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

Abstract

Background:The reason for the high prevalence of mild cobalamin (vitamin B-12) deficiency in the elderly is poorly understood. Objective: We aimed to determine the reason for this high prevalence. Design: 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. Results: Mild cobalamin deficiency, ie, low to low-normal plasma cobalamin concentrations (< 260 pmol/L) and elevated plasma MMA concentrations (> 0.32 mol/L), were found in 23.8% of subjects; 25.7% of subjects were not cobalamin deficient (plasma cobalamin ≥ 260 pmol/L and plasma MMA ≤ 0.32 mol/L). Six subjects (5.8%), including 1 with mild cobalamin deficiency, had dietary cobalamin intakes below the Dutch recommended dietary intake of 2.5 g/d. Mildly cobalamin-deficient subjects had lower total (diet plus supplements) cobalamin intakes (median: 4.9 g/d; 25th and 75th percentiles: 3.9, 6.4) than did non-cobalamin-deficient subjects (median: 6.3 g/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%; 2 = 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%) ( 2 = 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%) ( 2 = 0.5, P = 0.5). Conclusions: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.Am J Clin Nutr 1998;68:328-34.

Serum vitamin B12 concentrations and atrophic gastritis in older New Zealanders

“…Different prevalence rates of atrophic gastritis could reflect different rates of Helicobacter pylori infection in the various populations surveyed because H. pylori causes chronic gastritis and can lead to atrophic gastritis (Fennerty, 1994). However, the prevalence of H. pylori in a group of older New Zealanders (B50%) (Collett et al, 1999) is similar to that reported in studies carried out in the US (Everhart et al, 2000) and The Netherlands (van Asselt et al, 1998). Although atrophic gastritis was strongly associated with low serum vitamin B 12 in our study population, 77% of people with deficient (o148 pmol/l) and 94% with marginal vitamin B 12 (148-221 pmol/l) were classifed as having normal mucosa or superficial gastritis.…”

“…In 248 Kansas residents (465 y), the prevalence of atrophic gastritis was 9%; 5% had severe atrophic gastritis (Hurwitz et al, 1997). In 108 Dutch seniors (74-80 y), the prevalence of atrophic gastritis was 32% and 13% had severe atrophic gastritis using stricter criteria (PG I/II o1.6 and PG I o17) (van Asselt et al, 1998). In Finland, a 5-6% prevalence of severe atrophic gastritis was found in 425 older residents (460 y) using biopsies and a less stringent cut point of PG I o25 mg/l (Varis et al, 1991).…”

“…Using convenience samples, the prevalence of atrophic gastritis in the elderly has been estimated from 8 to over 40% (Krasinski et al, 1986;Faisal et al, 1990;Johnsen et al, 1991;Varis et al, 1991;Hurwitz et al, 1997;van Asselt et al, 1998). Some of these studies used examination of biopsies to establish the presence of atrophic gastritis while others used serological markers.…”

Relationship between methylmalonic acid, homocysteine, vitamin B12 intake and status and socio-economic indices, in a subset of participants in the British National Diet and Nutrition Survey of people aged 65 y and over

“…Table 3 of the present study indicate that some elderly respondents with raised MMA levels also have abnormal plasma urea and creatinine concentration, and therefore impaired kidney function. Many other studies have also detected a link between raised blood MMA levels and impaired kidney function (Stabler et al, 1986;Rasmussen et al, 1990a, b;Joosten et al, 1993;Lindenbaum et al, 1994;Koehler et al, 1996;Norman, 1998Norman, , 1999van Asselt et al, 1998;Herrmann et al, 2000;Hvas et al, 2000). According to Whitehead et al (1994), the 97.5th centile of plasma creatinine in adults aged 25 -55 y is approximately 122 mmol=l (males) and 100 mmol=l (females), and for plasma urea it is 7.6 mmol=l (males) and 6.8 mmol=l (females).…”

“…Functional B 12 deficiency in North America has also been highlighted (Pennypacker et al, 1992;Lindenbaum et al, 1994;Carmel et al, 1999;Stabler et al, 1999), especially in Caucasians (Carmel et al, 1999;Stabler et al, 1999). It is unlikely to be due to a simple lack of vitamin B 12 in the diet, and thus is more likely to relate to impaired absorption or retention of the vitamin, by mechanisms that remain poorly understood (Howard et al, 1998;van Asselt et al 1998). A recent study has demonstrated a correlation between severity depression and MMA, but not serum vitamin B 12 in older American women (Penninx et al, 2000), thus raising the possibility of subtle functional (neurological) effects of early vitamin B 12 deficiency.…”