Type 2 Diabetes
Description
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 respond poorly to insulin. The pancreas compensates by producing excess insulin (hyperinsulinemia), driving fat storage, liver fat accumulation, and systemic inflammation. Over time, β-cells become stressed, dysfunctional, and partially fail, raising fasting glucose and HbA1c. Systemic inflammation (IL-6, TNF-α), leaky gut, and endotoxins (LPS) worsen insulin resistance and damage insulin-signaling pathways.
Carbohydrates, leaky gut, and inflammation: High carbohydrate loads repeatedly spike glucose and insulin, driving oxidative stress, endothelial injury, and increased gut permeability. Bacterial endotoxins enter the bloodstream and create systemic inflammation, which further impairs insulin signaling and exacerbates Type 2 diabetes progression. Chronic inflammation accelerates complications such as neuropathy, nephropathy, retinopathy, and cardiovascular disease.
Fasting, ketogenic, and carnivore diets in Type 2: These metabolically targeted interventions address the root mechanisms of Type 2 diabetes:
- Lower glucose and insulin: Reducing carbohydrates rapidly lowers blood sugar and improves insulin sensitivity.
- Reduce inflammation and repair gut barrier: Ketosis lowers IL-6, TNF-α, and endotoxin load.
- Improve fat metabolism: Ketones supply stable, clean fuel and reduce oxidative stress.
- Promote cellular repair through autophagy: Fasting enhances mitochondrial function and clears damaged cellular components.
In Type 2 diabetes, fasting and low-carbohydrate diets can significantly improve or normalize blood sugar, often reducing or eliminating medication needs under medical supervision. By lowering insulin levels and inflammation, these strategies also support long-term β-cell recovery and improved metabolic flexibility.