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| Before You Begin Information presented here is for general educational purposes only. Each one of us is biochemically and metabolically different. If you have a specific health concern and wish my personalized nutritional recommendation, write to me by clicking here. |
Contents
Introduction
Pathophysiology of Dementia and AD
Diagnosis
What Are Your Chances of Dementia
and AD?
Memory Enhancement
and AD Prevention Protocol
1. Cell membrane instability
2. Atherosclerosis
3. Nutritional Deficiency
4. Deficiency in Antioxidants
5. Depression
6. Over-Medication and Drug Interaction
7. Metal Toxicity
8. Low Hormone Level
9. Under-Utilization of Mental
Capacity
10. Lack of Physical Activity
11. Genetic Factors
Discussion
Promising Treatments
Introduction
Less
than 30 years ago, the prevailing medical wisdom declared that "senility" was
the result of either normal aging or hardening of the arteries. Today we are
getting closer to truly understanding the causes of the major neurological disease
of old age, the aging brain, for which one of the many symptoms is failing memory.
As the brain ages, mental and physical functions
are impaired. The most extreme form of this process can lead to death.
While the rest of our body reaches its prime around age 30, starting its natural
progression of declining health soon thereafter,
our brain does not start loosing its major functions until our 60s.
The indicator of an aging brain is loss of brain tissue with men losing brain
tissue almost three times faster than women, according to a study conducted
at the University of Pennsylvania in 1999.
Four million Americans suffer from dementia, the hallmark of Alzheimer's
Disease (AD). This number is expected to swell fourfold by the year
2040. 12% of people aged 60 and above, and 50% of those over 80 years of
age, suffer from dementia, and the main cause is AD. Dementia is the fourth
leading cause of death in those over 60. AD alone kills 100,000 people per year
in the U.S.A. Onset of symptoms can start as young as 40 and continue for about
20 years before severe symptoms - such as loss of memory, inability to carry
out normal work and being irritable and suspicious - show.
Current treatment of dementia and AD include
drugs (medications such as Aricept, anti-inflammatory drugs such as ibuprofen),
hormones (DHEA, estrogen), nutritional supplementation (membrane stabilizers
such as Phosphatidylserine, herbs such as Gingko Biloba, Butcher's Broom, Cat's
Claw, amino acids such as L-Glutamine and Tyrosine, antioxidants such as Vitamin
A, C, E and Selenium) and brain exercises such as mental stimulation exercises.
Pathophysiology
of Dementia and AD
AD is a degenerative disease characterized by progressive mental deterioration,
memory loss, and dementia. Memory and abstract thought processes are impaired.
Symptoms include depression, disorientation of space and time, inability to
concentrate and communicate, loss of bladder and bowel control, memory loss,
personality change, and severe mood swings. Death usually occurs within 5 to10
years as the individual becomes totally incapacitated. Nerve fibers surrounding
the hippocampus, the brain's memory headquarters, become tangled and shrunken.
Information cannot be properly transmitted, new memory cannot be formed, and
old memories cannot be retrieved. Characteristic plaques of beta-amyloid
protein build up and damage nerve cells.
Diagnosis
There are no reliable and accurate markers,
in the form of blood tests, of dementia and AD. A brain scan is helpful in marking
the progression of the disease by indicating the brain's glucose metabolism
rate. A test measuring electrical activity in the brain can be helpful, but
not definitive. The measurement of the amount of beta-amyloid found in spinal
fluid is not a definitive diagnostic tool either.
Diagnosis of AD is not straightforward and rests largely on a combination of
clinical findings, confirmed by a specific set of physiological changes in the
brain.
What Are Your
Chances of Dementia and AD?
While
the average age of an AD patient is in the 70s, the disease begins to make its
appearance years earlier (in the 40s, 50s, or 60s) as mental problems such as
chronic forgetfulness and difficulty in handling routine chores. During
this borderline state, called mild cognitive impairment (MCI), people are not
demented but they do perform worse than their peers on memory tests. Family
members are the first to notice this impairment. People who meet the criteria
for MCI will degenerate into clinical AD at the rate of 10-15% percent a year,
according to Ronald Peterson, director of the Mayo Alzheimer's Disease Center.
By contrast, normal elderly people deteriorate at the rate of 1-2% per year.
If you have relatives with AD, your chance
of developing AD is higher than the general population. 49% of relatives of
AD patients develop the disease by age 87.
It is important not to over-diagnose AD.
