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How Healthcare Practitioners Can Help Patients Prevent Mental

Decline and Alzheimers Disease as they Age

James Meschino DC, MS, ND

As we age a number of factors predispose us to a decline in memory capacity and the

development of more severe forms of cognitive decline, such as dementia and Alzheimers
disease. One of these factors is the lifetime accumulation of free radical damage to brain cells
induced by the brains high use of oxygen. The same way that oxygen in the air causes apples
to rot or metal to rust, oxygen in the body damages our tissues in a similar fashion. The brain
uses about 20% of the bodys oxygen supply at any given moment to help brain cells metabolize
blood sugar into energy, which enables brain cells to keep functioning. But the side effect is a
build up of oxygen free radicals, which can damage brain cells and impair their function over
time. Free radical events are a known factor in Alzheimers disease and other forms of cognitive
decline.
Of importance is the fact that some studies show that individuals who supplement with
antioxidants (like vitamin C and vitamin E) have a lower incidence of Alzheimers disease as
they age. Thus, it may be wise to ensure that your patients get 1,000mg of vitamin C and 400IU
of vitamin E per day from a high potency multiple vitamin. The high potency multiple vitamin and
mineral should also contain a B-50 complex as a number of B-vitamins are required to
synthesize various of brain chemicals (neurotransmitters), which are essential to alertness,
concentration and cognition in general. For instance, the synthesis of dopamine, serotonin,
melatonin, epinephrine and nor epinephrine, all important neurotransmitters, require B-vitamins
as co-factors for their synthesis.
A second way in which we are predisposed to memory loss as we age is the decline in
synthesis of the memory chemical (neurotransmitter) acetylcholine, which really kicks in after
age 54. As we age the brain is less able to make this important memory chemical, setting us up
for memory loss and many of the manifestations of dementia and Alzheimers disease. There
appears to be a decline in the production of the enzyme that combines acetyl coenzyme A with
choline, known as acetyl transferase. As such, the brain makes less acetylcholine and memory
fails. In some cases, it is thought that the brain has trouble getting its hands on sufficient
amounts of choline in order to make acetylcholine. In any case the good news is that there are
several natural agents that have been shown in clinical studies to help the aging brain boost its
production of acetylcholine, thereby helping to combat age-related decline in memory
The most important natural agents include:

CDP-Choline (cytidine 5-diphosphocholine or citidinediphosphocholine or citicholine)

Phosphatidylserine
Bocopa Monnieri
Huperzine A

CDP-Choline is a normal component of the nerve cell membrane, which is important for
transmission of nerve impulses from one nerve to the next. It is also vital to the formation of the
memory chemical acetylcholine. Unfortunately, the aging brain is less able to synthesize the
CDP-Choline it requires. However, studies have shown that supplementation with CDP-Choline
can re-constitute brain levels of CDP-Choline, boosting levels of several important brain
neurotransmitters and improving nerve conduction ability. These results translate into enhanced

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mental acuity and improvement in a number of disorders involving memory loss and cognitive
decline.
Note that supplementing with most other forms of choline have not been shown to be effective.
Therefore, you can not substitute lecithin or other forms of phosphatidylcholine in place of CDP-
choline, as these forms dont appear to cross the blood-brain barrier as readily, and in clinical
trials they have not shown benefit.

Phosphatidylserine like CDP-Choline, Phosphatidylserine is a natural component of the

nerve cell membrane, and it too, is a victim of age-related decline in synthesis. Studies show
that supplementation with phosphatidylserine can also elevate brain levels of acetylcholine, and
has been shown to improve memory and cognition in clinical trials with afflicted individuals.

Bacopa Monnieri - the leaf of Bacopa, or water hyssop, has been used in the Indian medical
system of Ayurveda since the 6th century A.D. to help improve mental performance. Its active
ingredients (bacosides A and B) have been shown to enhance nerve transmission and are
potent antioxidants, which have been shown to protect brain cells from free radicals and other
toxic substances. Human studies indicate that Bacopa Monnieri can preserve memory function
and has been used in the treatment of various conditions involving memory loss.

