لخّصلي

The prevalence of vitamin B12 deficiency was 12% in this representative sample of an aged population. This is in accordance with the previously reported prevalence rates in other countries [1, 4, 5]. The proportion of previously undiagnosed vitamin B12 deficiency was remarkably large. Male gender, age 75 years or more and refraining from milk products doubled the probability for vitamin B12 deficiency, but no clinically relevant risk group for screening could be defined. Anaemia or macrocytosis did not predict vitamin B12 deficiency.

We used total vitamin B12 measurement as the first-line laboratory test because it is most commonly used by general practitioners in diagnosing vitamin B12 deficiency. It is inexpensive and widely available, but it has been considered not sensitive or specific enough to be used as the only laboratory test [2, 14]. The determination of tHcy or holoTC has been proposed as additional tests for subjects with borderline total vitamin B12 concentrations (150–250 pmol/l) [7]. However, the prevalence of hyperhomocysteinemia is high in the aged and increases with age. The main determinants for plasma tHcy concentrations are folate and vitamin B12 status as well as renal function [14]. The effect of impaired renal function and other diseases on tHcy seems to increase with age, which reduces its value as a laboratory test for vitamin B12 deficiency [15]. To overcome the unspecificity of tHcy, we also used low holoTC in subjects with borderline total vitamin B12 for the laboratory diagnosis of vitamin B12 deficiency.

False low total vitamin B12 concentrations have been found, but only a few reasons are known for them [16]. Recently, it has been shown that mild haptocorrin deficiency is more common than previously assumed and may explain as much as 15% of the low total vitamin B12 concentrations [16]. We are aware that our definition of vitamin B12 deficiency may have resulted in some overdiagnosis. Five subjects in this population could have been regarded as having false low total vitamin B12, because they had both normal tHcy and normal holoTC. We consider this justified since overdiagnosis of vitamin B12 deficiency is not as harmful as underdiagnosis, because no toxic effects have been reported from vitamin B12 supplementation. For this reason, we also consider additional holoTC and tHcy measurements efficient only in subjects with borderline total vitamin B12.

Vitamin B12 deficiency seems to be markedly underdiagnosed. In this study cohort, 78% of the subjects with vitamin B12 deficiency were previously undiagnosed. In clinical practice, more awareness is needed to prevent irreversible damage due to delayed diagnosis. Therefore, screening for even asymptomatic aged people has been suggested [5, 17]. Another option is to recognise the early clinical manifestations or possible risk factors. However, only a few recent studies have analysed possible clinical associates other than cognitive impairment. According to them, the signs and symptoms traditionally linked to vitamin B12 deficiency are not related to the occurrence of the disease [6, 18, 19].

Smoking, alcoholism and vegetarian diet were not associated with vitamin B12 deficiency in this aged population. These factors have been linked with an increased risk of vitamin B12 deficiency in younger adults [5, 8], but, to our knowledge, these relationships have not been previously investigated in aged populations. Milk product use is the rule rather than an exception among the Finnish aged, and it correlated positively with total vitamin B12 concentrations. Refraining from milk products doubled the probability for vitamin B12 deficiency.

Many previous studies have analysed the associations between cognitive function and vitamin B12 status [6, 20, 21], and the results have varied with the markers used. We used subjective memory impairment, MMSE and dementia diagnosis, which are rather insensitive measures for slight cognitive impairments. As in many other studies, we found no correlation between the MMSE score and total vitamin B12 or holoTC, but tHcy had an inverse correlation. In addition, vitamin B12 deficiency was not more frequent in subjects with poor subjective memory or low MMSE score. This is in contrast to a recent large study of people aged 75 years or more in the United Kingdom [21], in which the symptoms of memory impairment and low MMSE score were associated with all the measures of vitamin B12 status used in the study. The risk for cognitive impairment was greater in subjects with total vitamin B12 or holoTC concentrations in the lowest quartile and tHcy or methylmalonic acid concentrations in the highest quartile. In the same study, no association was found between any measures of vitamin B12 status and depression, but two previous population-based studies have shown depression to be a risk factor for vitamin B12 deficiency [22, 23]. Surprisingly, in our study, the probability for vitamin B12 deficiency was slightly lower than expected in subjects with depression and CHD. The result is most likely random error due to a large amount of variables analysed and does not obviate the need for screening for vitamin B12 deficiency in these subjects. Symptoms and signs of polyneuropathy were not recorded in this study. Bodily pain may be used as a poor indicator of polyneuropathy. Previously, bodily pain has been found to be more common in subjects with low vitamin B12 levels [24], but we found no association.