Environmental Causes and Prevention Measures for Alzheimer's Disease

George J. Brewer

• Publisher: Academic Press
• Year: 2017
• Print ISBN: 9780128111628
• eBook ISBN: 9780128111635
• Topic: Biological Sciences
• Subtopic: Neuroscience
• Index: Biological Sciences

Environmental Causes and Prevention Measures for Alzheimer's Disease examines the increased incidence of the disease in developed countries and aims to educate neuroscientists, medical practitioners and other educated individuals on new insights into environmental causation, primarily metals. This book looks into the web of evidence around the hypothesis of copper toxicity and the additional role that a high fat diet plays in disease progression and cognition loss. The data and its implications are discussed, along with potential prevention measures. This book will generate excitement and interest among neuroscientists, medical practitioners and other biomedical researchers.- Emphasizes the history and epidemiology of Alzheimer's disease, highlighting its epidemic proportions in developed countries- Discusses data on new environmental factors in developed countries- Provides prevention measures to potentially reduce Alzheimer's rates through diet

Chapter One

Introduction

Abstract

Chapter 1 is an introduction to the book. A brief description of Alzheimer’s disease (AD) is given, although a much more detailed description will be given in Chapter 2. It is pointed out that AD is a disease of cognition loss in people aged 60 and over, and a brief description of the brain pathology is given. Then the chapter briefly discusses what is in the rest of the book. A highlight is in Chapter 3, where surprising and important facts about AD are given—namely it is in epidemic prevalence in developed countries but rare in undeveloped countries, and the epidemic in developed countries has occurred in the last 100 years. It was rare before 1900. These facts cry out, “Something in the environment in developed countries is causing the epidemic”. Then there are two chapters searching for the environmental agent or agents, and then a chapter describing copper, particularly divalent copper or copper-2, as a major culprit. Then there are several chapters giving copper background and detailing how copper and, specifically, copper-2 are causative of AD. At this point in Chapter 1, the fascinating story of how chance and careful investigation led to the experimental demonstration that copper-2 in drinking water was causative of AD in an animal model. Chapter 1 then returns to the book overview. Chapter 8 puts together an overwhelming web of evidence that copper-2 is a major causal factor for the AD epidemic in developed countries that has emerged in the last 100 years. Chapter 9 shows how an increased body load of copper in general (irrespective of valence), occurring because of dietary changes in developed countries, is also contributing to the epidemic. Chapter 10 shows how nicely the copper hypothesis fits with known risk factors and current theories of AD causation. Chapter 11 is very important because it describes how people can almost completely avoid this disastrous disease by two easy steps that almost completely eliminate ingestion of copper-2. Dietary changes that reduce copper absorption are also discussed. The final chapter, Chapter 12, discusses how the federal government has failed to set proper standards for drinking water copper content and failed to assure safety of multimineral supplement pills by eliminating copper-2 in them.

Keywords

Alzheimer’s disease; Copper; Copper-2; Drinking water copper; Environmental causes of Alzheimer’s disease

He who finds a thought that enables him to obtain a slightly deeper glimpse into the eternal secrets of nature has been given great grace.

Albert Einstein

As stated above so well by Einstein, we scientists feel a touch of awe, or grace, when we uncover a new scientific truth. I now feel that sense of grace after uncovering a major environmental cause of Alzheimer’s disease (AD). AD is at a catastrophically increasing frequency and causes a disastrous loss of ability in our elderly to think and act effectively, thus robbing them of their golden years. Since the cause I have discovered can be easily corrected, or avoided, by individual persons, the grace I feel will be multiplied several fold if I can get this message out to the academic community and later the general public, and if it results in a major curbing of the disaster that is AD. So the purposes of this book are (1) to educate academicians and others about this newly discovered environmental cause, providing enough scientific evidence to convince, but not so much as to confuse and (2) to show people how to make the changes that will make all the difference in preventing AD.

In this introductory chapter, I will outline rather broadly what will be covered in the rest of the book. By the end of this chapter, you the reader will have the big picture, but not the details behind this major cause of AD. The details will be filled in as you read the rest of the chapters.

First of all, what is AD? In Chapter 2, we will provide more details about the disease that has reached epidemic proportions in many parts of the world, including the United States, but here we will just say enough to make sure everyone has a basic concept of the disease. It usually occurs in people aged 60 years and older, and usually begins with memory loss. If only mild memory loss is affected, it is called mild cognitive impairment (MCI). But MCI is usually a precursor to AD, as 80% of MCI patients convert to full AD at a rate of 15% per year. As the disease progresses, other cognitive functions in addition to memory begin to be lost. Decision making deteriorates, and the ability to perform even routine tasks is lost. Eventually the patient requires a full-time caretaker. Very often this is a family member, such as a spouse, so that the disease results not only in loss of enjoyment of the golden years of the patient but also puts a tremendous burden on the spouse or other members of the family, or whoever is the caregiver. This is particularly burdensome, because the AD patient may live for a decade or two requiring a full-time caretaker.

