Many of our patients and their families ask us about whether they should take any one of the many supplements, herbs, vitamins, or over-the-counter medications they have seen in the supermarkets or on television infomercials. Other patients are already taking some of these additives and wonder if they are doing any good or even whether they are harmful. Because many of these compounds have demonstrated or are purported to have antioxidant effects, and because oxidative stress is thought to be harmful to brain cells, there is a rational basis for hypothesizing that these drugs could slow progression of Alzheimer’s disease. We generally explain this rationale to the patient and family, but we also explain to them that, unlike medication approved by the US Food and Drug Administration (FDA), these supplements have not undergone careful evaluation, and, just like prescription medications, vitamins and supplements have benefits as well as risks and side effects, and the decision of whether to take them should be made by weighing the relative risks and side effects versus the benefits.
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Vitamin D:
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Increased risk of all-cause dementia and Alzheimer’s disease has been observed in those with vitamin D deficiency.
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We recommend vitamin D supplementation for our patients with vitamin D deficiency.
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Vitamin E:
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Two studies were positive in patients with Alzheimer’s disease, but both had issues and many other studies were negative.
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We do not recommend vitamin E for our patients.
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B complex vitamins—folic acid, B6, B12:
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There is much retrospective and theoretical data to suggest that these vitamins would be helpful in Alzheimer’s disease.
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A large 18-month study showed no benefit for patients with Alzheimer’s disease.
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We do not recommend B complex vitamins for our patients unless they have a vitamin B deficiency.
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Ginkgo biloba
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One study was positive in patients with Alzheimer’s disease, but many other studies were negative.
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We do not recommend ginkgo for our patients.
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DHA (phosphatidylcholine docosahexaenoic acid) (fish oil):
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Large, retrospective studies suggested that DHA may reduce the risk of Alzheimer’s disease.
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A large, multicenter, randomized, placebo-controlled trial showed no benefit.
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We neither encourage nor discourage taking DHA or eating fish for our patients.
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Anti-inflammatories:
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Several large retrospective studies suggested that non-steroidal anti-inflammatory drugs (NSAIDs) may help prevent Alzheimer’s disease.
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Several randomized controlled clinical trials for NSAIDs and cyclo-oxygenase (COX)-2 inhibitors showed no benefit related to Alzheimer’s disease.
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NSAIDs and COX-2 inhibitors have significant side effects and risks associated with them.
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We do not recommend NSAIDs or COX-2 inhibitors for our patients with Alzheimer’s disease.
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Vitamin D
A study published in September 2014 of over 1500 healthy older adults found that those who had vitamin D deficiency were between 1.7 (mild deficiency) and 2.2 (severe deficiency) times more likely to develop all-cause dementia and Alzheimer’s disease ( Fig. 18-1 ) ( ). However, a prior study found that vitamin D supplementation on healthy older women had no effect on cognition or the development of mild cognitive impairment (MCI) or dementia ( ). How do we reconcile these studies? The simple answer is most likely that supplementation of vitamin D is helpful if an individual’s levels are low. Vitamin D levels are, in fact, low in many older adults. Moreover, there are other proven benefits of vitamin D in the older adult, such as improving bone health (when combined with calcium), and there are few reported side effects of vitamin D when taken in recommended dosages. We therefore recommend that our older adults with memory problems (whether due to normal aging or disease) either have their vitamin D levels checked or simply take vitamin D supplementation. Because there have been no positive trials in improving cognition or reducing dementia, the exact dose and form of vitamin D to recommend (D2, ergocalciferol versus D3, cholecalciferol) is unclear at this time. The US Food and Drug Administration (FDA) recommends 400 IU (10 mcg) daily. Many guidelines recommend between 400 and 1000 IU daily, and most experts recommend the D3 (cholecalciferol) form. Note that there are some important and common drug interactions with vitamin D, including with digoxin, diltiazem, verapamil, thiazide diuretics, and others, so interactions should be checked prior to recommending vitamin D to your patient.
Vitamin E
A paper published in the New England Journal of Medicine in 1997 reported the results of a two-year, double-blind, placebo-controlled, randomized trial in 341 patients with mild to moderate Alzheimer’s disease receiving either high doses (2000 IU/day) of vitamin E (alpha-tocopherol), selegiline 10 mg/day, both, or placebo. The results showed no statistically significant difference in the outcomes among the four groups. However, after adjustment for unequal baseline MMSE scores by including MMSE as a covariate, all treatment groups—vitamin E, selegiline, and combined—showed better outcomes than the placebo ( ). In 2014 the Journal of the American Medical Association (JAMA) reported the results of a double-blind, placebo-controlled, randomized trial evaluating 613 patients with mild to moderate Alzheimer’s disease treated with vitamin E 2000 IU/day, memantine (Namenda) 20 mg/day, both, or placebo. The authors found that, compared to placebo, there was a slower rate of decline in the vitamin E group, but not in the memantine-alone group nor in the group treated with both vitamin E and memantine ( ). A randomized, double-blind, placebo-controlled study that evaluated vitamin E 2000 IU/day versus donepezil (Aricept) 10 mg versus placebo in over 750 patients with mild cognitive impairment over three years showed no benefit for vitamin E ( ).
How are we to best understand these somewhat conflicting data? How do we interpret a study in which there were no effects of treatment until a covariate analysis was performed to correct for unequal baseline, and then all treatments showed effects? What does it mean that another study found benefit for vitamin E alone but not when combined with memantine; does that mean that vitamin E is beneficial but memantine counteracts its beneficial effect? In our view, the data show that vitamin E provides no benefit in patients with mild cognitive impairment, and the data for the use of vitamin E in patients with mild to moderate Alzheimer’s disease remain unclear. Vitamin E may increase the risk of cardiac events in individuals with vascular disease or diabetes ( ), and vitamin E may cause problems with bleeding and/or easy bruising in some individuals ( ).
Based upon the available data, regardless of whether they are cognitively healthy or they have been diagnosed with mild cognitive impairment or Alzheimer’s disease, we do not recommend vitamin E supplementation for our patients, and if they are already taking vitamin E solely to prevent or retard Alzheimer’s disease, we recommend that they discontinue it.
Related posts:
Approach to the Patient with Memory Loss, Mild Cognitive Impairment, or Dementia
Jakob-Creutzfeldt Disease
Progressive Supranuclear Palsy
Legal and Financial Issues in Memory Loss, Alzheimer’s Disease, and Dementia
Evaluating the Behavioral and Psychological Symptoms of Dementia
Other Disorders That Cause Memory Loss or Dementia
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