Recently, VERY EXCITING NEWS about Alzheimer’s Disease (AD) has finally arrived—and Hope is winning-out in the war against this awful disease.
NUTRIENTS are at the Heart of this Hope & Lifestyle Choices centered around Plant-based Eating are at the crossroads. The EXCITING NEWS is that it is No Longer True that nothing can be done about Late-Onset Alzheimer’s Disease (LOAD) even for some with moderately advanced dementia.
Finally, after decades & decades of research, & billions upon billions spent in failed attempts to find effective medications, success at last, but it took a Programmatic Approach (which is addressed below) to successfully deal with the Multiple Processes underlying LOAD.
NO SINGLE THING
No Single Medication has worked well previously because Alzheimer’s is NOT a Single Disease: Early-Onset Alzheimer’s Disease (onset ~ 50 yrs of age) is caused by different genes than Late-Onset Alzheimer’s (onset ~ 65 yrs of age and older) & even LOAD comes in several subtypes. However, all types of Alzheimer’s share a final common pathway: at the heart of all Alzheimer’s resides a 40+ input Amyloid Precursor Protein Master-Molecular-Switch whose ultimate activity results in one of two outcomes—brain health vs. brain degeneration. Either brain health (neuroplasticity) is preserved, or inflammation & toxicity result in the build-up of garbage heaps both inside & outside of brain cells, ultimately antagonizing them to death—meaning causing brain cells to activate cellular downsizing programs (suicide programs) to be exact. If you wonder why they would do such a thing, just imagine what would happen if your waist (sewage) and trash-collection services got discontinued—toxic garbage would consume your property, first outside the house until you ran out of space, and then also within—how long until somebody would get sick? How long before the neighborhood homeowner’s association would demand you leave? How long until you opt to abandon your house all together, even if it means leaving your prized possessions (in the case of Alzheimer’s Dementia, this correlates to your memory, your cognition & your personality)?
ARE YOU AT RISK FOR LATE-ONSET ALZHEIMER’S DISEASE?
That depends, are you an adult offspring of a parent who suffered Alzheimer’s? Has anyone else in the family been diagnosed with Alzheimer’s Disease? LOAD used to be classified as ‘non-familial,’ because it didn’t ALWAYS run in families. But we have since learned that genes play a significant role, they just are not what are called, ‘highly penetrant’ genes, meaning they don’t alone cause disease, unlike the mutated genes of Early-Onset Alzheimer’s Disease, in which case the mutations alone almost invariably do result in manifestation of the disease.
These are important issues because we know that Alzheimer’s develops over DECADES before symptoms of memory loss begin to manifest—meaning one isn’t free from concern just because their memory appears to be working in their 50s and 60s. This is critically important, because early intervention is KEY to the potential for Reversing the underlying Disease Process & Key to Prevention too.
SUBTYPES of ALZHEIMER’S DISEASE
Dr. Dale Bredesen is an accomplished Neurologist, Neuroscience Researcher & Author of The End of Alzheimer’s: The First Program to Reverse & Prevent Cognitive Decline. Dr. Bredesen subclassifies Alzheimer’s into 3 predominate subtypes: ‘Atrophic’ or ‘Cold’ subtype (think lack of nutrients), ‘Inflammatory’ or ‘Hot’ subtype, and a ‘Vile,’ or ‘Toxic’ subtype.’ Of course, these subtypes co-occur and overlap significantly, hence the term, ‘predominate.’
THE REASON TO SUBTYPE ALZHEIMER’S DISEASE
The reason to subtype is because FUNCTIONAL BIOMARKERS for each subtype can be measured & steps can be taken to counter any imbalances caused by nutrient deficiencies (‘Atrophic’ or ‘cold’ subtype), or disturbances of other varieties. Methylmalonic Acid is an example of a functional biomarker which indicates a deficiency of functionally effective, bio-actively methylated, Vitamin B-12—or Methyl-B12, which is critically important for the recycling of methionine and homocysteine, and this is important because elevated levels of homocysteine correlate directly with dementia as well as cardiovascular disease.
Biomarkers representing ‘Inflammation’ (or the ‘hot’ subtype) can be identified and quantified & strategies involving intelligent food planning and the use of nutrient supplements for the sake of quashing the cellular wildfire that is chronic inflammation. Sedimentation Rate & CRP are two arbitrary conventional examples of biomarkers for inflammation. Calprotectin is an example of a functional biomarker for intestinal inflammation. There are many other examples that could just as well have been chosen to illustrate the point.
Many Urinary Organic Acids serve as Functional Biomarkers which indicate the presence of specific biochemical pathway disturbances, and this has a unique way of telling us what we need to ‘fix.’