Huperzine A - this natural substance was initially discovered within a club moss that grows in
Asia, which has been used traditionally to aid memory loss problems. Since being isolated,
Huperzine A is now synthesized for use in natural health products and has shown a remarkable
ability to support brain levels of acetylcholine (the memory chemical). It does so by partially
inhibiting the enzyme that breaks down acetylcholine (acetylcholinesterase), which results in
higher acetylcholine brain levels. Its positive effects on memory and brain function have been
shown in a number of human clinical trials.

Consider Recommending a Brain Support Supplement to Patients 55 and Older

Alzheimers disease affects 6-8% of the population over 64 years of age and 47% of people who
live to be 85 or older. Part of maintaining ones quality of life requires putting nutrition and
lifestyle practices in place that maintain a highly functional body and mind. Many wellness-
striving individuals focus on preserving their bodies, and dont realize that their brain is also
responsive to wellness interventions. Due to the fact that the aging process is associated with
decreased synthesis of the memory chemical acetylcholine, as well as important phospholipids
(CDP-Choline, Phosphatidylserine), which are required for optimal nerve impulse transmission, I
suggest that patients begin ingesting a supplement at age 55 that can help combat memory loss
and other related problems. Key ingredients in a memory support supplement include CDP-
Choline, Phosphatidylserine, Bacopa Monnieri and Huperzine A. All of these have been shown
to be safe, effective natural ingredients, when taken at appropriate dosages, and unlike Ginkgo
Biloba and Vinpocetine, do not increase risk for bleeding disorders. The only caveat is that
these supplements can not be used in conjunction with drugs commonly used to treat
Alzheimers disease.
One final note includes the fact that brain support nutrients of this type are best used in
conjunction with an antioxidant/B-vitamin enriched Multiple Vitamin and Mineral Supplement as
well as an Essential Fatty Acid Supplement containing borage seed, flaxseed and fish oil.
Nutrients from these supplements have also been shown to support brain function and
discourage the development of age-related cognitive decline problems, including Alzheimers
disease.

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References:
Agnoli A, et al. New strategies in the management of Parkinsons disease: A biological
approach using a phospholipid precursor (CDP-Choline) Neuropsycholbiology 1982;8(6):289-96
Canty DJ, et al. Lecithin and chloine in human health and disease. Nutr Reviews 1994;52:327-
339
Citicoline, Alzheimers disease, and cognitive performance. Life Extension 2000:6(9):69,2(Alt
Health Watch data base)
Encyclopedia of Nutritional Supplements. Prima Publishing 1996;Murray M:137-141
Foiravanti M, Yanagi M. Cytidinediphosphocholine (CDP-Choline) for cognitive and behavioral
disturbances associated with chronic cerebral disorders in the elderly. Cochrane Syst Revi
2002;(2):000269 In: The Cochrane Library, 1,2002. Oxford: Update Software
Present Knowledge in Nutrition (5th edition). The Nutrition Foundation, Inc 1984;Choline:383-
399
Secades JJ, et al. CDP-Choline: pharmacological and clinical review. Methods Find Exp Clin
Pharmacol 1995;17(Suppl B):1-54
Zeisel SH, et al. Choline,an essential nutrient for humans. FASEB J 1991;5:20093-2098
Cenacchi T, Bertoldin T, Farina C, et al. Cognitive decline in the elderly: A double-blind,
placebo-controlled multicenter study on efficacy of phosphatidylserine administration. Aging
1993;5:123-33
Crook T, Petrie W, Wells C, Massari DC. Effects of phosphatidylserine in Alzheimers disease.
Psychopharmacol Bull 1992;28:61-6
Crook TH, Tinklenberg J, Yesavage J, Petrie W, Nunzi MG, Massari DC. Effect of
phosphatidylserine in age-associated memory impairment. Neurology 1991;41:644-9
Engel RR, Satzger W, Gunther W, Kathmann N, Bove D, Gerke S, et al. Double-blind cross-
over study of phosphatidylserine vs. placebo in subjects with early cognitive deterioration of the
Alzheimer type. Eur. Neuropsychopharmacol, 1992;2:149-55
Funfgeld EW, Baggen M, Nedwidek P, Richstein B, Mistlberger G. Double-blind study with
phosphatidylserine (PS) in parkinsonian patients with senile dementia of Alzheimers type
(SKAT). Prog Clin Biol Res 1989;317:1235-46
Maggioni M, Picotti GB, Bondiolotti GP, Panerai A, Cenacchi T, Nobil P, et al. Effects of
phosphatidylserine therapy in geriatric patients with depressive disorders. Acta Psychiatr Scand
1990;81:265-70
Nunzi MG, Milan F, Guidolin D, et al. Effects of phosphatidylserine administration on age-
related structural changes in the rat hippocampus and septal complex. Pharmacopsychiat
1989;22:125-8
Valzelli L, Kozak W, Zanotti A, Toffano G. Activity of phosphatidylserine on memory retrieval
and on exploration in mice. Meth Find Extl Clin Pharmacol 1987;9:657-60
Vannucchi MG, Casamenti F, Pepeu G. Decrease of acetylcholine release from cortical slices
in aged rats: Investigations into its reversal by phosphatidylserine. J Neurochem 1990;55:819-
25

