LEF Magazine April 1998
Exploring The Future
There is a major paradigm shift in the way the medical profession is approaching aging, and the annual A4M conference has been a prime forum for its display. Here are ample reasons why.
By Thomas Donaldson, Ph.D.
The annual conference of the American Academy of Anti-Aging Medicine, held in Las Vegas, was typically far-ranging in its presentations. The conference covered topics from brain aging and repair to Alzheimer's detection and prevention, hormone replacement therapy, and anti-aging surgery techniques. Perhaps most controversial was the discussion of actual head transplants.
Here is an overview of those presentations of interest to life extensionists.
Thomas H. Crook, Ph.D., a consultant to several pharmaceutical companies, including Lederle Labs and Bristol Myers Squibb, discussed clinical test reports on phosphatidylserine in the prevention, arrest, and treatment of Alzheimer's disease. He detailed just how our memory deteriorates as we age. His early work on this issue had been with monkeys, but he now has devised human tests that relate easily to those given to monkeys.
Humans show a dramatic decline over time in their ability to remember relations between numbers and symbols. They also show a decline in several tasks based on memory for names, and again on the ability to remember a telephone number long enough to dial it.
One particular test, requiring the subject to remember some information while doing something else unrelated showed considerable decline with age. All of these declines are approximately linear, with no special ages at which we suddenly start failing these tests. Even when conducted on patients between ages 20 and 29, Crook's tests showed an average decline of 25 percent. (As with many such tests, speed played a role: only a short time is allowed for subjects to remember. It would be interesting to use similar tests with no time limit; one simple explanation for part of the decline may simply come from slower thinking as we grow older.)
In exploring ways to prevent this mental slowdown, Crook first tested hyperbaric oxygen, which did not work. He then tried a variety of memory drugs, including piracetam and hydergine, for their ability to preserve younger levels of memory. Phosphatidylserine turned out to be the only drug he found that provably increased memory abilities. In controlled tests at 300 mg/day, Crook found that phosphatidylserine improved performance on various memory tests. It worked best on those with lower scores. Treatment early in the course of Alzheimer's disease showed an effect; late treatment showed no measurable effect.
Besides performance of aged subjects on memory tests, those caring for these patients all noticed a clear improvement. Patients, too, noticed the improvement. These test patients and others were kept on phosphatidylserine for some time afterwards. The best strategy in dosage apparently consists of initial doses of 300 mg a day, followed after several weeks by a constant dose of 100 mg a day. The tests, with a starting dose of 100 mg a day, took about 12 weeks to have an effect; after that, 100 mg a day and 300 mg a day showed little difference.
This talk and Kay's talk were notable because they discussed a (partial) therapy, something we might actually do to help prevent our own memory from deteriorating, with no further basic experiments needed.
In another presentation, Thierry Hertoghe, M.D., of the Academy of General Medicine of Belgium, in Brussels, reviewed the effects of hormone replacement across all the different known hormones. He looked not only at bodily effects such as that on circulation and heart disease, but also on memory. Low levels of thyroid hormones, for instance, can cause both a lack of emotion and a lack of intelligence.
By the age of 85, 30 percent of elderly people become demented. One interesting feature of dementia due to Alzheimer's disease, alcohol, and others, is the low level of the hormone melatonin, produced by the pineal gland. Melatonin acts as a quite powerful antioxidant, and is low at all times in patients with Alzheimer's disease. It may protect our brain by acting as an antioxidant. DHEA (Dihydroepiandrosterone), a precursor of several hormones, has a profound effect against cancers, heart disease, and diseases of our arteries (scanty hair in the armpits provides one useful symptom of low DHEA). DHEA occurs in high levels in our brain, and low DHEA also involves a loss of memory. It improves the metabolic level of neurons and can sometimes make EEG tracings more normal.
Dr. Marguerite Kay, who presented her research on the effects of vitamin E, suggests that Alzheimer's disease is an illnes of the entie bod, not of the brain alone.
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