100 Simple Things You Can Do to Prevent Alzheimer's and Age-Related Memory Loss

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PUBLISHER'S NOTE

As stated by the author, "On many levels, Alzheimer's research is an exciting grab bag of uncertain theories, despite a hard-core center of scientific belief. Certainty about cause and preventive interventions has not yet been engraved in stone." So while this book includes preventive measures based on research by credentialed investigators, the information and advice contained in this book should not be interpreted as a definitive way to prevent Alzheimer's but rather as a guide to suggested measures that may help prevent Alzheimer's. This book is not intended to replace the services of a physician, nor does it constitute a doctor-patient relationship. Information in this book is provided for informational purposes only. You should consult your physician or health care professional regarding your care, in particular, with respect to any symptoms that may require diagnosis or medical attention. This book was current as of June 2010, and as new data become available through research, experience, or changes to product contents, some of the information in this book may become outdated. Any action on your part in response to the information provided in this book is at your discretion. You should consult your physician or health care professional concerning any information contained in this book, and follow their professional advice. The publisher makes no representations or warranties pertaining to any information contained in this book and is not liable for any direct or indirect claim, loss, or damage resulting from the use of information contained in this book.

Please note that the author is not active as an investor, owner, consultant, writer, or management participant in any nutritional supplement company or enterprise, and does not profit financially from the promotion or sale of any nutritional supplements.

INTRODUCTION

WHAT TO DO WHILE WE WAIT FOR A CURE

There's an amusing saying: "Of all the things I've lost, I miss my mind the most." For some reason, this has always slightly disturbed me, and lately more than ever. Quite accidentally, as the result of a routine blood test for cholesterol factors a few years ago, I discovered that I carry a gene that makes me exceptionally vulnerable to Alzheimer's disease. So do my two younger sisters. The gene, ApoE4, is carried by about 25 percent of Americans, and although it is not the only gene associated with Alzheimer's, it is the most dominant one so far discovered.

That doesn't mean, of course, that I or others so genetically marked are doomed to develop Alzheimer's. But knowing I have inherited this tiny time bomb, which may already be slowly and methodically deconstructing my brain cells and vaporizing my intellect, has dramatically focused my attention on ways to neutralize this threat to my aging brain.

Perhaps I have long sensed I could be a target. For nearly forty years, as a medical and nutrition writer concentrating on the predicament of aging, I have closely followed the research findings on Alzheimer's and age-related memory loss—from the increasingly exciting investigations into basic biochemical causes to the new surge of research into how to deter, slow, or even reverse the pathology and symptoms of memory loss.

As a senior medical correspondent for CNN, I did a documentary in the 1980s on the scientific quest for an Alzheimer's cure. My most memorable moment was when world-renowned Alzheimer's researcher Peter Davies, PhD, at Yeshiva University's Albert Einstein College of Medicine reached into a freezer and produced a slice of an Alzheimer's brain, given up at autopsy. It showed large holes—enlarged ventricles carved out by the disease. "Like a piece of Swiss cheese" he volunteered as he put the cold remains into my hand. The image of that diseased brain remains indelibly in my mind. I have often wondered exactly how the biological architect of disease worked to create the void that robbed that particular brain of its function and humanity, and if science would ever be able to stop or prevent the devastation that perhaps might be going on inside my own brain.

Fortunately, many researchers at leading medical centers have wondered the same thing, and applied their inventive minds to solving the Alzheimer's puzzle. Over the past twenty-five years, they have learned much about the pathology of Alzheimer's—and have spun many theories about what makes neurons get sick, become dysfunctional, and die; why brains become abnormally shrunken; and why learning and memory disappear. The pursuit of understanding the disease, of course, is a prelude to an antidote or a cure—possibly a vaccine or pharmaceutical potions that may one day magically halt the damage and perhaps even restore a dreadfully emaciated brain back to robust health.

Many experts I talk to think they will ultimately conquer Alzheimer's, which now afflicts 35 million people around the world and threatens to become a global tsunami of 115 million by 2050, as increasing life expectancy leaves us with an ever-expanding aged population.

Yet the dilemma of what to do in the meantime has not escaped Alzheimer's investigators. Many are shifting their focus to the imperative of prevention—the idea that we should try to head off the awful consequences of the disease before it transforms our brains beyond the point of no return. "It is far easier to rescue a sick neuron than a dead neuron," says prominent brain researcher David Bennett, MD, at Rush University Medical Center in Chicago. He and other leaders in the field are vigorously pursuing new ways to identify, prevent, and postpone brain changes and symptoms of age-induced neurodegeneration before they are irreversible.

