Principles of Dietetics · 14 min read
Macronutrients, Digestion and Metabolism
This chapter covers the biochemistry behind every later clinical decision: how carbohydrates, proteins and lipids are classified and judged for quality, where each nutrient is digested and absorbed, how hormones coordinate the process, which pathways run in the fed and fasting states, and how energy expenditure is measured. Expect questions that ask you to predict the nutritional consequence of a resected or diseased GI segment, interpret a respiratory quotient, or identify the limiting amino acid in a food.
Carbohydrates
Carbohydrates provide 4 kcal/g and are the preferred fuel for the brain, red blood cells and exercising muscle. The RDA of 130 g/day (adults) is based on the average minimum glucose use of the brain; the AMDR is 45–65% of energy. Glycogen stores are limited: roughly 100 g in the liver (maintains blood glucose) and 400 g in skeletal muscle (used only by that muscle, because muscle lacks glucose-6-phosphatase).
| Class | Examples | Composition / Notes |
|---|---|---|
| Monosaccharides | Glucose, fructose, galactose | Glucose is the circulating sugar; fructose is metabolized mainly in the liver and bypasses the phosphofructokinase control step; galactose comes from lactose |
| Disaccharides | Sucrose, lactose, maltose | Sucrose = glucose + fructose; lactose = glucose + galactose (β-1,4 bond); maltose = glucose + glucose |
| Oligosaccharides | Raffinose, stachyose, fructooligosaccharides (FOS), galactooligosaccharides (GOS) | 3–10 sugar units; not digested by human enzymes; fermented in the colon (gas, prebiotic effect) |
| Polysaccharides – starch | Amylose (linear α-1,4), amylopectin (branched α-1,6) | Plant storage glucose in grains, legumes, tubers; resistant starch escapes small-bowel digestion |
| Polysaccharides – glycogen | Liver and muscle glycogen | Highly branched animal storage form; negligible in the diet |
| Dietary fiber | Cellulose, hemicellulose, pectin, gums, β-glucans, lignin (non-carbohydrate) | Nondigestible; AI 14 g per 1,000 kcal (≈25 g women, 38 g men aged 19–50) |
| Feature | Soluble / Viscous Fiber | Insoluble Fiber |
|---|---|---|
| Examples | Pectin, gums, psyllium, β-glucan (oats, barley), inulin | Cellulose, hemicellulose, lignin |
| Sources | Oats, barley, legumes, apples, citrus, psyllium | Wheat bran, whole grains, vegetable skins, nuts |
| Physiologic effects | Forms gels, delays gastric emptying, binds bile acids, blunts postprandial glucose, fermented to SCFA | Adds bulk, speeds transit, softens stool |
| Clinical use | Lowers LDL cholesterol, improves glycemic control, can help both diarrhea and constipation | Constipation, diverticular disease prevention |
- Glycemic index (GI): blood glucose response to 50 g available carbohydrate from a food compared with glucose (= 100). Low ≤55, medium 56–69, high ≥70.
- Glycemic load (GL) = GI × grams of available carbohydrate per serving ÷ 100. Low ≤10, high ≥20.
- Worked example: watermelon GI ≈72 but a 120-g serving contains about 6 g carbohydrate → GL = 72 × 6 ÷ 100 ≈ 4.3 (low).
- GI is lowered by fiber, fat, protein, acid, intact grain structure, cooling (retrograded starch) and less ripeness; raised by processing and longer cooking.
