Will I Get Alzheimer’s?

Hello. My name is Anthony R. Ellis, M.D., and I am a psychiatrist who specializes in the treatment of mental health problems and brain illnesses in people over the age of 55. I wasn’t always interested in working with the older and wiser portion of our population, but ever since my father was diagnosed with, and later died from, Alzheimer’s disease, this area of psychiatry has been my primary focus. I am writing this e-book to answer a question that I am asked frequently by the spouses, family members, and other loved ones of patients with Alzheimer’s disease.

In addition to struggling with the effects of Alzheimer’s disease on their parent, relative or spouse, the next thing that seems to come up during family conference meetings on our geriatric psychiatry unit is “Will I get Alzheimer’s?” This is an intriguing question for many of us as the number of cases of Alzheimer’s disease is expected to go from roughly 5 million affected patients in the year 2000 to approximately 20 million patients in the year 2030. It’s also an interesting question because it is very difficult to answer. However, by looking through the available psychiatric and neurological research, and by sharing insights that I’ve gained through treating thousands of patients with Alzheimer’s disease, I hope to help you answer this question for yourself.

I intend to make the case that all of us would, in fact, develop signs of Alzheimer’s disease if we lived long enough. That sounds depressing. However, I also hope to relay the current information with regard to prevention strategies and give you a perspective that will alleviate worry and anxiety and allow you to focus on doing what you can to mitigate your risk and otherwise forget about this question and this problem, no pun intended. You can consider this an “unauthorized biography” of Alzheimer’s disease, as some of my ideas may not be in agreement with everything else you read about Alzheimer’s disease. Rest assured that the things that I have placed in this book are based on my interactions and dealings with patients affected by this illness, including my own father and many of his siblings.

Chapter 1: What is Alzheimer’s Disease?

Alzheimer’s disease is an illness of the brain that slowly robs you of your ability to function. Many times in medicine we label something with the name “disease” and imply that it is a clearly definable syndrome with a specific cause and known treatment. This may not be the best way to think of Alzheimer’s disease. It has previously been called dementia, senile dementia, and a variety of other names across human history, having to do with loss of function in old age. Alzheimer’s “disease” is likely a group of conditions that vary in their exact cause, age of onset, and rapidity of progression. For example, there are some patients who develop “pre-senile onset Alzheimer’s disease” who are known to have a specific genetic mutation that causes the illness. These patients have a change in the processing of a protein that can be found in everyone’s brain called beta amyloid. This protein normally causes very little difficulty. In the patients with this type of mutation, the amyloid protein is processed differently and becomes toxic to the brain and accumulates in clumps that cause inflammation and brain cell death.

In other patients who develop this early onset type of Alzheimer’s disease, there is a known mutation that affects another protein that is inside the structure of the brain cell called tau protein. There is a group of tubes inside brain cells that transport neurotransmitters and nutrients that allow the cell to function. In the patient’s with the abnormal tau protein, these intracellular transport processes are disrupted as these tubes become tangled and don’t function as well.

This specific form of Alzheimer’s disease is different than the form of Alzheimer’s disease that tends to show up after the age of seventy-five. The older onset form seems to be associated with aging and cumulative vascular damage to the brain. There are still amyloid protein deposits and neurofibrillary tangles, but also “vascular damage”. Vascular damage here refers to decreased blood flow and oxygen transport to areas of the brain as a result of blockages in very small arteries. Patients with high blood pressure, diabetes, high cholesterol, or those who smoke cigarettes, generally have more of these blockages at an earlier age and develop more over time than people who don’t have these “vascular risk factors.”

