Anorexia of aging in long term care: is dronabinol an effective appetite stimulant?--a pilot study.

INTRODUCTION: Anorexia and subsequent weight loss increase the risk of death in long term care (LTC) residents. In patients who fail to respond to nutritional intervention, orexigenic drugs are sometimes prescribed. There is limited data regarding the safety and efficacy of these drugs in older adults. OBJECTIVE: To examine the effect of a 12-week course of dronabinol on LTC residents with anorexia and significant weight loss. DESIGN, SETTING, PARTICIPANTS: Retrospective observational study on residents in five LTC facilities in a major metropolitan area. RESULTS: Twenty-eight subjects (22F, 6M) were involved in the study. Mean age 79.5 +/- 19.8 years (range 46-98 y). Mean body weight, serum albumin and serum prealbumin at baseline were 105.7 +/- 24.7 lbs, 3.39 +/- 0.47 g/dl and 22.15 +/- 7.92 mg/dl respectively. 15 subjects (53.5%) gained weight on dronabinol, of which 10 (67%) gained more than 5 lbs and 6(40%) gained more than 10 lbs. Five (33%) subjects gained less than 5 lbs. Residents who lost weight on dronabinol were younger than those who gained weight (70.9 +/- 5.62 y and 90.8 +/- 7.84 y respectively; p = 0.007) Overall, the mean weight gain on dronabinol was 3 +/- 8.01 lbs (p=0.2). Eleven subjects lost weight (mean loss 3 +/- 2.6 lbs). Of the subjects who lost weight 7 (64%) died compared with 4 (26%) in the subgroup who gained weight. CONCLUSIONS: Dronabinol therapy was well tolerated. Overall, there was a trend toward weight gain in LTC residents treated with 12 weeks of dronabinol. Failure to respond to dronabinol may indicate increased risk of death.

Impaired cognitive function and mental performance in mild dehydration.

Dehydration is a reliable predictor of impaired cognitive status. Objective data, using tests of cortical function, support the deterioration of mental performance in mildly dehydrated younger adults. Dehydration frequently results in delirium as a manifestation of cognitive dysfunction. Although, the occurrence of delirium suggests transient acute global cerebral dysfunction, cognitive impairment may not be completely reversible. Animal studies have identified neuronal mitochondrial damage and glutamate hypertransmission in dehydrated rats. Additional studies have identified an increase in cerebral nicotinamide adenine dinucleotide phosphate-diaphorase activity (nitric oxide synthase, NOS) with dehydration. Available evidence also implicates NOS as a neurotransmitter in long-term potentiation, rendering this a critical enzyme in facilitating learning and memory. With ageing, a reduction of NOS activity has been identified in the cortex and striatum of rats. The reduction of NOs synthase activity that occurs with ageing may blunt the rise that occurs with dehydration, and possibly interfere with memory processing and cognitive function. Dehydration has been shown to be a reliable predictor of increasing frailty, deteriorating mental performance and poor quality of life. Intervention models directed toward improving outcomes in dehydration must incorporate strategies to enhance prompt recognition of cognitive dysfunction.