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A Breakthrough approach to reducing risk of Alzheimer's diseaseA Nutritional Approach to Alzheimer's Disease

Dr. Steve Blake, ScD

 

 

June 2012

"It was good meeting you today and I very much appreciated your informative discussion of nutritional approaches to prevention and treatment of Alzheimer's disease and related dementias."
BRENT P. FORESTER, MD Instructor in Psychiatry, Harvard. Director Mood Disorders Division, Geriatric Psychiatry Research Program and Site Director, McLean Hospital,
Harvard Medical School.

      $9.95 to download the entire PDF book. Your comments are welcome.

      Please see below for a two-page article and the table of contents.

      Nutrition and Alzheimer's Disease
      By Dr. Steve Blake, ScD

      We all know that our diet can affect our chances of getting diabetes and heart disease. What about Alzheimer's disease? Evidence from medical journals indicates that we may be able to dramatically cut our risk of Alzheimer's disease—simply by getting enough of four vitamins. Further reduction of risk may be possible with a diet high in antioxidant fruits and vegetables. Are there dietary factors that increase our risk? Yes, the saturated fats in meat and dairy products can double our risk of developing Alzheimer's disease. In fact, high blood cholesterol levels can triple the risk. Let’s take a look at how this dreaded disease develops?
      How amyloid plaques develop
      Brain cells have certain long proteins embedded in their surrounding membranes. These long proteins are called "amyloid precursor proteins." They cause no trouble while in the membranes. The trouble begins when enzymes inside brain cells begin snipping off protein chains. These snipped-off proteins are called amyloid-beta. The snipped-off amyloid-beta proteins form clumps between the brain cells. These clumps are called amyloid-beta plaques and they are one signature feature of Alzheimer's disease.
      The amount of amyloid-beta formed is controlled by secretase enzymes inside brain cells. If there is more secretase, then we produce more amyloid-beta. If these secretase enzymes are quenched, then the risk of forming amyloid-beta plaques is greatly reduced. [The following sentence could be in a box or otherwise highlighted] The interesting part is that we can control these enzymes and thus the build-up of amyloid plaque.
      We need two B-vitamins to quench the secretase enzymes, and thus the formation of amyloid plaque. Vitamin B12 and folate work together to create SAMe (s-adenosylmethionine). SAMe quenches the genes that produce secretase enzymes inside our brain cells.
      Many diets do not supply enough folate. However, it is simple and easy to get enough folate from green leafy vegetables and beans. It is not so easy to get enough vitamin B12 and to absorb it properly. A cheap and safe sublingual vitamin B12 supplement is good insurance against Alzheimer's disease. People with dementia might consider taking SAMe supplements. SAMe needs to be taken in the morning and can react with certain drugs.
      Just getting enough folate and vitamin B12 can cut the risk of Alzheimer's disease by one quarter.
      Advanced Glycation Endproducts
      When sugars react with proteins or fats, they can cause advanced glycation endproducts. The acronym AGE is appropriate as these malformed proteins are a major cause of aging. These AGEs can lodge in the amyloid plaques in the brain. The AGEs then create massive amounts of free radicals that cause the cooking and shrinking of an Alzheimer's brain. First, it is a good idea to get enough folate and vitamin B12 to lower the production of amyloid plaques. Second, it is important to reduce our internal production and intake of AGEs.
      AGEs are made inside our bodies when blood sugar is high. After drinking a big, sugary drink, AGE formation will be higher than normal. These AGEs can circulate to the brain and build up in amyloid plaques. Happily, when we eat slow-releasing carbohydrates, we do not tend to create AGEs inside our bodies. Beans, vegetables, and yams are examples of slow-releasing carbohydrate sources that are safe to consume. White bread, white rice, and sugary desserts are examples of foods that boost blood sugar and AGE formation.
