Green Tea May Help Prevent Alzheimer’s

Green Tea—A Good “Witches’ Brew”

Green Tea May Help Prevent Alzheimer’s
Lab experiments show green tea and, to a lesser extent,
black tea hold promise for aging brains
By Will Block

ead any good tea leaves lately? How’s this for fortunetelling: If you ingest more tea, you will live a longer, healthier, happier life and become fabulously wealthy. OK, perhaps we’re lying about the wealth part, but the rest of it is true—probably. That may fall a bit short of the certainty you would like, but probabilities, based on scientific evidence, are the best anyone can do in the dicey business of living well and long.

Did you notice that we said “ingest” tea rather than “drink” tea? It’s not that there’s anything wrong with drinking tea—quite the contrary—but only that you would have to drink an awful lot of it (perhaps 10 cups a day) in order to optimize the health benefits from this wondrous brew, which is second only to water as the most widely consumed beverage on earth. A more convenient way to obtain the benefits tea has to offer is by ingesting tea-extract supplements (and you can still drink tea to your heart’s content).

This Will Amaze You

Taking tea, whether as a beverage or a supplement, gives you what one scientist has called a “witches’ brew” (but these are good witches) of chemical compounds whose broad spectrum of health-giving benefits—especially if it’s green tea—are probably unmatched in any other food. Green tea contains compounds that are antioxidant, antibacterial, antiviral, antimutagenic, and anticarcinogenic. Well-controlled clinical trials have shown that green tea can help prevent cancers of the pancreas, colon, small intestine, stomach, breast, and lung.1 No other supplement can make such a claim. There is also evidence that it can help prevent skin cancer,2 and laboratory studies have shown that it induces death in human prostate cancer cells.3

Furthermore, green tea helps protect against diabetes, atherosclerosis, heart attack, and stroke. It bolsters the immune system, protects against neurodegeneration, and promotes a sense of tranquility (even though, paradoxically, it’s considered to be a stimulant)—and it even helps burn fat, through a process called thermogenesis. All these aspects of green tea (and, to a lesser extent, black tea) have been discussed in previous articles in this magazine.*


*See, e.g., “Green Tea Helps Burn Fat” (July 2001), “Green Tea: What’s New Under the Sun?” (August 2001), “Green Tea May Help Control Blood Sugar” (February 2003), “Green Tea May Help Keep Your Ticker Ticking” (March 2003), “Lose Weight with 5-HTP and EGCG” (April 2003), “Theanine May Help You Fight Off Disease” (July 2003), and “Tea Extract Helps Reduce Cholesterol Levels” (December 2003).


Green Tea Is a Chemical Treasure Chest

The compounds principally responsible for this cornucopia of health benefits belong to a class of strongly antioxidative polyphenols called catechins. One catechin stands out from the rest as a kind of biochemical superstar: epigallocatechin gallate (EGCG), which has been described as possibly the most potent natural anticancer agent yet discovered. Fortunately, it turns out that EGCG is the most prevalent of the catechins in green tea.

The catechin content of black tea is much lower than that of green tea, owing to the oxidative fermentation process by which tea leaves are converted from green to black (sometimes the fermentation is carried out only partially, the result being oolong tea). The fermentation destroys most of the catechins (mainly by causing their polymerization) and, therefore, most of their biological activity. But in another stroke of good fortune, it turns out that the polymeric compounds to which some of the catechins are converted—called theaflavins and thearubigins—have significant health virtues of their own. Thus black tea, although it has only about one-sixth the antioxidant power of green tea, is still a potent beverage in its own right.

Another particularly beneficial compound—and this one is found equally in green, oolong, and black teas, because it’s unaffected by the fermentation—is theanine, a rare amino acid found only in tea (Camellia sinensis), two other Camellia species, and one species of mushroom. Theanine is primarily responsible for tea’s ability to boost our immune function.

Add Another Benefit to the List?

To the already impressive list of benefits derived from tea can now be added a potential protective effect—two effects, actually—against Alzheimer’s disease, owing to research recently conducted in England.4 These effects involve two different kinds of enzymes (the role of all enzymes is to catalyze biochemical reactions). Please bear in mind that the results discussed below were obtained with chemicals in test-tube experiments, which are not nearly as trustworthy, from a clinical point of view, as experiments with living cells or, better yet, experimental animals or, ultimately, human beings. Thus, although the results look promising, only further research can tell whether the promises will be fulfilled.


Green tea gives you what one
scientist has called a “witches’ brew”
(but these are good witches) of
chemical compounds whose broad
spectrum of health-giving benefits
may be unmatched in any other food.


Tea Inhibits Acetylcholinesterase . . .

The standard treatment for Alzheimer’s disease is with acetylcholinesterase inhibitors, such as galantamine. These are compounds that interfere with the action of acetylcholinesterase (AChE), the enzyme responsible for catalyzing the chemical breakdown of the neurotransmitter acetylcholine (ACh). The effect of this interference is to maintain higher levels of ACh, which is vital, because ACh deficiencies are responsible for the loss of memory and other cognitive functions in Alzheimer’s. (See the sidebar.)

