Multi-modal Approach to Alzheimer's
The purpose of this article is to explain why current medical approaches to Alzheimer's Disease are not effective and how a more novel approach can bring you some real hope.
My Personal Motivation
On a personal note, I began to make some dramatic lifestyle changes over 20 years ago as I could tell that my brain was shutting down when I was still in my mid 50s. I have a strong family history of cognitive decline so knew I had better figure this out and soon. For me it was learning more about gluten sensitivity and get a better understanding of diet and dietary supplementation.
AD Too Common
Alzheimer's Disease (AD) affects about 15% of the mature adult population so it is likely that you or someone you know will be affected.
Types of AD
It will be helpful to talk about the different types of AD. Early-Onset AD often starts when a person is in their 40's or 50's. This type affects about 5% of total AD cases. Early-Onset may or may not have identifiable genetic patterns. More common is Late-Onset AD and begins after the age of 65. No particular gene or genes are involved and there may or may not be a family history. Most rare is FAD or Familial Alzheimer's Disease. FAD affects about 1% of AD cases and has strong genetic traits. Many researchers believe that early-Onset and Late-Onset forms should really be referred to as conditions rather than diseases. The disease terminology should really be reserved for FAD.
Late-Onset AD
When we talk about AD in this article, we are referring mostly to Late-Onset Alzheimer's. This cause of this type has baffled modern medicine, but the goal of this article is to help explain why the cause is probably not that mysterious. We just won't find a magic pill that will fix it. You will need a holistic approach meaning bringing several factors into focus.
Theories About Causes
A couple of ideas about the nature of AD have remained in the forefront of scientific investigation and treatment. These are the plaque buildup theory and the germ theory, that is an infection. Despite many millions of dollars invested over a few decades on these theories, no meaningful treatments have emerged. In fact, AD like other neuro degenerative diseases like ALS, Huntington's, spinocerebellar ataxia and spinal muscle ataxia have a persistent and spectacular failure rate with current, single-modality treatments.
Single Mode Remedies Fail Spectacularly
In spite of fantastic failure of these treatments, the vast majority of current research continues to be geared to these single-modality approaches. In fact, most scientists spend their entire careers looking at one aspect of neurodegeneration like reactive oxygen species, metal binding, plaque accumulation or infectious processes etc.
We need to look at the problem from a new perspective. Many of these concepts come from Dr. Dale Bredesen who has published the only study to date that demonstrated a reversal of AD in several people.
UCLA Article About Successful Alzheimer's Trial
Multi-Modal Reasoning
The reasoning goes like this. For us to be high functioning people, our brains have to be able to sort which memories to retain and which to discard. When this sorting mechanism gets out of balance, memory problems will result. Multiple factors are always at play controlling this sorting process and they are all interdependent. Many chronic diseases depend on the interplay of many factors. An example is the balance of bone building (osteoblastic activity) and bone destruction (osteoclastic activity). The bone has cells that specialize in laying down new bone and other cells that specialize in absorbing bone tissue. This balance depends on many factors including diet, hormones and age and when the balance is disturbed excessive bone formation or excessive bone absorption will result. Excessive bone absorption with respect to bone building is a hallmark of osteoporosis.
Creating New Memories
Likewise in the brain we have the creation of new synapses and the destruction of existing synapses. We can call these effects synaptoblastic and synaptoclastic and like bone these result in healthy brain tissue when they are in balance. Current thought is that the control of synaptoblastic and synaptoclastic signaling is the result of dozens, if not hundreds of inputs.
Think of your brain like a company. The CFO considers all factors and if the company is running in the red, he or she will first stop all new hires, or in the brain analogy, stops new memories and new synapses.
A person has spent a life selecting the most critical memories so those are maintained, things like language instead of details about a sit-com rerun from last night.
Some Technical Jargon
If you would like to read further about some of the technical aspects, you can search things like APP (amyloid precursor protein), APOE, A-beta (beta amyloid protein), SAPP beta, SIRT1, netrin 1, NF Kappa beta, tau proteins and more. The interplay of these factors is complex and the leads to the multi-modal treatment plan that is introduced a little later. Fortunately, it is not necessary to understand the mechanisms to have success in treatment.
The brain depends on an extensive synaptic network that consists of a few quadrillion synapses. When the metabolic machinery can no longer effectively support that kind of activity, the brain sends out 4 biochemicals to begin the process of downsizing the number of synapses. You can interfere with these biochemicals and buy some time, but you still haven't addressed why the downsizing was deemed important. One of these biochemicals is beta amyloid protein or A-beta (pronounced A-beta like the letter A). Changing Abeta activity with drug therapy has not changed AD outcomes very much if at all.
