Anorexia Nervosa

Anorexia and generalized eating disorders involve severe metabolic and inflammatory dysfunction, not just psychological factors. High-carbohydrate intake and chronic insulin spikes drive systemic inflammation, neuroinflammation, and gut permeability. Many anorexia patients show leaky gut, elevated endotoxins, and inflammatory cytokines (IL-6, TNF-α) that disrupt appetite regulation in the brain. Neuroinflammation impairs the hypothalamus, creating anxiety, loss of hunger cues, and distorted satiety signals. Carbohydrate-driven insulin resistance further breaks the hormonal feedback loops involving ghrelin (hunger hormone) and leptin (satiety hormone), leading to incorrect hunger signals, food aversion, and dysfunctional appetite patterns.

The body also misinterprets carbohydrates as if they were protein due to a shared hepatic pathway: the liver processes excess protein through gluconeogenesis, and high carbohydrate intake activates the same metabolic signaling. As a result, the hypothalamus falsely interprets carbohydrate intake as large amounts of protein. For every gram of carbohydrate consumed, the brain reads it as if the body had eaten 8–10 grams of protein—the equivalent of 50–60 grams of meat. A typical high-carb meal containing 100 grams of carbohydrates is therefore misread as 80–100 grams of protein, equal to 500–600 grams of meat. This produces massively distorted satiety signals, tricking the brain into believing it has consumed nutrient-dense food when in reality almost no essential amino acids have been eaten.

In contrast, animal-based diets (protein + fat), which humans adapted to over millions of years, send correct satiety signals. Protein triggers accurate mTOR activation, supports neurotransmitter synthesis, and normalizes ghrelin and leptin. Fat stabilizes blood sugar, eliminates insulin spikes, reduces neuroinflammation, and repairs gut permeability. Ketosis (through fasting or carnivore/ketogenic diet) lowers inflammation, repairs the gut barrier, restores hypothalamic sensitivity, and re-establishes proper hunger and satiety cues. This metabolic state reverses the distorted signaling caused by carbohydrates and helps normalize appetite regulation in anorexia and eating disorders.