6 Alzheimer’s Disease Prevention and Management
Multi-micronutrients, Diet, and Lifestyle Recommendations
Alzheimer’s disease is a neurodegenerative disease characterized by a progressive loss of nerve cells from the cortex region of the brain. Over 90 percent of Alzheimer’s disease is acquired and only about 5 to 10 percent is inherited. It is the major cause of dementia and is found in individuals who are sixty-five years or older; indeed, Alzheimer’s disease is the leading cause of death among that age group.
Despite extensive research and the publication of thousands of research studies on the causes of Alzheimer’s disease, it has not been possible to reduce its incidence or rate of progression. Drugs used in treatment are based on the disease’s symptoms rather than its causes. Therefore, additional approaches based on prevention and improved management should be developed. To do so, it’s important to first identify the biochemical and genetic defects that contribute to the death of nerve cells in the brains of Alzheimer’s patients. Research studies have shown that these factors include increased oxidative stress, mitochondrial dysfunction, chronic inflammation, beta-amyloids (smaller fragments of amyloid precursor protein), proteasome inhibition, high cholesterol levels, and mutations in two genes--presenilin-1 and presenilin-2--that can be passed from parents to their children.
Among these contributing factors, I propose that increased oxidative stress is one of the earliest biochemical defects to trigger the development of Alzheimer’s. Therefore, mitigating oxidative stress should be one of the first preemptive approaches to reducing the incidence of this disease.
How to Reduce Oxidative Stress
Oxidative stress in the body occurs when the antioxidant system fails to provide adequate protection against damage produced by free radicals. Increased oxidative stress in the body can be most effectively reduced by elevating the levels of antioxidant enzymes as well as dietary and endogenous (made in the body) antioxidant chemicals, because they work in part by different mechanisms. For example, antioxidant enzymes reduce free radicals by catalysis--converting free radicals to nontoxic compounds--whereas dietary and endogenous antioxidant chemicals reduce free radicals by directly scavenging them.
In response to increased oxidative stress, existing levels of dietary and endogenous antioxidant chemicals are depleted, and they cannot be replenished or elevated without supplementation. To counteract this depletion I recommend a supplemental preparation of micronutrients containing multiple dietary and endogenous antioxidants, including vitamin D, B vitamins, certain minerals and polyphenolic compounds in the form of resveratrol and curcumin, and omega-3-fatty acids.
Rationale for Using Multiple Antioxidants
The antioxidants in my proposed formulation act through different mechanisms. For instance, their distribution in various organs and cells, their affinity for various types of free radicals, and their biological half lives are different. Furthermore, beta-carotene is more effective in scavenging oxygen radicals than most other antioxidants. Beta-carotene can perform certain biological functions that cannot be achieved by vitamin A, and vitamin A can perform certain biological functions that cannot be performed by beta-carotene. Vitamin A can induce differentiation in certain normal and cancer cells, whereas beta-carotene and other carotenoids do not. Thus, beta-carotene and vitamin A have, in part, different functions in the body.
Also, different conditions of the body affect the behavior of these compounds. For instance, the gradient of oxygen pressure varies within the cells. Some antioxidants, such as vitamin E, are more effective as scavengers of free radicals in reduced oxygen pressure, whereas beta-carotene and vitamin A are more effective in higher atmospheric pressures.
Cells contain mostly water and some fat, and cellular components are distributed throughout. Vitamin C is necessary to protect cellular components in the water portion of the cells, whereas carotenoids, vitamin A, and vitamin E protect cellular components in the fat portion of the cells.
A Unique Formulation of Micronutrients
The formulation of micronutrients I’m proposing has no iron, copper, manganese, or heavy metals (vanadium, zirconium, and molybdenum). Iron and copper are not added because they are known to interact with vitamin C, generating excessive amounts of free radicals. In addition, iron and copper are absorbed more in the presence of antioxidants than in the absence of antioxidants. Therefore, it is possible that prolonged consumption of these trace minerals may increase the free iron or copper stores in the body, as there is no significant way for the body to eliminate these elements in men and for women after menopause. Increased stores of free iron or copper may increase the risk of some chronic diseases including Alzheimer’s disease.
Heavy metals are not added to the supplement because prolonged consumption of these metals may increase their levels in the body-- since again there is no significant mechanism for excretion--and high levels of these metals are considered neurotoxic.
Diet and Lifestyle Recommendations for Alzheimer’s Disease
In addition to antioxidants and micronutrients, I also recommend diet and lifestyle changes to minimize the chances of developing Alzheimer’s disease. Dietary recommendations include a balanced diet that contains low fat and high fiber with plenty of fruits and vegetables. A low-caloric diet appears to be useful in improving memory. Among fruits, blueberries and raspberries are particularly important because of their protective role against oxidative injuries in the brain.
Lifestyle recommendations include daily moderate exercise, reduced stress, no tobacco smoking, and reduced exposure to noise and electromagnetic pulse. As we discussed earlier, the growing use of electromagnetic field technology has raised concerns regarding its long-term adverse health effects. Exposure to electromagnetic fields may contribute to memory loss; for example, healthy male rats exposed to increasing levels of electromagnetic pulse showed decreased memory, and exposure to electromagnetic pulse also decreased learning ability in mice. These results suggest that exposure to these fields can increase oxidative stress, one of the preliminary risk factors for Alzheimer’s disease.