June 2009 Issue
Supplementing Memory Loss
By Jasmin Ilkay, MPH, RD
Vol. 11 No. 6 P. 16
By the time you finish reading this article, five people will have been diagnosed with Alzheimer’s disease (AD). The disease affects more than 5 million Americans, and, as baby boomers continue to age, that number is expected to triple by 2050, according to statistics from the Fisher Center for Alzheimer’s Research Foundation. If there is any hope for reversing this startling trend, scientists must explore additional ways to prevent, manage, and eventually cure this mind-crippling disease.
AD is a degenerative brain disorder that manifests as a progressive deterioration of memory and mental function, according to the second edition of the Encyclopedia of Natural Medicine. The most common form of dementia, AD impairs memory, thought, and speech; the disease’s final stage renders an affected individual totally helpless and unable to control bodily functions.
The disease is characterized by the formation of neurofibrillary tangles and amyloid plaques in the brain. These tangles and plaques are composed of various protein deposits and cellular debris. The result is the shrinkage and loss of nerve cells, including ones that produce neurotransmitters. As the nerve cells continue to die, the brain itself shrinks and the wrinkles along its surface start to smoothen, according to the Fisher Center.
Can Dietary Supplements Help?
Early detection is key to delaying the disorder’s progression. Drug therapy treatments typically include cholinesterase inhibitors (eg, Aricept, Reminyl, Exelon) combined with the drug Namenda, which targets a brain chemical known as glutamate. This treatment has been shown to be most effective in delaying the progression of AD. The role that certain dietary supplements may play in preventing and managing the disorder is also under investigation.
Ginkgo biloba is the most popular brain-boosting supplement sold in the United States, owing to manufacturers’ claims that it enhances memory and cognitive function. A study published in 1998 in the Archives of Neurology detailed the results of an extensive literature review, the authors of which aimed to ascertain whether current data support the claim that ginkgo enhances cognitive function in patients with AD. The authors found a significant improvement in cognitive function in subjects who took daily doses of 120 to 240 mg ginkgo biloba extract for three to six months.
However, a more recent study concluded that ginkgo does nothing to prevent the development of dementia and AD. The Ginkgo Evaluation of Memory (GEM) study evaluated more than 3,000 men and women aged 75 and older for eight years. One half of the group took 120 mg ginkgo twice daily, while the rest took a placebo. During the study, 523 subjects were diagnosed with AD or another form of dementia. Dementia developed in 246 of those receiving a placebo compared with 277 in the ginkgo group, according to the study published in The Journal of the American Medical Association. The study authors concluded that ginkgo should not be recommended for the purpose of preventing dementia or dementia-related diseases.
Some scientists argue that the GEM study was not conducted for a long enough duration and that the dosage of ginkgo could have been higher. More trials investigating ginkgo biloba’s role in treating or preventing AD are still underway. For now, anyone planning to take ginkgo biloba supplements should follow manufacturers’ instructions and consult their physician. Those taking anticoagulants should proceed with even more caution, as ginkgo may increase their risk of bleeding.
Huperzine A (HupA) is an extract that comes from a moss called Huperzia serrata. While not very popular in the United States, HupA has been used as an herbal supplement in China for centuries to treat fevers, inflammation, muscle strains, and swelling and to manage AD.
Preliminary studies suggest that HupA acts like a natural cholinesterase inhibitor. Cholinesterase inhibitors prevent the breakdown of the neurotransmitter acetylcholine and are commonly prescribed to patients with AD. In addition to HupA’s ability to resemble the actions of cholinesterase inhibitors, it also has antioxidant and neuroprotective properties. These potential actions imply that HupA may be useful as a preventive and disease-modifying treatment for AD, according to information from a clinical trial sponsored by the National Institute on Aging. In the United States, HupA is presently available over the counter as a nutraceutical. Its actions are so promising that some U.S. clinicians are already prescribing it to their patients with AD.