There is a group of normal, aging adults who feel forgetful but perform well
on cognitive tests. This "worried well" group develops AD at the rate of 3%
per year. Forgetting where you put your keys
is not AD. Not knowing what you should do with your keys can be a form of dementia.
Memory Enhancement and
AD Prevention Protocol
| Attention Because of tremendous individual variation, the use of nutritionals should therefore be personalized for your body. One person’s nutrient can be another person’s toxin. If you have a specific health concern and wish my personalized nutritional recommendation, write to me by clicking here. |
There is no set protocol that is suitable for everyone. Study the following 11 steps to pick the ones most suitable for you. Try to adopt one protocol at a time and practice it for at least 21 days continuously to get into a good habit for that one step before proceeding to the next applicable step.
The steps listed are not in order of importance.
1. Cell membrane instability.
Researchers at the Massachusetts Institute of Technology discovered that
levels of choline and ethanolamine are significantly lower in those suffering
from AD compared to normal people. Both choline and ethanolamine are used
for the synthesis of phospholipids (PL), which are major components of the cell
membranes of neurons in the brain. With four other phospholipids (PL-choline,
PL-ethanolamine, PL-inositols, and sphingomyelines), they fit side by side,
holding the cell membrane together with proteins and other membrane constituents
inserted and secured between. PL optimizes a variety of functions that occur
at the nerve membrane of each nerve cell.
Clinical trials indicate that phosphatidylserine (PS) benefits cognitive impairment
such as memory, learning, vocabulary skills, and concentration, as well as mood,
alertness, and sociability, after receiving 100 mg of PS three times a day.
One study in the Journal of Neurology (1991) reported that 149 patients who
took 300 mg of PS daily for 12 weeks showed clinical global ratings of improvement
in standard neuropsychological performance tests.
PS also works synergistically with vitamin B12 supplementation. Animal
studies showed improved memory acquisition and retention in rats with memory
impairment following lesioning of nucleus basilis and supplementing with PS
and vitamin B12. PS also has a positive effect alleviating depressive disorders
associated with the geriatric patient, as shown in a study in which patients
who were given 300 mg/day of PS for 30 days showed consistent improvement in
depressive symptoms, memory, and behavior.
Solution:
Phosphatidylserine: 30 - 120 mg a day to enhance cell membrane stability.
2. Atherosclerosis.
Dementia can result from arteriosclerosis
that cuts off blood supply to the brain. The death of brain tissue can also
arise from strokes, tumors, hypothyroidism, advance syphilis, and other causes.
Decrease of blood flow to the brain caused by hardening of the arteries is a
significant contributing factor to dementia and memory loss.
Ginkgo comes from a tree called Ginkgo Biloba. It has been used for more than
5,000 years and is the most popular prescription drug in Germany and France
for treating symptoms of aging and deteriorating memory. In 1988 alone, it was
prescribed more than 5 million times. Extensive studies conducted in animals
and humans have been published on ginkgo, confirming
gingko's ability to stimulate blood flow to the brain by dilating blood vessels,
and decreasing platelet aggregation, besides being a powerful antioxidant.
Researchers consistently find a link between treatment with gingko and improvement
in cognitive performance in test subjects. Two German studies in 1991 showed
that in older patients with a history of more than 2 years of brain disturbance,
after three months, those given gingko showed an improvement in mental function
of 72% compared to only 8% improvement in those given a placebo. As a result
of treatment with gingko, cerebral vascular flow is improved, early AD is slowed,
and memory is improved. The standardized form of gingko is called Egb761 and
contains 24% flavone glycosides. In one double blind study, 2 doses of 320 mg
or 600 mg of Ginkgo Biloba were given to 18 elderly adults with mean age of
69.3. 1 hour later, they were tested for speed of information processing. Results
showed that those given ginkgo had a significant
improvement in speed of information processing.
Usual intake of ginkgo is 30 - 60 mg 2 - 4 times a day. In Germany, common dosage
for AD is 240 mg a day. It generally takes
6-12 weeks before any benefit is seen. Adverse reactions include slightly upset
stomach, headache, and slight dizziness in elderly patients on 120 - 180 mg
or more a day.
Due to its blood thinning properties, those on blood thinners such as coumadin
or aspirin, should consult their physician first before starting gingko as a
dietary supplement.
A few other herbs that have brain-enhancing properties include butcher's broom,
cat's claw, and bilberry. Butcher's broom
contains alkaloids. It improves circulation and has been helpful in thrombophlebitis,
varicose veins, and vertigo. It is more effective when taken with vitamin C.
