Dementia is defined as an acquired persistent impairment of intellectual function with compromise in at least three of the following spheres of mental activity: language, memory, visuospatial skills, emotion or personality, and cognition.
Despite recent advances in our understanding of the pathophysiology of Alzheimer's disease (AD) and other dementing illnesses, current treatments for these disorders often fall short of expectation. Patients, family members and caregivers often find themselves unable to resist the lure of using so-called natural products to treat or prevent memory impairments and their behavioral and psychological symptoms. This article will focus on providing an overview of the current scientific evidence of commonly used supplements for memory impairment.
Lecithin is found in many animal and vegetable sources (e.g., peanuts, cauliflower, oranges, eggs, steak and beef liver). Commercial sources can come from soybeans, eggs and other animal sources. Lecithin(Drug information on lecithin) is a choline-containing phospholipid and a major dietary source of choline. It is postulated to accelerate the synthesis of acetylcholine in the brain (Higgins and Flicker, 2000).
A review of 12 studies of dementia of the Alzheimer's type (DAT) to determine the efficacy of lecithin showed an overall relative deterioration of activities of daily living (ADLs) and no improvement of cognition or global impairment (Higgins and Flicker, 2000). In that same review, one trial of Parkinson's dementia showed a nonsignificant improvement in orientation and memory tests. There was no evidence of an effect on functional performance. However, the reviewers did find possible statistical improvement in one trial of subjective memory complaints.
The proposed lecithin dose is 1.2 g/day to 2.4 g/day. Possible adverse reactions include gastrointestinal (GI) pain, nausea or diarrhea. No adverse interactions have been reported.
Also known as tocopherol and tocotrienol, vitamin E(Drug information on vitamin e) occurs in oils, fats, nuts and other seeds, as well as a variety of animal foods. Alpha-tocopherol, the medical form used, is fat-soluble, and can therefore enter the brain. Vitamin E functions biologically as an antioxidant, inhibiting the process of lipid peroxidation.
One study using 1000 international units (IU) bid of vitamin E over two years in subjects with moderate DAT found no difference in survival time. The combination of vitamin E (2000 IU/day) and selegiline(Drug information on selegiline) (Eldepryl) (10 mg/day) was shown to reduce the rate of decline of functions in patients with AD. However, combined therapy was not superior to either agent alone (Sano et al., 1997).
Data from the Honolulu-Asia Aging Study suggested that vitamins E and C have a protective effect for vascular and mixed dementias and may improve cognitive function in late life (Masaki et al., 2000).
The proposed dose of vitamin E is 1000 IU bid. While possible adverse reactions are rarely reported, vitamin E may cause GI disturbances, blurred vision, headaches and fatigue.
Theoretically, vitamin E might increase the risk of bleeding in people with vitamin K deficiency or bleeding tendencies. It may theoretically have an additive interaction with antiplatelet and anticoagulant medications.
Thiamine (Vitamin B1)
The role of vitamin B1, which is present in cereal grains, nuts, meats and legumes, in treating alcohol(Drug information on alcohol)ic amnesia is well established. Animal studies both suggested that vitamin B1 might facilitate the presynaptic release of acetylcholine and bind to nicotinic receptors enhancing anticholinesterase activity. These may have a role in the management of AD.
Studies researching vitamin B1 as a treatment for AD are mostly small with fewer than 50 subjects. Most studies used subjects with mild-to-moderately severe AD and measured cognition and behavior as the primary outcomes. Overall results showed no improvement in cognition; however, results should be considered as inconclusive due to poor design and small number of subjects (Rodriguez-Martin et al., 2001).
The proposed dose of vitamin B1 is 1 g tid. Vitamin B1 may cause a hypersensitivity reaction or dermatitis. Loop diuretics may increase urinary B1 excretion resulting in a deficiency that can affect cardiac function.
Also known as water hyssop, Bacopa monniera is an Ayurvedic herbal used for mental illness, epilepsy and cognitive enhancement.
