Lowered Plasma Vitamin C, but not Vitamin E, Concentrations in Dementia Patients
Charlton, K. E., Rabinowitz, T. L., Geffen, L. & Dhansay, M. A. (2004). Lowered Plasma Vitamin C, but not Vitamin E, Concentrations in Dementia Patients. Journal of Nutrition Health and Aging, 8 (2), 99-107.
BACKGROUND: Alzheimer s disease (AD), according to the free radical hypothesis, affects brain regions where free radical damage occurs. Antioxidant nutrients may help to protect these brain regions. OBJECTIVE: To investigate whether plasma vitamin C and E status is lowered in subjects with AD and dementia. DESIGN: A case control study was conducted in 93 institutionalized subjects aged 65 + yrs. The dementia group (N = 43) included 15 subjects with Alzheimer s Disease (AD) and 28 subjects with senile dementia, while the control group included 50 subjects with no cognitive impairment. Subjects with uncontrolled hypertension and/or diabetes were excluded from the study. Plasma vitamin C and E was determined using the 2,6- dichlorophenolindophenol and the HPLC methods, respectively. Dietary intake, including dietary supplements, was assessed using a 2-day plate-waste method. Cognitive function was measured using the MMSE and nutritional status assessed using the Mini Nutritional Assessment (MNA) tool. RESULTS: The control group had significantly higher scores for the MNA, MMSE and Activities of Daily Living, compared with the dementia group. Controls had a significantly higher plasma vitamin C concentration than dementia patients (median = 0.84 (IQR = 0.54) mg/dl and 0.56 (0.80) mg/dl, respectively; P<0.05). The dementia group were more likely to have sub-optimal plasma vitamin C levels (< 0.6 mg/dl) than control subjects (OR = 2.99; 95 % CI = 0.95 9.79; P<0.05), despite having similar dietary vitamin C intakes. Plasma vitamin C was positively associated with MMSE score (r = 0.21; P<0.05). No difference was found between the groups for either plasma or dietary vitamin E. CONCLUSION: Plasma vitamin C levels were lower in subjects with dementia compared to controls, which was not explained by their dietary vitamin C intakes. This data supports the free radical theory of oxidative neuronal damage. Further investigations of whether supplementation with this vitamin may prevent or delay the progression of cognitive decline in patients with AD and senile dementia appear warranted.