Galantamine Buys Time

An attractive feature of galantamine for the treatment of mild to moderate Alzheimer’s disease is that it tends to remain effective for longer periods than do other agents. Whereas the drugs donepezil and rivastigmine may halt the progress of the disease for about 6 months before the patient’s decline resumes, galantamine often improves the patient’s condition for several months, and it may take a year or so to decline back to the starting point, thus buying time for the patient.

In their desire to optimize the benefits of galantamine, researchers would like to conduct long-term clinical trials that are placebo-controlled (and, of course, double-blind). For ethical reasons, however, they’re limited to 6 months. With Alzheimer’s, keeping half the patients on placebo (thus denying them actual treatment) for longer than that is deemed unacceptable. So after 6 months, the researchers can either quit or switch to an “open-label” protocol, in which all the patients receive treatment (and they all know it). This open-label extension of the trial can then be continued for some time. Upon its conclusion, another research group may step in, extending the trial for a still longer period. That has occurred several times recently with Alzheimer’s trials of galantamine,* and here we report on yet another example.


*See “Galantamine May Help You Remain a Smart Cookie” (April 2004) and “Galantamine Offers Sustained Cognitive Benefits” (December 2004).


Researchers in Finland, the United Kingdom, and the United States collaborated on an open-label continuation trial that enrolled 491 men and women (average age 73) with mild to moderate Alzheimer’s disease who had previously been enrolled in either of two 12-month trials of galantamine.1 One of these was a 6-month, double-blind, placebo-controlled trial followed by a 6-month open-label extension, and the other was analogous, but on a 3-month + 9-month schedule. The continuation of those two trials lasted 24 months, resulting in a total trial period of 36 months. (It should be noted that the two original trials and the continuation trial were all funded and directed by the Johnson & Johnson subsidiary Janssen Pharmaceutica Products, which markets galantamine as the prescription drug Reminyl®.)

Without interruption from the previous trials, the patients received 12 mg of galantamine twice daily for 24 months. At the initial visit and again at 12 months and 24 months, they were evaluated to assess their status in two domains: (1) cognitive function (memory, attention, language, orientation, etc.); and (2) functional abilities (activities of daily living, as well as planning, organizing, etc.). The trial was completed by 314 (64%) of the patients.

In terms of cognitive function over the 36-month period, the patients improved for the first 3 months, then gradually declined back to the baseline level by 12 months, and continued to decline for the next 24 months. Their rate of decline, however, was slowed relative to that which would be expected to occur if they had been on placebo instead (this rate can be calculated). Their condition deteriorated at about half the expected rate, and by the end of the 36-month period, they had gained about 18 months worth of preservation of their cognitive function.

In terms of functional abilities, the patients held steady for about the first 6–12 months, then declined for the duration of the trial. Thus, they gained about 6–12 months worth of preservation of their abilities in this domain. The galantamine was well tolerated, by and large, and very few of the adverse events recorded were judged by the researchers to have been related to the therapy.

In conclusion, the researchers stated,

This open-label study demonstrates that 12 mg of galantamine administered twice daily for 36 months is effective, safe, and well tolerated in patients with mild to moderate Alzheimer’s disease. … there appears to be a potential for prolonged benefit with galantamine therapy … compared with lack of treatment over time.
  1. Pirttilä T, Wilcock G, Truyen L, Damaraju CV. Long-term efficacy and safety of galantamine in patients with mild-to-moderate Alzheimer’s disease: multicenter trial. Eur J Neurol 2004;11:734-41.

The British researchers found that an extract of green tea leaves strongly inhibited the action of human AChE, and a black tea extract was also effective, albeit somewhat less so. (They tried a coffee extract too, but it was far less potent than the teas.)

. . . And Butyrylcholinesterase

Acetylcholinesterase is but one of a family of enzymes called cholinesterases, another of which is butyrylcholinesterase (BuChE). As its name implies (by analogy with acetylcholinesterase), the function of BuChE is to catalyze the breakdown of butyrylcholine (BuCh), a close chemical relative of ACh that is also present in the brain but that does not function as a neurotransmitter. Inhibiting BuChE is desirable too, because it too catalyzes the breakdown of ACh, albeit less effectively than AChE does.*


*Just to complicate things further, it turns out that AChE also catalyzes the breakdown of BuCh, albeit much less effectively than BuChE does. Thus, both types of cholinesterases inhibit both ACh and BuCh, but at different levels of effectiveness.


The researchers observed that both green tea and black tea inhibit BuChE equally effectively, and about as effectively as they inhibit AChE. (By contrast, the anti-Alzheimer’s agent galantamine, which is a strong AChE inhibitor, is a very weak BuChE inhibitor—the ratio of effective strengths is about 50:1.)

