Alzheimer’s (AD) diet and dementia

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a gradual decline in memory and other cognitive and behavioral functions, leading to occupational and social disabilities.

AD is the most common form of dementia in the US with a prevalence of approximately 8-10% in adults over the age of 65 (1, 2) and is characterized by the presence of neurofibrillar degeneration, beta-amyloid plaques and neuronal loss. These changes lead to a relative reduction of many neurotransmitters in specific areas of the brain, such as acetylcholine in the hippocampus. Although the precise cause of AD is unknown, relationships with genetic, lifestyle and other factors have been found.

Genetics

AD is usually sporadic, but there are familial, early-onset forms related to several genes, including those encoding the amyloid precursor protein on chromosome 21, presenilin 1 on chromosome 14, and presenilin 2 on chromosome 1. Also , patients with trisomy 21 (Down Syndrome) and subjects with an increased number of apo-E alleles on chromosome 19, have a higher incidence of AD.

The disease appears more frequently in old age. Other possible risk factors include low schooling, history of head injury, female gender, and cardiovascular disease. Exposure to aluminum has also been proposed as a potential risk factor.

Research in Nutrition

Studies have shown that the risk of AD is higher in people who consume diets high in cholesterol, saturated fat and total calories and low in fiber, vegetables, and fruits (3, 4, 5) . This type of diet appears to play a role in the formation of beta-amyloid plaques and in causing oxidative damage to neurons (6, 7, 8, 9) . This is also supported by data demonstrating a reduced risk of AD with the use of lipid-lowering drugs (10, 11) and the preliminary results of a single study that demonstrated an increased incidence of dementia in heavy meat eaters , compared with vegetarians (12) .

At the 9th Annual Conference on Alzheimer’s Disease and Related Diseases, Harvard researchers discussed the role that fruits and vegetables can play in AD. The dr. Jae Hee Kang and her colleagues evaluated approximately 13,000 women participating in the Nurses Health Study. They calculated the intake of fruit and vegetables in women between 1984 and 1995 and correlated these values ​​with performance in cognitive function tests carried out between 1995 and 2003, when women were in the eighth decade of life. Women with the highest consumption of green leafy and cruciferous vegetables – both rich in folate and antioxidants such as carotenoids and Vitamin C – had a lower cognitive decline than women with low intake of these vegetables (13) .

Increased homocysteine ​​levels appear to be an independent risk factor for AD, as well as being a risk factor for vascular diseases of the central nervous system (another common cause of dementia) (14, 15) . Although inherited forms exist, acquired hyperhomocysteinemia is usually the result of low levels of Vitamin B12, Vitamin B6 and Folate, which are necessary for its metabolism. Good sources of folate include legumes, orange juice, asparagus, nuts, and green leafy vegetables, such as spinach. Sources of B6 include whole grains, soy foods, peanuts, tree nuts, bananas and avocados. Vitamin B12 is usually found in foods and products of animal origin, however valid alternatives include fortified cereals and soy milk or vitamin supplements.

Checking your total energy intake can also be helpful. For example, some populations of China and Japan have low average daily caloric intakes (1,600-2,000 calories per day) and a lower incidence of AD compared to inhabitants of the USA or Western Europe (whose diets typically have a higher content than 2,000 calories per day) (16) . A 2002 study of older Americans, followed for an average of 4 years, found that, compared with those who consume the fewest calories, those who consume the most have an increased risk of AD (3) .

Hormone Replacement Therapy (HRT) has failed the test

It was once thought that hormones administered after menopause (HRT) would improve cognitive function, but subsequent studies have led to several conclusions. In one study, 120 patients with mild to moderate AD were randomly given low-dose estrogen, high-dose estrogen, or placebo for 12 months. There was no significant difference in cognitive and function test results in those who received estrogen versus those who did not (17) . Similar results are reported in the Archives of Neurology. Researchers administered equine estrogen to 120 women with AD for a year, but found no improvement in general cognitive function, memory, attention, or other tests (18)..

For the attention of doctors

A definitive diagnosis of AD is only possible through an autopsy or brain biopsy demonstrating the typical pathological changes described above. However, a diagnosis of probability can be made in the presence of some or all of the following symptoms:

  • Gradual memory loss (especially recent memory)
  • Difficulties in language ranging from difficulty in finding names to silence
  • Deficits in visual and motion-spatial tasks (for example, difficulty driving or dressing)
  • Difficulty in executive functions (for example, ability to judge, reason, plan and execute tasks)
  • Personality changes, up to psychiatric manifestations (for example, paranoia, depression, visual hallucinations, illusions).

Take care of the whole family

Because there may be a genetic predisposition to develop AD, family members of patients may be at increased risk of developing the disease. To minimize this risk they should be encouraged to follow a diet low in fat and cholesterol and rich in vitamins and antioxidants, as described above. In addition, patients and their caregivers should be referred to the Alzheimer’s Association ( www.alzheimer.it ) for guidance on support groups in their area.

 

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