Diabetes

Diabetes mellitus is a metabolic disease characterized by chronic high blood sugar due to problems with insulin production, insulin action, or both.

Type 1 diabetes - autoimmune β-cell destruction: In Type 1 diabetes, the immune system attacks and destroys the insulin-producing β-cells in the pancreas. Cytokines such as IL-1β, IFN-γ, and TNF-α activate immune cells that target β-cells and trigger apoptosis. IL-17-driven inflammation and reduced IL-10 (anti-inflammatory) support a chronic autoimmune loop, gradually erasing β-cell mass and leading to absolute insulin deficiency. Environmental triggers—viral infections, leaky gut, and chronic systemic inflammation—can increase intestinal permeability, expose immune cells to dietary/microbial antigens, and contribute to this autoimmune attack.

Type 2 diabetes - insulin resistance and β-cell exhaustion: In Type 2 diabetes, chronic high-carbohydrate intake and repeated insulin spikes lead to insulin resistance—cells stop responding properly to insulin. The pancreas compensates by producing even more insulin (hyperinsulinemia), which drives fat storage, liver fat accumulation, and further inflammation. Over time, β-cells become stressed, dysfunctional, and can partially fail, causing fasting glucose and HbA1c to rise. Systemic inflammation (IL-6, TNF-α), leaky gut, and endotoxins (LPS) worsen insulin resistance and damage insulin signaling pathways. The result is a vicious cycle of high glucose, high insulin, inflammation, and progressive β-cell burnout.

Carbohydrates, leaky gut, and inflammation: High carbohydrate loads and ultra-processed foods repeatedly spike blood sugar and insulin, promoting oxidative stress and endothelial damage. This disrupts the gut barrier (leaky gut), allowing bacterial products into the bloodstream that fuel systemic inflammation, which impairs insulin signaling and, in Type 1, can amplify autoimmune activity against β-cells. In both types, chronic inflammation accelerates complications such as neuropathy, nephropathy, retinopathy, and cardiovascular disease.

Type 1 β-cell regeneration and fasting-mimicking diet (FMD): Experimental studies in mice have shown that cycles of a fasting-mimicking diet (low-calorie, low-protein, low-carbohydrate, high-fat, keto-like) can temporarily shut down normal insulin/IGF-1 signaling and trigger a regenerative program in the pancreas. These FMD cycles reactivate dormant Ngn3+ pancreatic progenitor cells, which can differentiate into new insulin-producing β-cells. In diabetic mouse models, FMD restored insulin production and improved glucose control. Early human pilot studies in people with diabetes report increased C-peptide (a marker of residual insulin production) and improved glucose regulation after repeated FMD cycles, suggesting partial β-cell functional recovery. However, this regenerative process can only succeed under carnivore/keto metabolic conditions; as soon as carbohydrates are reintroduced and inflammation rises, the newly formed β-cells become vulnerable and are attacked and destroyed again. The body is biologically adapted to expect fat and protein—not carbohydrates—so chronic carbohydrate intake rapidly reactivates the autoimmune destruction. This is still experimental and not a guaranteed cure, but it shows that β-cells are not always permanently lost and may be partially regenerated under the right metabolic conditions.

Fasting, ketogenic, and carnivore diets - metabolic treatment: Fasting, ketogenic diets, and carnivore diets directly target the core mechanisms driving both Type 1 and Type 2 diabetes:

• Lower glucose and insulin: Reducing carbohydrates sharply lowers blood sugar and insulin demand, improving insulin sensitivity and relieving β-cell stress.
• Reduced inflammation and leaky gut: Ketosis lowers inflammatory cytokines, improves gut integrity, and decreases endotoxin load, which can calm autoimmune activity and improve insulin signaling.
• Fat-based metabolism: Ketones provide a stable, clean fuel that bypasses defective glucose metabolism, stabilizes energy levels, and reduces oxidative stress.
• Autophagy and cellular repair: Fasting and deep ketosis activate autophagy, clearing damaged cellular components, improving mitochondrial function, and potentially supporting β-cell health and regeneration.

In Type 2 diabetes, these interventions can significantly improve or even normalize blood sugar, often allowing reduction or discontinuation of medications under medical supervision. In Type 1 diabetes, they do not replace the need for insulin, but they can reduce inflammation, lower insulin requirements, stabilize blood sugar, and, together with approaches like FMD, may support partial β-cell regeneration and better overall metabolic control.