      AGEs can also be taken in from certain foods. The presence of water or steam prevents AGEs from forming during cooking. Plant foods are generally safe from high amounts of AGEs because of their water content. When meat, chicken, or fish are fried, broiled, or barbequed, AGEs are produced in large quantities. High amounts of AGEs are also found in cheese. This is because milk sugar reacts with milk protein to produce AGEs during the aging process. This is another good reason to avoid these animal products.
      Avoiding fried meat and sugary drinks can reduce your risk of Alzheimer's disease by half or more.
      Antioxidants
      We have learned that free radicals are produced in amyloid plaques studded with advanced glycation endproducts. These free radicals cause the oxidation and inflammation in Alzheimer's dementia. Antioxidants are helpful to lower the risk of Alzheimer's disease as well as other chronic diseases such as cancer and arterial disease. There are two types of antioxidants. Some come to us in plant foods. Other antioxidants are created inside our bodies. The antioxidants created inside our bodies need certain minerals to function.
      Antioxidants are abundant in fruits and vegetables. Vitamin C and carotenes are examples of antioxidants found in plant foods, but they are not found in animal foods. Polyphenols are found in berries and grapes. Not coincidentally, consumption of berries and grapes has been found to lower the risk of Alzheimer's disease.
      The most important antioxidant for cell membranes is vitamin E. Vitamin E protects the cell membranes in the brain from attack by free radicals. This is especially important because the cell membranes in the brain are particularly vulnerable to free radicals. The best sources of vitamin E are walnuts, almonds, sunflower seeds, and hazelnuts. Certain cold-pressed oils are the only other dietary source. Most vitamin E supplements are not helpful because they contain only the synthetic form of alpha-tocopherol and little or none of the other tocopherols that make up vitamin E.
      Getting enough antioxidant vitamins can reduce the risk of Alzheimer's disease by four to eight times.
      One of the main antioxidants inside our bodies is called glutathione peroxidase. Glutathione peroxidase needs the mineral selenium to function. The high amount of free radicals generated in Alzheimer brains depletes glutathione peroxidase and selenium. Many nuts and seeds are high in selenium, especially Brazil nuts and brown sesame seeds.
      The other important antioxidant enzyme formed within our bodies is called SOD (SuperOxide Dismutase). SOD needs three minerals to function. Copper, zinc, and especially manganese are needed to quench free radicals with this enzyme. Manganese has been found to be lacking in some diets, particularly high-meat diets. Whole grains, spinach, peanut butter, and sunflower seeds are good sources of these three minerals.
      Other dietary influences
      It is interesting that DHA from fish or fish oil has been found to be unhelpful in preventing or treating Alzheimer's disease. A recent, pivotal study showed that DHA is useless in treating Alzheimer's disease.
      Medical plants are vegetables with concentrated nutrients. There are two medical plants that have been shown in several double-blind studies to be quite helpful for Alzheimer's patients. One of these plants is the most-purchased medical plant in Europe. Gingko biloba increases circulation in the brain. Nine double-blind, randomized, placebo-controlled trials showed that ginko biloba helped both in delaying the onset of Alzheimer’s disease and in treating it. Ginkgo biloba is contraindicated if there are bleeding tendencies or with blood-thinning medication.
      Another medical plant used for Alzheimer's disease is gotu kola (centella asiatica). One study found that gotu kola lowered amyloid-beta in the hippocampus of the brain. The Hippocampus is a memory area of the brain. Another study using gotu kola showed an improvement over six months in moderate Alzheimer's disease, rather than the all-too-common degeneration.
      Diet can also influence our intake of pollutants. Certain pollutants have been found to double the risk of Alzheimer's disease. Solvents and pesticides were found to double the risk. Pesticide exposure is vastly lower in plant foods than in animal products. 

                 
      As we have seen, it is possible to greatly reduce the risk of this dreaded dementia.