Cat's claw is an herb that contains polyphenols and proanthocyanidins as active
ingredients. It enhances the action of white blood cells, and acts as an antioxidant
and anti-inflammatory. Bilberry contains fatty acids essential for cell wall
integrity.
The Amino acid L-Taurine works synergistically with gingko, Vitamin B12, and
zinc to help prevent AD. L-Taurine is an ion and pH buffer in the heart, skeletal
muscle, and central nervous system. It also helps to prevent abnormal blood
clotting. It lowers blood pressure and reduces risk of atherosclerosis. It facilitates
the digestion of dietary fat and prevents the formation of cholesterol gallstones.
For these reasons, L-Taurine is commonly used as an adjunct nutrient in
brain health. Common intake is 200 - 500 mg a day, while therapeutic doses
are as high as 3,000 - 5,000 mg a day.
Solution:
a. Control your blood
pressure.
b. Supplement with Ginkgo Biloba 30
- 60 mg two to four times a day if you are not on blood thinner. (Clear with
your physician first)
c. Supplement with L-Taurine, Cat's Claw, and Butcher's Broom, and Bilberry.
3. Nutritional Deficiency.
A common cause of memory loss is insufficient supply of necessary nutrients
to the brain. If the blood is "thick" with cholesterol and triglycerides, the
amount of nutrient-rich blood that can pass through the blood brain barrier
decreases. Malnourishment of the brain can occur, especially if the condition
is chronic in nature.
Deficiencies in amino acids and B vitamins,
especially Vitamins B6 and B12, are other modifiable causes of dementia. Deficiency
of Vitamin B12 produces pseudo-AD symptoms.
25% of people over age 60 - 69 and 40% of people over age 80 are deficient in
Vitamin B12, since older
people produce insufficient intrinsic factor, a substance necessary for the
absorption of Vitamin B12 from the intestines.
No one should accept a diagnosis of AD without first
undergoing a trial of intensive nutritional therapy, especially Vitamin B12
injections.
Solution:
Make sure you are not deficient in Vitamin B6 or B12. Trial of Vitamin B12 supplementation
or injection may be indicated.
4.
Deficiency in Antioxidants
Levels of antioxidants Vitamin
A, E, and the carotenoids
(including beta-carotene) are also low in people with dementia and AD.
These nutrients act as free radical scavengers, a deficiency of which may
expose the brain cells to increased oxidative damage.
Long term longitudinal studies in Switzerland spanning 22 years, from 1971
to 1993, and involving 442 subjects aged 65 to 94, have shown that higher
ascorbic acid and beta-carotene plasma levels are associated with better performance
in terms of memory and recall. Laboratory studies in aged rats support evidence
that chronic antioxidant treatment can improve cognitive function during aging,
supporting the free radical hypothesis of aging as it relates to brain function.
In addition, people with AD have been found
to be deficient in potassium, boron, and selenium.
Solutions:
a. Supplement with essential antioxidants:
i. Vitamin C:
2,000 - 4,000 mg
ii. Vitamin E: 400 - 800 IU
iii. Beta Carotene:
15,000 - 40,000 IU
iv. Selenium: 100 - 300 mcg
b. Additional antioxidants that may
be beneficial include:
i. Grape Seed Extract: 50 - 200 mg
ii. Coenzyme Q10: 30 - 150
mg
iii. L-Lipoic Acid: 50 - 250 mg
iv. Green Tea Extract: 30 - 150 mg
| Attention Because of tremendous individual variation, the use of nutritionals should therefore be personalized for your body. One person’s nutrient can be another person’s toxin. If you have a specific health concern and wish my personalized nutritional recommendation, write to me by clicking here. |
Research
shows that stress and depression
may cause some forms of memory loss. Prolonged depression or stress
leads to elevated levels of plasma cortisol, a "stress" hormone produced by
the adrenal glands. Cortisol appears to shrink the hippocampus, the central
unit in the brain that is associated with AD. Elevated levels of cortisol
during prolonged depression appear to wear down the hippocampus. When depression
is treated, cognitive function, including memory, improves. The earlier symptoms
are recognized, the more likely the deterioration can be slowed. Much more
research is needed, as it is still unclear if all patients with AD have elevated
plasma cortisol levels. Phosphatidylserine enhances cortisol-receptor sensitivity
and restores hypothalamic sensitivity to cortisol through its membrane stabilization
properties, resulting in reduced damage and restoration of healthy, normal
cortisol levels.
| Attention Because of tremendous individual variation, the use of nutritionals should therefore be personalized for your body. One person’s nutrient can be another person’s toxin. If you have a specific health concern and wish my personalized nutritional recommendation, write to me by clicking here. |
Avoid
alcohol, smoke, processed food, environmental toxins such as aluminum
and mercury.
