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【预订】The End of Alzheimer's Program

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作者Dale E. Bredesen, MD; Foreword by David Perlmutter, MD

出版社Penguin Publishing Group

ISBN9780593541876

出版时间2022-09

装帧平装

定价128元

货号YB-86095

上书时间2024-06-28

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The instant New York Times bestseller

The New York Times Best Selling author of The End of Alzheimer's lays out a specific plan to help everyone prevent and reverse cognitive decline or simply maximize brainpower.

In The End of Alzheimer's Dale Bredesen laid out the science behind his revolutionary new program that is the first to both prevent and reverse symptoms of Alzheimer's disease. Now he lays out the detailed program he uses with his own patients. Accessible and detailed, it can be tailored to anyone's needs and will enhance cognitive ability at any age.

What we call Alzheimer's disease is actually a protective response to a wide variety of insults to the brain: inflammation, insulin resistance, toxins, infections, and inadequate levels of nutrients, hormones, and growth factors. Bredesen starts by having us figure out which of these insults we need to address and continues by laying out a personalized lifestyle plan. Focusing on the Ketoflex 12/3 Diet, which triggers ketosis and lets the brain restore itself with a minimum 12-hour fast, Dr. Bredesen drills down on restorative sleep, targeted supplementation, exercise, and brain training. He also examines the tricky question of toxic exposure and provides workarounds for many difficult problems.  The takeaway is that we do not need to do the program perfectly but will see tremendous results if we can do it well enough.

With inspiring stories from patients who have reversed cognitive decline and are now thriving, this book shifts the treatment paradigm and offers a new and effective way to enhance cognition as well as unprecedented hope to sufferers of this now no longer deadly disease.
纽约时报即时畅销书

纽约时报畅销书作者阿尔茨海默病的终结阐述了帮助每个人预防和扭转认知能力下降或简单地最大化脑力的具体计划。

在阿尔茨海默病的终结中，Dale Bredesen 阐述了他革命性的新计划背后的科学原理：是第一个能够预防和逆转阿尔茨海默病症状的药物。现在，他列出了他对自己的患者使用的详细计划。它易于理解且详细，可以根据任何人的需求进行定制，并将增强任何年龄段的认知能力。

我们所说的阿尔茨海默氏病实际上是对多种大脑损伤的保护性反应：炎症、胰岛素抵抗、毒素、感染以及营养物质、激素和生长因子水平不足。布雷德森首先让我们找出需要解决哪些侮辱，然后制定个性化的生活方式计划。 Bredesen 博士重点关注 Ketoflex 12/3 饮食（它会引发酮症并让大脑通过至少 12 小时的禁食进行自我恢复），深入研究恢复性睡眠、有针对性的补充、锻炼和大脑训练。他还研究了有毒物质暴露的棘手问题，并为许多难题提供了解决方法。结论是，我们不需要完美地完成该计划，但如果我们能做得足够好，就会看到巨大的结果。

通过扭转认知衰退并正在蓬勃发展的患者的鼓舞人心的故事，这本书发生了转变治疗范式，并提供了一种新的有效方法来增强认知，并为这种现已不再致命的疾病的患者带来了前所未有的希望。

作者简介
Dale E. Bredesen, M.D., is internationally recognized as an expert in the mechanisms of neurodegenerative diseases such as Alzheimer's disease, and the author of the New York Times bestsellers The End of Alzheimer's (Avery, 2017) and The End of Alzheimer's Program (Avery, 2020), as well as The First Survivors of Alzheimer’s (Avery, 2021). He has held faculty positions at UC San Francisco, UCLA, and the University of California San Diego, and directed the Program on Aging at the Burnham Institute before coming to the Buck Institute for Research on Aging in 1998 as its founding president and CEO. He is currently a professor at UCLA.

精彩内容
The famous basketball coach, player, and executive Pat Riley exhorted his players to adopt the following attitude when the game is on the line: “Imagine that your head is underwater and you will not be able to breathe again unless you win.” That is some motivation indeed! And it is the attitude we must have about Alzheimer’s disease as well, and in fact about neurodegenerative diseases as a whole— these have all been untreatable terminal illnesses, and if we do not approach them as a societal emergency we will see 13 million demented Americans by 2050, their families destroyed, Medicare bankrupt, and a multi-trillion-dollar global burden of dementia. Yet our “standard of care” is to treat without determining the cause of or contributors to Alzheimer’s, to limit our treatment to a drug or two, to avoid targeted programs of treatment, to refuse clinical trials of multifaceted therapeutics, and to repeat the same old tired, ineffective approaches again and again. Where is the innovation? Where is the inspiration? Perhaps we need a pep talk from Pat Riley?