Eric B. Larson, MD, and Thomas J. Montine, MD, leading Alzheimer's investigators at Seattle's Group Health Research Institute and the University of Washington, expressed that view in a recent editorial in the Journal of the American Medical Association. The dramatically increasing global life expectancy, they wrote, makes it "difficult to overstate the urgency of finding solutions that prevent, delay, slow, and treat Alzheimer's disease and related dementias."

You may be surprised to know that many researchers now see Alzheimer's and other forms of dementia as diseases of "lifestyle" as well as genetics. That may soften some of our fear and feelings of helplessness surrounding the disease. Surveys show that Americans over age fifty-five, including me, fear Alzheimer's more than any other disease, even cancer, stroke, and heart disease. At the same time, most of us subscribe to the prevailing view that we are virtually powerless to protect ourselves against a disease seemingly so mysterious and cruel as to preclude any possibility of avoiding its onset. That is understandable, but authorities now say it is mostly a myth.

Researchers are increasingly struck by the fact that Alzheimer's has some of the same lifestyle origins as heart disease and diabetes, such as obesity, high bad LDL cholesterol, high blood pressure, and physical inactivity—although admittedly, the stakes seem higher when the target is your brain. Nothing can surpass the threat of losing your entire self—your intellect, personality, or reasons for staying alive. And that acknowledgment is what makes many Alzheimer's researchers so zealous in their quest for new strategies of prevention and early intervention.

WHAT IS ALZHEIMER'S, ANYWAY?

Alzheimer's disease is the most common form of dementia (which means "deprived of mind"), accounting for 60 to 80 percent of all cases of dementia. According to strict scientific definition, Alzheimer's dementia is a slow, progressive deterioration and shrinkage of the brain, characterized by two peculiar types of neuronal damage—clumps and plaques of a sticky gunk called beta-amyloid, and tangles, formed by another brain toxin known as tau. It is decidedly a disease of aging; age is the number one risk factor. Symptoms are rare before age sixty-five. After that, your chances of Alzheimer's double every five years. About half of all people over age eighty-five have Alzheimer's, according to the Alzheimer's Association. This does not mean, however, that Alzheimer's is a part of "normal aging." Alzheimer's is a chronic disease, and abnormal memory impairment is a warning sign.

Researchers used to define Alzheimer's as a single form of dementia, but in reality it's more complicated, says Larson. It is most often an overlapping combination of Alzheimer's dementia; vascular dementia, a disease of blood vessels in the brain; and something called Lewy body dementia, characterized by protein deposits also found in Parkinson's disease. The global symptoms of all dementias are much the same: severe deficits in cognition, particularly memory, and often motor activity that interfere with normal behavior and functioning.

Your vulnerability to Alzheimer's and other dementias is influenced by your genes. But genes are not the final deciders. They can be muted or magnified and partially subdued by your lifestyle and environment. It's also important to distinguish between early-onset Alzheimer's, before age sixty, and late-onset, after age sixty. Early-onset is caused by genetic mutations and is thus quite strongly inherited, but is rare, accounting for only 5 percent of all cases. The overwhelming threat for nearly all of us is late-onset Alzheimer's, which can be influenced by so-called susceptibility genes, such as ApoE4. This means that people with these genes are more predisposed, but by no means predestined, to develop Alzheimer's. Also, it may be possible to curtail the expression of such genes early in the disease process, essentially "curing" Alzheimer's before it becomes irreversible.

Most important, researchers no longer view Alzheimer's as a sudden brain catastrophe of old age; they now see it as a continuum of disease that spans decades and is influenced by early, midlife, and late-life factors such as nutrition, infections, education, diabetes, and mental and physical activity. The impact of these lifetime influences on your brain is typically silent until you reach your sixties, seventies, and eighties. Like other chronic diseases, Alzheimer's is a long time arriving.

Twenty to thirty years of slow and surreptitious neurodegeneration may pass before Alzheimer's brain pathology releases its symptoms to public view. Brain functioning worsens as neurons shrink and die primarily in the brain's cognitively sensitive regions, including the frontal cortex and hippocampus, prime victims of Alzheimer's.

In stunning new discoveries, made possible by brain-imaging technology and cerebrospinal-fluid analyses, scientists can now see the earliest origins of detrimental changes in the brain that produce symptoms years later. Using sophisticated PET scans, prominent researcher John C. Morris, MD, director of the Alzheimer's Disease Research Center at Washington University in St. Louis, sees deposits of toxic beta-amyloid, a hallmark of Alzheimer's, in the brains of a large percentage of older people who have yet to show any signs of mental impairment.

