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 potentially bring you some hope.
Alzheimer’s Disease (AD) affects about 15 percent of the mature adult population, so it is likely that you or someone you know will be affected.
While AD is reasonably well known, there are several different types, each with their own set of challenges. 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 and may or may not be identifiable by genetic patterns. Late-Onset AD is more common and begins after the age of 65. No particular gene or genes are involved and there may or may not be a family component. 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 be referred to as conditions rather than diseases and that disease terminology should really be reserved for FAD.
When we talk about AD in this article, we are mostly referring to Late-Onset Alzheimer’s. The 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. To treat Late-Onset Alzheimer’s, you will need a holistic approach that brings several factors into focus.
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 – an infection. Despite many millions of dollars invested over a few decades on these theories, no meaningful treatments have emerged. In fact, Alzheimer’s Disease, like other neuro degenerative diseases such as ALS, Huntington’s, spinocerebellar ataxia and spinal muscle ataxia, have a persistent and spectacular failure rate with current, single-modality treatments.
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 AD scientists spend their entire careers looking at one aspect of neurodegeneration such as reactive oxygen species, metal binding, plaque accumulation or infectious processes.
We need to look at the problem from a new perspective, which many AD scientists have been unwilling to do. With these new perspectives come more concepts and potentially, more effective treatment options. Several doctors are already doing this and have come up with new concepts that have the potential to be effective treatments. 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.
The reasoning for a holistic approach 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 disease 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 which brings with it a collection of issues such as osteoporosis.
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. So why would one treatment method be universally effective?
If you would like to read further about some of the technical aspects, you can search for things like APP (amyloid precursor protein), APOE, Abeta (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 four 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 Abeta (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 three or four issues.
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.
For example, 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. Abeta 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.
The following is a list of items that need to be looked at and addressed to get the proper brain health improvement for an increase in cognitive restoration. Each of these will require its own discussion, but 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 they 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. In the meantime, spend some time researching these factors and learn what your body needs to maintain a healthy brain.