       

      Contents
      Introduction ........................................................................... 3
      Chapter 1: An overview of Alzheimer’s disease .................... 9
      Drugs and Alzheimer’s disease .......................................... 9
      Changes to the brain in Alzheimer’s disease ................... 11
      What are amyloid plaques............................................... 13
      Meet tau tangles ............................................................. 14
      An epidemic of Alzheimer’s disease ................................ 16
      A broad approach to reducing the risk of Alzheimer’s disease........ 19
      Four steps to avoid Alzheimer’s disease ......................... 24
      Supplementary nutrients ................................................. 26
      Chapter 2: Folate, vitamin B12, homocysteine, and SAMe . 26
      How amyloid plaques are made ...................................... 27
      How two B-vitamins reduce the formation of amyloid plaques..... 29
      Folate and vitamin B12 transform excess homocysteine into
      SAMe. ..................................................................................... 31
      Homocysteine and Alzheimer’s disease .......................... 33
      Are we getting enough Folate and Vitamin B12? ............ 35
      Are we getting enough vitamin B12 ................................ 37
      SAMe and Alzheimer’s disease ........................................ 40
      Chapter 3: Advanced Glycation Endproducts ...................... 43
      Absorption of AGEs.......................................................... 44
      Formation of AGEs ........................................................... 45
      AGEs as a cause of the brain damage in Alzheimer’s disease...... 49
      Cooking methods to reduce AGEs in food ....................... 50
      Chapter 4: Antioxidants and Alzheimer’s disease ............... 52
      Vitamins E and C protect brain cell membranes from free radical
      attack ..................................................................................... 53
      Causes of excess free radicals ......................................... 54
      Radiation and medical testing as sources of free radicals...... 55
      Plant Antioxidants Defend Us from Free Radicals ........... 56
      Vitamin E and Alzheimer’s disease .................................. 57
      Why synthetic vitamin E is ineffective......................... 58
      Food sources of vitamin E ........................................... 62
      Vitamin C and Alzheimer’s disease .................................. 64
      Dietary sources of antioxidants ....................................... 66
      Plant antioxidants ............................................................ 69
      Antioxidants made in your body ..................................... 73
      Protecting our little energy factories, the mitochondria75
      Coenzyme Q10, the only fat-soluble antioxidant made in the
      body ................................................................................... 76
      Antioxidants in diets ........................................................ 78
      Chapter 5: Saturated fat and cholesterol ............................ 80
      Blood cholesterol and risk of Alzheimer’s disease .......... 82
      Chapter 6: Medical plants to treat Alzheimer’s disease...... 84
      Ginkgo biloba ................................................................... 84
      Gotu kola ......................................................................... 86
      Saffron ............................................................................. 88
      Chapter 7: Exercise and Alzheimer’s disease ...................... 90
      Chapter 8: DHA from algae or from fish oil ......................... 92
      Chapter 9: Environmental toxins and Alzheimer’s disease . 94
      Aluminum, does it cause Alzheimer’s disease? ............... 94
      Chapter 10: Nutritional approaches to Alzheimer’s disease .. 97
      Reference citations ............................................................ 100