Protein and Protein Quality
Protein provides 4 kcal/g and is about 16% nitrogen (so grams protein = grams nitrogen × 6.25). Of the 20 amino acids, nine are indispensable: histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan and valine. Conditionally indispensable amino acids (arginine, cysteine, glutamine, glycine, proline, tyrosine) become essential in prematurity, critical illness or metabolic disease; tyrosine, for example, is essential in phenylketonuria. The adult RDA is 0.8 g/kg/day (AMDR 10–35% of energy); needs rise in pregnancy and lactation (1.1 and 1.3 g/kg), growth, illness, wound healing and training.
| Measure | What It Compares | Key Points |
|---|---|---|
| Amino acid score (chemical score) | mg of limiting indispensable amino acid in 1 g test protein ÷ mg in reference pattern | Identifies the limiting amino acid: lysine in grains; methionine/cysteine (sulfur amino acids) in legumes; tryptophan in corn |
| PDCAAS | Amino acid score × fecal true digestibility | Scale 0–1, truncated at 1.0. Casein, whey, egg white and soy protein isolate = 1.0; wheat gluten ≈0.25. Used by FDA for protein %DV |
| DIAAS | Uses true ileal digestibility of each indispensable amino acid | Not truncated, so high-quality proteins can exceed 100%; ≥100 excellent, 75–99 good, <75 no quality claim (FAO). More accurate than PDCAAS |
| Biological value (BV) | Nitrogen retained ÷ nitrogen absorbed | Whole egg is the classic high-BV reference |
| Net protein utilization (NPU) | Nitrogen retained ÷ nitrogen consumed | Combines digestibility and BV |
| Protein efficiency ratio (PER) | Weight gain of growing rats per gram protein eaten | Historical; still used for infant foods |
Complementary proteins pair foods whose limiting amino acids differ (grains + legumes, such as rice and beans or hummus and pita). Complementation does not have to occur at the same meal; adequate variety across the day meets needs.
- N balance = (protein intake ÷ 6.25) − (urinary urea nitrogen + 4). The 4 g covers fecal, skin and non-urea urinary losses.
- Worked example: intake 90 g protein → 90 ÷ 6.25 = 14.4 g N. UUN 10 g → losses 10 + 4 = 14 g. Balance = 14.4 − 14 = +0.4 g (positive).
- Positive balance: growth, pregnancy, recovery. Negative balance: catabolic stress, burns, inadequate intake. Invalid with renal failure or large unmeasured losses (fistulas, burns).
Lipids and Lipoproteins
Lipids provide 9 kcal/g; the adult AMDR is 20–35% of energy, with saturated fat <10% and trans fat as low as possible. About 95% of dietary fat is triglyceride (glycerol + three fatty acids). Linoleic acid (omega-6) and α-linolenic acid (ALA, omega-3) are essential; AMDRs are 5–10% and 0.6–1.2% of energy. Conversion of ALA to EPA and DHA is limited (single-digit percentages), so preformed EPA/DHA come from fatty fish, algae oil or supplements. Essential fatty acid deficiency (scaly dermatitis, hair loss, poor wound healing, thrombocytopenia) can develop within weeks on fat-free parenteral nutrition.
| Type | Structure | Major Sources | Lipid Effect |
|---|---|---|---|
| Saturated (SFA) | No double bonds; solid at room temperature | Butter, cheese, fatty meats, coconut and palm oil | Raises LDL cholesterol (lauric, myristic, palmitic); stearic acid is relatively neutral |
| Monounsaturated (MUFA, omega-9) | One double bond (oleic acid) | Olive, canola and high-oleic oils, avocado, nuts | Lowers LDL when replacing SFA |
| Omega-6 PUFA | First double bond at carbon 6 from methyl end (linoleic → arachidonic acid) | Soybean, corn, sunflower oils; nuts, seeds | Lowers LDL when replacing SFA |
| Omega-3 PUFA | First double bond at carbon 3 (ALA, EPA, DHA) | ALA: flax, chia, walnuts, canola. EPA/DHA: salmon, sardines, mackerel | EPA/DHA lower triglycerides; anti-inflammatory eicosanoids |
| Trans fat | Trans double bond from partial hydrogenation | Industrial sources largely removed; small natural amounts in dairy and ruminant meat | Raises LDL and lowers HDL |
| Medium-chain triglycerides (MCT) | C6–C12 fatty acids | MCT oil, coconut oil (partly) | Absorbed into portal blood without bile salts or chylomicrons; no essential fatty acids |
Phospholipids (lecithin = phosphatidylcholine) form membranes and act as emulsifiers. Cholesterol builds membranes and is the precursor of bile acids, steroid hormones and vitamin D; the liver synthesizes most body cholesterol, and dietary cholesterol raises blood cholesterol less than saturated fat does.