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Dar A, Channa S. Calcium antagonistic activity of Bacopa monniera on vascular intestinal
smooth muscles of rabbit and ginea-pig. J Ethnopharmacol 1999;66(2):167-74
Dietary Supplement Information Bureau. www.content.intramedicine.com: Bacopa monnieri
Kidd PM. A review of nutrients and botanicals in the integrative management of cognitive
dysfunction. Altern Med Rev 1999 Jun;4(3):144-61
Mukherjee GD et al. Clinical trial on brahmi. I. J Exp Med Sci 1966;10(1):5-11
Stough C, Lloyd J, Clarke J, Downey LA, Hutchison CW, Rodgers T, et la. The chronic effects of
an extract of Bacopa monniera (Brahmi) on cognitive function in healthy human subjects.
Psychopharmacology (Berl) 2001 Aug;156(4):481-4
Tripathi YB, et al. Bacopa monniera linn. As an antioxidant: Mechanism of action. Indian J Exp
Biol 1996 Jun;34(6):523-6
Vohora D, Pal SN, Pillai KK. Protection from phenbytoin-induced cognitive deficit by Bacopa
monniera, a reputed Indian nootropic plant. J Ethnopharmacol 2000 Aug;71(3):383-90
Ashani Y, Peggins JO, Doctor BP. Mechanism of inhibition of cholinesterases by huperzine A.
Biochem Biophys Res Commun, 1992:184:719-26
Bai DL, et al. Huperzine A, a potential therapeutic agent for treatment of Alzheimers disease.
Curr Med Chem, 2000 Mar;7(3):355-74
Cheng DH, Ren H, Tang XC. Huperzine A, a novel promising acetylcholinesterase inhibitor.
Neuroreport 1996;8:97-101
Cheng DH, Tang XC. Comparative studies of huperzine A, E2020, and tacrine on behavior and
cholinesterase activites. Pharmacol Biochem Behav 1998;60:377-86
Dworkin N. Restoring memory. Psychology Today 2000 Jul/Aug;32(4):p28
McCaleb R. Huperzia looks promising for improving memory. HerbalGram, 10/31/1995;35:p14
Pirisi, Angela. Plant wisdom: Memory moss. Yoga Journal, 08/31/1999;147:p95
Sun QQ, Xu SS, Pan JL, et al. Huperzine-A capsules enhance memory and learning
performance in 34 pairs of matched adolescent students. Acta Pharmacol Sin 1999;20:601-3
Tang XC. Huperzine A (shuangyiping): A promising drug for Alzheimers disease. Chung Kuo
Yao Li Hsueh Pao, 1996 Nov;17(6):481-4
Wang Z, Ren G, Zhao Y et al. A double-blind study of huperzine A and piracetam in patients
with age-associated memory impairment and dementia. In: Kanba S, Richelson E (eds.) Herbal
Medicines for Nonpsychiatric Diseases. Tokyo: Seiwa Choten Publishers 1999:39-50
Xu SS, Gao, ZX, Weng Z et al. Efficacy of tablet huperzine-A on memory, cognition, and
behavior in Alzheimers disease. Chung Kuo Yao Li Hsueh Pao 1995;16:391-5

