High dose vitamin B supplements do not impede the cognitive decline in Alzheimer disease (AD) patients, according to a study published in the October issue of The Journal of the American Medical Association.
Elevated homocysteine levels are believed to play a role in the disease process of AD. As vitamin B reduces the levels of the amino acid by enhancing its metabolism, Paul S Aisen, at the Department of Neurosciences, University of California, San Diego (UCSD), and colleagues, sought to study if vitamin B supplementation benefited the cognitive function in AD patients.
A double-blind randomized study, involving 409 participants was conducted across multiple clinical research sites of the United States. All participants had mild to moderate AD and normal vitamin B12, folate and homocysteine levels. Sixty percent of the participants received vitamin B supplementation (5 mg/d of folate, 25 mg/d of vitamin B6, 1 mg/d of vitamin B12) and the rest were given placebo for a total duration of 18 months. A drop in the score on Alzheimer Disease Assessment Scale (ADAS-cog) was the primary outcome measure. Only 340 participants (202 in the treatment group and 138 in the placebo group) completed the study. There was a significant reduction in the homocysteine levels in participants who received vitamin B supplements (mean [Standard Deviation], –2.42 [3.35] in treatment group vs –0.86 [2.59] in placebo group; P<0.001). However, this did not translate into decelerated cognitive decline as determined by the ADAS-cog score (0.372 points per month for placebo group vs 0.401 points per month for active treatment group, P=0.52). Thus, the results of this study do not justify high dose vitamin B supplementation in patients with AD.
The relationship between homocysteine levels and dementia of AD has been extensively studied over the past few years. A German study by Schulz RJ (Current Opinion in Clinical Nutrition and Metabolic Care, 2007) reported that homocysteine is not an ideal marker for screening cognitive function but can be a surrogate marker for organ insufficiency and malnutrition. Also, Li L and colleagues (Dementia and Geriatric Cognitive Disorders, 2008) from the University of Alabama at Birmingham, USA, concluded in their study that rising homocysteine levels are related more to aging than cognition. Their conclusion was based on the findings that the homocysteine levels increased with age and the inverse relationship between the Mini-Mental State Exam scores and plasma homocysteine levels did not persist after adjustments for various factors.
Being the most common cause of dementia, Alzheimer disease causes cognitive and behavioral impairment sufficiently severe to affect the patient’s social and occupational functioning. The risk of developing the disease increases with age, with nearly 50% of those aged above 85 years having the disease. About 5 million Americans are affected by AD, which is estimated to reach 15 million by 2050, as the US population ages. Many patients require caregivers, and it is estimated that this unpaid labor force has an economic value of $306 billion. The exact cause of the disease is yet to be elucidated but recent studies have exposed several risk factors linked to genetics, environment and diet, some of which still need to be confirmed by larger studies. Until then, caregiving and end of life issues will remain the priority in the management of this neurological illness.
References
1. Aisen PS, Schneider LS, Sano M, et al. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial. JAMA. 2008 Oct 15;300(15):1774-83.
2. Hirono N, Hashimoto M, Yasuda M, Kazui H, Mori E. Accelerated memory decline in Alzheimer’s disease with apolipoprotein epsilon4 allele. J Neuropsychiatry Clin Neurosci. 2003 Summer;15(3):354-8.
3. Li L, Cao D, Desmond R, et al. Cognitive Performance and Plasma Levels of Homocysteine, Vitamin B(12), Folate and Lipids in Patients with Alzheimer Disease. Dement Geriatr Cogn Disord. 2008 Oct 16;26(4):384-390. [Epub ahead of print].
4. Schulz RJ. Homocysteine as a biomarker for cognitive dysfunction in the elderly. Curr Opin Clin Nutr Metab Care. 2007 Nov;10(6):718-23.
5. Alzheimer’s disease. CDC website. Last accessed October 23, 2008.
