Helping Patients Prevent Mental Decline and Alzheimer’s 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 Alzheimer’s disease. One of these factors is the lifetime accumulation of free radical damage to brain cells induced by the brain’s 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 body’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 CDPcholine, as these forms don’t 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 Alzheimer’s 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 one’s quality of life requires putting nutrition and lifestyle practices in place that maintain a highly functional body and “mind”. Many wellnessstriving individuals focus on preserving their bodies, and don’t 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 CDPCholine, 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 Alzheimer’s 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 Alzheimer’s disease.
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References: Agnoli A, et al. New strategies in the management of Parkinson’s 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;52:327339 Citicoline, Alzheimer’s 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:383399 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 Alzheimer’s 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 crossover 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 Alzheimer’s 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 agerelated 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;55:81925
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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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 ALZHEIMER’S 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s disease. The brains of Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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. Meschino’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 omega3 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, Alzheimer’s patients have been shown to have less DHA (an omega-3 fat) in the regions of the brain most affected by Alzheimer’s 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, QiuLan 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 Alzheimer’s disease, and is considered to be the main culprit leading to brain cell disruption, which manifests as memory loss, confusion, personality changes and other Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s disease. The study by Pavlik et was able to show additional features and benefits of Vitamin E supplementation in Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s disease patients not taking the Vitamin E supplement. B. Combining Vitamin E supplementation (2000 IU per day) with standard drugs used to treat Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s patients who did not take the 2000 IU per day of Vitamin E. D. In the Alzheimer’s disease patients who used only Vitamin E supplementation (2000 IU per day) and did not take any Alzheimer’s 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 Alzheimer’s Disease Cooperative Study A landmark study in the year 2000 known as the Alzheimer’s Disease Cooperative Study was one of the first published studies to show that providing Alzheimer’s 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 Alzheimer’s patients. The presence of excessive ß-amyloid protein formation (an extracellular insoluble protein) is a hallmark feature of the Alzheimer’s brain. A proposed mechanism of ß-amyloid toxicity is that it induces free radicals, which disrupt cellular lipid, protein, and DNA. In addition to ß-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 Alzheimer’s 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 radical–mediated damage, either directly or indirectly.
Conclusion The recent study (2008) by Pavlik et al adds to the body of evidence indicating that supplementing Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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 Alzheimer’s 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. Don’t 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 Nature’s 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 Alzheimer’s 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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