| Lipoprotein | Origin and Main Cargo | Apolipoprotein | Function / Clinical Note |
|---|---|---|---|
| Chylomicron | Intestine; dietary triglyceride (largest, least dense) | B-48 | Delivers dietary fat via lymph to tissues; remnants cleared by liver |
| VLDL | Liver; endogenous triglyceride | B-100 | Raised by excess energy, refined carbohydrate, alcohol, insulin resistance |
| IDL | VLDL remnant | B-100, E | Converted to LDL |
| LDL | From IDL; cholesterol-rich | B-100 | Delivers cholesterol to tissues via LDL receptors; primary atherogenic target |
| HDL | Liver and intestine; densest, highest protein | A-I | Reverse cholesterol transport to the liver (LCAT esterifies cholesterol) |
| Lipoprotein(a) | LDL-like particle with apo(a) | B-100 + apo(a) | Genetically determined, independent risk factor; minimally diet-responsive |
Digestion and Absorption by Organ
The small intestine is the main site of digestion and absorption; folds, villi and microvilli expand its surface area roughly 600-fold. Knowing where each nutrient is absorbed lets you predict deficiencies after resection, bariatric surgery or disease: duodenal bypass compromises iron and calcium, ileal resection compromises vitamin B12 and bile salts, and colectomy compromises water and sodium.
| Site | Secretions / Enzymes | Key Digestive Events | Main Absorption |
|---|---|---|---|
| Mouth | Salivary α-amylase, lingual lipase, mucus | Chewing; starch digestion begins (α-1,4 bonds) | Negligible |
| Esophagus | Mucus | Peristalsis; lower esophageal sphincter limits reflux | None |
| Stomach | HCl and intrinsic factor (parietal cells), pepsinogen (chief cells), gastric lipase, gastrin (G cells), mucus | Acid (pH 1.5–3.5) denatures protein, activates pepsin, kills microbes, releases B12 from food protein; chyme formed | Small amounts of water, alcohol, some lipid-soluble drugs |
| Duodenum | Pancreatic amylase, lipase, colipase, trypsin, chymotrypsin, carboxypeptidase; bicarbonate; bile; brush-border enzymes | Bulk of digestion; bile emulsifies fat; bicarbonate neutralizes acid | Iron, calcium, magnesium, zinc, copper, phosphorus, folate, thiamin, riboflavin, fat-soluble vitamins (begins) |
| Jejunum | Brush-border disaccharidases (lactase, sucrase, maltase) and peptidases | Completion of carbohydrate and protein digestion; micelle formation | Most monosaccharides, amino acids and peptides, fatty acids, water-soluble vitamins, fat-soluble vitamins |
| Ileum | — | Absorbs what escapes the jejunum (ileal adaptation after jejunal loss) | Terminal ileum: vitamin B12–IF complex and bile salts (enterohepatic circulation); also fat-soluble vitamins |
| Colon | Mucus; microbiota | Fermentation of fiber and resistant starch to SCFA (acetate, propionate, butyrate = main colonocyte fuel) | Water, sodium, potassium, SCFA; bacterial vitamin K and biotin |
Gastric emptying is slowed most by fat, then protein, then carbohydrate, and by high osmolality, large volume and acid or fat in the duodenum. Liquids leave faster than solids.