Morris's pioneering work documents that long before symptoms appear, there is a prolonged prelude of disguised normalcy (with seeds of destruction that show up on brain scans), frequently followed by a decade or so of gradual decline called mild cognitive impairment (MCI) or, more accurately, "early Alzheimer's disease." It is during this long time span of pre-symptomatic changes and mild impairment that he and others hope to identify the most vulnerable individuals and to use interventions to postpone the onset of Alzheimer's for many years or to prevent it entirely—which essentially means delaying serious symptoms until you die of something else.

As Maine geriatrician Laurel Coleman, MD, who sits on the board of the Alzheimer's Association, puts it, "Let's say you're dialed in to get Alzheimer's disease at eighty-two. You may be able to push that back until maybe you're ninety-two." Prominent Alzheimer's researcher Suzanne Tyas, PhD, at the University of Waterloo in Ontario, suggests it may be possible to push the symptoms of Alzheimer's so far into the future that they "don't happen until an age when most of us will no longer be alive."

The prospect of intervening to turn the clock back on Alzheimer's has tremendously exciting implications. "It's estimated that if we could delay the onset of Alzheimer's for even five years, it would reduce the number of new cases by half," says leading researcher Suzanne Craft, PhD, at the University of Washington.

YOU CAN RESCUE YOUR OWN BRAIN

As heartbreaking and devastating as Alzheimer's is, optimism is growing that we can lessen the risk and possibly save ourselves. A new slogan, entirely in sync with the latest scientific thinking, is showing up on blogs: "We have found a cure for Alzheimer's, and it is prevention." Top Alzheimer's investigators are now telling us that whether we develop the disease is not entirely random and capricious, not a matter of fate or destiny, nor an inevitable consequence of aging.

Yes, we may face an epidemic as baby boomers age, and yes, there may also be a partial or complete cure in our future. But the fact is, our susceptibility to Alzheimer's, like heart disease, cancer, and diabetes, though somewhat at the mercy of genes, is also partly influenced by factors within our control. And the disease's long lead time gives us years of opportunity in which to make a difference. Especially remarkable is that the state of your health in middle age—your forties and fifties—appears to foreshadow the health of your brain in your seventies and eighties.

Further, science clearly suggests that the daily decisions you make, even the small ones, can help build a brain able to function successfully into your nineties, or for an entire lifetime. Top scientists have documented the surprising power we have over our brains' destiny. For example, by eating the right foods, having a large social network, doing the right exercise, taking the right supplements, and controlling your blood sugar, depression, and stress, you can lower your chances of Alzheimer's, perhaps delaying it for so long that it does not become manifest during your lifetime.

Remarkable studies at the University of Washington School of Medicine find that eating a high-saturated-fat, high-sugar diet boosts brain levels of beta-amyloid, a toxic protein blamed for spreading the devastation of Alzheimer's. Eating certain other foods appears to lessen the toxic amyloid threat to brain cells. After surprising experiments, distinguished brain researcher Carl Cotman, PhD, at the University of California, Irvine, judged physical exercise more effective than any known drug in protecting the brain from damage leading to Alzheimer's and memory loss.

Especially intriguing is evidence that even severe pathology is not destiny. Some elderly brains function well even though riddled with the brain-damaging plaques and tangles consistent with a diagnosis of Alzheimer's. The explanation, suggest scientists: a particular lifestyle, which may include a higher education, a large social network, and intellectual activities, can bolster the brain's so-called cognitive reserve enough to overwhelm its physical wounds, so it appears to function normally long past the time it should. It makes you realize that nobody can predict what miracles the human brain can perform when pushed, prodded, soothed, and stimulated.

Rush University neuropsychologist Robert S. Wilson, PhD, says it best: "We now understand that brain activity depends not just on genes, but on how you live your life…. A lot of the disease we call Alzheimer's is outside plaques and tangles."

Clearly, the health of your brain, like that of your heart, is a far more personal choice than you probably realize. We all can do some things to help our brains negotiate the hazards of advancing age.

WHY THIS BOOK?

In recent years, I have noticed the increasing mountain of research on what we might do to deter and defer Alzheimer's. This research has always piqued my interest because of the genetic throw of the dice that triples my own risk. I often thought that when I had collected 100 scientifically supported possibilities for outliving and avoiding Alzheimer's and age-related memory decline, I would put them in a book to help answer this question: what do we do while we await the anticipated Alzheimer's cure?