A recent multicenter, double-blind, placebo-controlled, therapeutic trial was conducted to determine HupA’s ability to improve cognitive function in 210 patients with AD. The patients received either 200 or 400 mcg HupA or a placebo twice daily for 16 weeks. One half of the subjects also received concomitant treatment with Namenda. Results showed no statistical difference in the mean change on the AD Assessment Scale-Cognitive (ADAS-Cog) scores after 16 weeks of treatment with 200 mcg HupA. However, data demonstrated that the higher 400-mcg dose showed cognitive enhancement on the ADAS-Cog vs. placebo, according to the Mount Sinai School of Medicine Alzheimer’s Disease Research Center.
So far, preliminary studies conducted in the United States confirm what the Chinese have believed for years: HupA is a promising therapy for preventing and slowing the progression of AD. Longer trials with more participants are needed to further determine HupA’s role in treating AD. Individuals wishing to take HupA should first consult their physician.
Essential Fatty Acids
Fatty acids are abundant in the brain. They are incorporated into phospholipids, which form a barrier protecting the cells from the external environment.
Researchers have studied the role of essential fatty acids in AD management for years. Most fatty acid research focuses on the preventive role of DHA. Until recently, the specific mechanism by which DHA helped prevent AD was unknown. However, recent studies have begun to unlock the anti-Alzheimer’s mechanism in DHA and other essential fatty acids.
An article published in The Journal of Neuroscience detailed a study in which researchers found that even low doses of DHA derived from fish oil increased the production of the neuronal receptor LR11. The LR11 protein is found at reduced levels in patients with AD and is known to eradicate the protein that forms amyloid plaques. The researchers examined the effects of DHA in multiple biological systems and by adding it directly to neurons grown in the laboratory, including human neuronal cells.
Another study performed by scientists at the Gladstone Institute of Neurological Disease and the University of California found that the complete or partial removal of an enzyme that regulates fatty acid levels improved cognitive deficits in a mouse model of AD. Removing the enzyme lowered levels of arachidonic acid, possibly allowing neurons to function more normally. While fatty acid levels can be regulated by diet and the intake of supplements, the inhibition of arachidonic acid levels could prevent some of the neurological impairments in AD.
Phosphatidylserine (PS) is another essential fatty acid and the principal component of the membranes that surround the nerve cells. A PS deficiency has been linked to cognitive impairment, since low levels result in nerve cell deterioration. Proponents of PS suggest that therapeutic doses could protect nerve cells from degenerating, thus preventing or slowing the progression of AD. A small clinical trial reported promising results in AD patients treated with PS derived from soy. However, larger controlled studies are needed to determine whether PS has a role in AD treatment and prevention.
Fatty acids, especially DHA, could have a profound impact on the prevention and treatment of AD. Because DHA supplementation is considered relatively safe, many patients with AD or those at risk for AD may decide to supplement with DHA. Those who decide to take a DHA omega-3 fatty acid supplement should choose a reputable company whose products are free of heavy metals (eg, mercury, lead, cadmium).
Epidemiological research has demonstrated that AD is less common in India than in Western countries. A research group supported by the National Institute on Aging and the National Institute of Neurological Disorders and Stroke found that curcumin, the key ingredient in turmeric, may have anti-inflammatory and antioxidant properties. Researchers found that curcumin was able to cross the blood-brain barrier and bind directly to beta-amyloid peptides in test tube and transgenic mice. When fed to aged mice with significant plaque accumulation, the curcumin was able to reduce amyloid levels and the overall amount of plaque, the researchers found.
Looking to the Future
As AD becomes more prevalent, research becomes even more important. Of the dietary supplements mentioned, HupA and DHA appear to have the most potential for preventing and treating patients in the early stages of AD. With the development of earlier detection methods, these potential treatments could have a profound impact on the prevention and management of AD.
— Jasmin Ilkay, MPH, RD, is the director of nutrition for Fitwize 4 Kidz and a freelance writer who specializes in weight management, sports nutrition, eating disorders, and general nutrition counseling.