| Hormone | Source | Stimulus | Main Actions |
|---|---|---|---|
| Gastrin | G cells, gastric antrum | Peptides, gastric distension, vagal input | ↑ HCl secretion, gastric motility, mucosal growth |
| Secretin | S cells, duodenum | Acid in duodenum | ↑ Pancreatic bicarbonate; ↓ gastric acid |
| Cholecystokinin (CCK) | I cells, duodenum and jejunum | Fat and protein in duodenum | Gallbladder contraction, pancreatic enzyme release, slows gastric emptying, satiety |
| Glucose-dependent insulinotropic polypeptide (GIP) | K cells, duodenum and jejunum | Glucose and fat | Incretin: ↑ insulin when glucose is elevated |
| Glucagon-like peptide-1 (GLP-1) | L cells, ileum and colon | Nutrients in the gut | Incretin: ↑ insulin, ↓ glucagon, slows gastric emptying, ↑ satiety (target of GLP-1 receptor agonists) |
| Motilin | M cells, duodenum | Fasting (cyclic) | Migrating motor complex (housekeeping waves between meals) |
| Somatostatin | D cells, stomach, intestine, pancreas | Acid, nutrients | Broadly inhibits GI secretion and hormone release |
| Ghrelin | Stomach (fundus) | Fasting | ↑ Hunger; ↑ growth hormone release |
| Peptide YY | L cells, ileum and colon | Nutrients | ↓ Appetite, slows transit (ileal brake) |
| Leptin | Adipose tissue | Proportional to fat mass | Long-term ↓ appetite, ↑ energy expenditure; obesity shows leptin resistance |
Metabolic Pathways
| Pathway | Location | State | Key Facts |
|---|---|---|---|
| Glycolysis | Cytosol | Fed / all states | Glucose → 2 pyruvate, net 2 ATP + 2 NADH; anaerobic → lactate |
| Citric acid cycle | Mitochondrial matrix | All | Final common pathway for carbohydrate, fat and protein; needs thiamin, riboflavin, niacin, pantothenic acid |
| Glycogenesis / glycogenolysis | Liver, muscle | Fed / fasting | Insulin promotes storage; glucagon and epinephrine promote breakdown |
| Gluconeogenesis | Liver (and kidney) | Fasting, stress | Glucose from lactate, glycerol, glucogenic amino acids (alanine, glutamine); not from even-chain fatty acids |
| Lipogenesis | Liver, adipose | Fed (energy excess) | Acetyl-CoA → fatty acids; insulin-driven |
| Lipolysis / β-oxidation | Adipose / mitochondria | Fasting, exercise | Carnitine shuttles long-chain fatty acids into mitochondria; palmitate yields ≈106 ATP |
| Ketogenesis | Liver mitochondria | Prolonged fasting, very low carbohydrate, uncontrolled type 1 diabetes | Acetoacetate, β-hydroxybutyrate, acetone; brain adapts to ketones and spares protein |
| Transamination / deamination | Liver, muscle | All | B6 (PLP)-dependent; amino group → ammonia → urea cycle (liver) |
Amino acids are glucogenic (most), ketogenic (leucine and lysine only) or both (isoleucine, phenylalanine, tyrosine, tryptophan, threonine). In the fed state, insulin promotes glucose uptake, glycogenesis, lipogenesis and protein synthesis; in fasting and stress, glucagon, cortisol and catecholamines drive glycogenolysis, gluconeogenesis and lipolysis. During starvation, protein breakdown falls as ketones replace glucose for the brain; in metabolic stress (sepsis, trauma), catabolism persists despite feeding.
Energy Balance, RQ and Indirect Calorimetry
Physiologic fuel values (Atwater): carbohydrate 4, protein 4, fat 9 and alcohol 7 kcal/g. Resting energy expenditure rises with fat-free mass, fever (≈7% per °F, 13% per °C), burns, sepsis, hyperthyroidism and growth; it falls with age, starvation and hypothyroidism. Direct calorimetry measures heat output; indirect calorimetry (the clinical reference method) measures oxygen consumption (VO₂) and carbon dioxide production (VCO₂).
- Respiratory quotient (RQ) = VCO₂ ÷ VO₂.
- Abbreviated Weir equation: REE (kcal/day) = [3.941 × VO₂ + 1.106 × VCO₂] × 1.44 (VO₂ and VCO₂ in mL/min).
- Worked example: VO₂ 250 mL/min, VCO₂ 200 mL/min → RQ = 0.80. REE = (985.3 + 221.2) × 1.44 ≈ 1,737 kcal/day.