I finally did find 100 simple things people can do to build brains that are more resistant to aging and primed to function successfully over a long lifetime. I am well aware that you may not want to try them all at once and that there are some you may never try. Think of this book as a large buffet table. You may want to sample everything in it, or again, you may not. I suggest you try anything that strikes you as interesting and appealing. It's true that some things may work better for some people than others, depending on unknown genetic differences and individual preferences. It is impossible to say at this stage of the research which things will be most effective for you, although any type of mental stimulation, regular physical exercise, social engagement, and a high-antioxidant diet seem to have the edge.

As everyone knows, science is full of surprises. For years, mainstream medicine thought that gastrointestinal ulcers were caused by diet and stress. It took an Australian physician a decade to prove to the establishment skeptics that ulcers are caused by the bacterium Helicobacter pylori and treatable with antibiotics. Thus I don't refrain from including some scientific theories that are on the sidelines of mainstream research. On many levels, Alzheimer's research is an exciting grab bag of uncertain theories, despite a hard-core center of scientific belief. Certainty about cause and preventive interventions has not yet been engraved in stone.

However, this book includes only preventive measures based on research by credentialed investigators, most of whom are affiliated with leading scientific institutions. Offbeat preventive ideas do not get exposure here unless they come from scientifically valid sources.

Do I religiously do all of the things I suggest in this book? Mostly, and certainly in the area of nutrition and diet. I have recently taken up tennis again after a decade of being away from it. Yoga is new for me, as is water aerobics. At this writing, I have yet to filter my drinking water, and I can't do a crossword puzzle or play Scrabble (and never could). I am hoping that writing this book has given me a major infusion of mental activity, although I have lost some sleep over it (not good for the brain). I have no trouble being social (a good thing for the brain), although by definition a writer's life means spending many hours sedentary and alone. I don't take many nature walks and probably spend way too much time at the movies, and even though I like to think that films are mentally stimulating, I have no evidence to prove it. Most important to me, my seventy-eight-year-old brain seems to be functioning reasonably well, despite my genetic handicap. And I want to keep it that way. Still, I am aware that life, like science, holds surprises. Whether Alzheimer's is waiting in my future is unknown. But I am doing my best to outlive it, and I am inviting you to do the same.

1

GET SMART ABOUT ALCOHOL

It can boost brain cells or destroy them

Your brain may like a little alcohol, but not a lot. Study after study shows that moderate drinkers are less apt to develop Alzheimer's. Recent research at Wake Forest University Baptist Medical Center found that older people who drank eight to fourteen alcoholic beverages per week—one or two a day—had a 37 percent lower risk of dementia than nondrinkers. The bad news: stepping into the "heavy drinker" category—more than fourteen drinks a week—doubled the odds of developing dementia compared to not drinking.

UCLA researchers find that heavy drinking pushes you two to three years closer to Alzheimer's. And heavy drinkers who also carry the ApoE4 Alzheimer's gene can expect the onset of dementia four to six years earlier. Further, in the large Framingham Heart Study, a community health study spanning several decades, heavy drinking (more than fourteen drinks a week) predicted shrinkage in the memory regions of the brain.

British doctors writing in the British Journal of Psychiatry recently warned that heavy and binge drinking among older people is creating "a silent epidemic" of alcohol-related dementia that causes as much as 10 percent of all cases of dementia.

Even adults who usually drink lightly or moderately but go on occasional binges face a higher risk of dementia. A Finnish study showed that adults who binged in midlife at least once a month—drinking, for example, more than five bottles of beer or a bottle of wine at one sitting—were three times more likely to develop dementia, including Alzheimer's, twenty-five years later. Passing out from alcohol at least twice in one year hiked the chances of developing dementia by ten times.

On the other hand, a daily cocktail or glass of wine may help delay dementia. Research finds that alcohol is an anti-inflammatory (inflammation promotes Alzheimer's) and raises good HDL cholesterol, which helps ward off dementia. High antioxidants in red wine give it additional anti-dementia clout. Such antioxidants, including resveratrol, act as anticoagulants and artery relaxants, dilating blood vessels and increasing blood flow, which encourages cognitive functioning. That makes many researchers favor red wine over white wine, which has comparatively few antioxidants. (See "Make It Wine, Preferably Red," here.)

What to do? Understand that alcohol in low doses over an adult's lifetime appears brain protective, but large doses at one time kill or cripple brain cells, leaving you more vulnerable to cognitive dysfunction and Alzheimer's decades later. The toxic impact is long lasting. If you do drink, stick to low or moderate amounts, sipped slowly, preferably with food. That means no more than one drink a day for women, two for men. One drink usually means a twelve-ounce beer, a shot of liquor, or five ounces of wine.

