PREFACE

Why Should You Read This Book?

Although humankind suffers many neurological diseases, this book focuses on the neurodegenerative Parkinson’s disease and Huntington’s disease. About 1 million people suffer from Parkinson Disease, with about sixty thousand new cases diagnosed annually in the USA and three to four million people remaining undiagnosed. Huntington’s disease, on the other hand, is estimated to have an incidence of about fifteen hundred per year.

The direct and indirect cost of Parkinson’s disease is estimated to be about $25 billion per year, while the annual cost of treating Huntington’s disease may vary. The average annual medical cost per individual is about $10,500, but it could be as much as $47,000 if the cost of care givers is included.

Parkinson’s disease is considered a slow progressive chronic neurodegenerative disease, appearing later in life and characterized by the loss of dopamine neurons from the brain, which causes involuntary tremors of the limbs and trunk as well as non-motor deficits and neurological symptoms, including impaired sense of smell, memory loss, and psychiatric symptoms. Parkinson’s is the most common form of neurodegenerative disease after Alzheimer’s disease.

In contrast, symptoms of Huntington’s disease--an incurable and fatal genetic disease caused by a gene mutation--appear in young adult life and become progressively worse. The major symptoms of Huntington’s include movement disorders, cognitive dysfunction, and psychiatric problems. The movement disorders are characterized by uncontrolled movement or tics in the fingers, feet, face, or trunk, which become more intense when the individuals are anxious or disturbed. As the disease progresses, other symptoms appear, such as clumsiness, jaw clenching (bruxism), loss of coordination and balance, slurred speech, difficulty swallowing and eating, uncontrolled continual muscular contractions (dystonia), difficulty walking, stumbling, and falling. The cognitive dysfunctions are characterized by progressive loss of memory, including the ability to concentrate, answer questions, and recognize familiar objects.

At present, there is no adequate strategy for the prevention of Parkinson’s disease and the mitigation of Huntington’s disease symptoms, and their treatment options remain unsatisfactory. In this book I propose a unified hypothesis that increased oxidative stress and chronic inflammation are primarily responsible for the initiation and progression of these diseases. Therefore, mitigating oxidative stress and chronic inflammation appears to be a logical solution to reduce development or progression in both. The proposed strategy, in combination with standard therapy, may improve management outcomes more than just standard therapy alone.

To reduce oxidative stress and chronic inflammation, it’s essential to increase the body’s levels of all antioxidant enzymes and all standard dietary and endogenous antioxidants. This goal cannot be achieved by the use of the one or two antioxidants that have been used in clinical studies. Therefore, I have proposed that a preparation of micronutrients containing multiple dietary and endogenous antioxidants, B vitamins with high doses of vitamin B3 (nicotinamide), vitamin D, selenium, and certain polyphenolic compounds (curcumin and resveratrol), should be employed in clinical studies to reduce the risk of development and/or progression of Parkinson’s and Huntington’s. These micronutrients are capable of increasing the levels of all antioxidant enzymes by activating a nuclear transcriptional factor-2/antioxidant response element pathway as well as by enhancing the levels of standard dietary and endogenous antioxidants.

Even though some laboratory data exist to suggest that even the genetic basis of neurological disease can be prevented or delayed by micronutrient supplements, the increase in the amount of micronutrients that I propose flies in the face of conventional theory, for most neurologists believe that antioxidants and vitamins have no significant role in the prevention or improved management of neurodegenerative diseases. These beliefs are primarily based on a few clinical studies in which supplementation with a single antioxidant, such as coenzyme Q10 in Parkinson’s disease, produced only modest beneficial effects in the study group. Another study demonstrated that vitamin E alone was ineffective in reducing the progression of Parkinson’s disease.

The fact of the matter is that patients with neurodegenerative diseases may have a high oxidative environment in the brain, thus the administration of a single antioxidant should not be expected to produce any significant beneficial effects. This is due to the fact that an individual antioxidant in the presence of a high oxidative environment may be oxidized, and then act as a pro-oxidant rather than as an antioxidant. Also, the levels of the oxidized form of an antioxidant may increase after the prolonged consumption of a single antioxidant; this can subsequently damage brain cells. Coupled with this is the fact that a single antioxidant cannot elevate all antioxidant enzymes as well as a multitude of dietary and endogenous antioxidants.

In this book I discuss oxidative stress, inflammation, properties and function of antioxidants and certain phenolic compounds, structure and function of normal human brain, and the incidence, cost, and causes of each neurodegenerative disease. In addition, this book presents evidence in support of a hypothesis that increased oxidative stress and chronic inflammation in the brain play an important role in the initiation and progression of neurodegenerative diseases. I also provide formulations of micronutrients containing multiple dietary and endogenous antioxidants and B vitamins, vitamin D, selenium, and certain polyphenolic compounds (curcumin and resveratrol) specific to each neurodegenerative disease.

I hope that this book will serve as a guide to the consumers who are interested in using micronutrients to reduce the risk of developing Parkinson’s or the mitigation of the symptoms of Huntington’s disease.