The early onset forms of Alzheimer’s disease are more than likely related to a variety of relatively rare genetic mutations. These cases make up less than 5% of all cases of Alzheimer’s disease. This early onset form related to a genetic mutation is more likely to be inherited than the later onset form of Alzheimer’s disease. The later onset form accounts for the bulk of patients who are diagnosed with Alzheimer’s. It is clear that if you have a relative who develops early onset Alzheimer’s disease, you are at increased risk for developing Alzheimer’s disease yourself. I treated a patient once who was in his late 50s when I first met him and he had developed his first symptoms when he was in his early 50s. He had a history of late onset Alzheimer’s disease in one parent and early onset Alzheimer’s disease in the other parent. He had a particularly rapid course and passed away at around the age of sixty-two, having spent approximately the last eighteen months of his life in a nursing home.

At present, genetic testing is not widely available for family members of patients with early onset Alzheimer’s disease, although this testing may be more widely available over time due to advances in this field. It may be possible at some point in the future for all children of someone who has early onset Alzheimer’s disease to be tested, as is currently the case for children of patients affected by Huntington’s chorea. Huntington’s chorea is another form of dementia that is inherited and its inheritance pattern is known. It is interesting to note that many children of patients affected by Huntington’s chorea choose not to have the genetic test done, because they simply don’t want to know what is in store for them.

Much less is known about the genetic risk for the later onset form of Alzheimer’s disease. I personally believe that it is because this is a heterogeneous group, meaning that this is a broad group of illnesses or types of Alzheimer’s disease that vary, as noted previously. In addition, the degree to which a person has vascular damage in the brain (damage related to problems with clogged blood vessels as previously described) affects the age at which one shows symptoms. The amount of vascular damage also affects the course of the illness in terms of how rapid one loses function and memory capacity.

Chapter 2: Known Risk Factors For Alzheimer’s Disease

There are some known risk factors for the development of Alzheimer’s disease that can be culled out of the many studies that have been done to help with predicting the future. Unfortunately, our current ability to predict the future for a given patient is not very good. It leaves you with the option of trying to reduce your risk factors and improve your general brain health, and that’s all. As I said before, having one or both parents affected by the early age of onset type of Alzheimer’s disease is clearly a strong risk factor, and would require that the patient with this family history gets a periodic screening after the age of forty-five to try to detect the illness as early as possible. This would allow treatment to begin at the earliest possible time.

Another potent risk factor is having two copies of apolipoprotein E4. Apolipoproteins are transporters of cholesterol and other fatty substances in the blood system and in the brain. These lipid or fat carriers are inherited from our parents. We inherit one copy of the type of apolipoprotein from each parent. There are three known types of apolipoprotein: E2, E3, and E4. It appears that apolipoprotein E2 has some protective value against the development of Alzheimer’s disease, apolipoprotein E3 seems to be neutral, and apolipoprotein E4 seems to definitely be the “bad guy.” If you were to get a copy of apolipoprotein E4 from each parent, making you what we call homozygous for apolipoprotein E4, then your risk of Alzheimer’s is approximately eight times the risk of the general population. I saw a statistic in one study that indicated that if you had two copies of apolipoprotein E4, your risk of developing Alzheimer’s by age ninety was fifty percent. Unfortunately, I personally believe that your risk of developing Alzheimer’s by age ninety is fifty percent anyway, so I am not sure of the usefulness of that statistic. Statistics of that sort come and go and it doesn’t become clear until more date and information are available on what risk factors are, and how much each increases risk. I do believe that having two copies of apolipoprotein E4 is a risk factor and I hope that at some point in the future, a test will become available so one can find out their apolipoprotein status and use that information in an overall personal brain health care plan. At present, the test is generally only available in research settings.

Other risk factors for Alzheimer’s disease are the known vascular risk factors. Vascular disease in the brain causes small blockages that restrict oxygen supply to the deep white matter around the ventricles (fluid-filled spaces close to the center of the brain). A person who has an MRI that has “periventricular white matter hyperintensities suggestive of chronic ischemic change” basically has little white dots around these fluid-filled spaces in the brain that indicate brain damage and these contribute in a cumulative way to problems with concentration and memory. Many of these small areas of damage can cause vascular dementia, even in the absence of clear discrete strokes. In my experience, people who have a history of high blood pressure, diabetes, high cholesterol, cigarette smoking, and/or are overweight or sedentary in their lifestyle, have more of these “deep white matter hyperintensities” or “unidentified bright objects” on their CT scans or MRI scans of the brain. In the book titled, Aging with Grace: What the Nun Study Teaches Us About Leading Longer, Healthier, and More Meaningful Lives,
they described a population of patients who were aging in a controlled environment. That is, generally the nuns did not smoke, did not drink, had similar health care, diet, and environment, and only differed in their duties in the overall scheme of the convent.

