Nutrition Strategies to Reduce Alzheimer Risk

Nutrition plays a role in all chronic diseases,1 and it may help lower the risk of cognitive decline and the development of late onset Alzheimer’s disease (AD).2 The brain requires adequate nutrition for formation and maintenance of nerve cells and neurotransmitters.3

Dementia is a progressive, incurable neurodegenerative disorder that encompasses many symptoms that relate to impaired cognitive function.3 AD accounts for about 70% of dementia diagnoses.2 The hallmark signs of AD are beta-amyloid protein deposition in the form of plaques, intracellular deposits of tau protein as neurofibrillary tangles in the brain, and neuronal loss.4 Genetics, environment, education and lifestyle factor into AD risk.5

Diagnosis of AD requires two components: progressive memory loss and loss of at least one of the following: understanding words; performing complex tasks that require muscle coordination; recognizing and using familiar objects; or planning, organizing and completing normal activities.6 AD is classified as early onset AD (commonly related to familial gene mutations and typically occurring before age 65) or late onset AD, which presents after age 65 and is not related to gene mutations.7

AD begins with gradual memory loss and deterioration of cognitive functions, eventually causing complete disability and then death.4 Because there is no cure for AD, the focus must be on risk reduction. Research has identified lifestyle and behavior modifications that can reduce the risk of developing late onset AD and slow its progression. This article focuses on dietary considerations that may help reduce the risk or slow the progression of late onset AD.

With advancing age comes increased oxidative stress, leading to oxidative damage. Oxidative stress is an imbalance in production of reactive oxygen species (ROS) or free radicals and antioxidants that work to remove ROS or free radicals.5 Oxidative stress promotes the production of amyloid-beta, which causes plaque buildup in patients with AD.4 Antioxidants protect the brain from oxidative damage and amyloid-beta toxicity caused by free radicals.8 When antioxidants are not able to remove enough ROS, this causes oxidative stress that leads to neurodegenerative changes in the brain.5

SEE ALSO: Understanding Alzheimer’s Disease

The body normally possesses oxidative defenses against free radicals, but with aging the overuse of these due to continued accumulation of free radicals eventually depletes the body’s normal defenses, leading to increased oxidative stress and damage.9 Environmental exposures to free radicals that cause oxidative stress and damage are air pollution,10 UV radiation,11 tobacco smoke and pesticides.12

Evidence has shown a link between oxidative stress and amyloid-beta toxicity, accumulation of tau as neurofibrillary tangles, and dysfunction of mitochondria.4 Mitochondria are essential for many cellular functions, including cell survival and death. They produce ROS and are vulnerable to oxidative stress. Dysfunction of mitochondria may be related to amyloid-beta and tau accumulation, which causes an increase in production of ROS, leading to oxidative stress and eventual neuronal death. Buildup of amyloid-beta results in neuronal loss, synaptic degeneration and cognitive decline.4

Antioxidants play a crucial role in removing and preventing formation of ROS, resulting in decreased oxidative stress, amyloid-beta production, and formation of neurofibrillary tangles, and they also help restore mitochondria function.4 One meta-analysis showed that low levels of plasma antioxidants in patients with AD were caused by an increased use of antioxidants from an overproduction of free radicals. Also present were low levels of the antioxidants vitamins A, C and E, believed to result from the overuse of antioxidants. This suggests that AD patients may benefit from increased intake of these vitamins. Vitamins A, C and E may also be beneficial in reducing AD risk.9 It is also suggests that oxidative stress may be an early change that occurs in the development of AD.Other studies have identified a link between a diet high in flavonoids, such as that found in blueberries, strawberries, spinach and red wine, and a decreased risk of age-related cognitive decline.1

Omega 3 Fatty Acids
Fatty acids are necessary for neural membrane integrity, with protective effects against oxidative damage.8 The two types of fatty acids are saturated and unsaturated. Polyunsaturated fatty acids (PUFAs) and monounsaturated (MUFAs) are the primary types of unsaturated fatty acids. Omega 3 and omega 6 are PUFAs.

Omega 3 has anti-inflammatory properties and neuroprotective properties.13,14 Omega 3 is found in plants, nuts, seeds, seafood and fish, and omega 6 is found in animals.13 One systematic review found that an increase in omega 3 may slow cognitive decline in older adults without AD.15 The Italian Longitudinal Study on Aging showed that dietary intake of low saturated fats, high antioxidants and unsaturated fatty acids, especially PUFAs, helped improved cognitive function.1

Research shows that the metabolism of nutrients by the liver is altered in patients with AD, resulting in decreased levels of DHA. DHA is an omega 3 fatty acid used for abnormal protein processing including amyloid-beta and tau. Another meta-analysis found a correlation between low levels of DHA and a decline in MMSE scores, suggesting that AD patients may need increased dietary intake of DHA to slow disease progression.9

