Abstract
ObjectivesTo determine prevalence of vitamin B12 and folate deficiency and associations with cognitive performance in participants recruited for the Cognitive Health in Ageing Register: Investigational, Observational, and Trial Studies in Dementia Research: Prospective Readiness cOhort Study (CHARIOTPRO) SubStudy (CPRO-SS).DesignCross-sectional analysis of data collected in the screening phase for the CPRO-SS.SettingParticipants were recruited from the Chariot Register at Imperial College London comprising approximately 39,000 community dwelling volunteers.ParticipantsCommunity dwelling individuals aged 60–85 years with B vitamin biomarker measures available were included (n=1946). After medical history and other exclusions, 1347 cognitively healthy participants were included for analysis of cognitive data.MeasurementsCognitive status was assessed with the Repeatable Battery for Neuropsychological Status (RBANS). Assays included vitamin B12 and folate, followed by serum methylmalonic acid and homocysteine levels for those with low vitamin B12. Gender-specific linear regression analysis was performed for associations between cognition and biomarkers. Non-gender specific regression for groups graded by B vitamin deficiency severity were also performed.ResultsVitamin B12 deficiency (<148pmol/L) was found in 17.2% of individuals and folate deficiency (<10nmol/L) in 1% of our participants. Low vitamin B12 was associated with poorer memory (p<0.03) in men. A high BMI predicted poorer attention and visuospatial indices (p<0.05). A regression analysis by B12 level revealed associations with poorer attention (β −6.46; p=0.004) for the deficient group and with immediate memory (β −2.99; p=0.019) for those categorised as severely deficient.ConclusionOlder men and women are prone to vitamin B12 deficiency with associated subtle and different domain-specific disruptive effects in measures of memory and attention. Elevated homocysteine and methylmalonic acid contributed to poorer cognitive performance. Novel groups at particular risk of cognitive deficit were identified for future interventional studies in this field.
Highlights
Background deficiencyIf not recognised and treated, these deficiencies may lead to a preventable cause of cognitive impairment [9].The worldwide prevalence of B12 deficiency is estimated There are two B12-dependent enzymatic reactions important to be around 6%
Associated with lower Attention indices (-6.462, Confidence Intervals (CI) -10.844, -2.080; p=0.004). (Table 3) There was a borderline significance for association of the Severely deficient group with lower total Repeatable Battery for Neuropsychological Status (RBANS) scores (-2.321 CI -4.812, 0.170; p=0.068). In this prospective study of older community dwelling participants, we found the overall prevalence of vitamin B12 deficiency to be 17.2%, which high, is in line with previously reported literature [1], We found a high degree of B12 insufficiency/low normal status, as described by Smith & Refsum [13]
Low B12 levels were associated with high body mass index (BMI) and both factors independently predicted worse cognitive performance, whilst folate had both positive and negative effects on specific cognitive domains
Summary
The worldwide prevalence of B12 deficiency is estimated There are two B12-dependent enzymatic reactions important to be around 6%. Prevalence is higher in adults over to maintaining health. The and methylation of homocysteine (Hcy) to form methionine deficiency of folate is reported to be significantly rarer since by methionine synthase. The latter reaction requires the the institution of fortification of grains in many countries world presence of folate. Vitamin B12 deficiency will limit these wide [5]. The most recognised clinical manifestation of vitamin cellular reactions resulting in increased concentrations of
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