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Disuse Atrophy, Your Brain, And Your Future
Disuse Atrophy, Your Brain, And Your Future
Disuse Atrophy, Your Brain, And Your Future
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Disuse Atrophy, Your Brain, And Your Future

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Disuse Atrophy, Your Brain, and Your Future explains disuse atrophy and how it can and will affect all tissue types on the cellular level and shows you how to prevent it, particularly when it comes to that most amazing of cells, the neuron. This book explains how you can slow the decline of the cells in your brain and live a full and vigorous mental life, no matter how old you are.
LanguageEnglish
PublisherBookBaby
Release dateJul 1, 2017
ISBN9781543901351
Disuse Atrophy, Your Brain, And Your Future

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    Disuse Atrophy, Your Brain, And Your Future - Kenneth A. Bartholomew

    Wooden

    Introduction

    Disuse Atrophy is a condition that will affect everyone who lives beyond the age of 20 or 30, and there may be parts of the body that suffer disuse atrophy even before that time. Atrophy is a shrinking away or drying up of tissue. Stedman’s Medical Dictionary, 25th Edition, defines atrophy (from the Greek atrophia, fr. a- priv. or without + trophe, nourishment or literally ill-fed) as a wasting of tissues, organs, or the entire body, as from death or the reabsorption of cells, diminished cellular proliferation, decreased cellular volume, pressure, ischemia, malnutrition, lessened function, or hormonal changes. Stedman’s then goes on to list 66 types of atrophy, but nowhere in that list is the term disuse atrophy used. Yet I will show you that disuse atrophy can and does affect every organ of the body, including the multiple specialized areas of the brain, and that there is something you can do about it.

    The seed for this book was lodged in my brain during the first year of medical school in 1972, and like a pinyon pine seed in a stony mountain crag, it took root and would not let go. 44 years later it is still there, slowly sending its roots deep for water, not letting go. I began the first draft in 1989 and finished around 2000, but could not get it published because, as I was told, You are not a neuroscientist. Then I learned more about e-publishing during a writer’s conference, and like the examples in these pages, I refused to give up.

    Over the last 40 years of medical practice, I have treated countless patients with the drug-free, common sense approach found in these pages. The fact that Stedman’s does not even list disuse atrophy is an example of how the medical establishment for decades studied disease, while the maintenance of health often went unaddressed. I believe that disuse atrophy is a huge source of debility in the general population, and nothing in my research has caused me to alter that opinion.

    I know of no more encouraging fact

    than the unquestionable ability of

    man to elevate his life by a conscious endeavor.

    – Henry David Thoreau

    Walden

    Chapter 1

    Grandpa And The Woodcutter

    The aging process first began to intrigue me in grade school. Each day as I walked to school I would see the bent and gray man splitting his firewood with his double-bladed axe, good weather or bad. I don’t remember his name, but I still remember so clearly that he looked much too old to be doing such strenuous work. Year after year, into my high school years, I watched him swing that axe to stoke his morning fire, and it slowly dawned on me that he could do it every day because he did it every day. If he had stopped for 6 months he would have had much more difficulty getting started again.

    I realized the same thing more personally when we would start a new season in sports. Muscles and ligaments that had been forgotten for months were stiff and sore for the first few days as we forced our bodies back into shape. It was during this time that my grandfather made what I would come to believe was a fatal mistake. He retired.

    Grandpa Whitney had been a scholarly and compassionate judge, and it seemed there was no one who knew him who did not respect him. He rarely drove to the court house, walking in good weather or bad, and he walked home for lunch. Each evening he would go for a walk after dinner with my grandmother and whichever of many grandchildren might be visiting. During the day he would be busy at the court house, using both body and brain, hearing cases or researching them. But when he retired, literally to his rocking chair, it seemed that you could see him age daily. Before the next two years were out, he was in the hospital constantly, his memory began to slip, and then he was dead.

    For years I wondered what his fate might have been had he stayed active. His age may have necessitated giving up his seat on the bench, but he need not have quit going to the court house, reading and researching cases, nurturing younger judges. But he didn’t do that, and he had no hobbies other than reading, nothing to get him out of that rocking chair. Even then I wondered, Which came first, the chicken or the egg? If my suspicions were correct, I was glad that he retired at 75 instead of 65.

    In high school, another question kept coming to mind. Why do some kids turn out so well, and others so poorly? Children from nearly identical backgrounds can turn out to be such very different adults, and others, from very poor and very wealthy backgrounds, can turn out the same. I wondered what the common denominator might be, and I realized that I was intrigued with how the mind worked.

    I have been trained in general medicine and surgery. The practice of medicine in a small town gives one enormous opportunity for human observation - at least as much as a neuroscientist in an animal lab. It definitely broadens one’s view. All of my theories came about as a result of this human observation, and only later did my research for this book help solidify what I had been led to believe by objective observation. Therefore, I take full blame for wherever my theory may be wide of the mark. But whether I am proven right or wrong as future cellular research unfolds the inner workings of brain cells, I believe what follows is a sound and workable model of thinking about the body and the brain and how best to preserve their healthy functioning. Let us look, then, at atrophy and some aspects of aging, and see how disuse atrophy differs from them.