2

CONSIDER ALPHA LIPOIC ACID AND ALCAR

These two supplements work together to rejuvenate your aging brain

If you could take one antioxidant to ensure good cognitive functioning as you age, what would it be? The answer seems clear to prominent researchers at Oregon State University's Linus Pauling Institute. Alpha lipoic acid, also known as lipoic acid, is the strongest antioxidant rejuvenator of aging brains we have ever seen in aged animals, says institute researcher Tory Hagen, PhD, noting that it's especially powerful when combined with the supplement acetyl-l-carnitine (ALCAR).

Hagen has pioneered the study of lipoic acid and ALCAR, along with biochemistry professor Bruce Ames, PhD, at the University of California, Berkeley. Now eighty, Ames discovered ALCAR in the 1990s being sold as a "smart drug" in Italy. In groundbreaking research, he and Hagen showed that old, sluggish rats became as physically and mentally active as rats half their age within a few weeks of being fed ALCAR and lipoic acid. "It's like a seventy-five-year-old having the energy of a forty-year-old," says Ames.

He explains that brain cells require ALCAR as fuel to keep tiny energy generators called mitochondria humming along. As we age, we synthesize 50 percent less ALCAR. Deficient in fuel, our cellular energy factories become dysfunctional and leave neurons sputtering in disorganized communication. Mitochondrial distress in brain cell synapses is one of the earliest biochemical clues that Alzheimer's is on the march, according to recent research. Boosting ALCAR in brain cells helps revive mitochondrial functioning, creating a surge in overall mental and physical energy, claims Ames. ALCAR also blocks the formation of Alzheimer's tau tangles in test tubes.

The critical job of alpha lipoic acid in brain cells is to stand guard over the mitochondrial energy plants, protecting them against damage from the continual onslaught of free-radical chemicals. Lipoic acid is one of the few known antioxidant molecules able to zip through the blood-brain barrier to fend off such destruction. Lacking the antioxidant protection found in lipoic acid, the mitochondria factories tend to collapse and shut down, leaving your brain in a constant state of "brownout."

Hagen also discovered another way lipoic acid appears to prevent and reverse brain damage. It "chelates," or flushes, iron deposits out of the brain. As you age, iron accumulates in neurons and accelerates the "oxidative damage" blamed for cognitive decline and dementia. After Hagen fed old rats high doses of lipoic acid for just two weeks, the iron in their brains dropped dramatically to the levels normally seen in young rats.

In humans, alpha lipoic acid has been shown to help lower blood pressure, blood sugar, and triglycerides; reverse insulin resistance; and prevent diabetic neuropathy. Some doctors routinely give 600 milligrams of lipoic acid a day to diabetics to help prevent complications.

What to do? Consider taking either or both of these supplements to boost brain-cell functioning. You can find them separately and together in health food stores or drugstores and online. If you buy ALCAR alone, be sure the label says acetyl-l-carnitine and not just plain L-carnitine.

Both alpha lipoic acid and acetyl-l-carnitine are considered safe at the recommended daily doses of 200 mg per day for lipoic acid and 500 mg per day for ALCAR, although you can take lower doses if you want. If you take higher doses to address a medical problem, such as diabetes, do so only with the advice and monitoring of a health professional.

The University of California, Berkeley, has patented a combination pill of 200 mg of alpha lipoic acid and 500 mg of aceytl-l-carnitine, the doses recommended by Ames. It is called Juvenon and is available at http://juvenon.com. Ames says he donates any money he receives from its sale to human testing of the supplement. Several other companies market combinations of lipoic acid and ALCAR.

3

ASK QUESTIONS ABOUT ANESTHESIA

Could anesthesia bring on Alzheimer's?

It's not uncommon to be in a mental fog when you come out of surgery. Typically, the anesthesia wears off quickly, although it can linger for days or weeks. On occasion, doctors see cases like the sixty-five-year-old woman who, six months after hip surgery, develops memory loss and is later diagnosed with Alzheimer's. Is it coincidence? Or could anesthesia cause permanent damage, accelerating the onset of Alzheimer's—especially in those genetically susceptible or already suffering the mild cognitive loss that precedes dementia?

The possibility worries some experts. Roderic G. Eckenhoff, MD, a professor of anesthesiology at the University of Pennsylvania School of Medicine in Philadelphia, says, "We give these drugs to millions of patients every year and blithely ignore that they could have long-term effects." He notes that lab animals subjected to common inhaled anesthetics show increased death of brain cells, detrimental clumping of toxic beta-amyloid and tau, and long-lasting cognitive dysfunction, including memory loss. Eckenhoff fears that such anesthetics may accelerate the onset of dementia and Alzheimer's, especially in vulnerable elderly brains.