Exercise as it relates to Disease/Exercise or Diet to manage Alzheimer's Disease?

Alzheimer's Disease (AD) is the most common form of Dementia accounting for approximately 50-70% of all cases.[1] AD involves the development of a progressive neuropsychiatric disorder that is characterised by: gradual memory impairment, loss of acquired skills and emotional disturbances.[1] People with AD lose their ability to remain independent and become increasingly unpredictable.[1] As AD progresses over the years, it leads to lose of mobility and eventually death.[1]


Risk Factors edit

The prevalence of AD increases with age, it is more common in individuals over the age of 65.[2] In 2009, 96% of individuals diagnosed with AD were 65 years or older.[2] 64% of these individuals were women.[2] The proposed cause of AD is associated with the accumulation of β-amyloid proteins outside the neurons in the brain, interfering with neuron to neuron communication.[2] In addition, the formation of tangles occurs. This involves the accumulation of tau proteins inside the neuron which blocks the transportation of essential molecules throughout the brain.[2] This causes neuron branches to decline leading to cell death and the development of AD.[2]

AD was the third leading cause of death in 2010, associated with 9,003 deaths.[3] This number increased from 3,740 in 2001.[3] 31% of deaths in people with AD are associated with comorbid conditions including influenza and pneumonia.[2] Hypertensive disease and Ischaemic heart disease both contributed to 12% of deaths and malignant cancers approximately 5% of deaths in people with AD.[2]

Diagnosis and Treatment edit

In the diagnosis of AD, physicians commonly referred to the criteria outlined in DSM-IV, including:[2]

  • Symptoms must include decline in memory and decline in at least:[2] Ability to generate coherent speech or understand spoken or written language[2] - Ability to recognise or identify objects, assuming intact sensory function[2] - Ability to execute motor activities, sensory function, and comprehension of the tasks; and[2] - Ability to think abstractly, make sound judgements, and plan or carry out complex tasks.[2]
  • The decline in cognitive abilities must be severe enough to interfere with daily life.[2]

A comprehensive management plan should be developed as soon as possible after AD diagnosis. To design an appropriate management plan an assessment of: daily function, cognition, comorbid conditions, disorders of mood and emotions, and caregiver status should be performed.[4] As the disease progresses, the management plan should be modified to address new issues.[4] Lifestyle choice can decrease the risk and slow down cognitive and behavioral decline in AD.[4][5]

Exercise or Diet edit

Physical activity is associated with a reduced risk for developing AD and delaying cognitive decline by reducing brain atrophy, improving memory and other cognitive functions.[6] Adults who exercise around the age of 40, are less likely to develop AD after age 65 compared to sedentary peers.[7] Small amounts of physical activity of 1.3hr of vigorous, 2.4hr of moderate or 4hr of light per week demonstrate a reduced risk.[6] Physical activity has been correlated to the rate of cognitive decline in mild cognitive impairment (MCI), dementia and AD.[6] Patients that participate in small preliminary exercise show a reduced rate of cognitive deterioration. This is due to the proposed patterns of activation and stimulation improving brain plasticity and increasing cerebral blood flow.[6] Greater amounts and intensities of physical activity show a stronger correlation and reduced inflammation and increased concentration of neurotransmitters and insulin growth factor.[6] This resulting in decreased cortical β-amyloid burden slowing down the progression of AD.[2][6]

The Mediterranean diet has been suggested to reduce the risk of MCI, AD and lower mortality of AD.[6][8] Current evidence identifies correlations between diet and MCI, AD and decline.[8] In general a higher intake of nutritious food including: fruit, vegetables, nuts, fish and legumes and less consumption of meat, high fat dairy and confectionary was associated with lower cognitive deficits and a reduced risk of AD.[8]