    All that is human must retrograde if it does not advance.

    – Edward Gibbon

    Decline and Fall of the Roman Empire

    Chapter 2

    Atrophy

    Atrophy (at’-roe-fee) is a wasting of tissue, a drying up, a loss of integrity and a diminution in the size of a tissue. It can be broken down into six basic types:

    Avascular Atrophy

    Denervation Atrophy

    Abuse Atrophy

    Aging Atrophy

    Malnutritional Atrophy

    Disuse Atrophy

    It is very important to look at atrophy this way because, although aging is really a composite of all six types, there is something we can do about four of them. Experience shows us that we will be more stimulated to do that something if we understand what we are doing. You will find that although it is complex, you do not need a degree in neuroanatomy to see inside your brain. And I hope you will learn as this book unfolds that there are few things you cannot understand, and few things you cannot do.

    AVASCULAR ATROPHY: Avascular means without blood flow. This may be due to trauma crushing or cutting the arteries so that blood cannot get into the tissue, blocking the flow of fresh oxygen, sugar, proteins, amino acids and vitamins essential for that tissue’s well-being. Or it can be due to the veins being blocked, pinched, or clotted in such a way that the blood cannot exit the tissue, causing a damming or sludging effect and restricting the flow of nutrients.

    If the heart slows down or stops long enough, lack of oxygen delivery leads to cell damage. The area of the body most sensitive to temporary circulation stoppage is the brain - cell death can occur in three to five minutes. Muscle and bone are more resilient - if the interruption is brief, they can recover. During orthopedic surgery, a pressure cuff is often placed on a limb to prevent blood loss and virtually no flow occurs for up to two hours, yet those tissues are little worse for the wear. Peripheral nerve tissue is somewhere in between. One of my patients underwent knee surgery two years ago and only recently regained function of one of the nerves leading to the foot. The nerve and muscle on that side of her lower leg and foot may be permanently weak due to the atrophy that occurred during the loss of blood flow. We term this damage Necrosis if there is actual cell death. Atrophy, on the other hand, is a shrinking or wasting, but not cell death. Necrosis would tend to be quick or acute, whereas atrophy would tend to be chronic, a long, drawn-out wasting. My patient’s outer, or lateral, leg muscle is smaller and weaker on that side and probably will be for life.

    The most common type of avascular damage to the tissues is due to slow blockage of the arteries with eventual occlusion.

    This is the classic arteriosclerosis, or hardening of the arteries, in which a high cholesterol level is implicated. Plaque, a fatty deposition, penetrates the intima or inner lining of the arterial wall and slowly builds up, blocking the channel and restricting blood flow. When plaque first begins to accumulate, there is no damage for many years because we are born with more blood flow than we need. However, years later, when there is only a tiny opening remaining, platelets and red blood cells can pile up against the rough pinhole and form a clot, suddenly closing off the area served by that vessel. When this happens in the heart, it is called a heart attack or Myocardial Infarction (MI). When it happens in the brain, it is called a Stroke. Tissue has died. Avascular Necrosis has occurred.

    If the artery does not close off completely, but the narrowing reaches a critically small level, there may be only a few red blood cells able to get through the opening per minute. This very reduced oxygen and nutrient supply causes a steady wasting of the tissue downstream from the blockage. Avascular Atrophy is occurring.

    I stated earlier that we can do something about four of the forms of atrophy. Avascular atrophy is one of them. If it progresses to avascular necrosis, it is too late and only rehabilitation is possible. An ounce of prevention is worth years of rehab.

    Since high blood pressure (Hypertension), Diabetes, smoking, and high cholesterol levels (particularly LDLC or Low Density Lipoprotein Cholesterol) accelerate this process, it is imperative to start as young as possible with a sensible diet low in fats and overall calories, regular exercise that burns off excess fats and opens arteries, and regular blood pressure measurements, keeping the blood pressure under 130/80 ideally, or at least under 140/85. If you are diabetic, you need to keep your calorie intake low, your weight as trim as possible, and your blood sugars in a reasonable range (although keeping it very low has not been proven to prolong life and has some bad consequences). Lastly, tobacco smoke contains hundreds of toxins, some of which are obviously carcinogens, but others cause intense injury to the arterial wall, accelerating the above process so much that smoking probably kills more people by cardiovascular damage than by lung damage.

    We know that this process begins in childhood, not middle age and certainly not old age. Autopsies done on children who died of accidental deaths revealed plaque already starting to accumulate by age five. Therefore it is our responsibility to not only take care of ourselves, but to begin teaching our children good lifestyle habits early on.

    I remember too clearly the case of a twenty-five year old medical student from Texas, because, at the time, I was a twenty-five year old medical student from Utah. He was a good athlete, trim and in excellent condition until the day he collapsed playing basketball. He was dead at twenty-five! An autopsy revealed that his blood vessels were so clogged with plaque that they were described at autopsy as looking like an old man’s arteries. His family was then tested and found to have the gene that codes for astronomical levels of both cholesterol and triglyceride fats.

