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 common late-life 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 have Alzheimer’s. Also it may be possible to curtail the expression of such genes by intervening 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 Alzheimers 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 a hundred 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 a hundred 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.