Nutritious foods, Balanced diet reduces the risk and decline in AD

Resveratrol a natural phenol has been researched in treatment for cognitive degeneration. Resveratrol can be found in blueberries, dark chocolate and peanuts.[9] It's identified that treatment of 24 mg/kg of resveratrol for 45 days reduced β-amyloid plaque pathology in specific regions of the brain.[2][9] Supporting neurodegenerative disease may be delayed or mitigated with use of dietary measures that protect against β-amyloid plaque formation.[2][9]

Vitamin E and vitamin B are crucial nutrients for the brain. Vitamin E is an antioxidant associated with reduced Alzheimer’s risk and slowed cognitive decline.[7] Vitamin E can be found in nuts or seeds, mangoes, papayas, avocados, tomatoes, red bell peppers, spinach, and fortified breakfast cereals. Vitamin B, specifically folate, B6, and B12 are essential for cognitive function.[7] These vitamins work together to reduce levels of homocysteine, an amino acid linked to cognitive impairment. Folate can be found in leafy greens, beans, peas, citrus fruits and cantaloupe.[7] Vitamin B6 comes from green vegetables, whole grains, bananas, nuts and sweet potato. Vitamin B12 can be found in meats and dairy products, fortified foods like cereals or supplement form.[7]

Recommendations edit

Research has shown that physical activity and diet are independent factors that reduce the rate and progression of AD.[6] Together they provide a greater benefit in managing AD, by slowing down tangle and plaque formations in the brain.[6] Individuals who develop AD that previously exercised and practiced good nutrition generally demonstrate greater benefits with a slower decline of cognitive and behavioural functioning.[6] Recommendations to manage AD include:

  1. Minimize saturated fats and trans fats[8]
  2. Vegetables, legumes, fruits, and whole grains should be the primary staples of the diet[8]
  3. A small handful of nuts and sees provides a healthy source of Vitamin E[7]
  4. A reliable source of Vitamin B12, such as fortified foods or supplements providing at least 2.4 μg/day[7]
  5. Engage in aerobic exercise equivalent to 40 minutes of brisk walking 3 times per week[7]
  6. Reassess Individual for a management plan tailored to specific needs and requirements[4][5]

References edit

  1. a b c d Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM, et al. Inflammation and Alzheimer’s disease. Neurobiology of aging. 2000;21(3):383-421
  2. a b c d e f g h i j k l m n o p q r Thies W, Bleiler L. 2011 Alzheimer's disease facts and figures. Alzheimer's & dementia: the journal of the Alzheimer's Association. 2011;7(2):208
  3. a b Statistics ABo. People Identified as having Dementia or Alzheimer's Disease. Australia2009; Available from: http://www.abs.gov.au/AUSSTATS/abs@.nsf/Lookup/4102.0Main+Features50Dec+2012
  4. a b c d Cummings JL, Frank JC, Cherry D, Kohatsu ND, Kemp B, Hewett L, et al. Guidelines for managing Alzheimer's disease: part I. Assessment. Am Fam Physician. 2002;65(11):2263-72
  5. a b DEFICITS C. Guidelines for managing Alzheimer's disease: Part II. Treatment. Am Fam Physician. 2002;65(12):2525-34
  6. a b c d e f g h i j Scarmeas N, Luchsinger JA, Schupf N, Brickman AM, Cosentino S, Tang MX, et al. Physical activity, diet, and risk of Alzheimer disease. JAMA: the journal of the American Medical Association. 2009;302(6):627-37
  7. a b c d e f g h Committee P. Dietary Guidelines for Alzheimer's Prevention. Australia: Physician's Committee for Responsible Medicine; 2013; Available from: http://www.pcrm.org/health/reports/dietary-guidelines-for-alzheimers-prevention
  8. a b c d e Gu Y, Scarmeas N. Dietary patterns in Alzheimer’s disease and cognitive aging. Current Alzheimer Research. 2011;8(5):510
  9. a b c Karuppagounder SS, Pinto JT, Xu H, Chen H-L, Beal MF, Gibson GE. Supplementation of resveratrol reduces plaque pathology in a transgenic model of Alzheimer's disease. Neurochemistry international. 2009;54(2):111-8