In the patients who had very little vascular damage in their brain, the amount of neurofibrillary plaques and tangles seem to dictate the level of dysfunction to some degree. For example, if you had no vascular damage in your brain and only plaques and tangles from Alzheimer’s disease, then your degree of disability and problems with memory and functioning were roughly proportional to the amount of plaques and tangles found after autopsy. However, if you had a significant amount of vascular damage in the brain that was found on a microscopic basis in terms of thickening of the arteries, blockages, etc., some of these patients with very few plaques and tangles had a marked amount of concentration, memory and functional problems and were clearly demented.

The important story with regard to these vascular risk factors seems to be that, if you have any of them, they should be reduced to the degree possible to reduce the risk to your aging brain. For example, if you have high blood pressure or diabetes, they should be aggressively controlled through available treatments in order to reduce damage to your brain over time. The advice is similar for high cholesterol. Obviously, if you smoke, you should quit, not only for the positive effects on overall brain function as you age, but in addition, smoking is the single most preventable cause of death and disease in the United States. If you are overweight, you should make changes to your diet and exercise regimen to lose weight and approach ideal body weight as best you can. Generally, this means cutting out saturated fat and switching to lower fat products, reducing the amount of simple carbohydrate intake, and avoiding fast food, sugary drinks, etc. Most patients can lose weight with relatively minor dietary changes if they can make the changes habitual.

One has only to increase the amount of exercise by walking or by some other form of exercise that you enjoy, and reduce sugar and fat in the diet. This was more difficult when there was not a large amount of low-fat or low-sugar products available, but this excuse no longer holds with the availability of these products being widespread. Generally, many of them taste the same as the full-fat or full-sugar product. A sedentary lifestyle, which contributes to obesity, is also not very good for the brain and thus, the recommendation above with regard to exercise holds true to reduce risk of damage to your brain over time related to not getting enough exercise.

If one were to spend as much time on mitigating and reducing brain illness risk factors such as these as we do watching reality television shows, sports, or other television programs, then the health of our brains as we age would improve markedly. Other known risk factors for Alzheimer’s disease include head trauma and having Down’s syndrome. Head trauma increases risk for each individual head trauma of a severe nature. Any head trauma that was severe enough to cause loss of consciousness counts as a risk factor for increasing Alzheimer’s disease risk. Patients with Down’s syndrome have three copies of chromosome 21. There is a genetic risk factor on chromosome 21 that is increased in these patients and most of the patients with Down’s syndrome develop Alzheimer’s disease in their 50s and 60s. As you can see, there are known risk factors that one can reduce in order to increase the likelihood that you’ll make it into your 70s or 80s with a relatively intact brain and improve your quality of life and, potentially, your longevity.

Chapter 3: What Can I Do to Delay or Prevent Alzheimer’s Disease?

As noted in the previous chapter, reducing vascular risk factors is probably your #1 prevention strategy. In order to do this, you should reduce your overall saturated fat intake. What is saturated fat? Saturated fat is fat that you can see. For example, when you look at a hunk of hamburger that is raw, all the little white dots that you see are fat. When you look at a chicken breast, the fat that you frequently cut off, that yellow mushy stuff is saturated fat. When you look at a piece of salami, all the little white dots in the salami are saturated fat. Other places where one finds a lot of saturated fat include cheese and dairy products.