- Valid test: rested, fasting (or on stable feeding), steady state; physiologic RQ range 0.67–1.3. A value outside this range signals a measurement error (air leak, hyperventilation).
| RQ | Interpretation |
|---|---|
| ≈0.7 | Fat oxidation; also ketosis, starvation, underfeeding |
| ≈0.8 | Protein oxidation |
| ≈0.85 | Mixed diet |
| ≈1.0 | Carbohydrate oxidation |
| >1.0 | Net lipogenesis from overfeeding (especially excess carbohydrate/dextrose) or hyperventilation; raises CO₂ load in patients with respiratory compromise |
Acid–Base Basics
Normal arterial values: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L. The bicarbonate buffer (CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻) is the main extracellular buffer; the lungs adjust CO₂ within minutes and the kidneys adjust bicarbonate over days. Read pH first, then decide whether PaCO₂ or HCO₃⁻ explains it.
| Disorder | pH | Primary Change | Compensation | Nutrition-Related Causes / Implications |
|---|---|---|---|---|
| Metabolic acidosis | ↓ | ↓ HCO₃⁻ | ↓ PaCO₂ (hyperventilation) | Diabetic ketoacidosis, diarrhea or fistula losses, renal failure, lactic acidosis, thiamin deficiency; use acetate salts in PN |
| Metabolic alkalosis | ↑ | ↑ HCO₃⁻ | ↑ PaCO₂ (hypoventilation) | Vomiting, nasogastric suction, diuretics, hypokalemia; use chloride salts in PN |
| Respiratory acidosis | ↓ | ↑ PaCO₂ | ↑ HCO₃⁻ (renal) | COPD, hypoventilation, sedation; avoid overfeeding, which increases CO₂ production |
| Respiratory alkalosis | ↑ | ↓ PaCO₂ | ↓ HCO₃⁻ (renal) | Hyperventilation from anxiety, pain, early sepsis, high altitude |
Nutrigenomics and Nutrigenetics
Nutrigenomics studies how nutrients and bioactive food components affect gene expression; nutrigenetics studies how inherited genetic variation alters nutrient requirements and responses. Epigenetics changes gene expression without changing DNA sequence (DNA methylation, histone modification); methyl donors such as folate, B12, choline and methionine participate. Most single gene–diet associations have small effects, so direct-to-consumer genetic diet advice should be interpreted cautiously and integrated with standard assessment.
| Gene / Variant | Nutrition Relevance |
|---|---|
| MTHFR (C677T) | Reduced enzyme activity; higher homocysteine when folate status is low; adequate folate intake is the response |
| LCT (lactase persistence) | Determines whether lactase activity continues into adulthood |
| HFE (C282Y, H63D) | Hereditary hemochromatosis: avoid iron and high-dose vitamin C supplements, limit alcohol; treated with phlebotomy |
| FTO | Associated with obesity risk; physical activity attenuates the effect |
| APOE (ε4) | Higher LDL response to saturated fat and higher cardiovascular and Alzheimer risk |
| PAH | Phenylketonuria: lifelong phenylalanine restriction, tyrosine supplementation (inborn error) |
- Match deficiency to site: ileal resection or Crohn disease → B12 and bile salt (fat) malabsorption; duodenal bypass → iron and calcium deficiency; gastrectomy or atrophic gastritis → loss of intrinsic factor and acid.
- PDCAAS is truncated at 1.0 and uses fecal digestibility; DIAAS uses ileal digestibility and is not truncated. Grains are limited in lysine, legumes in sulfur amino acids.
- RQ >1.0 = overfeeding (lipogenesis); RQ ≈0.7 = fat oxidation or underfeeding. Weir equation converts VO₂ and VCO₂ to kcal.
- Know the incretins (GIP, GLP-1), CCK (fat → gallbladder and enzymes) and secretin (acid → bicarbonate).
- MCT bypass micelles and chylomicrons and enter portal blood, but provide no essential fatty acids.
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