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 OMEGA-3 FATS MAY REDUCE RISK OF AGE-RELATED COGNITIVE DECLINE,

DEMENTIA AND ALZHEIMERS DISEASE

James Meschino DC, MS, ND

Biological Mechanisms Addressing Neuroprotective Effects of Omega-3 Fats

Several recent studies have suggested that higher intake and blood levels of omega-3 fatty
acids may help to reduce risk of age-related cognitive decline, dementia and Alzheimers
disease. (1-5). Three of four epidemiological studies have suggested a protective effect for
omega-3 fatty acids, in this regard. (6) The major dietary sources of these fatty acids are fish
and shellfish from both salt water and fresh water. EPA and DHA can also be synthesized from
the elongation and desaturation of alpha-linolenic acid, which is present in some vegetable oils.
(7) Flaxseed oil is an especially rich source of alpha-linolenic acid, an omega-3 fatty acid.
DHA is 22 carbons long and has six double bonds, with the first one occurring between
carbon three and four from the omega end (the methyl end) of the fatty acid chain. It is the most
prominent fatty acid in the brain, retina, and spermatozoa and is necessary for vision, cognition,
and sperm motility. The neurons and synaptosomes of the cerebral cortex are especially rich in
DHA, where it is incorporated into the membrane phospholipid structure. The brains of
Alzheimers patients have been shown to contain a lower content of DHA in the grey matter of
the frontal lobe and the hypocampus than do the brains of patients without Alzheimers disease.
The brains of Alzheimers patients also demonstrate a build-up of amyloid protein complex and
an inflammatory component.(7)
The Framingham Heart Study showed that persons with plasma phosphatidylcholine
DHA in the top quartile of values had a significantly (47%) lower risk of developing all-cause
dementia than did those in the bottom quartile and significantly greater protection was obtained
from consuming 2.9 fish meals per week than from consuming only 1.3 fish meals per week, on
average. (7)
Several mechanisms have been proposed to explain how omega-3-fats can reduce nerve cell
degeneration associated with these conditions.
Omega-3 fatty acids are known to provide anti-inflammatory effects due to their conversion to anti-inflammatory eicosanoids
within the body. The eicosanoids formed from omega-3 fatty acids also improve blood flow by dilating vessels, and decreasing
platelet stickiness (anti-thrombotic), and provide other benefits associated with cardiovascular health, such as improving
endothelial function and lowering triglyceride blood levels. All of these effects are also associated with prevention of cognitive
decline largely via preserved blood flow circulation to brain tissue (lower risk of cerebrovascular disease).

However, omega-3 fatty acids also play a direct role in nerve cell structure and function.
Eicosapentaenoic acid (EPA) and docsahexaenoic acid (DHA) have been shown to improve the
composition of nerve cell membranes, and stimulate the development, regeneration and
function of nerve cells by stimulating synaptic plasticity and increasing neurotransmission, as
well as increasing memory abilities. In short, long chain omega-3 fatty acids are structural
components of neuronal and other cell membranes, affecting membrane fluidity, nerve
transmission and nerve cell function in a positive way. They also modulate the production of
eicosanoids and inflammatory cytokines and help preserve blood flow to the brain.
There is also the suggestion that oxidative stress (from oxygen and other free radicals),
significantly contributes to neuronal damage seen in cases of cognitive impairment and
Alzheimers disease, by depleting the brain of vulnerable highly unsaturated fatty acids (e.g.