Beta-Secretase Leads to (Ugh!) Amyloid-Beta

The second avenue by which green tea (but not, in this case, black tea) might help prevent Alzheimer’s disease is by inhibiting the action of beta-secretase, an enzyme that catalyzes the breakdown of amyloid precursor protein (APP). That name is self-explanatory, and the result of this chemical breakdown is amyloid, better known as amyloid-beta, a small protein with a dreadful reputation. Amyloid-beta is the primary constituent of the gunky deposits, called senile plaque, that are a characteristic feature of the brains of Alzheimer’s victims.

It is believed that oxidative damage caused by free radicals is at least partially responsible for the formation of this destructive substance, which, in an odd twist of biochemistry, is itself apparently responsible for causing further oxidative damage to the brain. Amyloid-beta is also implicated in the formation of neurofibrillary tangles, another distinctive pathological feature of brains ravaged by Alzheimer’s disease.

Both AChE and BuChE are found in senile plaques and neurofibrillary tangles, incidentally, but their chemical properties are somewhat different from those of the AChE and BuChE molecules found in normal brain cells (which means that their molecular structures must be at least slightly different). These differences may lead to the abnormal protein processing that is thought to play a major role in the pathogenesis of Alzheimer’s disease.5

Green Tea Alone Inhibits Beta-Secretase

The British researchers found that their green tea extract inhibited human beta-secretase by 27% after 5 minutes of incubation, and it reached a maximum of 38% after 60 minutes. They stated that only a few other beta-secretase inhibitors have been reported in the scientific literature, all of them synthetic chemicals of limited therapeutic potential, owing to their high molecular weights, which are likely to restrict their ability to cross the blood-brain barrier. They stated further that they know of no reports of any natural beta-secretase inhibitors derived from plants. Thus, for the time being, green tea is the only plant that offers the potential for providing this valuable function.


Green tea has such a remarkable
record of therapeutic versatility that
it should surprise no one if
Alzheimer’s is added to the list.


Just how valuable it may be is illustrated by experiments described by the British authors. When other researchers genetically modified laboratory mice to overproduce APP, the result was not only increased amyloid-beta levels, but also the development of the pathological hallmarks of Alzheimer’s disease, including plaque deposits and neural damage and loss. By contrast, mice that were genetically engineered to be unable to produce APP had no amyloid-beta in their brains (and no observed side effects). Other researchers found in laboratory experiments that selective inhibition of beta-secretase by a synthetic compound suppressed amyloid-beta secretion in human embryonic kidney cells.

Bet on Green Tea

In their own experiments, the British researchers were unable to determine which compounds in tea are responsible for the effects they observed. It’s therefore impossible to know whether these effects would likely be seen in human beings, because we don’t know whether or not the compounds in question will cross the blood-brain barrier, thereby gaining access to the brain. That is but one of many factors that will determine whether or not green tea has clinical efficacy in this particular arena.

On the other hand, green tea has such a remarkable record of therapeutic versatility in other arenas that it will probably surprise no one if it becomes a factor in this one as well. So for the sake of your health and happiness, and perhaps even your longevity, it would be wise to make green tea a part of your daily life. Cheers!

References

  1. PDR for Herbal Medicines, 2nd ed. Medical Economics Co., Montvale, NJ, 2000, p 370.
  2. Elmets CA, Singh D, Tubesing K, Matsui M, Katiyar S, Mukhtar H. Cutaneous photoprotection from ultraviolet injury by green tea polyphenols. J Am Acad Dermatol 2001 Mar;44(3):425-32.
  3. Paschka AG, Butler R, Young CY-F. Induction of apoptosis in prostate cancer cell lines by the green tea component (-)-epigallocatechin-3-gallate. Cancer Lett 1998;130:1-7.
  4. Okello EJ, Savelev SU, Perry EK. In vitro anti-beta-secretase and dual anticholinesterase activities of Camellia sinensis L. (tea) relevant to treatment of dementia. Phytother Res 2004;18:624-7.
  5. Wright CI, Guela C, Mesulam MM. Protease inhibitors and indoleamines selectively inhibit cholinesterases in the histopathologic structures of Alzheimer disease. Proc Natl Acad Sci USA 1993;90(2):683-6.

Dual-Action Galantamine

Galantamine provides a heralded dual-mode action for boosting cholinergic function: it inhibits the enzyme acetylcholinesterase, thereby boosting brain levels of acetylcholine, and it modulates the brain's nicotinic receptors so as to maintain their function. The recommended daily serving ranges from a low of 4 to 8 mg of galantamine to begin with to a maximum of 24 mg, depending on the individual's response.

For an added measure of benefit, it is a good idea to take choline, the precursor molecule to acetylcholine, as well as pantothenic acid (vitamin B5), an important cofactor for choline. Thus it is possible to cover all bases in providing the means to enhance the levels and effectiveness of your acetylcholine.


Will Block is the publisher and editorial director of Life Enhancement magazine.

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