Abstract
Dementia occurs in about 2.4 percent of persons aged 65 to 69 years but in 22 percent of those aged 80 years and over (Kay et al., 1964 and 1970). The importance of these observations is emphasized by the increasing proportion of the population reaching old age. This brings an increasing demand on health care facilities and long term residential care. The causes of dementia are unknown. It has been suggested that one of the changes in dementia is a reduction in the cholinergic, serotoninergic and other transmission systems. Preliminary studies by Lehmann (1979) suggested that a proportion of old people may not absorb tryptophan (a precursor of serotonin) normally and that this is associated with dementia. This is of considerable potential interest in relation to diet because primary dietary lack, or a failure to absorb certain nutrients, might contribute to the aetiology of the disease. The possible effect of nutrition on brain function in the elderly and on the dementing process, is confounded by the fact that dementing old people have often been in hospital for sometime and have become institutionalised. Any deficiency in the provision of food and its nutrient content may therefore affect mental state as well as physical well being. Dietary intakes of 23 patients with senile dementia and 12 residents in part III accommodation were compared to those of healthy community controls of similar age. The patients with senile dementia had lower mean intakes of energy, protein, fibre, ascorbic acid and nicotinic acid. The poor dietary intake of ascorbic acid was reflected in lower levels of plasma ascorbic acid. Both patients and controls had low intakes of folic acid, yet only in patients was a lower level of red cell folate shown. Dietary intakes of thiamin were similar between the groups, yet one third of the patients had intakes below the recommended daily amount (DHSS, 1979). These results are of interest when investigating the effect of nutrition on mental performance. The group of residents had significantly lower mean intakes of ascorbic acid, thiamin, pyridoxin, vitamin B12, folic acid, nicotinic acid, protein and iron, copper and zinc. These findings were reflected in lower circulating levels of ascorbic acid and folic acid in the residents. In both cases the poor dietary intakes for patients and residents was partly attributed to inadequate portion size and for residents poor menu design. There is no clear evidence that any nutritional deficiency is found specifically in patients with senile dementia, though there are suggestions that folic acid deficiency may play a role in the development of the condition. A preliminary investigation into the effect of vitamin supplementation on patients with dementia showed an improvement in mental function over a two month period, for those on active preparation. However, the results did not reach a level of significance and it is suggested that a longer period of supplementation on a larger group of patients with early dementia is necessary. The association between ageing, senile dementia and nutritional status merits further investigation in the light of nutritional inadequacies both in patients and residents in part III accommodation. There is a need for a total reappraisal of the provision of food to the elderly in institutions.