Turmeric—A Natural Powerhouse
Turmeric Protects Your Brain Cells
Double-barreled curry spice is an antioxidant and an anti-inflammatory
By Will Block
ne thing leads to another." That old saying usually comes up in the context of sexual shenanigans, when things just spiral out of control—sometimes with a happy ending, sometimes not. But there are other arenas as well—our health, for example—where things can get out of control unless we take prudent measures to keep a lid on them. Are you in the mood for a slightly spicy prudent-measures article? (Sorry, no sex included.)
Being committed to a long, healthy, happy life means, among other things, being cognizant of a stark fact to which most people seem oblivious: the human brain is as susceptible to disease as any other organ of the body, and it needs to be protected and maintained in the same way the rest of the body is: through good nutrition (including judiciously chosen dietary supplements) and regular exercise (mental gymnastics). Doing this will most likely prevent one thing from leading to another, namely, aging leading to mild cognitive impairment leading to dementia leading to a tragic and premature death. (Keep that sequence in mind.)
Aging Is Inevitable
Like politicians lying, aging is inevitable. Also inevitable, it seems, is some degree of benign memory loss (commonly called age-related memory loss), owing to the wear and tear on the brain of just having lived for a long time. All that thinking and loving and wondering and worrying, etc., take their toll, albeit to very different degrees: some people seem blessed with brains that remain quick, strong, and agile well into old age, just as some oldsters remain remarkably physically fit (often the two go hand-in-hand, probably not coincidentally).
Dementia Is Not
What is not inevitable (in most cases), however, is dementia, of which the Big Two are Alzheimer’s disease and vascular dementia. The latter is easy to prevent: maintain good cardiovascular—and thus cerebrovascular—health through diet and exercise (and, of course, no smoking). Do that, and you will probably have no atherosclerosis, no heart attack, no stroke, and no vascular dementia, and you will have a leg up on preventing Alzheimer’s disease as well. (In real life, these two forms of dementia are often commingled, and it can be difficult to make an accurate diagnosis except at autopsy.)
Vascular dementia is primarily due to well-understood “plumbing” problems in the circulatory system. Alzheimer’s is a more complex disease, the origins of which, although still largely a mystery, are related to oxidative stress and inflammatory processes in neurons (brain cells). In a convoluted web of causes and effects, these two biochemical phenomena are related to two hallmark features of the Alzheimer’s-ravaged brain: senile plaques and neurofibrillary tangles, and they lead to the ultimate hallmark: the death of neurons in certain regions of the brain, notably those governing memory and other cognitive functions.
But Mild Cognitive Impairment Usually Leads to Dementia
In the discussion above, did you notice how we skipped from aging to dementia, with a brief digression on age-related memory loss? What happened to mild cognitive impairment, which was one of the links in that one-thing-leads-to-another chain? Let’s backtrack.
Unlike age-related memory loss, which is considered to be normal and no significant threat to brain health, mild cognitive impairment (MCI) is a recognized disease state. In its most common form, its primary characteristic is memory loss (more severe than normal, but still “mild”), with other cognitive functions usually being impaired to a less significant degree. It is a major threat to brain health, because it usually (but not always) leads to Alzheimer’s disease: over a 6-year period, about 80% of MCI patients will progress (degenerate is a better term) to Alzheimer’s.*
Because MCI is a much less severe condition than Alzheimer’s, however—it’s a transitional phase between normalcy and dementia—it has received nowhere near as much attention from the scientific community as Alzheimer’s has. That, however, is changing, with the growing awareness that anything that could prevent MCI from occurring would therefore probably also prevent Alzheimer’s. Seen from a different perspective, anything that’s potent enough to help alleviate Alzheimer’s (galantamine, e.g.) could probably alleviate—and better yet, prevent—its precursor, MCI. That premise remains to be proved through clinical trials, but it’s a reasonable one that few would disagree with.
Turmeric—“The Spice of Life”
Turmeric (Curcuma longa)
Meanwhile, more research is being focused on the possible benefits of nutritional supplements that can impact either of the two above-mentioned chemical processes that are implicated in cognitive decline: oxidation and inflammation of brain neurons. Of special interest are nutrients that can impact both of these processes, because intervention strategies for Alzheimer’s disease (and MCI) may require targeting both oxidation and inflammation.
Among the nutrients that may fill this bill, the most notable is a member of the ginger family: turmeric
(Curcuma longa), the Indian spice that gives some mustards their bright yellow color. Turmeric is better known as one of the principal ingredients (along with cumin, coriander, and other spices) of curry powder, a staple throughout much of India and Southeast Asia, where since ancient times it has been called “the spice of life.”
