Pamela Hutchison, BSc, ND
Age-related cognitive decline begins, remarkably, in the late 20s and early 30s. As we age, we lose brain function from cellular injury due to inflammation, toxin exposure, insufficient sleep, injury, and other noxious influences. The development of any dementia is owing to genetic predisposition plus the cumulative effects of these lifelong processes. As preventive medical experts, NDs are well positioned to treat early cognitive decline, before pharmaceuticals are required, and to help those at risk to avoid dementia or at least minimize its effect on their lives.
In general, current research in cognitive decline and dementia supports the traditional naturopathic approach of “treating the whole person.” Cognitive capacity is influenced by neurotransmitter activity, general brain health, cardiovascular health, education, diet, nutrient levels, smoking, exercise levels, blood glucose level, and immune system function, to name a few. Our brains act within the greater whole of the body, so a healthier body equals a healthier brain, and vice versa.
This 2-part article presents strategies for assessing, preventing, and treating cognitive decline in its various manifestations. Because many of our patients in their 60s and 70s are fearful of dementia and often report memory problems, our first step should be to determine who indeed is at risk or is actually in early decline.
When interviewing the patient, ask about family history of dementias, heart disease, obesity, diabetes mellitus, mental illness, and neurological disorders. Discuss personal history of smoking, other drug use, medications, head injuries, strokes, toxin and heavy metal exposures, cardiovascular events, mental health, and general medical conditions. When discussing memory loss and cognitive dysfunction, assess onset (fast or slow) and severity (see rating scales for cognitive decline in Sidebar 1).
Rating scales provide a baseline of how a patient is currently functioning. Sidebar 1 lists some brief rating scales you can perform in the office. Most people in very early cognitive decline will do well on all the scales, but those with mild cognitive impairment will struggle. These are valuable tools to quantify current cognitive function and to reassure patients who test well that they are not experiencing clinical dementia.
The physical examination should be thorough and include all items listed in Sidebar 2, as well as any procedures indicated by the interview. Take note of ambulation when the patient is entering and leaving the room, and attend to what the patient’s facial expression is and how he or she acts during the visit. Repetition of the same information during the visit may indicate memory loss. If tremor, gait changes, flat facial expression, or affect blunting is evident, consider additional assessments for Parkinson disease.
Laboratory tests are useful to rule out nondementia-related causes of cognitive dysfunction, broadly assess risk, focus treatment, and motivate the patient to make changes. Sidebar 3 lists laboratory tests that are generally indicated when assessing cognitive decline or risk of cognitive decline. The tests that have so far proven to be of some predictive value are largely those used to assess vascular risk and inflammation. These include levels of homocysteine, C-reactive protein (CRP), and interleukin 6 (IL-6).
Homocysteine levels have been found to correlate with various changes in the brain and its function. High homocysteine levels are associated with atrophic brain changes (a hallmark of Alzheimer disease) and silent brain infarcts in healthy middle-aged adults.1 Among older patients, elevated homocysteine concentrations within normal levels have been seen to predict the rate of global cognitive decline in neuropsychological test results and in those with Alzheimer disease.2,3 In a study4 of older patients investigating whether homocysteine concentration (and other markers) predicted conversion from cognitively healthy to mild cognitive impairment to Alzheimer disease, homocysteine levels were higher in those who converted from cognitively healthy to Alzheimer disease vs in those who did not.
The predictive value of homocysteine level alone for future cognitive decline is a modest 5%,5 although it may be more sensitive to subclinical Alzheimer disease (in older populations) over other forms of dementia.6 Because homocysteine level is elevated in mental illnesses and vascular disease in general, it is important to view it as one of several markers that, when elevated together, indicate a heightened risk of cognitive decline.