In addition, there is a hypothesis that the increased amount of simple sugars in our diet increase oxidative stress in our bodies. The idea here is that human beings were designed to forage for their own food and run down and catch their own food, and when you look at the difference between what our bodies were designed for and what we currently do, there is a wide difference. I have not had to catch much of my own food recently. I generally go to the grocery store, although I have learned to stay to the outside aisles of the grocery store and stay away from the cookie aisle and the prepared foods in boxes because of their high amounts of saturated fats, high fructose corn syrup, and other simple sugars.

In addition, processed foods generally contain what is called trans-fat. This artery clogging form of fat should be removed from your diet. The food industry, for ease of use and for shelf life purposes, has taken perfectly good types of oil, such as palm oil, soybean oil, and others, (better oils include canola oil, flaxseed oil and olive oil)and hydrogenated them or “saturated them” with hydrogen to increase their stability and their workability in the products that you find on the shelves in boxes and bags. This trans-fat is not easy to metabolize and this is currently felt to be one of the major dietary hazards in the American diet. Recently there is more awareness of the possibility that trans-fats could increase hardening of the arteries, coronary artery disease, arteriosclerosis, etc. These will be regulated by the Food and Drug Administration and most packages will have to state the amount of trans-fats contained in products.

When I go to the grocery store, I always look at anything that’s in a bag, box, or carton and read down the ingredients looking for the amount of trans fat. If trans fat amount is not listed on the label, I look in the ingredients and look for the hidden trans fat, which is usually described as “partially hydrogenated oil.” It is frequently palm oil, soybean oil, or other low-quality oils that are not particularly heart healthy. Most people now know that heart healthy oils, such as canola oil and olive oil, are much more useful in general to cook with, even though corn oil can be used and is less expensive. Personally, I use mostly canola oil and olive oil in all of my cooking, depending on whether I want oil with taste (olive oil) or one without taste (canola oil). By reducing saturated fat and simple sugars in your diet, you will reduce your heart disease risk and, in addition, reduce the propensity to perform blockages in the arteries that feed the deep portions of the brain. In addition, by making these adjustments, you can lose weight, which will reduce another risk factor. Obviously one can avoid activities during which there is a high likelihood of head injury. Personally, I am not particularly big on high-speed water skiing, snow skiing where there are a lot of trees, skateboarding, mountain biking through the woods at the speed of a car, or any other potentially hazardous activities that put my brain at risk. I have discovered over time that it is very difficult to get another brain, and that the one I have is likely the only one I’ll have for my whole life. I expect to take care of mine so that it will take care of me.

Chapter 4: Running Your Brain

Exercise can be very useful in reducing both cardiac and brain health risks. The average American, at present, does not get enough exercise. I heard about a recent study that showed that only approximately 25% of Americans that should be exercising are getting adequate amounts of exercise. The amount of exercise that is currently recommended is thirty minutes of aerobic exercise per day. I know a lot of people like to count walking up and down stairs and walking around at work as exercise. Also, people who work outside and do manual work try to count this as exercise at times. Remember, the human body was designed to run, to move, to catch food, to walk and forage for seeds and nuts, etc., not to sit at home in front of the television or to sit at a desk all day. The only way to get adequate exercise is to pick up some sort of aerobic exercise that you do four or five days a week, or at minimum, two to three days a week. In order to do this, the exercise has to be something that you enjoy. If it’s something that you don’t have any emotional investment in, you’re not likely to get past the three month hump that it takes to make an exercise program a habit. My favorite types of exercise for general body and brain health include walking, swimming, running, hiking, and biking. Most of these sports don’t require a lot in terms of equipment and are generally safer than some previously mentioned leisure activities.

I am a runner and have been since 2001. Prior to 2001, I was a TV watching couch potato who took the elevator at work. I also ate fast food several times per week and was generally not taking good care of myself, which actually requires a lot of time and effort. I joined a running program in 2001 in order to get group support for my new healthy endeavor. Over the last few years, with this group support, I have gone from my former 10-pound overweight, high stress, fast-food eating status, to having run several half marathons and I’m in the best shape that I’ve been in since I was in my 20s.

