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Nutritional Status is Associated With Severe Dementia and Mortality

The Cache County Dementia Progression Study

Sanders, Chelsea L., MS*; Wengreen, Heidi J., RD, PhD*; Schwartz, Sarah, PhD*; Behrens, Stephanie J., MS*; Corcoran, Chris, ScD*; Lyketsos, Constantine G., MD; Tschanz, JoAnn T., PhD* The Cache County Investigators

Alzheimer Disease & Associated Disorders: October-December 2018 - Volume 32 - Issue 4 - p 298–304
doi: 10.1097/WAD.0000000000000274
Original Articles

Purpose: Studies have reported faster cognitive/functional decline in persons with dementia (PWD) with malnutrition. We investigated whether baseline nutritional status predicted severe dementia and mortality in a population-based sample.

Patients: A maximum of 300 PWD were assessed annually for up to 8.6 years.

Methods: Nutritional status was assessed using a modified Mini-Nutritional Assessment (mMNA). Severe dementia was defined as: “severe” rating on the Clinical Dementia Rating or Mini-Mental State Examination score ≤10. Using Cox proportional hazards models, we examined the association between baseline mMNA score (or its subcomponents) with each outcome. Covariates included demographics; dementia onset age, type, and duration; APOE genotype; and residency with caregiver.

Results: Compared with “well-nourished,” “malnourished” PWD had 3-4 times the hazard of severe dementia [hazard ratio (HR), 4.31; P=0.014] and death (HR, 3.04; P<0.001). Those “at risk for malnutrition” had twice the hazard of severe dementia (HR, 1.98; P=0.064) and 1.5 times the hazard of death (HR, 1.46; P=0.015). mMNA subcomponents of food group intake, weight loss, body mass index, mobility, health status, protein consumption, and mid-arm circumference predicted one or both outcomes.

Conclusions: Nutritional status is an important predictor of clinical outcomes in dementia and may provide an avenue for intervention.

*Utah State University, Logan, UT

The Johns Hopkins University, Baltimore, MD

Supported by NIH grants R01AG21136 and R01AG11380, and the Johns Hopkins Alzheimer’s Disease Research Center P50AG005146.

The authors declare no conflicts of interest.

Reprints: JoAnn T. Tschanz, PhD, 2810 Old Main Hill, Logan, UT 84322 (e-mail: joann.tschanz@usu.edu).

Received December 5, 2017

Accepted July 30, 2018

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