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EPA and DHA). Some researchers suggest that by replenishing brain cells with EPA and DHA
via higher intake levels, individuals may help protect themselves against cognitive decline to a
significant degree. (8-11)
Adding support to the epidemiological and experimental studies that suggest that omega-3 fatty
acids can reduce risk of cognitive decline, the April 2007 issue of the American Journal of
Clinical Nutrition contained the findings of two large prospective studies that evaluated intake of
omega-3 fatty acids and subsequent risk of cognitive decline, dementia and Alzheimers disease
in older human subjects. Taken together, the findings of MA Beydoun et al (the Atherosclerosis
Risk in Communities Study) and those of BM van Gelder et al (the Zutphen Elderly Study)
indicate that a moderate intake of EPA and DHA were strongly associated with reduced risk of
cognitive decline. (9, 10)
The ARIC Study
The Atherosclerosis Risk in Communities Study analyzed plasma fatty acids in cholesterol
esters and phospholipids in whites residing in Minneapolis MN from 1987 through 1989. From
1990 through 1992 and from 1996 through 1998, 3 neurophysiological tests were administered.
Effectively, this study assessed the association between plasma fatty acids and cognitive
decline in adults aged 50-65 years of age at baseline and conducted a subgroup analysis. A
striking finding among the 2251 study subjects was that higher levels of omega-3 fatty acids
were associated with reduced risk of decline in verbal fluency, particularly in hypertensive and
dyslipedemic subjects, whose tissues are exposed to greater oxidative stress from these
conditions. In contrast, the risk of global cognitive decline increased with elevated palmitic acid
(a saturated fat) and in subjects with higher levels of arachidonic acid (an omega-6 fatty acid
found in meat and dairy products). (9) It should be noted that palmitic acid is a saturated fat that
is highly associated with thrombosis and the elevation of LDL-cholesterol, both of which can
lead to atherosclerosis obstruction, increasing the tendency to develop dementia (11)

The Zutphen Elderly Study

In the Zuthen Elderly Study data on fish consumption of 210 male participants, who were
aged 70-89 years of age in 1990, and data on cognitive functioning collected in 1990 and
1995 were assessed. The intake of EPA and DHA was calculated for each participant.
Results showed that fish consumers had significantly less 5-year subsequent cognitive
decline than did non fish consumers and a linear trend (dose-dependent trend) was observed
for the relation between the intake of EPA and DHA and cognitive decline. More specifically,
the results showed that elderly men who consumed an average of approximately 400 mg per
day of omega-3 fatty acids from EPA and DHA had significantly less cognitive decline over
the five year period than did those consuming an average of approximately 20 mg per day of
omega-3 fatty acids.
At present the American Heart Association recommends the consumption of fish (preferably
fatty fish) at least twice per week, a recommendation that is compatible with the results of the
Zutphen Elderly Study. To achieve 400 mg per day of EPA and DHA, one would have to
consume 6 servings per week of lean fish (average serving size 140 gm or about 5 ounces) or
one serving per week of fatty fish, such as mackerel or herring. (10) One can also achieve this
level of intake by consuming a mere 20 gm of Chinook salmon (less than one ounce) or 100 gm
of cod (a little more than 3.5 ounces). As such, two to three meals of fish per week would supply
approximately 380 mg of EPA/DHA per day, on average. (7)

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Summary
A number of epidemiological studies and experimental studies suggest that higher intake levels,
brain levels and blood levels of EPA and DHA may help preserve cognitive function as we age,
and reduce risk of dementia and Alzheimers disease. A number of biological mechanisms have
been proposed to explain the protective effects of EPA and DHA in regards to these
neurodegenerative conditions. More recently, two prospective studies, involving older and
elderly humans (the ARIC and Zutphen Elderly Studies) have shown a strong correlation
between higher plasma and intake levels, respectively, of EPA and DHA, and subsequent
decreased cognitive decline. The Zutphen Elderly Study highlighted the fact that an average
daily intake of 400 mg of EPA and DHA appears to be a significant threshold level at which a
marked protective effect is observed. Some experts suggest that for people who are allergic to
fish and/or shellfish and those who cannot or will not obtain sufficient intake of fish, that they
consume 1000 mg per day of fish oil from supplementation (Connor WE, Connor SL, 2007). A
supplement containing fish oil and flaxseed oil may also be a consideration providing the total
amount of EPA and DHA reaches a minimum threshold intake value of 400 mg per day. Health
practitioners should bear this information and these dosage levels in mind when making
recommendations about specific essential fatty acid supplement products to their patients.

