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Nutrition and Cognition in Older Persons

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Nutrition and Cognition in Older Persons Nutrition and Aging: I.H. Rosenberg; A. Sastre (eds), Nestle´ Nutrition Workshop Series Clinical & Performance Program, Vol. 6, pp. 121–134, Nestec Ltd.; Vevey/S. Karger AG, Basel, 2002. Nutrition and Cognition in Older Persons John E. Morley GRECC, St. Louis VA Medical Center, and Division of Geriatric Medicine, Saint Louis University, St. Louis, Mo., USA The concept that ‘we are what we eat’ is by no means a new one and appears to be particularly true when one examines the effect of food intake on cognitive function. Even in the case of mild protein energy malnutrition, poor nutritional state is associated with a decline in cognitive function [1]. Food intake, or the lack thereof, can modulate thought processes in multiple ways (Table 1). This chapter will focus on a number of mechanisms that appear to play a role in modulating cognition in older persons. Modulation of Memory by Gastrointestinal Peptide Release Cholecystokinin (CCK) has been shown to enhance memory retention [2]. It produces this effect by stimulating ascending fibers in the vagus nerve (Fig. 1). These then send messages to the nucleus tractus solitarius and from there to the amygdala and the hippocampus [3]. When mice are fed immediately after learning a task, they demonstrate improved memory [2]. This enhanced retention can be abolished by utilizing a CCK antagonist. Circulating CCK levels are elevated in older persons and increase to a greater degree following fat administration [4]. CCK levels are elevated to a greater degree in malnourished compared to healthy older individuals [5]. Food intake improves cognition in humans [6]. It would seem possible that utilizing finger food high in fat (a potent CCK releaser) may be useful to reinforce positive behaviors in older persons with early deterioration in cognition. A number of other gastrointestinal peptides also modulate memory after peripheral administration. These include gastrin releasing peptide [7] and amylin [8]. The potential ability to manipulate this release of gastrointestinal hormones to modulate memory represents a fertile research ground. 121 Nutrition and Cognition in Older Persons Table 1. Mechanisms by which food can modulate cognition 1. Release of gastrointestinal peptides that can modulate cognition 2. Alterations in gastrointestinal luminal bacteria resulting in increased gut cytokine release 3. Decreased nutritional status leading to impaired immune function, infections and cytokine release 4. Effects of circulating glucose 5. Effects of fasting on brain membrane fatty acid concentration 6. Vitamin deficiencies 7. Free radical scavengers 8. ‘Natural’ memory aids 9. Protein toxicity 10. Food-drug interactions ⇑Memory Nucleus tractus Amygdala solitarius Ascending vagus CCK Fat Fig. 1. The mechanism by which cholecystokinin (CCK) enhances memory. Cytokines and Cognition Cytokines, such as interleukin-2, have been demonstrated to produce cognitive impairment and delirium after administration to humans [9]. There are three possible mechanisms by which cytokines may have their release 122 Nutrition and Cognition in Older Persons altered by food. Probiotics and biotics alter the gut flora often reducing local gastrointestinal cytokine release and decreasing the possibility that infectious bacteria enter the circulation. Starvation increases the ability of bacteria to translocate from the gastrointestinal lumen into the systemic circulation. Persons with malnutrition have a decrease in the immune system making them more prone to developing systemic infections and cytokine release. It has been suggested that cytokines produce their effects on the central nervous system indirectly similar to CCK by stimulating the ascending fibers of the vagus [10]. Recently we have studied the mechanism(s) by which interleukin-1 (IL-1) produced impaired memory retention. Direct adminis- tration of IL-1 into the septum results in impaired retention. Utilizing both mouse and human antibodies and hIL-1, we were able to demonstrate that intraperitoneally administered IL-1 produces its effects both by stimulating ascending nerve fibers and releasing itself in the septum and by a direct effect after it has crossed the blood brain membrane. Cytokine modulation of cognition following food ingestion represents another mechanism worthy of further exploration. Effects of Circulating Glucose Hypoglycemia is well established as a cause of delirium. On the other hand, continuously elevated glucose levels also are associated with cognitive impairment [11, 12]. This appears to be a direct glucotoxic effect as in mice made diabetic with streptozotocin, a single injection of insulin restores their impaired performance on retention tests to normal [13]. In