Memory and the ability to do tasks appropriately are all part of what is called cognition, so the AD patient loses more and more cognition as the disease progresses. But what is going on in the brain of the AD patient to cause this loss of cognition? Are there abnormalities that can be seen in the brain? Yes, scans of various types will show shrinkage of the brain. And at autopsy, typical abnormalities are seen in the brains of AD patients. Besides shrinkage, a prominent abnormality that is seen is what are called “amyloid plaques.” A piece from a protein called amyloid precursor protein is clipped off. This piece is called beta amyloid, and large numbers of beta amyloid pieces clump together to form amyloid plaques. These plaques are uniquely present in AD brains, and so characteristic that many experts think they play a critical role in the disease process, causing damage to the brain. Found bound to these plaques are large quantities of three metals, zinc, copper, and iron. The binding of copper and iron in these plaques causes them to generate what are called “oxidant damaging radicals” in the brain. This oxidant damage does appear to be involved in the injury to the AD brain. More details are given about amyloid plaques in Chapter 2 and the metals bound to them in Chapter 4.

A second prominent abnormality found in AD brains at autopsy is called “neurofibrillary tangles.” These are tangles of the hairlike outgrowths from the neurons (brain cells) of the brain. Amyloid plaques and neurofibrillary tangles are so specific for AD that it allows the pathologist to make a certain diagnosis of AD. In fact, this is the only way the diagnosis of AD can be made with 100% certainty. However, doctors who have expertise with AD patients can nowadays make the diagnosis in live patients with about 95% accuracy.

In Chapter 3 we will provide interesting new facts about the epidemic of AD that most people, and even doctors who treat lots of AD patients, don’t realize. These facts provide a whole new perspective about AD. These facts shout out, “AD is caused by something new in our environment!” This new perspective is both depressing and exciting. Depressing because it turns out the epidemic, and the loss of their golden years by our elderly, is mostly caused by something we are doing to ourselves. Exciting because there are some simple things we can do to reverse the epidemic.

In a nutshell, these interesting new facts are

1. AD is at epidemic proportions in developed but not undeveloped countries.

2. AD at a high frequency is a relatively new disease phenomenon, reaching epidemic levels in the last 100 years. AD was nonexistent, or very rare, before the year 1900. The evidence for this is very good.

3. The absence of AD in the 1800s is not due to the lack of elderly people in high-enough frequency to have been affected by the disease.

4. The absence of AD in the 1800s is also not due to it not being noticed, or attributed to “normal aging.”

This set of facts lead to a clear conclusion, almost “shout it out” as said earlier, that some thing or things in the new environment in developed countries, not present in undeveloped countries, is, or are, strongly causal of the AD epidemic.

I would like to emphasize to readers how important the above conclusion is. It is more important than finding out that cigarette smoking causes cancer, heart disease, and stroke. At least these killers often kill relatively fast, and generally patients retain their thinking ability until the end. That is, they remain human until the end. Not so with AD. Patients are gradually stripped of their memories and thinking ability over a period that may last up to two decades. They lose what makes them human and become no more than pet animals. Is that the way we want our loved ones to end up their lives, with a caretaker caring for them for years and years like a pet animal?

So surely, if a major cause of the disease is something in the environment, we as a society and as individuals should leave no stone unturned to find the cause and remove it, so as to prevent as many cases of this degrading disease as possible. Well, we now know a major environmental cause. As we will discuss in Chapters 6–9 in detail, it is ingestion of inorganic copper, together with a high meat diet. In Chapter 11, we tell you how to eliminate these risks, which can be done in a relatively simple, inexpensive manner. This message needs to be disseminated in our society, so that people can learn how to avoid this very bad disease.

