Organic compounds composed of carbon, hydrogen, and oxygen (general formula Cn(H2O)n) that serve as primary energy substrates and structural components. Carbohydrates include monosaccharides (glucose, fructose), disaccharides (lactose, sucrose), and polysaccharides (starch, glycogen, cellulose), with vastly different metabolic and health effects depending on type and context.
Carbohydrate digestion begins with salivary amylase (breaks starch to maltose), continues with pancreatic amylase in small intestine, and completes with brush border enzymes (sucrase, lactase, maltase) cleaving disaccharides to monosaccharides (glucose, fructose, galactose). Glucose is absorbed via SGLT1 (active, sodium-coupled) and GLUT2 (passive) in enterocytes. In circulation, glucose triggers insulin release, driving GLUT4-mediated uptake in muscle and adipose. Glucose is stored as glycogen (muscle, liver) or converted to fat via de novo lipogenesis when glycogen stores are full. Fructose bypasses insulin-regulated steps, going directly to liver for metabolism—excessive fructose drives hepatic lipogenesis, uric acid production, and metabolic dysfunction. Different carbohydrate types create different fermentation products in colon: sweet smell indicates carbohydrate fermentation; toxic compounds (cadaverine, putrescine) indicate protein fermentation.
Carbohydrate quality and timing are critical in cPNI. Refined/processed carbohydrates drive insulin resistance, inflammation, and metabolic syndrome through: (1) Chronic hyperinsulinemia from constant SGLT1 activation, (2) AGE formation, (3) Postprandial inflammation, (4) Dysbiosis from rapid fermentation. Context matters: Type II muscle fiber injury creates TNF-alpha signaling demanding carbohydrates for glycolytic repair—post-injury carbohydrate restriction impairs healing. Conversely, chronic high-carbohydrate intake without glycogen depletion (exercise) drives fat storage and metabolic dysfunction. Timing principle: carbohydrates should match energetic demand (post-exercise, injury repair) rather than being consumed constantly.
- Include monosaccharides (glucose, fructose), disaccharides (lactose, sucrose), polysaccharides (starch, glycogen)
- Digested by amylase (salivary, pancreatic) and brush border enzymes (lactase, sucrase, maltase)
- Glucose absorbed via SGLT1 (active) and GLUT2 (passive) in small intestine
- Fructose bypasses insulin regulation, metabolized directly in liver
- Excessive fructose drives hepatic lipogenesis, uric acid, metabolic syndrome
- Carbohydrate fermentation in colon produces sweet-smelling gases
- Type II muscle fibers produce TNF-alpha demanding carbohydrates post-injury
- Constant carbohydrate intake (>21 meals/week) prevents metabolic switching
- Refined carbohydrates drive AGE formation, inflammation, insulin resistance
- Context matters: post-exercise and post-injury carbohydrates support recovery
- glucose — primary monosaccharide from carbohydrate digestion
- fructose — monosaccharide that bypasses insulin regulation
- insulin — hormone released in response to blood glucose elevation
- SGLT transporters — actively transport glucose from intestinal lumen
- GLUT4 — insulin-dependent glucose transporter in muscle and adipose
- glycogen — storage form of glucose in muscle and liver
- de novo lipogenesis — conversion of excess carbohydrate to fat
- brush border enzymes — complete final digestion of carbohydrates to monosaccharides
- pancreatic enzymes — amylase breaks down starches in small intestine
- Type II fibers — glycolytic muscle fibers that preferentially use carbohydrates
- TNF-α — produced by Type II fibers post-injury, signaling carbohydrate demand
- insulin resistance — develops from chronic high carbohydrate intake and hyperinsulinemia
- metabolic syndrome — driven by excessive refined carbohydrate consumption
- AGEs — advanced glycation end-products formed from glucose-protein reactions
- fermentation — undigested carbohydrates undergo bacterial fermentation in colon
- FODMAP — fermentable carbohydrates that cause GI symptoms when malabsorbed
- short-chain fatty acids — produced from bacterial fermentation of resistant starch
- metabolic flexibility — ability to switch between carbohydrate and fat oxidation
- postprandial hyperglycemia — blood glucose spike after high-carbohydrate meals
- time-restricted eating — limits carbohydrate-driven insulin signaling to feeding window
- Module 2
- Module 5
- Module 6