Steroidal saponins derived from the leaves are the active principle ingredient thought to enhance nerve impulse transmission, and hence to improve memory and cognition. Animal and human studies conducted in India in the early 1980s reported memory enhancing effects with improved concentration and working memory (Singh and Dhawan, 1982; Singh and Singh, 1980). Further studies are needed to explore the pharmacology and clinical usefulness of this supplement.
The proposed dose of Bacopa monniera is 12 g/day of the dried plant in syrup. Possible adverse effects and interactions are unclear from the literature available.
Perhaps the most widely recognized plant in folk medicine, ginseng (Panax ginseng) refers to several different species originating in different countries. The root is considered the most valuable in traditional medicine and has been used in the treatment of a great number of symptoms and diseases. The contents of the particular root are dependent on the species, age, location of plant, and method and timing of harvest and processing. Over the last decades, laboratory and human studies have documented a range of pharmacological effects from the ginsenosides, the steroid-like compounds found in ginseng. Ginseng is known as an adaptogen. Animal studies report a reversal of scopolamine-induced memory deficits in rats, an increase in acetylcholine uptake and improved learning performance. In humans, two randomized, controlled trials reported some improvement in cognitive function over eight and 12 weeks of ginseng use. Another study, looking specifically at 50 elderly subjects, reported improvement over baseline measures (Vogler et al., 1999).
The proposed ginseng dose is 400 mg/day. Possible adverse effects from taking ginseng include headache, hypoglycemia, tremor, sleep disorders and GI disorders. Ginseng may interact with warfarin(Drug information on warfarin) (Coumadin), diabetic agents and insulin, diuretics, digoxin(Drug information on digoxin), phenelzine(Drug information on phenelzine) (Nardil), and alcohol.
An endogenous substance that participates in cellular energy production, acetyl-l-carnitine is structurally related to acetylcholine; hence it may enhance cholinergic neurotransmission. It may also promote mitochondrial membrane stabilization.
Several animal and laboratory studies suggested a possible role in delaying cognitive decline. A large-scale study enrolled 229 subjects with probable AD between 45 years of age and 65 years of age. Subjects were randomized to 1 g tid or placebo. No differences in the rate of decline of cognitive function were noted (Thal et al., 2000). This finding is contrary to outcomes reported in previous smaller studies that indicated a slowing of cognitive decline. Further studies are needed to evaluate the possible role of acetyl-l-carnitine in the management of memory impairment.
The proposed dose of acetyl-l-carnitine is 1.5 g/day to 4 g/day divided in three doses. Possible adverse reactions may include confusion, depression, agitation or aggression in patients with AD. No adverse interactions have been reported.
Ginkgo biloba extracts are prepared from the green leaves of the maidenhair tree. More than 40 individual components of ginkgo have been identified so far. Actions of the components of ginkgo include antioxidant properties, vasodilation, antagonism of platelet-activating factor and an increase in density of muscarinic receptors.
A recent review of nine randomized, double-blind, controlled studies suggested that ginkgo extract is more effective than placebo in delaying the deterioration of AD, vascular dementia and mixed types. A small effect was observed after six months in a meta-analysis looking at subjects with mild-to-moderate AD (Ernst and Pittler, 1999). Wettstein (2000) compared placebo-controlled studies of available cholinesterase inhibitors with studies of the standardized ginkgo extract EGb 761 and found similar periods of delay in disease progression, although another well-designed study failed to find any benefit in elderly subjects with mild-to-moderate dementia (van Dongen et al., 2000). Large doses of ginkgo (>600 mg) resulted in subtle improvement in speed of information processing but not in other cognitive functions. Overall, studies looking at memory improvement in nondemented healthy adults have been inconclusive.
The proposed dose of ginkgo is 120 mg/day to 240 mg/day divided in three doses of the standardized extract containing 24% flavonoids and 6% terpenoids. Possible adverse reactions include headache, dizziness, palpitations, restlessness, weakness, central nervous system hemorrhage and seizures. Ginkgo should be used with caution with medications that inhibit clotting or enhance bleeding.