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Gut hormones released in response to food that coordinate the stomach, pancreas, liver, appetite and glucose control. The main incretins are GLP-1 and GIP; their effects depend on meal composition, insulin sensitivity and medications.

A vitamin-like compound involved in cell signaling, insulin sensitivity, ovarian function, nervous-system activity and fat metabolism. Myo-inositol and D-chiro-inositol are discussed most often, especially in PCOS and insulin resistance.

A pancreatic hormone that regulates glucose, energy storage and use, protein synthesis, lipolysis and liver metabolism. It is not an enemy by itself; problems arise with deficiency, excess, insulin resistance or inappropriate therapy.

A state in which tissues respond poorly to insulin forces the pancreas to produce more hormone to control glucose. It is linked with visceral fat, fatty liver, blood pressure, triglycerides, sleep, stress and muscle mass.

A state in which muscle, liver, and fat tissue respond poorly to insulin, forcing the pancreas to secrete more of it. It can hide behind normal fasting glucose for years, so waist size, triglycerides, HDL, fasting insulin, HOMA-IR, and post-meal responses matter.

The insulin response to a specific meal depends not only on carbohydrates, but also on protein, fat content, digestion speed, time of day, sleep, stress and metabolic health. In LCHF, the goal is not zero insulin, but a predictable and appropriate post-meal response.

Insulin sensitivity describes how effectively muscles, liver, and adipose tissue respond to insulin. It improves through lower visceral fat, strength training, sleep, adequate protein, carbohydrate control, inflammation management, and medication-aware monitoring, not through one supplement.

A routine that places meals within a limited eating window may improve appetite control, glucose stability and total energy intake, but it is not a mandatory part of LCHF. Safety depends on medications, sleep, protein, electrolytes, stress and eating behavior history.

An eating pattern with a limited eating window may reduce snacking, support appetite control, and improve metabolic flexibility. It should not be confused with chronic under-eating: safety depends on medication, pregnancy, diabetes, body weight, stress, sleep, and food quality.

The gut microbiota participates in fiber fermentation, short-chain fatty acid production, bile acid metabolism, immune regulation and food tolerance. On keto and LCHF, the practical issue is not a mythical balance of “good” and “bad” bacteria, but tolerated food diversity, stool quality, absence of inflammatory symptoms and gradual change.

The everyday term gut flora describes microorganisms living in the intestinal lumen and on the mucosa, influencing fermentation, stool, bile acids, immune reactions and food tolerance. In low-carbohydrate eating, the practical goal is not perfect bacteria, but regular stool, absence of pain, tolerated fiber and gradual diet adjustment.

This part of the digestive system does far more than digest food: it regulates absorption, barrier defense, motility, bile acids, immune signaling and interaction with the microbiome. On low-carbohydrate diets, the practical focus is stool quality, fat tolerance, fiber, electrolytes and warning signs of inflammation rather than vague “cleansing.”

Plant polyphenols from soy, clover and some legumes can interact with estrogen receptors, but their effects depend on dose, microbiota, hormonal status and product form. Whole-food sources and concentrated supplements need different interpretation.