Alzheimers
ResearchA lot of research has already taken place over the years. Here
are some of the results of such research. A research team from an Alzheimer's
Disease Research Center under Dr. Lopez (Ref.1) analyzed the results of the treatments
and the research of Alzheimers patients over 2 decades. They found that there
were at least 6 subgroups where Alzheimers was associated with some other significant
conditions. The majority was the patients with Alzheimers disease due to cerebrovascular
disease. Next there were the groups with Alzheimers due to alcoholism (15%), depression
(7%), thyroid disorders (4%), a history of head trauma (6%), and due to pernicious
anemia ( 6%, due to vitamin B12 deficiency). The researchers found that over
20 years the first three subgroups, namely the ones with cerebrovascular disease,
with depression and with Alzheimers due to alcoholism had a decreased life expectancy,
whereas the others had a normal life expectancy. There are many research papers
that have described that the senile plaques, which are found on the cortex of
brains of Alzheimer patients, are made up of beta-amyloid substance and of neurofibrillary
tangles (don't worry if this is confusing). To put it simple: This protein
material is like glue, which prevents the neurons from working properly and causes
the memory loss and the confusion so typical for Alzheimers patients. Over the
years the question then arose where does this glue substance" beta-amyloid"
come from? Ref. 2 points out that for many years it was thought that this abnormal
protein would have come from the liver and was then deposited in the brain. There
is now evidence presented in Ref. 2 that the beta-amyloid actually comes directly
from the cells in the brain where it is found and also deposited. Ref. 3 showed
that beta-amyloid is not useless at all. It actually has a very important antioxidant
function in normal brains and keeps lipoproteins, an important chemical substrate
of the brain, from getting oxidized. Recent research from the University of Pittsburgh
School of Medicine linked these plaques with a loss
of nitric oxide production in the brain, which would lead to a reduction
of perfusion of brain blood vessels. This in turn can lead to a loss of oxygen
and nutrients in the brain trissue. The Alzheimers patient's brain appears
to have a regulation problem where through some genetic or other mechanism, the
autoregulation of amyloid-peptides and other similar peptides appears to have
gotten lost. There seems to be an overproduction of these peptides until they
no longer are soluble. The insoluble surplus of these beta-amyloids
is then deposited as the glue-like senile plaques that clog up the
patient's thinking. In Ref.4 the authors presented convincing evidence that low
levels of a subtype of amyloid peptides was found to be lower in Alzheimer patients
and in Lewy body dementia patients. Ref. 5 showed, similar to the already mentioned
Ref. 3, that this subtype of amyloid peptides prevents lipoproteins in the cerebrospinal
fluids from being oxidized. Ref. 5 went further in describing the mechanism of
how this is achieved. The authors suggest that this subgroup of amyloid peptides
protects the very sensitive so-called "microtubules", an important cell
component of nerve cells in the CNS, from being destroyed. If this protective
system is not functioning, nerve cells are lost and this affects thinking, memorizing
and other cognitive functions of the brain.With the newer
test methods it is now possible to depict these senile plaques at
a stage when clinical symptoms are not present yet, which is very useful for early
diagnosis in high risk families. At a conference in Vancouver/BC (Ref.
16) Dr. Howard Feldman who is involved in several clinical trials involving newer
treatments for Alzheimer patients reviewed the beneficial effects of a combination
of Memantine and Donepezil. The medications seem to prevent the amyloid aggregate
formation and thus allow the brain to function more normally. Once the senile
neuritic plaques (the "gluey substance") have formed, an inflammatory
reaction takes place that leads to neurodegeneration. This last stage is irreversible.
The key is to diagnose Alzheimers early with the
above mentioned newer methods, to reduce or eliminate the inflammation and to
prevent neurodegeneration from taking place. Cholesterol lowering drugs are a
newer way to cut down on plaque formation, secretase inhibitors are another way.