      Reference citations

      1 Nonoptimal Lipids Commonly Present in Young Adults and Coronary
      Calcium Later in Life: The CARDIA (Coronary Artery Risk Development in Young Adults), Pletcher et al. Annals of Internal Medicine, August 3, 2010, vol. 153 no. 3 137-146.
      2 Mechanisms by which Dietary Fatty Acids Modulate Plasma Lipids,
      Fernandez and West, J. Nutr. 135:2075-2078, September 2005.
      3 Folate, vitamin B12, and serum total homocysteine levels in confirmed
      Alzheimer Disease, Clarke, et al. Archives of Neurology, November 1998, volume 55.
      4 Homocysteine, folate, and vitamin B-12 on mild cognitive impairment,
      Alzheimer Disease, and vascular dementia, Quadri, et al. American Journal of Clinical Nutrition, Vol. 80, No. 1, 114-122, July 2004.
      5 Homocysteine and folate as risk factors for dementia and Alzheimer
      Disease, Ravaglia, et al. American Journal of Clinical Nutrition, Vol. 82, No. 3, 636-643, September 2005.
      6 Protein Phosphatase 2A Methyltransferase Links Homocysteine
      Metabolism with Tau and Amyloid Precursor Protein Regulation, Sontag et al. The Journal of Neuroscience, March 14, 2007, 27(11):2751–2759.
      7 S-adenosylmethionine/homocysteine cycle alterations modify DNA
      methylation status with consequent deregulation of PS1 and BACE and
      beta-amyloid production, Fuso et al. Molecular and Cellular Neuroscience 28
      (2005) 195– 204.
      8 Protein Phosphatase 2A Methyltransferase Links Homocysteine
      Metabolism with Tau and Amyloid Precursor Protein Regulation, Sontag et al. The Journal of Neuroscience, March 14, 2007, 27(11):2751–2759.
      9 S -Adenosylmethionine Is Decreased in the Cerebrospinal Fluid of
      Patients with Alzheimer’s Disease. Linnebank et al. Neurodegenerative Dis
      2010;7:373–378.
      10 S-Adenosyl methionine (SAMe) versus celecoxib for the treatment of
      osteoarthritis symptoms: A double-blind cross-over trial. Najm et al. BMC
      Musculoskeletal Disorders 2004, 5.
      11 Does Accumulation of Advanced Glycation End Products Contribute to
      the Aging Phenotype? Semba et al. J Gerontol A Biol Sci Med Sci. 2010
      September;65A(9):963–975.
      12 Orally absorbed reactive glycation products (glycotoxins): An
      environmental risk factor in diabetic nephropathy, Koschinsky et al. Proc. Natl. Acad. Sci. USA 94 (1997).
      13 Active glycation in neurofibrillary pathology of Alzheimer disease:
      N-(Carboxymethyl) lysine and hexitol-lysine, Castellani et al. Free Radical
      Biology and Medicine Volume 31, Issue 2, 15 July 2001, Pages 175-180.
      14 Advanced Glycosylation End Products and Nutrition—A Possible
      Relation with Diabetic Atherosclerosis and How to Prevent It, Xanthis, Vol. 72, Nr. 8, 2007, Journal of Food Science.
      15 Dietary Advanced Glycation End Products and Aging, Luevano-Contreras
      et al. Nutrients 2010, 2, 1247-1265.
      16 Active glycation in neurofibrillary pathology of Alzheimer disease:
      N-(Carboxymethyl) lysine and hexitol-lysine, Castellani et al. Free Radical
      Biology and Medicine Volume 31, Issue 2, 15 July 2001, Pages 175-180.
      17 Amplifiers of Systemic Inflammation– The Role Advanced Glycation and
      Lipoxidation End Products in Foods, Stig Bengmark, Kuwait Medical Journal 2008, 40 (1): 3-17.
      18 Age- and Stage-dependent Accumulation of Advanced Glycation End
      Products in Intracellular Deposits in Normal and Alzheimer’s Disease Brains,
      Luth 2005 Cerebral Cortex February 2005;15:211—220.
      19 Advanced Glycosylation End Products and Nutrition—A Possible
      Relation with Diabetic Atherosclerosis and How to Prevent It, Xanthis, Vol. 72, Nr. 8, 2007, Journal of Food Science.
      20 Gofman, J. W. and E. O’Conner. X-Rays: Health Effects of Common
      Exams. San Francisco: Sierra Club Books, 1985.