For more information on this or other related topics, visit Dr. Meschinos website
at: http://www.meschinohealth.com/

References
1. Conquer JA, Tierney MC, Zecevic J, Bettger WJ, Fisher RH. Fatty acid analysis of blood plasma
of patients with Alzheimers disease, other types of dementia, and cognitive impairment. Lipids
2000;35:1305-12
2. Heude B, Ducimetiere P, Berr C. Cognitive decline and fatty acid composition of erythrocyte
membranes the EVA Study. Am J Clin Nutr 2003;77:803-8
3. Tully AM, Roche HM, Doyle R, et al. Low serum cholesteryl esterdocosahexaenoic acid levels in
Alzheimers disease: a case-control study. Br J Nutr 2003;89:483-9
4. Kalmijn S, van Boxtel MP, Ocke M, Vershcuren WM, Kromhout D, Launer LJ. Dietary intake of
fatty acids and fish in relation to cognitive performance at middle age. Neurology 2004;62:275-80
5. Kalmign S, Feskens EJ, Launer LJ, Kromhout D. Polyunsaturated fatty acids, antioxidants, and
cognitive function in very old men. Am J Epidemiol 1997;145:33-41
6. He K, Song Y, Daviglus MI, et al. Fish consumption and incidence of stroke: a meta-analysis of
cohort studies. Stroke 2004;35:1538-42
7. Connor WE and Connor SL. The importance of fish and docosahexaenoic acid in Alzheimers
disease. Am J Clin Nutr;85:929-30. 2007
8. Brunner E. Oily fish and omega 3 fat supplements. BMJ;332:739-740.2006
9. Beydoun MA, Kaufman JS, Satia JA, Rousamond W, Folson AR. Plasma n-3 fatty acids and the
risk of cognitive decline in older adults: the Atherosclerosis Risk Communities Study. Am J Clin
Nutr 85:1103-11. 2007
10. Van Gelder BM, Tijuis M, Kalmijn S, Kromhout D. Fish consumption, n-3 fatty acids, and
subsequent 5-y cognitive decline in elderly men: the Zutphen Elderly Study. Am J Clin Nutr; 85:
1142-7. 2007

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 11. Scientific Advisory Committee on Nutrition, Committee on Toxicity. Advice on fish consumption:
benefits and risks. London, Stationery Office, 2004
www.food.gov.uk/multimedia/pdfs/fishreport2004full.pdf (accessed 9 Feb 2006)
..

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 DHA Omega-3 Fat Shown To Block Amyloid Synthesis In
Alzheimers Disease Prevention
James Meschino DC, MS, ND

Recent studies indicate that higher intake and blood levels of omega-3 fats are associated with
reduced risk of age-related cognitive decline, dementia and Alzheimers disease. The
Atherosclerosis Risk in Communities Study, which followed 2251 individuals (aged 50-65),
showed that higher blood levels of omega-3 fats were associated with reduced risk of decline in
verbal fluency. The Zutphen Elderly Study, which followed 210 elderly men (aged 70-89) for five
years, showed that men who consumed an average of approximately 400 mg per day of omega-
3 fats (from fish) had significantly less cognitive decline over the five year period than did those
consuming approximately 20 mg per day. The Framingham Heart Study showed that persons
with blood levels of omega-3 fats (phosphatidylcholine DHA) in the top 25% had a significantly
(47%) lower risk of developing all-cause dementia than did those in the bottom 25%. In addition,
Alzheimers patients have been shown to have less DHA (an omega-3 fat) in the regions of the
brain most affected by Alzheimers disease (the frontal lobe and hypocampus).
Experimental studies have shed light on the ways in which omega-3 fats may reduce risk of
these conditions. For example, omega-3 fats have been shown to reduce brain inflammation,
increase blood circulation to brain cells, inhibit abnormal clots in blood vessels within the brain.
More recently, omega-3 fats were shown to improve nerve transmission among brain cells and
support brain cell repair mechanisms.
The most recent finding, however, was reported in the Journal of Neuroscience (Dec. 2007, Qiu-
Lan Ma and fellow researchers), showing that omega-3 fats inhibit the build up of amyloid
plaque in brain cells. The accumulation of amyloid plaque (a protein) in brain cells is a hallmark
feature of Alzheimers disease, and is considered to be the main culprit leading to brain cell
disruption, which manifests as memory loss, confusion, personality changes and other
Alzheimers signs and symptoms. These researchers discovered that omega-3 fats (particularly
DHA) increases the number of receptors (the LR11- receptor) on human and murine (mice)
brain cells, which in turn transmits signals within the cell that block the accumulation of amyloid
protein.
Taken together, my advice is to ingest at least 400 mg per day, on average, of omega-3 fats.
This means consuming 3-4 fish servings per week. In addition, I personally take 2-3 capsules
per day of a supplement containing 400 mg each of fish oil, flaxseed oil and borage seed oil. For
those allergic to fish and seafood I strongly recommend flaxseed oil supplementation (1200 mg,
2-3 capsules per day) as an alternative.

