Recent studies suggest that the rate of Alzheimer’s disease in America is expected to increase to one new case every 33 seconds by 2050, or a million new cases every year. While conventional medications address many of the symptoms associated with Alzheimer’s, all current therapies fall short of providing a solution that will halt or reverse the disease. To alter this dire socioeconomic scenario, we need an integrated and comprehensive approach that addresses many of the very complex factors that may be driving the changes in brain structure and function seen in Alzheimer’s disease.
Investigations into the possible causes of Alzheimer’s disease have yielded little fruit. One reason for the lack of success is that the brain deterioration seen in Alzheimer’s disease is thought to begin several decades before any symptoms become noticeable. Research has also discovered a number of potential factors that may or may not play a role in each person’s particular case. Several of the most important factors include neurofibrillary tangles, senile amyloid plaques and clumps, inflammation, and oxidative stress. Other critical factors may be mitochondrial dysfunction, low levels of acetylcholine or sex hormones, nerve cell over-excitability, and certain infections. Importantly, several of these factors may not work alone, but may have some influence on each other.
Most of the symptoms related to Alzheimer’s dementia have been linked to the damage and loss of nerve cells and the loss of connections between nerve cells in the brain. In some people, much of this destruction may result from abnormal tangles or clumps of protein in or around neurons. Neurofibrillary tangles form when a needed protein, called ‘tau’, begins to twist and fold incorrectly inside nerve cells. Normally, tau’s job is to help transport nutrients and neurotransmitters (e.g., acetylcholine) on special conveyor belts within each neuron. If tau begins to clump and form tangles, critical internal transport systems are disrupted and begin to fail, and nerve cells may slowly die. One of the influential factors that may increase tau’s susceptibility to misfold is inflammation. Abnormal protein clumps may also form in the space around neurons, from another needed protein called ‘amyloid’. During day-to-day activities, amyloid protein helps nerve cells survive, grow, and repair injuries. However, when mutations occur or when nerve cell membranes are damaged, amyloid may clump into sticky plaques with the consistency of tree sap. As the senile plaques build up, they can block connections between nerve cells, and damage or destroy cells they squeeze and push against. By causing these problems, unnatural plaques may actually stimulate the immune system that in turn will trigger oxidative stress and inflammation.
Because inflammation appears to be present alongside many other factors thought to cause Alzheimer’s disease, lowering levels of chronic (long-term) inflammation is a reasonable goal within any comprehensive Alzheimer’s treatment protocol. An intensive therapeutic approach should also recognize that all cells in the body, including cells in the brain, are built, operated, and maintained by the food we eat. Therefore, the daily diet may provide the opportunity to supply a series of very special building materials that can be used to optimally construct nerve cells, and support their normal daily function.
Interestingly, the material making up each brain cell is mostly fat. A myriad number of different fat types are needed to build a brain cell, but up to 50% of each neuron should be one specific omega-3 fat called DHA or docosahexaenoic acid. In most people, the human body often needs substantial quantities of DHA in the diet, because unlike many other fats, it is poorly made by body cells. To support normal brain cell structure, excellent dietary sources of DHA and its partner EPA (eicosapentaeonic acid) include fish and other seafood, and quality fish oil supplements. Above and beyond acting as an integral part of normal brain cell structure, DHA and EPA are regularly removed from these structures and converted into a whole range of powerful signal molecules. These signals move throughout each brain cell and act to lower inflammation. In contrast, higher levels of another type of fat (arachidonic acid), is made from common dietary vegetable oils and can be removed and converted into signal molecules that raise inflammation. Comprehensive approaches to address Alzheimer’s disease might therefore be improved by supporting higher levels of DHA and EPA from fish and fish oil in brain tissues, and relatively lower levels of arachidonic acid from vegetable oils.
For each individual, the appropriate use of DHA and EPA from fish oil, alongside other supportive dietary ingredients such as acetyl-L-carnitine, huperzine A, lipoic acid, and N-acetylcysteine, may form a solid and integral foundation for comprehensive nutritional strategies designed to confront Alzheimer’s disease.
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