Some people who are unable to run because of health issues might choose walking. The difference in calorie consumption between running and walking is only around 50%. In other words, generally speaking, you burn approximately 100 calories per mile when you’re running and about 50 calories per mile when you’re walking. Because walking takes about 30-40% more time to complete, your overall caloric burn is reduced, and I believe that many people could become runners if they started with a run-walk program that emphasized a slow and gradual increase in the running component of the equation. For success stories with regard to this approach, the reader is referred to my book, “Running the CRIM: Stories From the Coolest Race in Michigan.” This is about ordinary people who had made a similar transition through the use of a running group or CRIM training program. This book is available on Amazon.com. For people who can’t run or walk because of physical disabilities related to arthritis or other physical problems of that nature, swimming is a viable alternative. Usually, one can find a place to swim within a reasonable distance, but if not, there may be other lower-impact aerobic activities available at local community centers or through local classes advertised in the newspaper put on by local school districts, etc. Some patients who are unable to run or walk are able to use an elliptical trainer, which is also a lower impact activity that mimics the exercise that you can get with running or walking with less impact on your physical limitations.

Here is another caveat with regard to running, and running your brain. I saw a study recently in the scientific literature that showed that when they took a group of mice that had a specific medical problem that caused their brains to deteriorate, much in the same way that Alzheimer’s causes deterioration in humans, that mice who exercise frequently on a treadmill had a better course over time with their illness. The implication from the study was that the running increased the oxygen supply to the mouse brain and nurtured and supported new brain cell growth. The mice who did not exercise would still have some intermittent brain cell growth to replace losses related to the brain damaging illness, but the new brain cells did not survive, implying that they are especially susceptible to damage from low oxygen environments.

While our brains are more complicated than the mouse brain, it is interesting to note that the type of exercise was running, and this model does tend to approximate the human brain model and parallels our understanding of Alzheimer’s and the interplay with vascular risk factors. For example, if you are going to develop Alzheimer’s at age 75, but through the use of frequent and consistent exercise you created a highly oxygenated brain by growing new blood vessels into the small nooks and crannies and improving the health of the blood vessels that already existed, when your brain began to try to replace brain cells damaged by the Alzheimer’s disease process, these new brain cells would survive instead of dying out. Thus, you could stay one step ahead of the Alzheimer’s and have a slower decline. It may not cure the illness, but it may decrease the slope or rate of decline.

Why is this important? Alzheimer’s is generally a 10-year illness. So, if you were going to develop the illness at age 75, you would be dysfunctional and dependent on others sometime around age 80 or 81. Let’s say, for example, through the use of some nutritional supplements that are antioxidant in nature, and through a consistent exercise regiment, you could push the age of noticeable onset of Alzheimer’s out three or four years. What that would mean is three or four more years of functional time without being dependent on others. This means that you are able to drive longer, you’re able to manage your own finances longer, and you’re still able to do things that you enjoy, which makes these years meaningful and useful.

In this example, you would then not show any symptoms until around age 80 and would not become dysfunctional or dependent on others until around age 85 or 86. Personally, I am betting on that extra five or six years of functioning to decrease the burden of my care in my later years on my family, and increase my quality of life in my seventh and eighth decades should I be lucky enough to live that long. Some people might say, “Let me see if I have this straight. You want me to reduce the amount of fat in my diet, reduce the amount of sugar in my diet, lose weight, take better care of my high blood pressure or diabetes, quit smoking, and take up exercise routinely, and I’ll have five more functional years in my 70s or 80s?” and then decide that that’s not worth it. Well, they would have a point. However, I would ask a person with that perspective to take a trip through four of five local nursing homes and see how poorly some of the people are doing there in terms of quality of life.

My guess is that they’ll have the same reaction that I have when I see people who are disabled by dementia. Seeing people disabled in this way increase personal fears about aging. I’d like to reduce these fears and decrease the likelihood that other people will have to pity me, and so I’m going to follow my own recommendations and I hope you will, too. Now you know what I mean by “running your brain”.