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B-vitamin status in relation to cognitive health over 4 years in healthy older adults

Published online by Cambridge University Press:  24 September 2014

C. F. Hughes ,
M. Ward ,
L. Hoey ,
F. Tracy ,
A. Molloy  and
H. McNulty
C. F. Hughes
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine, BT52 1SA
M. Ward
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine, BT52 1SA
L. Hoey
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine, BT52 1SA
F. Tracy
Affiliation:
Causeway Hospital, Coleraine, BT52 HIS
A. Molloy
Affiliation:
School of Biochemistry and Immunology, Trinity College Dublin, Dublin 2, Ireland.
H. McNulty
Affiliation:
Northern Ireland Centre for Food and Health, University of Ulster, Coleraine, BT52 1SA
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Abstract

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Proceedings of the Nutrition Society , Volume 73 , Issue OCE2: Irish Section Meeting, 18–20 June 2014, Changing Dietary Behaviour: Physiology Through to Practice , 2014 , E102
Copyright
Copyright © The Authors 2014 

Advancing age is associated with a decline in cognitive function which can range from mild cognitive impairment to dementia. Epidemiological evidence suggests that sub-optimal B-vitamin status may be associated with greater cognitive impairment in both healthy older adults and in patients with dementia( Reference Herrmann and Obeid 1 ). In addition, evidence from randomised control trials has demonstrated a beneficial effect of B-vitamin supplementation on cognitive function( Reference de Jager, Oulhaj and Jacoby 2 , Reference Durga, van Boxtel and Schouten 3 ) but the evidence is not entirely consistent( Reference Ford, Flicker and Alfonso 4 ). The aim was to investigate B-vitamin status in relation to cognitive decline over a 4 year follow-up period in healthy older adults. We hypothesised that poorer B-vitamin status at baseline would lead to a greater than expected rate of cognitive decline.

In a retrospective study, healthy older adults (n = 154; aged 60–88years) who had been previously screened for cognitive function were reassessed four years after initial assessment. Cognitive function was assessed at both timepoints by the Mini-Mental State Examination (MMSE), the most widely used cognitive screening tools in a clinical setting. Participants were initially recruited as being cognitively healthy at baseline, i.e. having an MMSE score between 25–30.

At the 4 year follow-up assessment, when participants were aged 73·4 ± 7·1 years, mean cognitive MMSE scores had declined from 29·1 ± 1·3 to 27·5 ± 2·3 (P < 0·001). Although most participants showed a typical rate of cognitive decline expected for healthy older adults (i.e. a decrease of 0·2–0·6MMSE points per year)( Reference Park, O'Connell and Thomson 5 ), cognitive decline occurred at an accelerated rate in a sub-set of participants (i.e. greater than 1 MMSE point per year; n = 38). Baseline predictors of accelerated cognitive decline were investigated (Table).

For each B-vitamin biomarker, lowest tertile (or highest tertileHcy) was compared with other two tertiles. Values were considered significant if P ≤ 0·05.Abbreviations; CI: confidence interval; Hcy: homocysteine.

After adjustment for age, a low baseline concentration of vitamin B6, as measured using pyridoxal-5-phosphate (PLP;<43·3 nmol/l) was associated with a 4-fold higher risk of having accelerated cognitive decline. Neither folate nor vitamin B12 concentrations were significantly associated with cognitive decline. In conclusion, lower vitamin B6 status at baseline was strongly associated with an accelerated rate of cognitive decline over the 4 year period. Vitamin B6 may be an important (often overlooked) protective factor in maintaining cognitive function in ageing.

References

1. Herrmann, W, Obeid, R. (2011) ClinChem Lab Med 49, 343–4.Google Scholar
2. de Jager, CA, Oulhaj, A, Jacoby, R, et al. (2012) Int J Geriatr Psychiatry 27, 592–600.Google Scholar
3. Durga, J, van Boxtel, MPJ, Schouten, EG, et al. (2007) Lancet 369, 208–16.Google Scholar
4. Ford, AH, Flicker, L, Alfonso, H, et al. (2010) Neurology 75, 1540–7.CrossRefGoogle Scholar
5. Park, HL, O'Connell, JE, Thomson, RG. (2003) Int J Geriatr Psychiatry 18, 1121–34.CrossRefGoogle Scholar