addition, three studies in older humans found that improved glucose control resulted in improved cognitive ability [14–16]. In addition to this, long-term poorly controlled diabetes results in permanent cognitive dysfunction secondary to vascular dementia [17]. Increases in glucose within the normal range, such as occur during a glucose tolerance test, improve memory in animals [18], young [19] and older [20] humans. Patients with dementia of the Alzheimer’s type appear to have abnormalities of glucose metabolism [21]. Raising the glucose levels in these patients improves cognition [22]. This effect appears to be predominantly due to the increase in insulin levels produced by elevating glucose levels [23]. Fat and the Neuronal Cell Membranes There is increasing evidence that fatty acid ratios in the diet can modulate the production of neurotransmitters, neuropeptides, enzymes and neuronal membrane composition [24]. In infants, some studies have suggested that dietary supplementation of long-chain polyunsaturated fatty acids may enhance cognitive function [25, 26]. 123 Nutrition and Cognition in Older Persons ↑Amyloid precursor protein ↑β-Amyloid ↓∆9-Desaturase ↓Unsaturated fatty acids ↓Membrane fluid ↓Neurotransmitter function ↓ Fig. 2. Pathophysiology of the cognitive defects due Cognition to β-amyloid overproduction. Based on studies in the SAMP8 mouse. In the Rotterdam Study the effect of food intake on the development of dementia was studied in 5,386 nondemented persons 55 years and older [27]. Dementia was associated with total fat (RR2.4), saturated fat (RR1.9) and cholesterol (RR1.7) intake. Fish consumption was inversely related to incident dementia (RR0.4). In a smaller group of elderly people in Spain lower intakes of saturated fat and cholesterol were found in persons with a normal MiniMental Status Examination [28]. The Italian Longitudinal Study on Aging examined the relationship of dietary macronutrients to cognitive function in 5,632 subjects aged 65–84 years [29]. In this study, high monounsaturated fatty acid intake was protective against age-related cognitive decline. These data are supported by a study in rats that demonstrated that a diet with high concentrations of saturated fatty acids impaired a wide range of learning and memory functions [30]. Yamomoto et al. [31] reported that a diet high in α-linolenate (18:3 n − 3) increased survival time and learning 124 Nutrition and Cognition in Older Persons ability in older rats. Sardine oil which increases brain levels of docosahexanoic acid enhanced membrane fluidity and maze-learning ability in mice [32]. Dietary docosahexanoic acid increased levels of hippocampal acetylcholine and improved passive avoidance response in stroke-prone spontaneously hypertensive rats [33]. The SAMP8 mouse develops early impairment in acquisition and learning [34]. This impairment is related to overproduction of β-amyloid [35, 36]. Activity of 9-desaturase is reduced by nearly 50% with age in these mice [37]. This is due to a specific decrease in mRNA. The decline in 9-desaturase is accompanied by the expected decline in the brain levels of unsaturated fatty acids. Dietary supplement with perilla oil (rich in α-linolenate) resulted in improved learning ability in the SAMP8 mouse [38]. Figure 2 provides a schema by which β-amyloid overproduction appears to result in cognitive decline. Yehuda et al. [39] provided a short-term supplementation to 100 patients with Alzheimer’s disease with a compound containing a 1:4 ratio of n − 3 and n − 7 fatty acids. Patients showed improvements in mood, cooperation, appetite, sleep, ability to navigate at home and short-term memory. Not all patients demonstrated a response. Overall these studies strongly support a role of membrane mobility in the development of age-related cognitive decline and in dementia. Dietary intervention appears to hold the potential to reverse these defects. Cholesterol and Cognition In vitro, in cell cultures, cholesterol can modulate the production of β- amyloid [40, 41] and hypercholesterolemia accelerates the β-amyloid pathology in a transgenic mouse model [42]. Cholesterol depletion inhibits the genera- tion of β-amyloid in hippocampal neurons [43]. Sparks [44] found that dietary cholesterol induced Alzheimer-like β-amyloid immunoreactivity in the rabbit brain. Studies examining the effect of cholesterol lowering in middle age support the concept that this will result in decreased atherosclerosis and decreased vascular dementia [45]. The direct effects of cholesterol-lowering agents on cognition are less clear. Two studies failed to show an effect of cholesterol- lowering agents on cognition [46, 47] while two showed deleterious effects [48, 49]. Vitamins Vitamin deficiencies were among the first clearly recognized causes of delirium. Thus pellagra (nicotinic and deficiency)
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