Medication may not be the only way to help prevent and treat this frightening disease.
Losing one’s mind, or “going senile,” may be the most feared consequence of aging. Only a few decades ago, it was widely assumed that this loss of mental capacity—also called dementia—resulted from a progressive hardening of the arteries that is an inevitable part of the aging process. According to this theory, once a person reaches a certain age their arteries will get so hard and narrow that they can no long provide brain cells with an adequate supply of oxygen. These delicate cells then begin dying off at the rate of tens of thousands per year. Eventually, the person loses so much of their brain tissue that their ability to think and remember becomes seriously impaired.
Scientific studies have indeed confirmed that diseased blood vessels are more likely to become clogged, resulting in strokes, which can in turn lead to a deterioration in cognitive function. Although this mechanism does play a role in many cases of memory loss and senility, extensive research conducted over the last twenty years has revealed that the vast majority of cases—at least 75 percent—of age-related dementias result instead from a chronic neurodegenerative disorder called Alzheimer’s disease (AD). Once considered to be a rare and mysterious condition, it is now recognized that AD is responsible for a rapidly growing epidemic of dementia in this country and around the world. Current estimates are that AD affects about 4 million Americans. Given that the elderly population is rapidly increasing and that AD strikes up to 50 percent of people aged eighty-five and older, the number of afflicted people is expected to triple in the next thirty to forty years.
Unfortunately, the discovery that AD and not hardened arteries is the culprit behind age-related dementia has led to an increase in our collective anxiety. This is reflected throughout the medical literature on AD, where an attitude of gloom and doom prevails. AD is not well understood, it’s difficult to diagnose, and it’s even more difficult to treat. Most people die from it within eight to ten years after the diagnosis is made. At least there have been concerted efforts to educate the public about how to prevent and treat hardened arteries, but with AD, very little information has been disseminated about the role of lifestyle factors in prevention and treatment.
The mainstay of conventional therapy for AD involves the use of a class of prescription drugs called cholinesterase inhibitors. These drugs work by blocking an enzyme that breaks down acetylcholine, one of the primary chemicals that the brain uses to store memories. Because acetylcholine is depleted in the brains of people with AD, taking a substance that increases it can potentially enhance or restore short-term memory and cognitive function. Currently available drugs in this category include tacrine, donepezil, rivastigmine, and galantamine.
Interestingly, galantamine, the newest drug to achieve approval for treatment of AD in the United States, is an extract from daffodil bulbs (Narcissus tazetta).
Despite the promise offered by these drugs, their effects have been modest at best. Although regular use can lead to mild improvements in mental function and behavior for 30 to 50 percent of patients, this only lasts for an average of two years. Once the drug stops working, the person’s condition tends to rapidly deteriorate. In other words, all these drugs do is buy time by keeping symptoms at bay. And, at an average cost of $4 per day, they do so at a steep price. They can also cause numerous side effects including nausea, vomiting, sweating, watery eyes, increased salivation, and diarrhea. Tacrine, the first drug to be routinely prescribed for AD, was later found to cause severe liver damage in a number of patients. Consequently, tacrine has largely been supplanted by its successors.
Clearly, there is a need for better ways to deal with this disease. We need therapies that address the underlying mechanisms instead of temporarily covering up the symptoms. Instead of trying to plug the leaks in the dam, we need to understand why the river is overflowing. We need to figure out ways to identify the disease in its earliest stages, so we can slow it down or stop it before it inflicts so much damage that it becomes impossible to treat.
Although we don’t know the exact cause of AD, a large body of research is starting to provide some answers. This research indicates that AD is a chronic inflammatory disorder, in which the brain is literally eaten away by a slow, smoldering fire, which can go on for ten to twenty years. This fire is fueled by highly reactive molecules called free radicals, which are normal byproducts of respiration but can be increased when there is an inadequate supply of antioxidants. Free radicals are also produced by overactive immune cells in the brain, which have been incited into action by multiple triggers, including environmental “excitotoxins,” toxic heavy metals, rancid fats, excessive refined carbohydrates, chronic infections, and head injuries. Because the brain has so much reserve capacity, symptoms such as memory loss don’t appear until many, many cells have died. This is part of the reason that the disease is so hard to treat—by the time it is diagnosed, it has already been wreaking havoc for decades.
As our understanding of the factors that influence this process increases, so does the realization that simple lifestyle changes can have a big impact. For example, studies have shown that high doses of the antioxidant vitamin E (1,000 to 2,000 IU) can slow the progression of AD. Additional studies have suggested that antioxidant-rich foods such as blueberries, purple grape juice, spinach, ginger (Zingiber officinale), green tea (Camellia sinensis), turmeric (Curcuma longa), and rosemary (Rosmarinus officinalis) can also have anti-inflammatory effects in the brain. In other words, foods that neutralize free radicals can help put out the smoldering fire that perpetuates this disease. And they do this without any additional toxic effects.
One especially promising therapy is standardized ginkgo extract (Ginkgo biloba). Although ginkgo has been used in Traditional Chinese Medicine for more than 2,500 years, its use as a nutraceutical for brain disorders didn’t begin until a little more than thirty years ago, when German researchers discovered that a 50:1 concentrate had potent biological properties. Since that time, more than fifty clinical studies have shown that concentrated ginkgo extract has beneficial effects for patients with dementia from early-stage AD and strokes.
Critics of the studies on ginkgo, most of which were published in Germany, have been quick to point out that its effects have not been dramatic. However, these criticisms usually leave out a very important finding: When given to patients with similar degrees of cognitive dysfunction, ginkgo’s effect is statistically comparable to that of the cholinesterase inhibitors. Another missing point, which I think is even more crucial, is that ginkgo is not just treating symptoms. Because ginkgo is a potent antioxidant, it also has the potential to slow down the underlying disease process.
In my opinion, the real question is not whether we should be choosing between ginkgo, donepezil, galantamine, or, for that matter, high-dose vitamin E as the ideal treatment for AD. Once the person has full-blown symptoms, there is no reason why we shouldn’t pull out all the stops and use all of these approaches together. There are no significant negative interactions that should keep us from giving ginkgo and vitamin E alongside the cholinesterase inhibitors.
What’s more, there are a number of other herbs that could potentially be added to create a truly optimal treatment regimen. For example, bacopa (Bacopa monnieri), also known as brahmi or water hyssop, has been shown in animal and human studies to enhance cognition as well as being a potent antioxidant. Gotu kola (Centella asiatica) and ashwaganda (Withania somnifera), two other Ayurvedic herbs with long histories of use for nervous disorders, have not been as well studied as ginkgo or bacopa but appear to have similar properties.
In addition to using certain herbs and antioxidant-rich foods as adjunct therapies for AD, it is important to point out that they also have the potential to be excellent preventive medicines. Because they are inexpensive and very safe to use for extended periods of time, it is not necessary to wait until the person has clinical disease before recommending them. In fact, a strong case could be made that these “cognition enhancers” could be beneficial for anyone at risk of developing AD later in life. Rather than casting herbs such as ginkgo or bacopa in the same mold as prescription drugs and then trying to compare their effectiveness based on the same criteria, we need to think of them from an entirely different perspective—that is, as food and balm for the brain. It is time to shift the focus of our research toward developing a longitudinal, integrated strategy that can prevent our brains from catching fire in the first place, so that we can appreciate our golden years with alert minds and intact memories.
Robert Rountree, M.D., is a physician in private practice in Boulder, Colorado, where he practices integrative medicine. He is co-author of Smart Medicine for a Healthier Child (Avery, 1994) and Immunotics (Putnam, 2000), and is an Herb Research Foundation advisory board member.
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