Therefore, please don’t be concerned if you get your tests, take them to your doctor, and he or she is skeptical. If you ask your doctor to obtain these tests, don’t be surprised if he or she brushes you off with an all-knowing smile or even a look of disdain. As they say, “An expert is someone who does not want to be told anything new in his or her field of expertise.” This personalized approach to cognitive decline is a twenty-first-century approach, not yet in practice by the vast majority of doctors. As one neurologist said, “I wouldn’t order these tests because I would not know how to interpret them.” Another physician said, “These tests don’t tell you whether you have Alzheimer’s or not.” True; what they tell you is why you have cognitive decline (or risk for decline)—what all of the contributors are. Determining if you have Alzheimer’s does not help you to avoid it or reverse it; determining why is the key. Most people who already have Alzheimer’s disease or MCI (mild cognitive impairment, the harbinger of Alzheimer’s) or SCI (subjective cognitive impairment, which precedes MCI) turn out to have between ten and twenty-five contributors, and these are identified by the tests so that each can be addressed therapeutically.

Practitioners have attempted to treat dementia for thousands of years without knowing what caused it or contributed to it, but now, for the first time, we can actually treat the underlying mechanisms. Of course, when Ayurvedic physicians treated dementia thousands of years ago, they did not refer to it as Alzheimer’s disease—it was not until 1906 and 1907 that Dr. Alois Alzheimer published his famous papers—but Ayurvedic physicians clearly described and attempted to treat dementia, and what we now call Alzheimer’s disease is the most common syndrome of dementia.

Twenty years ago, our laboratory research led us to identify the APP (amyloid precursor protein) switch, and when we began to look at what factors flip this switch toward the Alzheimer’s side—the synaptoclastic side—we found that there are different groups of factors, and thus there are actually different types of Alzheimer’s disease.

   • Type 1 Alzheimer’s is inflammatory, or hot, so if you have ongoing inflammation, you are increasing your risk for Alzheimer’s disease. In fact, one of the major mediators of the inflammatory response is called NFκB (nuclear factor kappa-light-chain enhancer of activated B cells), and this increases the production of the very molecular scissors that produce the amyloid from APP, so there really is a direct link from inflammation to Alzheimer’s.
   • Type 2 Alzheimer’s is atrophic, or cold, so if you have sub- optimal levels of nutrients, hormones, or trophic factors (cell growth factors like NGF, nerve growth factor), you are in- creasing your risk for Alzheimer’s disease. Simply put, you do not have the support necessary to maintain the five hundred trillion (500,000,000,000,000) synaptic connections in your brain. On the positive side, optimizing those same nutrients, hormones, and trophic factors offers you the best chance for optimizing your memory and overall cognitive function.
   • Type 1.5 Alzheimer’s is glycotoxic, or sweet, so if you have high blood sugar or high fasting insulin, as 80 million Americans do, you are increasing your risk for Alzheimer’s disease. We call this type 1.5 because it has features of both type 1 and type 2: chronic inflammation (type 1) occurs be- cause the glucose actually attaches to many of your proteins, like remoras to a shark, causing an inflammatory response to these altered proteins (such as hemoglobin A1c, which is hemoglobin with a glucose stuck to it, and hundreds of other proteins). Reduced trophic support (type 2) occurs because your insulin—which is a critical growth factor for your brain cells—has been high chronically, causing your cells to lose their sensitivity to insulin.
   • Type 3 Alzheimer’s disease is toxic, or vile, so if you have exposure to toxins such as mercury, toluene, or mycotoxins (toxins made by certain molds such as Stachybotrys and Penicillium), then you are increasing your risk for Alzheimer’s disease. Since we are exposed to hundreds of toxins—from the mercury in seafood and dental amalgams to air pollution to the benzene in paraffin candles to the trichothecenes from the black mold growing in water-damaged homes, and on and on—we all experience this risk to a greater or lesser degree, so the key is to minimize exposure, identify the toxins to which we are exposed, and increase excretion and metabolism of the toxins.
   • Type 4 Alzheimer’s disease is vascular, or pale, so if you have cardiovascular disease, you are at increased risk for Alzheimer’s disease. Indeed, vascular leakiness represents one of the earliest changes identified in Alzheimer’s disease.
   • Type 5 Alzheimer’s disease is traumatic, or dazed, so if you have a history of head trauma—whether from a traffic accident or a fall or even repeated minor head injuries during sports—you are at increased risk for Alzheimer’s disease.
You can see from these different types of Alzheimer’s disease we identified, and the causes of each one, that virtually all of us a

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【预订】The End of Alzheimer's Program

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