| Message from Dr. Lam I hope you have enjoyed reading this article. If you have areas you don’t understand, comments (good or bad), or if you have a specific health concern, feel free to write to me by clicking here. |
About The Author
Michael Lam, M.D., M.P.H., A.B.A.A.M. is a specialist in Preventive and Anti-Aging Medicine. He is currently the Director of Medical Education at the Academy of Anti-Aging Research, U.S.A. He received his Bachelor of Science degree from Oregon State University, and his Doctor of Medicine degree from Loma Linda University School of Medicine, California. He also holds a Masters of Public Health degree and is Board Certification in Anti-aging Medicine by the American Board of Anti-Aging Medicine. Dr. Lam pioneered the formulation of the three clinical phases of aging as well as the concept of diagnosis and treatment of sub-clinical age related degenerative diseases to deter the aging process. Dr. Lam has been published extensively in this field. He is the author of The Five Proven Secrets to Longevity (available on-line). He also serves as editor of the Journal of Anti-Aging Research.
For More Information
For the latest anti-aging related health issues, visit Dr. Lam
at www.LamMD.com. Feel free to email
Dr. Lam at dr@LamMD.com if you have any questions.
Reprint Information
This article may, in its unabridged, unaltered form and in its entirety only,
be reprinted and republished without permission provided that it is for personal
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to the author, with copyright notice and www.LamMD.com
clearly displayed as source. Written permission from Dr. Lam is required
for all other use.
©2001 Michael Lam, M.D. All Rights Reserved.
References
Allain H et al. Effect of two doses of Ginkgo biloba extract
(Egb 761) on dual-coding test in elderly subjects. Clin Ther 1993 May-Jun; 15(3):
549-58.
Balch J., Balch P. Prescription for Nutritional Healing, Avery Publishing Group,
New York, 1997.
Breitner JC et al. Familial aggregation in Alzheimer's disease: comparison of
risk among relatives of early- and late-onset cases, and among male and female
relatives in successive generations. Neurology 1988 Feb; 38(2): 207-12.
Cavanaugh JC et al. Forgetting and use of memory aids in 20 to 70 years olds
everyday life. Int J Aging Hum Dev 1983; 17(2): 113-22.
Crook T et al. Effects of phosphatidlyserine in Alzheimer's disease. Psychopharmacol
Bull 1992; 28(1): 61-6
Deijen JB et al. Vitamin B6 supplementation in elderly men: effects on mood,
memory, performance and mental effort.
Elias PK et al. Blood pressure, hypertension, and age as risk factors for poor
cognitive performance. Exp Aging Res 1995 Oct-Dec; 21(4): 393-417.
Grassel E. Effect of Ginkgo biloba extract on mental performance. Double-blind
study using computerized measurement conditions in patients with cerebral insufficiency.
Fortschr Med 1992 Feb 20; 110(5): 73-6.
Maggioni, M et al. Effects of phosphatidylserine therapy in geriatric patients
with depressive disorders. Acta Psychiatr Scand 1990 Mar; 81(3): 265-70.
Masuda Y, et al. EGG phosphatidylcholine combined with vitamin B12 improved
memory impairment following lesioning of nucleus basalis in rats. Life-Sci.
1998; 62(9): 813-22.
Meneses A et al. Effects of aging and hypertension on learning, memory, and
activity in rats. Physiol Behav 1996 Aug; 60(2): 341-5.
Oken BS et al. The efficacy of Ginkgo biloba on cognitive function in Alzheimer's
disease.
Perrig WJ. The relationship between antioxidants and memory performance in the
old and very old. J Am Geriatr Soc 1997 June; 45(6): 718-24.
Powell LS et al. Alzheimer's Disease: A Guide for Families. Perseus Press, 1993.
Resnick SM et al. Estrogen replacement therapy and longitudinal decline in visual
memory. Neurology 1997 Dec; 49(6): 1491-7.
Satoh T et al. Walking exercise and improved neuropsychological functioning
in elderly patients with cardiac disease. J Intern Med 1995 Nov; 238(5): 423-28.
Socci DJ et al. Chronic antioxidant treatment improves cognitive performance
of aged rats.
Winter JC. The effects of an extract of Ginkgo biloba Egb761, on cognitive behavior
and longevity in the rat. Pysiol Behav 1998 Feb 1; 63(3): 425-33.
Warren Tom. Beating Alzheimer's. Avery Publishing Group, 1991.