Moreover, Detoxification Genes can be STRATEGICALLY induced (stimulated) by the tactical use of specific nutrients (this is the burgeoning science of nutrigenomics), which then reduces the ‘vile burden’ (‘Toxic’ subtype) of accumulated BIOTOXINS by enhancing their biotransformation and elimination which includes heavy metals such as Mercury and Lead, and other metals such as Cadmium, among an ever-increasing number and variety of other biotoxins, such as those derived from mold, or found in herbicides (glyphosate) for examples.
Nutrients make up the specific coenzyme & cofactor components required for their respective enzymes to function properly. Nutrients also act to regulate gene expression, notably including our own genetic capacity (antioxidant capacity) for protecting brain cells from oxidative damage, thereby preserving neuro-networks including those serving memory storage and & core aspects of personality.
Nutrigenomics is the scientific study of how nutrients function to either amplify or silence the expression of specific genes. Science has progressed greatly with unraveling which nutrients regulate which genes and with what outcome.
THE PROGRAMMATIC APPROAH THAT SUCCEEDED WITH ALZHEIMER’S
Although there are, in current clinical trials, a number of new gene therapies that are showing promising results indeed, it is Dr. Dale Bredesen’s innovative, programmatic approach to Alzheimer’s, called The ReCODE Protocol, upon which I most want to focus for 2 particular reasons:
- For one, because Dr. Bredesen’s ReCODE Protocol has already proven effective in clinical trials at preventing & reversing cognitive decline.
- Secondly, because the SUCCESS of the ReCODE Protocol at forestalling & reversing cognitive decline & memory loss, creates an important CALL TO ACTION!
Dr. Bredesen’s ReCODE Protocol is based upon Lifestyle Modifications (eating & sleeping routines, exercise & relaxation programs), Nutrient Optimization Strategies, and perhaps above all else, upon a near complete Avoidance of the Standard American Diet in favor of Plant-Based Eating—primarily.
WHY SO SAD?
THE STANDARD AMERICAN DIET is SAD due in part to its high saturated fat, its low fiber & its over-abundance of highly-refined carbohydrates, which together combine to promote insulin resistance & chronic inflammation, both of which are strongly implicated as major contributors in the prolonged development of neuro-degenerative process. LONG BEFORE symptoms of Mild Cognitive Impairment & Memory Loss manifest clinically in a person’s life, insulin resistance & chronic inflammation have been busy fueling metabolic havoc.
Now, you may read elsewhere: ‘There is no cure for Alzheimer’s Disease and no way to slow the nerve damage it causes in the
brain,’ but this simply is no longer true—Dr. Bredesen’s ReCODE protocol has already demonstrated efficacy in clinical trials at forestalling and reversing cognitive decline. Reversing cellular degeneration of short-term memory processes, requires regulating the genetic control governing protease metabolism of APP transmembrane receptors which protrude from cell surfaces, particularly near synapses. Approximately 40 molecular inputs (many of which are nutrients) insert for computational input into the ‘central command’—Master-Molecular Switch --the transmembrane Amyloid Precursor Protein receptor whose activity supports neuroplasticity when gene regulation of cleavage patterns results in a neuroprotective single splice of APP verses its opposite pattern—a 3-splice neurodegenerative function.
(‘Yes’ to neuroprotection and preservation is protease cleavage in one place resulting in two neuro-supportive, parts, (sAPPa and CTF), both of which encourage a favorable synaptoblastic equilibrium, thereby preserving neuroplasticity! ‘No,’ effectively, is the outcome of 3-splice protease cleavage of APP, creating 4 distinct parts, each of which contributes to neurodegeneration, and together function for the purpose of the activation of cellular ‘downsizing programs’—'cellular suicide programs’ to be exact, which give rise to the neurodegenerative disease process which serves to shrink the brain until there is nothing left of mind to shrink—advanced, end-stage dementia.)
But the exciting news is that a programmatic approach to optimizing APP metabolism is effective at modulating gene regulation and restoring neuroplasticity--resuming synaptogenesis, repairing cognitive impairment, including memory function, flipping the APP switch in the direction of single splice neuroprotection and perseverance of intact neuroplasticity.
To be fair, our medications today are thought to help maintain mental skills and slow ‘disease effect,’ but ‘disease effect’ is not the same thing as ‘disease progression.’ In truth, our current medications don’t address the underlying disturbances causing the Alzheimer’s disease response, such as ‘cholinesterase inhibitors’ for example, or NMDA-receptor antagonist—the two FDA-approved classes of medications can only provide improvement temporarily, and the latter shows evidence for sometimes worsening symptoms. Psychopharmacology, or the use of medicines aimed at regulating neurotransmitter receptors runs out of currency, so to speak, when nutrient re-supply becomes deficient. Meanwhile, exciting news has it that the neurodegenerative decline into dementia can be confronted head-on with programmatic strategies that optimize nutrients & uses nutrigenomic strategies not only to forestall Alzheimer’s progression, but also prevent it and even reverse the damaging consequences of APP metabolism gone awry (restore healthy clearance and elimination of intracellular garbage (neurofibrillary tangles) & extracellular trash (amyloid-beta plaques) in order to support and maintain & preserve synaptic structure and neuroplastic function, and therefore also neurocognition.