      21 A controlled trial of selegiline, alpha-tocopherol, or both as treatment
      for Alzheimer’s disease, Sano et al. April 24, 1997, JAMA Volume 336 Number 17.
      22 Molecular bases of the treatment of Alzheimer’s disease with
      antioxidants: prevention of oxidative stress, Jose Vina, et al. Molecular Aspects of Medicine 25 (2004) 117–123.
      23 Dietary Intake of Antioxidant Nutrients and the Risk of Incident
      Alzheimer Disease in a Biracial Community Study, Morris et Al. JAMA, June 26, 2002—Vol 287, No. 24.
      24 High plasma levels of vitamin E forms and reduced Alzheimer’s disease
      risk in advanced age, Journal of Alzheimer’s Disease, volume 20, #4 2010.
      25 Vitamins and Minerals Demystified, Blake, McGraw-Hill, 2008.
      26 Relation of the tocopherol forms to incident Alzheimer disease and to
      cognitive change, Morris et al. Am J Clin Nutr 2005;81:508 –14.
      27 Vitamin E Forms in Alzheimer's Disease: A Review of Controversial and
      Clinical Experiences, Usoro and Mousaa, Critical Reviews in Food Science and Nutrition Volume 50, Issue 5, 2010, Pages 414 – 419.
      28 Lowered plasma vitamin C, but not vitamin E, concentrations in
      dementia patients. Charlton et al. The Journal of Nutrition Health & aging,
      2004, vol. 8, no2, pp. 99-107.
      29 Vitamin E and vitamin C supplement use and risk of incident Alzheimer’s
      disease, Morris et al. Alzheimer Disease & Associated Disorders: September
      1998 - Volume 12 - Issue 3.
      30 Association of vitamin E and C supplement use with cognitive function
      and dementia in elderly men. Masaki et al. Neurology 2000;54:1265-1272.
      31 Dietary Intake of Antioxidants and Risk of Alzheimer Disease, Engelhart
      et al. JAMA. 2002;287:3223-3229.
      32 The total antioxidant content of more than 3100 foods, beverages,
      spices, herbs and supplements used worldwide, Carlsen et al. Nutrition Journal 2010, 9:3.
      33 Grape juice, berries, and walnuts affect brain aging and behavior,
      Joseph et al. Journal of Nutrition 139: 1813S-1817S 2009.
      34 Concord grape juice supplementation improves memory function in
      older adults with mild cognitive impairment, Krikorian et al. British Journal of Nutrition (2010), 103, 730–734.
      35 Nutritional status of selenium in Alzheimer's disease patients, Cardoso
      et al. British Journal of Nutrition (2010), 103: 803-806 .
      36 Coenzyme Q10 Attenuates β-Amyloid Pathology in the Aged Transgenic
      Mice with Alzheimer Presenilin 1 Mutation, Yang et al. J Mol Neurosci (2008) 34:165–171.
      37 Cognitive performance among the elderly in relation to the intake of
      plant foods. The Hordaland Health Study, Eha Nurk, British Journal of Nutrition (2010), 104, 1190–1201.
      38 Food Combination and Alzheimer Disease Risk, A Protective Diet, Yian
      Gu et al. Arch Neurol. 2010;67(6).
      39 Dietary Fats and the Risk of Incident Alzheimer Disease, Morris et al.
      Archives of Neurology 2003; 60: 194-200.
      40 Apolipoprotein E4 Allele, Elevated Midlife Total Cholesterol Level, and
      High Midlife Systolic Blood Pressure Are Independent Risk Factors for Late-Life Alzheimer Disease, Kivipelto et al. Annals of Internal Medicine 2002, vol. 137, no3, pp. 149-155.
      41 Association of Higher Levels of High-Density Lipoprotein Cholesterol in
      Elderly Individuals and Lower Risk of Late-Onset Alzheimer Disease, Reitz et al. Archives of Neurology. 2010;67(12):1491-1497.
      42 Independent inhibition of Alzheimer’s disease B- and G-Secretase
      cleavage by lowered cholesterol levels, Grimm et al. The Journal of Biological
      Chemistry Vol. 283, No. 17, pp. 11302–11311, April 25, 2008.
      43 Ginkgo biloba for dementia: a systematic review of double-blind
