2 diabetes: future approaches” by Clifford J. Bailey of Aston University.
It is, on the surface, an impressive piece — a meticulous summary of every drug class, every molecule, and every new combination that promises better glycaemic control for type 2 diabetes (T2D).
Yet buried in its introduction lies a quiet confession:
“Despite at least nine differently acting classes of glucose-lowering agents, many people with type 2 diabetes do not achieve or maintain sufficiently tight glycaemic control.”
This is the sentence that should have changed the direction of the entire paper — but it didn’t.
The Paradox of Progress
Bailey’s review catalogues a dazzling array of next-generation drugs — incretin co-agonists, amylin analogues, glucagon receptor modulators, mitochondrial activators, and even miRNA therapeutics. Each aims to patch a piece of the broken glucose regulation puzzle: enhance insulin secretion, suppress glucagon, slow gastric emptying, increase satiety, or stimulate β-cell preservation. The list is long, the chemistry elegant — and yet, the outcomes remain depressingly familiar.
We’ve been here before.
Every decade brings a new “breakthrough” molecule. Sulfonylureas, metformin, thiazolidinediones, DPP-4 inhibitors, GLP-1 analogues, SGLT2 inhibitors — all arrived with the same hope. And yet, the review admits what clinical reality has shown for decades:
“Normal glucose homeostasis is seldom reinstated.”
Despite the pharmacological fireworks, the natural history of type 2 diabetes remains unchanged — gradual progression, medication layering, and eventual insulin dependence. It’s like repainting a burning house while refusing to turn off the gas leak.
Insanity, Defined
Einstein’s famous remark — “Insanity is doing the same thing over and over and expecting different results” — feels painfully apt here.
Modern medicine continues to pour billions into downstream drug discovery while ignoring the upstream metabolic chaos that caused the disease. We treat the endpoints of dysfunction — hyperglycaemia, insulin resistance, fatty liver — as if they were the disease itself.
The irony is that our most celebrated drugs are synthetic imitations of what the body already does under natural regulatory states:
GLP-1 agonists mimic the appetite-suppressing and insulin-modulating effects of fasting.
FGF21 analogues copy the hepatic stress response to nutrient scarcity.
GDF15 elevation — seen as a “drug target” — actually rises naturally during caloric restriction and mitochondrial hormesis.
Mazdutide, retatrutide, and other multi-agonists blend glucagon, GIP, and GLP-1 signalling — the same adaptive balance that a low-insulin, high-ketone metabolic state achieves without injections.
We are literally engineering fasting in a syringe — and selling it as innovation.
What the Evidence Already Shows
If pharmacology keeps failing to “normalize” glucose metabolism, it’s not because the body can’t recover — it’s because we keep intervening at the wrong level. Over the past decade, clinical studies have repeatedly demonstrated that T2D remission is not only possible but reproducible.
1. Calorie Restriction and Energy Deficit
Roy Taylor’s Counterpoint and Counterbalance trials (Diabetologia, 2011; Cell Metabolism, 2018) showed that just 8 weeks of 800 kcal/day diet normalized fasting glucose and insulin secretion in most participants. Liver and pancreatic fat decreased dramatically; β-cell function returned. No drugs required.
2. Carbohydrate Restriction and Ketogenic Therapy
Hallberg et al. (Diabetes Therapy, 2018) reported 60% diabetes remission at 2 years under supervised ketogenic diets, with sustained HbA1c reduction (≈1.3%) and elimination of insulin or oral agents in nearly all participants.
3. Intermittent Fasting and Time-Restricted Feeding
Sutton et al. (Cell Metabolism, 2018) demonstrated that early time-restricted feeding improved insulin sensitivity and β-cell responsiveness — independent of weight loss.
4. Bariatric Surgery and Metabolic Reset
Mingrone et al., (NEJM, 2021) found that over 40% of surgical patients maintained remission at 10 years. The mechanism wasn’t mechanical — it was biochemical: incretin reset, gut-liver communication, metabolic re-entrainment.
5. Stress Regulation and Circadian Repair
Growing evidence shows that chronic psychological and circadian stress sustain hyperglycaemia through cortisol, adrenaline, and sleep disruption — yet stress and sleep remain the blind spots of diabetes care.
The Uncomfortable Truth
If these data are clear, why does mainstream medicine still behave as though type 2 diabetes is incurable?
Because the system profits more from management than resolution.
Lifestyle interventions are difficult to patent.
No one can trademark fasting, sunlight, muscle, or peace of mind.
Pharmaceutical innovation is celebrated because it can be monetized, scaled, and prescribed — not necessarily because it heals.
Yet, even Bailey’s review unwittingly confirms this irony: every next-generation incretin agonist is a pharmaceutical simulation of natural metabolic recovery. We are not inventing new biology — we are trying to outsource what the human body has always been capable of doing when given the right conditions.
The Upstream Approach
Real progress lies not in new drugs, but in restoring bioenergetic adaptability — the body’s ability to balance energy availability, allocation, and recovery. This is the essence of the upstream model:
These strategies don’t manage diabetes — they retrain metabolism. They don’t suppress symptoms; they restore the body’s rhythm of fasting, feeding, repair, and resilience.
The Way Forward
The 2025 review concludes, almost hopefully, that “new technologies including miRNAs, epigenetic modulators and AI compound design are in their infancy.”But perhaps the real frontier is not in silicon or synthesis — it’s in humility.
Type 2 diabetes is not a drug deficiency. It’s a metabolic communication breakdown — between energy intake and energy use, between stress and recovery, between abundance and repair.
As clinicians and scientists, we must stop calling symptom management a “cure.”We need to stop celebrating synthetic fasting while discouraging real fasting. And we must stop the collective insanity of walking the same path, expecting a different destination.
A Saner Medicine
A saner medicine would recognize that metabolic health cannot be outsourced to chemistry. It would prioritize early detection of bioenergetic imbalance, guide patients toward food-based and behavioral recovery, and use drugs only as bridges, not lifelong crutches.
The tools for remission already exist — they’re called time, rest, rhythm, and restraint. The tragedy is not that medicine doesn’t know how to reverse type 2 diabetes.
It’s that, despite all the evidence, it keeps pretending it can’t.
Bailey, C. J. (2025). Pharmacological therapies for type 2 diabetes: Future approaches. Diabetologia. https://doi.org/10.1007/s00125-025-06581-6
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