Continuing with the broad outline of the book, having presented in Chapter 3 the clear evidence leading to the conclusion that a new environmental agent or agents is causing the AD epidemic, in the next two chapters, Chapters 4 and 5, a logical search of what those agents might be is pursued. To be identified as a likely causative environmental factor, the factor (or agent) must pass two tests. First, does change in the factor or agent fit with the AD history and demographics demonstrated in Chapter 3. That is, is it now different between developed and undeveloped countries, and has it changed in developed countries over the last 100 years? The second test is the question of whether there are data of some type making the factor or agent a logical causative factor for AD. It must be recognized that in terms of this second test, not everything is currently known about all the ways AD can be caused. So just because a factor or agent fails this second test doesn’t rule it out as a possible candidate. It’s just that the case is greatly strengthened if the second test is positive as well as the first. In Chapter 4, the search will focus on metals. Several metals have been suspected of playing AD causative roles, and if exposure has changed, one or more of them could be a causative environmental factor. We will come out of this search by hitting pay dirt. Copper turns out to be the culprit, and in two ways. Exposure to copper-2 (divalent copper) is specifically AD causative, and a lifetime exposure to increased body copper levels is also AD toxic. Copper-2 and copper, in general, both pass tests for being environmental AD causative agents. Much is being written in the recent literature about the effect of diet and other lifestyle factors on AD. So, in Chapter 5, whether any lifestyle factors could explain the AD epidemic is examined. In Chapter 5 we hit pay dirt again, identifying increased meat eating with increased copper absorption as a likely new environmental AD causative factor.

In Chapter 6, detail about how copper-2 and copper in general fits as major environmental factors causing the AD epidemic will be provided and how increased meat eating fits as well, because it increases copper absorption.

Continuing with the broad outline of the book, in Chapter 7 background on copper in general is provided, since much of the book will be talking about copper. Copper’s role in the body as an essential element will be discussed. Unlike lead, which is purely a toxic metal, while copper can be toxic, for example as said here copper toxicity is a cause of AD, it is also critical to life, taking part in many vital reactions.

Also in Chapter 7, the difference between what is called “inorganic copper” and “organic copper” will be discussed. In brief, organic copper is the copper in food, safely bound to proteins and other organic molecules in the food. It is primarily copper-1. This organic copper is absorbed from the intestine and is taken immediately to the liver, where it is put in safe channels. Inorganic copper, which is copper-2, such as copper in drinking water or in mineral supplement pills, are simple salts of copper, not bound to anything. A portion of inorganic copper is absorbed directly into the blood, bypassing the liver, and directly contributing to the potentially toxic copper of the body. Think of it this way: Our bodies evolved to safely handle the copper in food. Our bodies have not evolved to safely handle inorganic copper, because in the prior eons of evolution, inorganic copper was not ingested. It is only during the 1900s and since that humans have been exposed to copper in drinking water, because of the spread of copper plumbing in developed countries, as well as the increasing habit in developed counties of taking a daily multimineral pill containing inorganic copper. The reason for the difference in the way the body handles inorganic copper and organic copper is now known. As explained by reviewing the simple chemistry of copper i...

Table of contents

• Cover image
• Title page
• Table of Contents
• Copyright
• Dedication
• Foreword
• Acknowledgments
• Chapter One. Introduction
• Chapter Two. A Little Background on Dementia and Alzheimer’s Disease
• Chapter Three. Interesting and Important Historical and Demographic Facts About the Epidemic of Alzheimer’s Disease in Developed Countries Pointing to Environmental Intoxicants Causing the Epidemic
• Chapter Four. Candidate Environmental Factors for the Alzheimer’s Epidemic Part 1: The Metals—Aluminum, Lead, Mercury, Zinc, Iron, and Copper
• Chapter Five. Candidate Environmental Factors for the Alzheimer’s Epidemic Part 2: Diet and Other Lifestyle Factors
• Chapter Six. Identification of Copper-2 and Copper in General, as Major Environmental Intoxicants in the Alzheimer’s Disease Epidemic: The Copper Hypothesis
• Chapter Seven. Background on Copper, Including Why Copper-2 Is So Specifically Neurotoxic
• Chapter Eight. Inorganic Copper, or Copper-2, Ingestion as a Major Causal Factor for the Alzheimer’s Disease Epidemic—The Web of Evidence
• Chapter Nine. Increased Copper Absorption Resulting From Dietary Changes in Developed Countries as Another Causal Factor in the Alzheimer’s Disease Epidemic
• Chapter Ten. The Copper Hypothesis Fits Nicely With Known Risk Factors and Theories of Alzheimer’s Disease Causation
• Chapter Eleven. Prevention Measures Action Items: Two Simple Steps to Eliminate Ingestion of Copper-2, and Dietary Changes to Reduce Copper Absorption
• Chapter Twelve. Failures: What the Government Has Not Done to Ensure Healthy Drinking Water and Nontoxic Multimineral Pills
• Chapter Thirteen. Treatment of Alzheimer’s Disease
• Chapter Fourteen. Summary and Conclusions
• Index