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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 are at some risk for Alzheimer’s, and indeed, this is one of the reasons that it is such a common disease. With the many toxins to which we are exposed, the processed foods, the high-carbohydrate and unhealthy fat content of the SAD (standard American diet), the leaky gut so many of us have, and the lipid abnormalities (“cholesterol,” although the cholesterol itself is actually not the problem), most of us have a significant risk for Alzheimer’s disease. The good news is that nearly all of us can avoid or reverse the problem, now that we understand the contributors. To do that, we simply need to address the underlying drivers of the disease process—it’s like patching thirty-six holes in your roof—the same ones that we profile in the subtyping described above, and the earlier we do this, the easier it is to achieve success. The overall goal of treatment can be summarized as removal, resilience, and rebuilding: removal of the exposures contributing to cognitive decline, resilience resulting from optimal health support, and rebuilding of the neural network.