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New Evidence That Vitamin E Supplementation Improves Outcomes In
Alzheimers Patients:
A 2008 study adds to the body of evidence

James Meschino DC, MS, ND

In a paper presented at 2008 American Academy of Neurology Annual Meeting.(Chicago, Il,

Poster Sessions III: Aging) researchers showed that Alzheimers disease patients who
supplemented their diet with 2000 IU per day of Vitamin E had a 26% lower mortality rate. As
explained by the lead researcher, Dr Valory Pavlik from the Baylor College of Medicine's
(Alzheimer's Disease and Memory Disorders Center, Houston, TX), many previous studies have
shown that Vitamin E supplementation can slow the progression of Alzheimers disease. The
study by Pavlik et was able to show additional features and benefits of Vitamin E
supplementation in Alzheimers disease patients and answered some common concerns about
the safety of using high dosages of Vitamin E, and combining Vitamin E with conventional drugs
used to manage this condition. In their study of 847 Alzheimers disease patients, who were
followed for 4.9 years, their results showed the following:

A. A 26% reduced mortality rate in the patients administered 2000 IU of Vitamin E per day
compared to Alzheimers disease patients not taking the Vitamin E supplement.

B. Combining Vitamin E supplementation (2000 IU per day) with standard drugs used to
treat Alzheimers disease (cholinesterase inhibitors) produced the best overall results
with respect to longevity and disease progression. Thus, it appears to be safe to
recommend Vitamin E supplementation to Alzheimers patients already taking a
cholinesterase inhibitor drug such as AriceptTM (donepezil), ExelonTM(rivastigmine)
ReminylTM(galantamine) and Ebixa (memantine hydrochloride)

C. Recent concerns about Vitamin E supplementation increasing risk of cancer and heart
disease were put to rest, as this study showed that individuals with Alzheimer disease,
who were in a high-risk age group for death from cardiovascular disease and cancer
(average age 73.5 8.6 years) showed a 26% lower mortality rate than Alzheimers
patients who did not take the 2000 IU per day of Vitamin E.

D. In the Alzheimers disease patients who used only Vitamin E supplementation (2000 IU
per day) and did not take any Alzheimers disease medication, these patients still
showed a 26% lower mortality rate than patients not taking the Vitamin E supplement,
along with significant disease management outcomes.

Overall the researchers concluded, Regimens that included vitamin E were associated with a
26% lower mortality rate. There was a suggestion that of vitamin E plus a cholinesterase
inhibitor was more beneficial than taking either agent alone.

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The Alzheimers Disease Cooperative Study

A landmark study in the year 2000 known as the Alzheimers Disease Cooperative Study was
one of the first published studies to show that providing Alzheimers patients with 2000 IU per
day of Vitamin E could slow the progression of their disease. The Alzheimer's Disease
Cooperative Study (ADCS) was formed in 1991 as a cooperative agreement between the
National Institute on Aging (NIA) and the University of California, San Diego. The ADCS is a
major initiative for Alzheimer's disease (AD) clinical studies in the Federal government,
addressing treatments for both cognitive and behavioral symptoms. Reporting in the American
Journal of Clinical Nutrition researchers published results showing that vitamin E
supplementation (2000 IU per day) may slow functional deterioration leading to nursing home
placement.

Why Vitamin E Supplementation?

The brains of Alzheimers disease patients frequently shows generalized atrophy, neuritic
plaques (dystrophic axons and dendrites surrounding an amyloid core), and neurofibrillary.
Evidence suggests that oxidative stress (free radicals) may lead to permanent cellular damage
in the brain that triggers some of the changes seen in the brain of Alzheimers patients. The
presence of excessive -amyloid protein formation (an extracellular insoluble protein) is a
hallmark feature of the Alzheimers brain. A proposed mechanism of -amyloid toxicity is that it
induces free radicals, which disrupt cellular lipid, protein, and DNA. In addition to -amyloid,
several other processes may also induce oxidative stress in AD. Activated microglial cells found
in association with neuritic plaques may release cytokines, prooxidants, and free radicals.
As well, other etiological factor such as cytoskeletal destabilization, energy deprivation,
or toxic inflammatory responses may all converge in a common final pathway involving free
radicals, as well.
Prior to the Alzheimers Disease Cooperative Study earlier clinical trials and epidemiologic
studies had suggested that several agents may help prevent the development of AD or slow
further deterioration. These agents include vitamin E, selegiline, estrogen, and anti-inflammatory
drugs. One property that they all share is the ability to protect against free radicalmediated
damage, either directly or indirectly.

