High intake of Vegetables and Fruit Key to Prevention
By Joel Fuhrman, M.D. www.drfuhrman.com
Conventional And Alternative Treatments Offer Little Benefit.
Conventional treatment for Alzheimer’s is only mildly helpful, and many complementary and alternative treatments currently in use are ineffective and not supported by long-term research studies. Prevention remains the best defense against dementia.
An anti-inflammatory diet rich in fruits and vegetables, optimization of blood pressure, improved serum lipids, regular exercise, avoidance of smoking, and reduction of alcohol consumption form the foundation of a preventative lifestyle. When your diet is low in green vegetables and fruits and high in processed foods and animal products, the low micronutrient and phytochemical intake allows your brain cells to build up free radicals. This oxidative stress to the brain eventually takes its toll. Oxidative damage is the earliest event in the progression of this disease. There currently is no cure for Alzheimer’s disease, but it can be prevented. If someone has the early signs of the disease, its progression and severity can be slowed.
Brain Health & Heart Health
Research is showing that the health of the brain, one of the body’s most highly vascular organs, is closely linked to the overall health of the heart and blood vessels. We now know that the decrease in oxygenation of the brain that occurs with atherosclerosis up-regulates the production of amyloid proteins that damage the brain in Alzheimer’s. Both atherosclerosis and elevated blood cholesterol levels are involved in the development of this disease, and cholesterol is directly involved in promoting amyloid plaque formation. In experimental models, animals fed high-fat and high-cholesterol diets exhibited impaired learning and memory performance compared to those fed control diets. They showed more amyloid plaque deposition in the brain, greater loss of neurons, and other Alzheimer’s related symptoms.1 One study of 444 Finnish men found that an elevated cholesterol level in midlife was associated with three times the risk of developing Alzheimer’s in late life.2
Diet A Key Factor
A number of studies have examined the relation of dietary fat intake to the development of the disease, and animal-food based fat has been implicated in many studies. High intake of saturated fat doubles the risk of Alzheimer’s disease, and even moderate intake of trans fat increased the risk by 2–3 times.3
People who consume diets rich in fruits, vegetables, seeds, and nuts have a significantly lower incidence of Alzheimer’s, and there are multiple studies that show that a proper diet is protective. Green vegetables are the foods with the most powerful degree of protection. What you choose to eat today affects your risk for Alzheimer’s disease later in life.
In recent studies involving over 4,000 New Yorkers, those who ate a better (mildly better by my standards) diet that was higher in fruits, vegetables, nuts, and beans and low in red meat had a 65 percent lower Alzheimer’s risk.4 Specific foods like blueberries have been shown to be especially protective against the symptoms of Alzheimer’s.5 Vegetable and fruit juice consumption also has been shown to offer protection, but not antioxidant vitamins such as E,C, or beta-carotene or tea consumption. You actually have to consume raw vegetables or their juices to get the powerful protection available.6 One study after another shows that for both vascular dementia and Alzheimer’s, the same dietary pattern that causes heart disease (high in animal fats and low in fruits and vegetables, especially green vegetables) also creates a biochemical environment favorable for dementia.7
The Right Type Of Fat Intake
The chief omega-3 in the brain is DHA, which is found in the fatty membranes that surround nerve cells, especially at the microscopic junctions where cells connect to one another. The content of DHA in the brain decreases with aging, and more so in patients with dementia.
DHA stimulates growth of the branches that connect one cell to another. Extensive branching creates a dense neuron network, which provides the basis of the brain’s capacity to process, store, and retrieve information.8 Recently, studies have shown that DHA increases production of LR11, a protein that is found in reduced levels in Alzheimer’s patients, which is known to destroy the protein that forms the “plaques” associated with the disease.9 In mice, even short-term DHA restriction causes significant memory deficits. DHA reduces amyloid accumulation even when given to old mice with high levels of amyloid plaque formation.10
A nine-year follow-up cohort study analyzed dietary questionnaires and DHA blood levels of 899 study subjects who were participating in the Framingham Heart Study. Individuals with the highest DHA levels had half as much dementia.11 In another study, DHA was administered to patients who already had mild to moderate Alzheimer’s disease. The supplemented group was shown to slow the rate of decline in the group of patients in the earliest stages of the disease.12
A large nationwide clinical trial is currently being conducted by the National Institutes of Health to evaluate whether DHA, taken over many months, slows progression of both cognitive and functional decline in people with mild to moderate Alzheimer’s. DHA supplementation likely won’t help that much when Alzheimer’s is well established. Brain cells do not regenerate. Prevention is still the best approach.
Significantly, the same dietary pattern for Alzheimer’s prevention— high intake of fruits, vegetables, legumes, seeds, and nuts, and low intake of saturated fat—is the same dietary pattern that has been demonstrated to be protective against Parkinson’s disease, according to the results of a new, prospective study reported in the December 2007 issue of the American Journal of Clinical Nutrition. A diet rich in micronutrients, high in vegetables, low in animal foods, and including DHA supplementation is the formula to beat Alzheimer’s disease and dementia. But the trick is to adopt this diet now, not after it is too late.
1. Bhat N. “High cholesterol linked to increased AD risk.” Neuroscience 2006; Abstract 711.6.
2. Notkola I, Sulkava R, Pekkanen J, et al. “Serum total Cholesterol, Apolipoprotein E epsilon 4 allele, and Alzheimer’s disease.” Neuroepidemiology 1998;17:14-20.
3. Morris MC, Evans DA, Bienias Jl, et al. “Dietary fats and the risk of incident Alzheimer’s disease.” Arch Neurol 2003; 60;194-200.
4. Scarmeas N, Stern Y, Mayeux R, et al. “Mediterranean diet, Alzheimer’s disease and vascular mediation.” Arch Neurol 2006;63:1709-1717.
5. Joseph J, Arendash G, Gordon M, et al.<.strong> “Blueberry supplementation enhances signaling and prevents behavioral deficits in Alzheimer’s disease model.” Nutr. Neurosci 2003;6:153-162. Geriatrics Aging 2006;9(2):110-113.
6. Dai Q, Borenstein AR, Wu Y, et al. “Fruit and vegetable juices and Alzheimer’s disease: the Kame Project.” Am J Med 2006:119(9):751-9.
7. Otsuka M, Yamaguchi K, Ueki A. “Similarities and differences between Alzheimer’s disease and vascular dementia from the viewpoint of nutrition.” Ann NY Acad Sci 2002:977:155-61. Nash DT, Fillit H. “Cardiovascular disease risk factors and cognitive impairment.” Am J Cardiol 2006;97(8): 1262-5. Sadowski M, Pankiewiz J, Scholtzova H, et al. “Links between the pathology of Alzheimer’s disease and vascular dementia.” Neurochem Res 2004;29(6):1257-66.
8. Darios F, Davletov B. “Omega-3 and Omega-6 fatty acids stimulate membrane expansion by acting on syntaxin 3.” Nature 2006; 440: 813-817.
9. Ma Q, Teter B, Ubeda O. “Omega-3 fatty acid docosahexaenoic acid increases SorLA/Lr11, a sorting protein with reduced expression in sporadic Alzheimer’s disease (AD); relevance to AD prevention.” Journal of Neuroscience 2007;27(52) 14299-14307.
10. Zamrine E. “Emerging drug therapies for dementia.”
11. Schaefer E, Bongard V, Beiser A, et al. “Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer’s disease.” Arch Neurol 2006;63:1545-1550.
12. Levi Y, Jonhagen M, Cederholn T, et al. “Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer’s disease: OmegAD Study.” Arch Neurol 2006;63:1402-1408.