Is it a coincidence that elderly residents of rural India, who eat large amounts of curry, appear to have the lowest incidence of Alzheimer’s in the world? No one knows for sure. A mere correlation proves nothing (think of the countless other factors, besides curry consumption, that differentiate rural Indians from urban Americans, say—what effect might those factors have?). Nonetheless, the correlation is intriguing to scientists, who believe that certain compounds found in the rhizomes (rootstalks) of the turmeric plant may indeed be responsible for conferring some degree of protection against Alzheimer’s.
The biochemical mechanism involved may be the same as that through which these compounds help to confer some protection against the dangers of spoiled meat (which is one reason, along with masking the bad flavor, why curry is used so extensively in regions where refrigeration is not available). That mechanism is antioxidation, the chemical neutralization of destructive free radicals, which are widely believed to play a major role in the pathogenesis of Alzheimer’s disease, as well in many other age-related conditions—including MCI.
Amyloid-beta—Killer of Neurons
The antioxidant/anti-inflammatory compounds in turmeric are a group of polyphenols called curcuminoids, named for the best known among them, curcumin. In a recent laboratory study at the University of Illinois, researchers tested nine curcuminoids isolated from turmeric root for their ability to protect cultured rat cells from damage caused by amyloid-beta (also called beta-amyloid); this small protein molecule is the principal constituent, along with some polysaccharides, of the senile plaques found in the brains of Alzheimer’s victims.
From the brain’s point of view, amyloid-beta is a disaster: it is believed to be formed in part through oxidative damage caused by free radicals, and it causes further free radical production, causing further oxidative damage, etc. In fact, amyloid-beta is neurotoxic—it kills neurons. In addition, it plays a role in the formation of neurofibrillary tangles, its evil, neurotoxic twin in the pathology of Alzheimer’s. All this death and destruction occurs primarily in cholinergic neurons (those for which acetylcholine is the neurotransmitter) in certain regions of the brain, notably the hippocampus, which govern vital aspects of memory and other cognitive functions.
Curcumin—An Amyloid-beta Killer?
Thus, one of the principal aims of Alzheimer’s research is to find agents that can inhibit or prevent the formation of amyloid-beta, and a growing body of evidence points to curcumin as a prime candidate in this regard. In the Illinois study, it turned out that five of the nine curcuminoids (including curcumin) were strongly protective against amyloid-beta neurotoxicity in the rat cells; one other was weakly protective, and three were inactive.*
UCLA Researchers Mess with Mice, Stifle Alzheimer’s
In another study, researchers at the University of California, Los Angeles, conducted a variety of biochemical tests of the action of curcumin in mice that had been genetically engineered (“transgenic” mice) to be highly susceptible to human-type Alzheimer’s disease.* They found evidence of potent antioxidant and anti-inflammatory activities of curcumin that enable it to interfere with the pathogenesis of Alzheimer’s through multiple biochemical mechanisms. An important consequence of these activities in the mouse brains was the strong suppression of amyloid-beta formation.
The UCLA researchers’ observations tended to confirm and amplify the conclusions reached in many prior studies. One such conclusion was that curcumin is safe even at very high dosages (its use by countless humans throughout their lives argues for its long-term safety as well). In that regard, curcumin is different from ibuprofen and many other nonsteroidal anti-inflammatory drugs (NSAIDs), which are effective in reducing the risk for Alzheimer’s disease but which pose a serious danger for long-term human use because of their tendency to produce gastrointestinal damage, including ulcers. (Curcumin is itself an NSAID and is widely used in the treatment of arthritis as well as other inflammatory disorders.)
UCLA Researchers Ratchet up to Rats, with Similar Results
In a study with rats, the same research group at UCLA placed various groups of middle-aged and elderly rats on diets containing curcumin or ibuprofen, or no supplement, for 2 months. They then used surgical methods to infuse soluble amyloid-beta directly into specific areas of the rats’ brains in order to create a simulated Alzheimer’s-like state of neurodegeneration (remember that amyloid-beta causes oxidative and inflammatory damage and kills neurons). The objective was to determine the extent to which curcumin and ibuprofen could protect the rats’ brains and their cognitive function from this biochemical assault (the control rats were infused with a neutral solution containing no amyloid-beta).
The results showed that curcumin, but not ibuprofen, provided strong protection from oxidative damage. On the other hand, the two agents provided equivalent protection from inflammatory damage (not surprisingly, considering that they’re both NSAIDs). Curcumin dramatically reduced the actual numbers of senile plaques in the rats’ brains—by 80% with a low dosage but by only 45% with a much higher dosage (the data for ibuprofen were not given). In a water-maze test of the rats’ spatial memory, the curcumin-fed rats fared much better than the no-supplement amyloid-beta-damaged rats, performing as well as the amyloid-beta-free control rats. (For some reason, the ibuprofen-fed rats were not given this test.)
The researchers concluded by saying,
Curcumin has a long history of safe use and is well tolerated in humans with limited or no side effects reported at effective anti-inflammatory and antioxidant doses. The data reported here argue that curcumin or another combined antioxidant/NSAID may prove useful for Alzheimer’s disease prevention or treatment.