A final note is that studies using vitamin B12 or folic acid to successfully decrease homocysteine levels did not find a relationship to improved cognitive status in older patients with dementia7 or in those with mild to moderate Alzheimer disease8; thus, homocysteine concentration should be considered a surrogate marker for cognitive decline and not a causative agent or an indicator that vitamin B12 or folic acid supplementation will be specifically effective in reversing cognitive change. That being said, there is some indication that folic acid alone may be beneficial for cognitive function in healthy older patients with elevated homocysteine levels and may improve outcomes for patients taking cholinesterase inhibitors.9
An elevated CRP level indicates inflammation and is a nonspecific indicator of risk for cognitive decline. It may be more specific to vascular dementia vs Alzheimer disease when IL-6 level is elevated as well.6 Older stroke-free nondemented individuals with higher CRP levels showed greater microstructural disintegration in the frontal lobes, as well as poorer scores on tests assessing executive function.10 A CRP level exceeding 3.3 mg/L seems to be correlated with mild cognitive decline in older subjects (age range, 70-89 years).
Similar to CRP, IL-6 is an indicator of systemic inflammation. Elevations in IL-6 level seem to be associated with non-Alzheimer dementia independently11 and in combination with elevated CRP level, as mentioned earlier. Co-elevations of CRP and IL-6 levels in a patient older than 65 years, along with indicators of cognitive decline through rating scales, physical examination, and intake interview, should raise suspicions of vascular dementia.
Once a full intake and laboratory study has been performed, a clinician has the tools to build a specific treatment plan for a patient that takes into account his or her specific risks for cognitive decline or dementia. The strategy provides a framework for tracking progress and motivates the patient to see his or her changes.For more than 10 years, Dr Pamela has practiced with a clinical focus on mental health, neurology, and neurobehavioral disorders in adults and children. She is the clinic director of Acacia Integrative Health Clinic in Victoria, British Columbia, Canada, a multidisciplinary clinic with a team approach to healthcare.
1. Seshadri S, Wolf PA, Beiser AS, et al. Association of plasma total homocysteine levels with subclinical brain injury: cerebral volumes, white matter hyperintensity, and silent brain infarcts at volumetric magnetic resonance imaging in the Framingham Offspring Study. Arch Neurol. 2008;65(5):642-649.
2. Oulhaj A, Refsum H, Beaumont H, et al. Homocysteine as a predictor of cognitive decline in Alzheimer’s disease. Int J Geriatr Psychiatry. 2010;25(1):82-90.
3. Ellinson M, Thomas J, Patterson A. A critical evaluation of the relationship between serum vitamin B, folate and total homocysteine with cognitive impairment in the elderly. J Hum Nutr Diet. 2004;17(4):371-383.
4. Blasko I, Jellinger K, Kemmler G. Conversion from cognitive health to mild cognitive impairment and Alzheimer’s disease: prediction by plasma amyloid beta 42, medial temporal lobe atrophy and homocysteine. Neurobiol Aging. 2008;29(1):1-11.
5. Nilsson K, Gustafson L, Hultberg B. Plasma homocysteine and cognition in elderly patients with dementia or other psychogeriatric diseases. Dement Geriatr Cogn Disord. 2010;30(3):198-204.
6. Ravaglia G, Forti P, Maioli F, et al. Blood inflammatory markers and risk of dementia: The Conselice Study of Brain Aging. Neurobiol Aging. 2007;28(12):1810-1820.
7. Kwok T, Lee J, Law CB, et al. A randomized placebo controlled trial of homocysteine lowering to reduce cognitive decline in older demented people [published online ahead of print January 7, 2011]. Clin Nutr. 2011. doi:10.1016/j.clnu.2010.12.004. Medline:21216507.
8. Aisen PS, Schneider LS, Sano M, et al. High-dose B vitamin supplementation and cognitive decline in Alzheimer disease: a randomized controlled trial: Alzheimer Disease Cooperative Study. JAMA. 2008;300(15):1774-1783.
9. Malouf R, Grimley Evans J. Folic acid with or without vitamin B12 for the prevention and treatment of healthy elderly and demented people. Cochrane Database Syst Rev. 2008;(4):CD004514.
10. Wersching H, Duning T, Lohmann H, et al. Serum C-reactive protein is linked to cerebral microstructural integrity and cognitive function. Neurology. 2010;74(13):1022-1029.
11. Sundelöf J, Kilander L, Helmersson J, et al. Systemic inflammation and the risk of Alzheimer’s disease and dementia: a prospective population-based study [published correction appears in J Alzheimers Dis. 2010;20(2):681]. J Alzheimers Dis. 2009;18(1):79-87.