      placebo-controlled trials, Ernst E, Pittler, Clinical Drug
      Investigation.1999;17:301-8.
      44 Ginkgo biloba, Sierpina et al. Am Fam Physician, 2003 Sept 1 68(5)
      923-926.
      45 Ginkgo biloba and Donepezil: a comparison in the treatment of
      Alzheimer’s dementia in a randomized placebo-controlled double-blind study,
      Mazza et al. European Journal of Neurology 2006, 13: 981–985.
      46 Centella asiatica Extract Selectively Decreases Amyloid β Levels in
      Hippocampus of Alzheimer’s Disease Animal Model, Dhanasekaran et al.
      Phytotherapy Research. 23, 14–19 (2009).
      47 Effect of different extracts of Centella asiatica on cognition and markers
      of oxidative stress in rats, Kumar and Gupta, Journal of ethnopharmacology, Volume 79, Issue 2, February 2002, Pages 253-260.
      48 Comparison on Cognitive Effects of Centella Asiatica in Healthy Middle
      Age Female and Male Volunteers, Dev et al. European Journal of Scientific
      Research Vol.31 No.4 (2009), pp.553-565.
      49 Effect of centella asiatica on mild cognitive impairment (MCI) and other
      common age-related clinical problems, Tiwari et al. Digest Journal of
      Nanomaterials and Biostructures Vol. 3, No.4, December 2008, p. 215 – 220.
      50 A 22-week, multicenter, randomized, double-blind controlled trial of
      Crocus sativus in the treatment of mild-to-moderate Alzheimer’s disease,
      Akhondzadeh et al. Psychopharmacology (2010) 207:637–643.
      51 Saffron in the treatment of patients with mild to moderate Alzheimer’s
      disease: a 16-week, randomized and placebo-controlled trial, Akhondzadeh,
      Journal of Clinical Pharmacy and Therapeutics Volume 35, Issue 5, pages
      581–588, October 2010.
      52 Exercise Plus Behavioral Management in Patients With Alzheimer
      Disease: A Randomized Controlled Trial, Teri et al. JAMA. 2003;290(15):2015-2022.
      53 Physical Activity, Diet, and Risk of Alzheimer Disease, Scarmeas et al.
      JAMA, August 12, 2009—Vol 302, No. 6.
      54 Effects of Aerobic Exercise on Mild Cognitive Impairment, A Controlled
      Trial, Laura D. Baker et al. Arch Neurol. 2010;67(1):71-79.
      55 Physical exercise and mild cognitive impairment: A population-based
      study, Geda et al. Archives of Neurology, Vol 67 (NO. 1), JAN 2010, 80-86.
      56 No Effect of DHA Supplementation in Slowing Alzheimer's Progression,
      Quinn et al. JAMA. 2010;304:1903-1911, 1952-1953.
      57 Neurodegenerative Memory Disorders: A Potential Role of
      Environmental Toxins, Caban-Holt et al. Neurologic Clinics 23 (2005) 485–521.
      58 Low aluminum levels in the human brain from controls and Alzheimer
      patients, Delacourte et al. The Journal of Applied Neuroscience, Vol.2005.1-14.
      59 Brain aluminum in aging and Alzheimer disease, John R. McDermott et
      al. Neurology, May 10, 2011, 76 (19).
      60 Content of Brain Aluminum Is Not Elevated in Alzheimer Disease,
      Bjertness et al. Alzheimer Disease & Associated Disorders: Fall 1996 - Volume 10 - Issue 3.
      61 Trace copper levels in the drinking water, but not zinc or aluminum
      influence CNS Alzheimer-like pathology, Sparks et al. The Journal of nutrition, health & aging 2006, vol. 10, no4, pp. 247-254.
      62 Evidence for Participation of Aluminum in Neurofibrillary Tangle
      Formation and Growth in Alzheimer’s Disease, Walton, J of Alzheimer’s Disease 22 (2010) 65–72.
      63 Link between Aluminum and the Pathogenesis of Alzheimer's Disease:
      The Integration of the Aluminum and Amyloid Cascade Hypotheses, Kawahara and Kato-Negish, International Journal of Alzheimer’s Disease. 2011; v2011.
      64 Aluminum in the Diet and Alzheimer's Disease: From Current
      Epidemiology to Possible Disease-Modifying Treatment, Frisardi et al. Journal of Alzheimer's Disease, Volume 20, Number 1 / 2010.