It’s Turmeric Time!
In that context, another antioxidant that has received much attention in the scientific literature recently is vitamin E (see the sidebar). As potent an antioxidant as vitamin E unquestionably is, however, it appears that curcumin is several times more potent still, which makes it all the more attractive as a potential preventive and therapeutic agent for Alzheimer’s and other neurodegenerative disorders.
Your Brain Needs Vitamin E—and C
Vitamin E has a well-earned reputation as a powerful antioxidant that plays an important role in heart health. Less well known, however, is its role in preserving brain health (not that these two aspects of health are separate—in fact, there is much common ground there). By combating oxidative stress in your brain—which churns out more free radicals than any other part of your body, owing to its disproportionately high rate of energy consumption—vitamin E helps to stave off the tendency toward cognitive decline.
The results of different studies on this subject have not been entirely consistent, however. An epidemiological study by researchers in Chicago showed that older people with the highest levels of vitamin E intake were at substantially lower risk for cognitive decline than those with the lowest levels. The authors drew the startling conclusion that the effects on cognitive decline from being at the highest level of daily intake of vitamin E (whether from food plus supplements or from food alone) were equivalent to a corresponding decline in age of 8 to 9 years—a handsome payoff from taking your vitamins!
More recently, a team of researchers studied the elderly residents of Cache County, Utah, who are known for their extraordinary longevity. It turned out that the risk for developing Alzheimer’s disease was dramatically lower than the norm among those who took substantial daily supplemental amounts of both vitamin E and vitamin C (which is also an antioxidant). No such effect was seen, however, among those who took one vitamin or the other, but not both, and there was only a modest effect among those who took a conventional multivitamin formulation without additional supplementation with E or C.
Contrary to several other studies demonstrating vitamin E’s antioxidant benefits for cognitive function when taken alone, the Cache County study suggested that vitamin E was effective (for that population, anyway) only in conjunction with vitamin C—which everyone should be taking in substantial quantities anyway, so it’s almost a moot point. So take all your vitamins! (For more on this subject, see
“Antioxidant Vitamin Combo Cuts Alzheimer’s Risk” in the March 2004 issue.)
- Morris MC et al. Vitamin E and cognitive decline in older persons. Arch Neurol 2002;59:1125-32.
- Zandi PP, Anthony JC, Khachaturian AS, Stone SV, Gustafson D, Tschanz JT, Norton MC, Welsh-Bohmer KA, Breitner JCS, for the Cache County Study Group. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements. Arch Neurol 2004;61:82-8.
Isn’t that nice? Just think—it could have been something awful, like cod liver oil. Instead, it’s a delightful spice that most people love to eat. If you’re not one of those people, however, and if, in any case, you don’t care to eat turmeric every day, the best way to assure yourself of its uninterrupted benefits is via supplementation. And for that, you’ve come to the right place.
- Petersen RC, Doody R, Kurz A, Mohs RC, Morris JC, Rabins PV, Ritchie K, Rossor M, Thal L, Winblad B. Current concepts in mild cognitive impairment. Arch Neurol 2001;58:1985-92.
- Frautschy SA, Hu W, Kim P, Miller SA, Chu T, Harris-White ME, Cole GM. Phenolic anti-inflammatory antioxidant reversal of Ab-induced cognitive deficits and neuropathology. Neurobiol Aging 2001;22:993-1005.
- Ganguli M, Chandra V, Kamboh MI, Johnston JM, Dodge HH, Thelma BK, Juyal RC, Pandav R, Belle SH, DeKosky ST. Apolipoprotein E polymorphism and Alzheimer disease: the Indo-US Cross-National Dementia Study. Arch Neurol 2000;57:824-30.
- Rinaldi P, Polidori MC, Metastasio A, Mariani E, Mattioli P, Cherubini A, Catani M, Cecchetti R, Senin U, Mecocci P. Plasma antioxidants are similarly depleted in mild cognitive impairment and in Alzheimer’s disease. Neurobiol Aging 2003;24:915-9.
- Park S-Y, Kim DSHL. Discovery of natural products from Curcuma longa that protect cells from amyloid-beta insult: a drug discovery effort against Alzheimer’s disease. J Nat Prod 2002 Sep;65(9):1227-31.
- Lim GP, Chu T, Yang F, Beech W, Frautschy SA, Cole GM. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse. J Neurosci 2001;21:8370-7.
- in ’t Veld BA, Ruitenberg A, Hofman A, Launer LJ, van Duijn CM, Stijnen T, Breteler MMB, Stricker BHC. Nonsteroidal antiinflammatory drugs and the risk of Alzheimer’s disease. N Engl J Med 2001;345:1515-21.
- Zhao BL, Li XJ, Ho RG, Cheng SJ, Xin WJ. Scavenging effect of extracts of green tea and natural antioxidants on active oxygen radicals. Cell Biophys 1989;14:175-85.
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.