BIOCHEMICAL DISTURBANCES ARE COMMON FEATURES IN AD.
Biochemical disturbances of physiological pathways are common features of Alzheimer’s, especially involving glucose metabolism. In fact, the enzyme which degrades Insulin (breaks down insulin as a first step in insulin’s recycling is the same enzyme that gets burdened with having ALSO to degrade the toxic junkpiles of amyloid-beta plaques found in the extracellular matrix of those with Alzheimer’s Disease.
Late-Onset Alzheimer’s Disease is well-recognized to involve MULTIPLE PHYSIOLOGICAL SYSTEMS, not the least of which include:
- Its general state of bioenergetics
- Its specific state of nutrition
- Its relative state of inflammation
- Its overall toxic burden
- Its gastrointestinal health & the health of its microbiome, to name but several.
But the single greatest risk factor for developing Late-Onset Alzheimer’s Disease (30% risk) has to do with a gene-variant APOE4. So, what exactly are the ACTIONS OF APOe4—the variant gene’s protein product?
ACTIONS OF APOe4
Apoe4 binds to the promotor regions of some 1700 other genes, reducing the production of their associated proteins—now this is quite a spectacular fraction of genes given only twenty thousand or so genes are thought to comprise us entirely, so affecting nearly 2000 other genes is huge!
ApoE4 reduces the clearance of amyloid-beta peptides, which become self-amplifying toxic heaps of trash that destroys the extracellular matrix, which is where neurons connect (synapse) with one another, such as in the construction of short-term memory storage in the hippocampus region of the brain.
The APOE4 gene variant does other unfriendly things:
ApoE4 enhances inflammation as it inhibits genes that limit inflammation, and stimulates genes that promote it.
ApoE4 causes the oxidation of cholesterol whose radical behavior damages vessels during transport through the circulation resulting in vasculitis. In the brain, cerebral vasculitis increases the risk of dementia by contributing to neurodegeneration; in the heart it raises the chance (for single copy ApoE4 carriers) to get cardiovascular disease to as high as 50%. Think about that further to recognize it for what it implies: ApoE4 carriers are among us to the tune of 75 million unsuspecting American carriers, and, worse still, while being at 30% risk for dementia, they are at 50% higher risk for cardiovascular disease, and living our lifestyle and eating the standard American diet condemns them to both.
Let’s bring this home! ApoE4 is a gene-variant that is carried by literally 75 MILLION Americans alone. ApoE4 is known to confer a 30% risk for developing dementia—but notice this still leaves a 70% requirement for additional conditions to occur to cause disease. Unfortunately, it appears that living the standard American lifestyle & eating the Standard American Diet (SAD) combine to do just that—that is, meet the additional 70% requirement necessary to cause disease. Said another way, AND THIS IS QUITE A REMARKABLE THING to SAY: Nearly a quarter of our entire American population are both unknowingly at risk & utterly unaware that by living our lifestyle & eating our Standard American Diet, we are virtually, unwittingly, guaranteeing ourselves a fate of dementia—and this is what explains…why we are witnessing a skyrocketing Alzheimer’s epidemic not only in America today, but also in areas of the world strongly influenced by our western culture! Our SAD Diet & typical lifestyle completes the remaining 70% risk for cognitive decline into dementia, such that the effective risk is a much HIGHER RATE—truly EPIDEMIC in Proportion!
But although we’ve learned Late-Onset Alzheimer’s Disease is an epidemic out of control, and we’ve learned the disease is no longer a helpless situation, still to this day, our conventional medical community still does not recommend routine APOE genotype screening as a preventative measure, presumably based on the previous and now disproven notion that Late-Onset Alzheimer’s is a hopeless disease.
CALL TO ACTION!
Because ALZHEIMER’S is no longer a HOPELESS cause, we are thus faced with a Serious Call to Action—Learn your ApoE genotype, especially if you’ve lost a parent to Alzheimer’s, and even if you haven’t any memory problems as you encounter your 60s, just in case you, like millions of others, must get serious about applying a ReCODE-like strategy of your own, now, in order to avoid a fate of dementia!
If you’d like to learn more about the ApoE4 gene-variant or Late-Onset Alzheimer’s Dementia, definitely read Dr. Dale Bredesen’s Book: The End of Alzheimer’s: The First Program to Reverse and Prevent Cognitive Decline.