Scurvy is a disease caused by severe vitamin C (ascorbic acid) deficiency, characterized by impaired collagen synthesis leading to bleeding gums, poor wound healing, skin hemorrhages, and weakened blood vessels. It results from the essential role of vitamin C in collagen hydroxylation.
Vitamin C (ascorbic acid) is an essential cofactor for prolyl hydroxylase and lysyl hydroxylase, enzymes that add hydroxyl groups (-OH) to proline and lysine amino acids during collagen synthesis. Without adequate vitamin C, these hydroxylation reactions cannot occur. Un-hydroxylated collagen cannot form the stable triple-helix structure required for tensile strength. The resulting defective collagen causes blood vessels to become fragile, wounds to fail to heal, and connective tissues to deteriorate. This explains why tissues 'fall apart' in scurvy.
Scurvy demonstrates the absolute requirement of vitamin C for collagen synthesis and tissue integrity. While severe scurvy is rare in developed countries, subclinical vitamin C deficiency (impaired hydroxylation without frank scurvy) may impair wound healing, increase bruising, and reduce tissue repair capacity. Understanding scurvy's mechanism explains why vitamin C supplementation (250 mg/day in wound healing protocols) supports collagen synthesis, immune function, and tissue repair. It also highlights why collagen supplementation alone is insufficient without adequate vitamin C for proper hydroxylation.
- Caused by severe vitamin C (ascorbic acid) deficiency
- Results from impaired collagen hydroxylation without vitamin C cofactor
- Symptoms: bleeding gums, poor wound healing, skin hemorrhages, weak blood vessels
- Hydroxylation of proline and lysine requires vitamin C
- Un-hydroxylated collagen cannot form stable triple-helix structure
- Tissues 'fall apart' without properly cross-linked collagen
- Demonstrates absolute requirement for vitamin C in collagen synthesis
- Prevented/treated with vitamin C supplementation
- Vitamin C — vitamin C deficiency causes scurvy through impaired collagen hydroxylation
- Hydroxylation — vitamin C-dependent hydroxylation is impaired in scurvy, preventing proper collagen formation
- collagen — scurvy results from defective collagen that cannot properly cross-link
- proline — vitamin C required for hydroxylation of proline to hydroxyproline in collagen
- Hydroxyproline — absence of hydroxyproline in scurvy prevents stable collagen triple helix
- lysine — vitamin C needed for hydroxylation of lysine for collagen cross-linking
- wound healing — scurvy demonstrates how vitamin C deficiency impairs wound healing through collagen defects
- Collagen synthesis — scurvy exemplifies failure of collagen synthesis without adequate vitamin C
- connective tissue — connective tissue deteriorates in scurvy due to defective collagen
- blood vessels — blood vessel fragility in scurvy due to weak collagen in vessel walls
- bleeding — scurvy causes bleeding from fragile, collagen-deficient blood vessels
- immune function — vitamin C deficiency in scurvy also impairs immune cell function
- Collagen I — type I collagen synthesis requires vitamin C; deficiency causes scurvy
- Collagen III — type III collagen formation also impaired in scurvy
- triple helix — hydroxylated collagen forms triple helix; lacking in scurvy
- tensile strength — collagen in scurvy lacks tensile strength due to improper cross-linking
- antioxidant — vitamin C is also antioxidant; deficiency in scurvy increases oxidative stress
- nutrition — scurvy is a classical nutritional deficiency disease
- Micronutrients — scurvy exemplifies importance of micronutrient adequacy for tissue structure
- Immunonutrition — vitamin C in immunonutrition protocols prevents scurvy-like impairment