To begin with meaningful treatment, we need to look at a wide range of metabolic factors. When people with cognitive problems are evaluated, they tend to have 10-25 significant identifiable issues. Healthy, asymptomatic people have maybe 3 or 4 issues.
We also want to optimize each factor. For example, the lab range for "normal" B12 is 200 to 900. We like to see it over 500 so you can die of B12 deficiency and be in normal range.
Each Person Will Be Different
Each person needs to be evaluated and treated according to what is found. This is different than just having a standard Alzheimer's diagnosis with a standard treatment. Such a one size fits all diagnosis, and treatment is a colossal mistake.
Side Notes: AD has been called Type III diabetes by Dr. Delmonte. The truth goes beyond this, but the observation is valid that metabolic factors are key components of AD. Dr. Gerstle of UCSF has shown that 100% of people with AD have central insulin resistance if you look at neuro exosomes. A-beta interacts with insulin receptor and inhibits downstream signaling.
Therefore, controlling blood sugar and insulin resistance will be important in Alzheimer's treatment. But again, it is too easy to fall into the trap of addressing one factor and not getting the results you desire.
What You NEED to Know
The following is a list of items that need to be looked at and addressed if necessary to get the proper brain health improvement for an increase in cognitive restoration. Each of these will require its own discussion. I have made a couple of short notes to give the reader an idea of where this is headed. I also have a list of supplements that should be considered. Which ones will be most beneficial will be different for each person. I will try to give guidelines for the do-it-yourself brain health builder.
Most of the factors that need to be evaluated are pretty obvious. That doesn't mean that haven't been overlooked for decades or maybe a person thinks they are doing just fine in that category when they are really just good at self-delusion. A person needs to learn what their brain really needs, not what they want the brain to need. Some of the factors that need be evaluated are:
Diet
Stress
Sleep
Exercise
Brain stimulation
Lab values of Homocysteine, B12, D3, CRP, Insulin, Zn and Cu, blood sugar and HbA1C
Hormone balance
GI Health
Nerve growth factor (NGF)
Brain structural components
Heavy metal toxicity
SirT1
Antioxidant support
We plan on starting a new website dedicated to just brain health. This is so critical that we don't want the message to get lost in the background of other health concerns and supplements.
The following links are from the APOE4 web site that has a nice guide to working on your brain health. Each section has some descriptions of possible problems. You will need a blood test with some specific markers to help you understand your risk. APOE4
2. Enhance autophagy, ketogenesis
5. Exercise
7. Homocysteine less than 6 (earlier version of the protocol was < 7)
(We recommend HydroxyB12 aka hydroxocobalamin instead of methyB12 for most people.)
9. CRP less than 1.0; A/G greater than 1.8 (earlier version of the protocol was > 1.5)
10. Fasting insulin less than 5; HgbA1c less than 5.6 (earlier version of the protocol was Fasting insulin <7; HgbA1c <5.5)
11. Hormone balance
12. GI health
(Percepta by Cognitive Clarity)
15. 25OH-D3 = 50-80ng/ml (earlier version of the protocol was 50-100)
(The amount of supplementation of D3 will vary with the person. Some people need 20,000 IUs per day to maintain a serum level of 80)
Pure Encapsulations Vitamin D3 125 mcg (5,000 IU)
16. Increase NGF : Allergy Research Group Advanced NeuroPlus
17. Provide synaptic structural components
Jarrow Formulas Citicoline (CDP Choline) 250mg
Allergy Research Group Advanced NeuroPlus
18. Optimize antioxidants: Tocotrienols, NAC, glutathione support, alpha lipoic acid
19. Optimize Zn:Cu ratio - 1:1 ratio
20. Ensure nocturnal oxygenation
21. Optimize mitochondrial function
CoQ or ubiquinol, a-lipoic acid, PQQ, NAC, ALCAR, Se, Zn, resveratrol, ascorbate, thiamine (pyrroloquinoline quinone)
22. Increase focus
24. Exclude heavy metal toxicity : Heavy Metal Toxicity?
EuroMedica Clinical Glutathione, link below!
25. MCT effects - Coconut oil
I know this is a lot to take in but work on this a step at a time and once you hit a certain combination, your efforts should begin to pay off. Remember it won't be easier 5 years from now.