A-beta-vaccination has been successful in a mouse model to prevent Alzheimers,
but in man 6% of subjects experienced encephalitis as a serious side-effect, so
the vaccination approach has to be improved. Metal
chelators are another new line of research to cut down on plaque
formation as mercury, zinc and copper toxicity has been shown to play a role in
this disease. There is also evidence that high
insulin levels in the blood contribute to Alzheimers and this may
be caused in turn from too much sugar intake. For those of you who may
be skeptical about the effects
of mercury from tooth fillings, here is a You tube link to convince you
otherwise. Mercury poisoning has been first detected in children with autism,
but lately more and more evidence has accumulated regarding Parkinson's disease
and Alzheimer's disease as neurological disorders that can be directly linked
to mercury fillings (the more fillings, the more severe the disease). Hormone
effects: The brain tissue has abundant amounts of hormone receptors,
particularly receptors for testosterone, estrogen, progesterone, cortisol, growth
hormone. The fact that women get Alzheimers first and men seem to get it at a
later point in time, would indicate to me that the lack of natural hormones after
menopause puts women at risk first for developing Alzheimer's disease. Women tend
to get menopause between the age of 40 and 55 (some even earlier). Men on the
other hand enter into andropause at a later stage in their lives, about age 50
to 65. According to the 2011
Alzheimer's Facts and Figures there were 5.2 million people over the age
of 65 who had Alzheimer's. Of these 3.4 million were women (65.4%) and 1.8 million
were men (34.6%). At the age of 71 and older 16 % of women had Alzheimer's disease,
compared to with 11 % of men. Dr. Hertoghe has published under Ref. 19 that women
need bio-identical estrogen, progesterone and a small amount of testosterone replacement
for preserving normal brain function after menopause. Men on the other hand need
bio-identical testosterone and a small amount of progesterone replacement after
andropause. Both sexes also need smaller amounts of DHEA and pregnenolone as supplements
as the adrenal glands are aging as well and cannot keep up normal hormone production
on their own. Dr. Hertoghe pointed out in several lectures (Ref.20) that hormone
replacement has increased in significance as people live much longer than in the
past.
Books like "Breakthrough" (Ref.17) by Suzanne Somers
have reviewed newer insights of antiaging medicine. This points out the importance
of detoxifying the body from heavy metals like mercury, lead and cadmium. Another
breakthrough in terms of a nutritional supplement comes in the shape of a semi-essential
nutrient, called phosphatylserine (PS), which prevents cognitive decline (Ref.18).
This is a phospholipid, which is present in all cell membranes, particularly in
brain cells. It has been extensively studied on Alzheimer patients and on patients
at risk for cognitive decline including EEG and PET scanner studies. As outlined
in Ref. 18 there have been many well-controlled studies regarding PS and improvement
of cognitive and brain activity function, motor skills and various cognitive measures.
Acetyl-cholinergic activity was boosted about 15-20 % when EEG studies were used.
PET scanner activity was showing significant improvements in brain metabolism
in subjects with relatively severe impairment. Only 300 mg of PS per day (in three
divided doses of 100 mg each) were necessary for this. For prevention in normal
subjects 100 mg daily are likely sufficient. All of the facts are not out
yet about Alzheimers, but it is exciting to see the recent progress both in terms
of early diagnosis and Alzheimers treatment. On the longterm prevention, as always
in medicine, will prevail as the most effective method regarding diminishing the
frequency of this disease. Here are steps that everybody can do today to
minimize the risk of developing Alzheimer's disease: 1. take 2000 IU of
Vit. D3 per day 2. get a T3 and T4 blood test to rule out hypothyroidism
(doctors often do not order T3) 3. Measure lead and mercury levels in urine
and stool, particularly if you have more than 3 amalgamate tooth fillings 4.
If you test positive for mercury, go for intravenous chelation therapy, which
specifically remove heavy metals from your system. 5. Regular exercise
and good nutrition have been linked to less Alzheimer's disease. 6. Omega-3-fatty
acids (molecularly distilled Omega-3 or cod liver oil capsules etc.) and/or fish
help you to preserve brain cells 7. Take the nutrient phosphatylserine
(PS) 100 mg once daily for prevention of Alzheimers and dementia. 8. Cut
out sugar and starchy food by following a low-glycemic diet so that elevated insulin
levels are brought back to normal. 9. Mayo Clinic research recently showed
that computer based memory exercises in seniors will lead to significantly less
Alzheimer's disease in the years down the road. 10. Progesterone cream (only
bio-identical, from compounding pharmacy) has anti-Alzheimer effects. Women would
incorporate this into their bio-identical hormone ngreplacement schedule following
menopause. Men would utilize the brain rejuvenating effect of testosterone into
their hormone replacement routine following andropause. Both also take small amounts
of oral DHEA and pregnenolone. |