Conclusion

The recent study (2008) by Pavlik et al adds to the body of evidence indicating that
supplementing Alzheimers disease patients with 2000 IU per day of natural Vitamin E, can slow
the progression of their disease and lower the mortality rate by 26% (over a five-year period).
Unfortunately, many medical doctors have not been exposed to these studies and thus, Vitamin
E supplementation is often left out of the management of many Alzheimers disease cases. In
these instances it is up to Complementary Health Care Professionals to provide patients and
family members with the research and recommendations that have been shown to be
meaningful, in regards to Vitamin E supplementation (as well as other effective natural
interventions). The study by Pavlik et al suggests that Vitamin E supplementation, at a dosage
of 2000 IU per day, is effective, safe, enhances the benefits of conventional Alzheimers drugs,
and does not increase the risk of cancer or heart disease in this older and elderly population.

For more information on this or other related topics, please visit: http://www.meschinohealth.com

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References:

1. Valory Pavlik, Rachelle Doody, Susan Rountree, Eveleen Darby. Vitamin E Use Is Associated
with Improved Survival in an AD Cohort. 2008 American Academy of Neurology Annual
Meeting.(Chicago, Il) Poster Sessions III: Aging and Dementia: Clinical II. # P03.076

2. Grundman M. Vitamin E and Alzheimer disease: the basis for additional clinical trials.
American Journal of Clinical Nutrition, Vol. 71, No. 2, 630S-636s. 2000.

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Summary

The Quick Checklist of How to Best Maintain Memory Function

Maintaining healthy brain function and memory over a lifetime requires that you be proactive.
Dementia and Alzheimers disease affect way too many people as they age, and we now see
that much of this could be avoided if people would use some targeted strategies during their
lifetime. Here are some important recommendations:

1. Take every precaution to avoid head injuries throughout your entire life
2. Always be learning something new or further developing an existing talent or skill set
3. Dont damage your brain with cigarettes, alcohol or illicit drugs, and try to use the least
number of medications as possible throughout your lifetime
4. Nourish your brain with omega-3 fats from fish, twice per week, on average
5. Take a high potency multiple vitamin that is antioxidant enriched and contains a B-50
complex (example: Adeeva Multiple Vitamin)
6. Take 2-3 capsules per day of an Essential Oil supplement to ensure adequate omega-3
fat and essential fatty acid support for your brain. I recommend a supplement that
combines fish oil, flaxseed oil and borage seed oil (example Adeeva Natures Essential
Oil)
7. Keep your fasting blood sugar level below 5.0 mmol/L (90 mg/dL). Elevated blood sugar
(glucose) and high insulin levels are strongly linked to Alzheimers disease development.
This means eating sugary foods and starchy foods in moderation if at all, performing
aerobic exercise for 30 mins at least 3-4 times per week, and having a waist
circumference under 36 inches if you are a man, and under 34 inches if you are a
woman. Have your doctor check your blood glucose level on your next appointment and
ask for the number.
8. Ensure that your blood cholesterol level is below 4.8 mmol/L (185 mg/dL). This means
avoiding high fat meat and dairy products, as well as deep fried foods and transfats.

After Age 55, Add The Following:

1. Take a Memory Support Supplement each day that contains meaningful doses of
CDP-choline, Phosphatidylserine, Huperzine A and Bocapa monnieri (example
Adeeva Memory Support Complex) to help your brain continue to make the
memory chemical acetylcholine as you get older
2. Learn a new skill such as a learning to play a musical instrument or a foreign
language something that is outside of your usual knowledge base

Participate in a mind-body activity that builds new neural circuits, such as playing ping-pong or
taking dance lessons or martial arts lessons.

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