Role of cobalamin intake and atrophic gastritis in mild cobalamin deficiency in older Dutch subjects

• Published in: The American journal of clinical nutrition 1998-08, Vol.68 (2), p.328-334
• Main Authors: VAN ASSELT, D. Z. B, DE GROOT, L. C. P. G. M, VAN STAVEREN, W. A, BLOM, H. J, WEVERS, R. A, BIEMOND, I, HOEFNAGELS, W. H. L
• Format: Article
• Language: English
• Subjects: Afdeling Humane voeding; Aged; Aged, 80 and over; Biological and medical sciences; Diet; Female; Gastritis, Atrophic - complications; Helicobacter Infections - complications; Helicobacter pylori; Human Nutrition; Human Nutrition & Health; Human Nutrition (HNE); Humane Voeding; Humane Voeding & Gezondheid; Humans; Male; Medical sciences; Metabolic diseases; Methylmalonic Acid - blood; Nutrition; Older people; Other nutritional diseases (malnutrition, nutritional and vitamin deficiencies...); Prevalence; Vitamin B; Vitamin B 12 - administration & dosage; Vitamin B 12 - blood; Vitamin B 12 Deficiency - epidemiology; Vitamin B 12 Deficiency - etiology; VLAG
• ISSN: 0002-9165; 1938-3207
• DOI: 10.1093/ajcn/68.2.328

The reason for the high prevalence of mild cobalamin (vitamin B-12) deficiency in the elderly is poorly understood. We aimed to determine the reason for this high prevalence. We examined cobalamin intake, the presence and severity of atrophic gastritis, the presence of Helicobacter pylori infection, and plasma cobalamin and methylmalonic acid (MMA) concentrations in 105 healthy, free-living, older subjects aged 74-80 y. Mild cobalamin deficiency, ie, low to low-normal plasma cobalamin concentrations (< 260 pmol/L) and elevated plasma MMA concentrations (> 0.32 micromol/L), were found in 23.8% of subjects; 25.7% of subjects were not cobalamin deficient (plasma cobalamin > or = 260 pmol/L and plasma MMA < or = 0.32 micromol/L). Six subjects (5.8%), including 1 with mild cobalamin deficiency, had dietary cobalamin intakes below the Dutch recommended dietary intake of 2.5 microg/d. Mildly cobalamin-deficient subjects had lower total (diet plus supplements) cobalamin intakes (median: 4.9 microg/d; 25th and 75th percentiles: 3.9, 6.4) than did non-cobalamin-deficient subjects (median: 6.3 microg/d; 25th and 75th percentiles: 5.4, 7.9) (P = 0.0336), mainly because of less frequent use of cobalamin supplements (8% compared with 29.6%; chi2 = 3.9, P = 0.048). Atrophic gastritis was found in 32.4% of the total study group: mild to moderate in 19.6% and severe in 12.7%. The prevalence of severe atrophic gastritis, but not mild-to-moderate atrophic gastritis, was higher in mildly cobalamin-deficient subjects (25%) than in non-cobalamin-deficient subjects (3.7%) (chi2 = 4.6, P = 0.032). The prevalence of immunoglobulin G antibodies to H. pylori was similar in mildly cobalamin-deficient subjects (54.2%) and in non-cobalamin-deficient subjects (44.4%) (chi2 = 0.5, P = 0.5). The high prevalence of mild cobalamin deficiency in healthy, free-living, older Dutch subjects could be explained by inadequate cobalamin intake or severe atrophic gastritis in only 28% of the study population. Other mechanisms explaining mild cobalamin deficiency in older people must be sought.