In this practical scientific guide, leading researcher in cancer, heart disease, and diabetes prevention Kedar N. Prasad, Ph.D., reveals the latest revolutionary discoveries on the use of antioxidants to prevent and treat Alzheimer's disease. He details how the proper combinations of vitamin and antioxidant supplements can greatly increase the effectiveness of standard medical treatments for Alzheimer's as well as delay or even prevent onset despite a family history of the disease.
Prasad shows how oxidative stress and chronic inflammation play a significant role in the initiation and progression of neurodegenerative diseases like Alzheimer,. He provides an easy-to-follow daily supplement regime to target free radical dam-age and inflammation and stop the progression of Alzheimer, and related complications such as altered sleep patterns, memory impairment, and behaviour changes like depression and anger. Reviewing the scientific research on supplements and Alzheimer's, he debunks the flawed conclusions of the neurological community that vitamins and antioxidants are ineffective, revealing how their studies focused on specific micronutrients used alone rather than synergistic combinations.
Offering the missing complement to the standard care of medications promoted by mainstream medicine, this guide provides a truly holistic approach to Alzheimer, prevention, treatment, and care.
Kedar n. Prasad, Ph.D., is the chief scientific officer of the Premier Micronutrient Corporation, the former director of the Center for Vitamins and Cancer Research at the University of Colorado School of Medicine, and the former president of the International Society of Nutrition and Cancer. The coauthor of Fighting Cancer with Vitamins and Antioxidants and author of Fight Diabetes with Vitamins and Antioxidants and Fight Heart Disease with Vitamins and Antioxidants, he lives in the San Francisco Bay Area.
Why Should You Read This Book?
Alzheimer's disease, a progressive disorder that attacks the neurons in the brain, accounts for 60 to 80 percent of all dementia cases. Although it typically affects older individuals, it also can affect younger people carrying mutated genes; indeed up to 5 percent of individuals afflicted with Alzheimer's disease have what is known as "early onset Alzheimer's," which can present with symptomatology when individuals are in their 40s or 50s. This is due to a familial Alzheimer's in which mutations in certain genes cause the onset of this disease earlier. Symptoms of Alzheimer's disease may include memory loss, a decrease in problem-solving abilities, difficulty completing ordinary chores and tasks, confusion, depression, spatial disorientation, difficulty speaking or writing, losing things, poor judgment, social withdrawal, and mood changes.
Alzheimer's disease remains a major medical concern in the United States, given that it strikes primarily older people (age sixty-five and over). This demographic is expected to increase from about 40.2 mil-lion in 2010 to about 89 million by the year 2050 (U.S. Census Bureau, 2010). Consequently, this disease will create huge health problems and be a burden on society in terms of the cost of its management.
At present, there is no adequate strategy for the prevention of Alzheimer's disease, and its 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 this disease. Therefore, mitigating oxidative stress and chronic inflammation appears to be a logical solution to reduce the disease's development and progression. The proposed strategy, in combination with standard therapy, may improve management outcomes more than just utilizing standard therapy alone.
In order 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 for the prevention or treatment of in some neurodegenerative diseases in humans. Therefore, I have proposed that a preparation of micronutrients containing multiple dietary and endogenous antioxidants, B vitamins with high doses of vitamin Be (nicotinamide), vitamin D, selenium, and certain polyphenolic compounds (curcumin and resveratrol) should be employed in clinical studies for reducing the risk of development and progression of Alzheimer's disease. These micronutrients are capable of increasing the levels of all antioxidant enzymes by activating a nuclear transcriptional factor-2/antioxidant response element (Nrf2/ARE) pathway, as well as by enhancing the levels of standard dietary and endogenous antioxidants.
Most neurologists believe that antioxidants and vitamins have no significant role to play in the prevention or the improved management of Alzheimer's disease. These beliefs are primarily based on a few clinical studies in which supplementation with a single antioxidant, such as vitamin E, produced modest beneficial effects or no effect. However, the brains of patients with a neurodegenerative disease such as Alzheimer's may be a characterized by a high oxidative environment. Therefore, the administration of a single antioxidant should not be expected to produce any significant beneficial effect. This is because an individual antioxidant in the presence of a highly oxidative environment may be oxidized to act as a pro-oxidant rather than an antioxidant. Coupled with this is the fact that levels of the oxidized form of the antioxidant may increase after the prolonged consumption of the single antioxidant. This increase can damage brain cells. In addition, a single antioxidant can't enhance the levels of antioxidant enzymes as well as the levels of dietary and endogenous antioxidants.,
In peer-reviewed journals I have published several reviews that challenge the current trend of using a single antioxidant for the prevention and/or management of neurodegenerative diseases in high-risk populations. These articles have failed to have any significant impact on the design of clinical trials, however, and the inconsistent results of the effects of a single antioxidant continue to be published. And although some books on neurodegenerative diseases and their causes and symptoms are available, none of them have critically analyzed the published data on the effects of antioxidants on neurodegenerative diseases. Nor have they questioned whether the experimental designs of the study on which the conclusions were based were scientifically valid; whether the results obtained from the use of a single antioxidant in a high-risk population may be extrapolated to the effect of the same antioxidant in a multiple antioxidant preparation for the same population; or whether the results of studies obtained on high-risk populations can be extrapolated to normal populations.
The growing controversies regarding the value of multiple micro-nutrients in the prevention and improved management of neurodegenerative diseases need to be addressed, and new solutions need to be proposed. This book articulates the reasons for the controversies mentioned above and proposes evidence and scientifically based, rational solutions for the prevention and improved management of Alzheimer's disease.
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