    But regardless of your genetics, you can improve on whatever hand you’ve been dealt. Controlling high blood pressure adds an average of eight years to your life, and smoking shortens your life by ten to twenty years. Additionally, the reduction in strokes and heart failure adds quality to those extra years. Even if we cannot control our own habits, don’t we owe it to our children to educate them properly from the start? The process is already underway inside their arterial walls.

    DENERVATION ATROPHY: Denervation atrophy is a little more straightforward. When a motor nerve is cut, the muscle it innervates or stimulates begins to waste. That muscle can have a perfectly normal blood supply and excellent nutrition, but still it shrivels. It even happens in newborns when a nerve is crushed during passage through the birth canal. Even though the blood vessels are healthy and all necessary nutrients are being delivered, without the electrical stimulation of the nerve the muscle does not get everything it needs. It needs activity to be healthy. Muscular contraction takes place when an electrochemical signal, originating in the brain or spinal cord, travels down the nerve and reaches the Motor End Plate.

    Muscle Body With Nerve And Motor End Plate

    A chemical called Acetylcholine is released from the motor end plate and jumps the gap to the muscle cell on the other side (much like the spark plug in your car’s engine) sparking or triggering a contraction of that cell via release of stored electrochemical charges on the surface of that cell. This electrical current then passes extremely rapidly from cell to cell in a chain reaction, causing each muscle cell to contract or shorten. The cumulative effect is thousands or millions of cells each moving a fraction of a millimeter, thus causing several inches of overall movement. However, when the electrical stimulation is lost, the cells simply sit there and get boggy, less circulation takes place, milking of waste byproducts from cells does not occur, and wasting or atrophy begins.

    Denervation Atrophy

    This gentleman had nerves in his right lower back slowly pinched off by a bad disk and arthritic narrowing of the spinal canal. His right leg has shrunk despite his being active, with a committed exercise program trying to keep it healthy. Without the nerve to stimulate it, the muscles are smaller and weaker than those in the left leg.

    Any process that causes nerve loss will start this cascade of events. Cutting or crushing or clogging a critical blood vessel to a nerve will lead to that nerve’s atrophy, therefore avascular atrophy can result in denervation atrophy.

    ABUSE ATROPHY: Abuse atrophy is even more straightforward. When a tissue is abused beyond a set point, a certain amount of cell loss occurs, either loss of cell integrity or outright cell death. A common example of this is the alcoholic liver. At first, the liver hypertrophies or goes into overdrive in response to the over-stimulation and hyperactivity it is forced to undertake to break down the excess toxins in the system. Much as a muscle enlarges when it is worked, so does the liver enlarge. At first. But as it is repeatedly overworked, overpowered and slowly poisoned by the excess alcohol, it begins to suffer damage. The cells that were once enlarged and at peak performance can no longer tolerate the chemical abuse and they begin to decline in functional capacity. They begin to shrink and scar. In the late phase, there is a combination of atrophy of some cells doing their job but doing it poorly, and necrosis or death of other cells. Dying or dead cells become scar tissue within a now very weakened, shriveled, and hardened liver. You can picture a similar chain of events in the lung tissue of a regular smoker whose lungs are blackened, stiff and scarred by the time they are 60. Congress passed laws about workplace conditions in coal mines to prevent black lung, but can do nothing about letting us do it to ourselves.

    AGING ATROPHY: Close your eyes for a minute and picture your parents or your grandparents. You know their skin is thinner, their lips less full with tell-tale wrinkles, their hair more thinly spaced and the fibers thinner and more brittle than they once were. Their muscles are more thin and cannot generate the strength they once could. They cannot sprint or bound up the stairs two at a time. Brain scan images show a definite thinning of the brain in older people, even in those who from all outward appearances are functioning perfectly normally. These are just some manifestations of normal aging. Some do it better than others, but we all age.

    Young Healthy Brain

    Elderly Healthy Brain

    The brain scans above are from a young, healthy person and a healthy 93-year-old lady, respectively. The gray areas represent brain tissue, the black areas represent fluid. Note the full complement of gray matter in the young person and the huge areas of fluid replacing brain tissue in the 93 year old. The old brain has atrophied markedly but this person can still talk, walk, feed herself, and enjoy music. This is a good example of physiologic reserve.

    Unfortunately, I have also seen CT Scans of 60 year old brains that show a similar degree of atrophy from alcoholism, and severe alcoholism also causes peripheral nerve damage as well as specific psychiatric changes in the brain. So although a glass of wine or two helps lower cholesterol and helps us relax and lower our blood pressure, too much of a good thing turns bad.

    We are born with more of every tissue than we need to get by. We have about six times as much kidney tissue, for example, than we need for normal cleansing of the blood. We also have far more muscle mass than we need for everyday locomotion. This is called physiologic reserve. We have a reserve of tissue to

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