Mohammed T. Abou-Saleh

Principles and Practice of Geriatric Psychiatry.Editors: Professor John R. M. Copeland, Dr Mohammed T. Abou-Saleh and Professor Dan G. BlazerCopyright & 2002 John Wiley & Sons LtdPrint ISBN 0-471-98197-4 Online ISBN 0-470-84641-0210 PRINCIPLES AND PRACTICE OF GERIATRIC PSYCHIATRYNutritional Factors in DementiaD. N. Anderson 1 and M. T. Abou-Saleh 21Mossley Hill Hospital, Liverpool, and 2 St George’s Hospital Medical School, London, UKThe prevalence of nutritional disorders among the elderly issubstantial, particularly among the elderly mentally ill (seeChapter 138a). Those with dementing disorders are at specialrisk. Dementia caused by a single nutrient deficiency is rare in theUK and USA and malnourishment will normally be the result of adementia and deranged eating patterns, rather than its cause. Theelderly in hospital or residential care are more likely to bemalnourished than those living in the community 1,2 .Reduced plasma and blood levels of folate 3–6 , vitamin B 3 12 ,vitamin C 2,5,7–10 , and vitamin E 8–10 in particular, have beenreported in association with dementia and cognitive impairment.Goodwin et al. 11 reported a direct relationship betweenwater-soluble vitamins and cognitive function in healthysubjects. Those with the lowest levels of plasma folate andvitamin B 12 scored significantly worse on the Halstead–Reitancategories test and the Wechsler memory test. As part of theBasle Longitudinal Project on Ageing, involving urban-dwellinghealthy elderly people, Perrig et al. 12 found that b-carotene andvitamin C levels were independently correlated with memoryfunction after controlling for compounding variables such asage, education and gender. High intake of monounsaturatedfatty acids was found to be associated with better memoryfunction in 300 people aged 65–84 years 13 . Unsaturated fattyacids appear important for maintaining the development andintegrity of neuronal function.Botez et al. 14 having found evidence of organic brain damage onpsychometric testing in folate deficient subjects, reported improvementfollowing 12 months’ supplementation. Of five patients whounderwent radionucleotide cysternography, three showedimprovement of cerebral atrophy. Supplementation with vitaminE has been associated with slower development of the pathologyof Alzheimer’s disease 15 .It is not easy to establish, from studies of this sort, whethernutritional deficiency is a cause or effect of cognitive impairment.Supplementation studies suggest that certain additional nutrientsmay influence cognitive performance and, whether causative ornot, nutrient deficiency may increase cognitive decline. Ifaetiologically significant, then the relevance of many of thesefindings may lie in the relationship with the oxidative stresshypothesis of Alzheimer’s disease and the significance of oxidativestress for the development of ischaemic vascular disease. There isincreasing evidence that reactive oxidizing species contribute tothe neuronal damage and formation of the amyloid plaques seenin Alzheimer’s disease 16,17 . Antioxidants could be important forpreventing this damage and antioxidant constituents of diet, suchas vitamins E and C and b-carotene may be of particularimportance. Vitamin C is actively concentrated in the brain 18 andis considered to be the most effective antioxidant in humanplasma 19 .Impaired antioxidant status 20 and low plasma vitamin C levels 21have been suggested as risk factors for coronary artery diseaseand, therefore, may be relevant to dementia of vascular origin.Similar associations have been reported with vitamin B 6 and folateconsumption 22 . Preliminary suggestions that vitamin E mayreduce the risk of stroke has obvious implications for thedevelopment of vascular dementia.The causative role of thiamine deficiency for the Wernicke–Korsakoff syndrome is established and it seems that somealcoholic dementias may result from Wernicke–Korsakofflesions 23 . Other B vitamins are capable of producing cognitiveimpairment and dementia 24 but are only likely to be significantcauses in industrially underdeveloped countries.Assessment of nutritional status should be part of the generalmanagement of dementing patients and nutritional deficiencycorrected whenever possible. The cause of undernutrition ismultifactorial and various interventions may help to improve apatient’s nutritional state 25 (see Chapter 138a). For a few patientsthis may lead to gratifying improvements of cognitive performance,but all are likely to benefit by a reduction of morbid riskand improvements in general health. It is likely that a clearerunderstanding of the relationship between dietary constituentsand dementia will contribute to methods of prevention andtreatment of this condition.REFERENCES1. Burns A, Marsh A, Bender DA. Dietary intake and clinical,anthropometric and biochemical indices of malnutrition in elderlydemented patients and non-demented subjects. Psychol Med 1989; 19:383–91.2. Hancock MR, Hullin RP, Ayland PR et al. Nutritional state ofelderly women on admission to mental hospital. Br J Psychiat 1985;147: 404–7.3. Sneath P, Chanarin I, Hodkinson MH et al. Folate status in ageriatric population and its relation to dementia. Age Ageing 1993; 2:177–82.4. Shorvon SD, Carney MWP, Chanarin I, Reynolds EH. Theneuropsychiatry of megaloblastic anaemia. Br Med J 1980; 28:1036–43.5. Kemm JR, Alcock J. The distribution of supposed indictors ofnutritional status in elderly patients. Age Ageing 1984; 13: 21–8.6. Abou-Saleh MT, Spalding E, Kellett J. Folate deficiency in dementia.Br J Psychiat 1986; 148: 336.7. Shaw DM, Tidmarsh SF, Thomas DE et al. Senile dementia andnutrition. Br Med J 1984; 288: 792–3.8. Jeandel C, Nicholas MB, Dubois F et al. Lipid peroxidation and freeradical scavengers in Alzheimer’s disease. Gerontology 1989; 35: 275–82.9. Riviere S, Birloyez-Aragon I, Nourhashemi F, Vellas B. Low plasmavitamin C in Alzheimer patients despite an adequate diet. Int J GeriatPsychiat 1998; 13: 749–54.10. Sinclair AJ, Bayer AJ, Johnston J et al. Altered plasma antioxidantstatus in subjects with Alzheimer’s disease and vascular dementia. IntJ Geriat Psychiat 1998; 13: 840–5.11. Goodwin JS, Goodwin JM, Garry PJ. Association betweennutritional status and cognitive functioning in a healthy population.J Am Med Assoc 1983; 249: 2917–21.12. Perrig WJ, Perrig P, Stahelin HB. The relation between antioxidantsand memory performance in the old and very old. J Am Geriat Soc1997; 45: 718–24.13. Solfrizzi V, Panza F, Torres P et al. High monounsaturated fatty acidintake protects against age-related cognitive decline. Neurology 1999;8: 1563–8.14. Botez MI, Botez T, Maag H. The Wechsler sub-tests in mild organicbrain damage associated with folate deficiency. Psychol Med 1984; 14:431–7.