Folate and B Vitamins
Homocysteine is a sulfur-containing amino acid that naturally increases with age.16 It is converted to methionine and cysteine with assistance of folate and vitamins B12 and B6.17 High levels of homocysteine cause atrophy of the brain.16,17 Deficiencies of folate and vitamins B12 and Bhave been linked to an increase in homocysteine levels, which causes poor episodic memory and perceptual speed.9 Low levels of B12 can cause neuron degeneration.5 A systematic review and meta-analysis found that elevated levels of homocysteine consistently increase the risk of AD, and folate and B vitamins help protect cognitive function by decreasing these levels.9,18

Mediterranean Diet
The Mediterranean diet consists of a high intake of fruit, vegetables, legumes and cereal; moderate to high intake of fish; high intake of unsaturated fatty acids, mostly in the form of olive oil; low to moderate intake of dairy products; low intake of meats and saturated fatty acids; and a low to moderate intake of red wine with meals.19,20 This diet contains high levels of omega-3 fatty acids, vitamin B6 and antioxidants, which lower the risk of mild cognitive impairment and AD. The fatty acids in this diet may improve immediate recall and processing speed.8 A systematic review and meta-analysis suggested that the Mediterranean diet is associated with a lower risk of developing AD and a slower progression from mild cognitive impairment to AD.20,21

Advise Patients Early
Many patients know that a healthy diet will decrease risk of chronic disease, but they may not know about the beneficial effects it can have on their cognitive function as they age. Dietary intake of antioxidants, folate, B vitamins, and omega 3 fatty acids has been linked to slowed cognitive decline and a reduced risk of AD. Adherence to the Mediterranean diet has also been proven beneficial. Education is an essential tool providers can use to help patients become familiar with dietary changes that may reduce their risk for, or slow the progression of, late onset AD.

1. Solfrizzi V, et al. Dietary fatty acids intakes and rate of mild cognitive impairment. The Italian Longitudinal Study on AgingExper Gerontol. 2005;41(6):619-627.

2. Engelborghs S, et al. Rationale and clinical data supporting nutritional intervention in Alzheimer’s disease. Acta Clin Belg. 2014;69(1):17-24.

3. Polidori M, Schulz J. Nutritional contributions to dementia prevention: main issues on antioxidant micronutrients. Genes Nutr. 2014;9(2):1-11.

4. Zhao Y, Zhao B. Oxidative stress and the pathogenesis of Alzheimer’s disease. Oxid Med Cell Longev. 2013;2013:316523. doi:10.1155/2013/316523.

5. Feng Y, Wang X. Antioxidant therapies for Alzheimer’s disease. Oxid Med Cell Longev. 2012;2012:472932. doi:10.1155/2012/472932.

6. Castellani R, et al. Alzheimer disease. Dis Mon. 2010;56(9):484-546.

7. Goldman J, Hou C. Early-onset Alzheimer disease: When is genetic testing appropriate? Alzheimer Dis Assoc Disord. 2004;18(2):65-67.

8. Yaffe K, Hoang T. Nonpharmacologic treatment and prevention strategies for dementia.

Continuum. 2013;19(2):372-381.

9. Lopes da Silva S, et al. Plasma nutrient status of patients with Alzheimer’s disease: Systematic review and meta-analysis. Alzheimer’s Dement. 2014;10(4):485-502.

10. Moulton P, Yang W. Air pollution, oxidative stress, and Alzheimer’s disease. J Environ Public Health. 2012;2012:472751. doi:10.1155/2012/472751.

11. Almenar-Queralt A, et al. UV irradiation accelerates amyloid precursor protein (APP) processing and disrupts APP axonal transport. J Neurosci. 2014;34(9): 3320-3339.

12. Anstey K, et al. Development of a new method for assessing global risk of Alzheimer’s disease for use in population health approaches to prevention. Prev Sci. 2013;14(4):411-421.

13. Sanford A, Flaherty J. Do nutrients play a role in delirium? Curr Opin Clin Nutr Metabol Care. 2014;17(1):45-50.

14. Lourida I, et al. Mediterranean diet, cognitive function, and dementia: A systematic review. Epidemiology. 2013;24(4):479-489.

15. Fotuhi M, et al. Fish consumption, long-chain omega-3 fatty acids and risk of cognitive decline or Alzheimer disease: a complex association. Nat Clin Pract Neurol. 2009;5(3):140-152.

16. Roman GC, et al. Translating current knowledge into dementia prevention. Alz Dis Assoc Disord. 2012;26(4):295-299.

17. Refsum H, et al. Facts and recommendations about total homocysteine determinations: an expert opinion. Clin Chem. 2004;50(1):3-32.

18. Beydoun M, et al. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014;14:643.

19. Sofi F, et al. Effectiveness of the Mediterranean diet: Can it help delay or prevent Alzheimer’s disease? J Alz Dis. 2010;20(3):795-801.

20. Singh B, et al. Association of Mediterranean diet with mild cognitive impairment and Alzheimer’s disease: A systematic review and meta-analysis. J Alz Dis. 2014;39(2):271-282.

21. Lourida I, et al. Mediterranean diet, cognitive function, and dementia: A systematic review. Epidemiology. 2013;24(4):479-489.

Melissa Meador is a family nurse practitioner at Mobile Medical Consultants in Charleston, S.C.

About The Author