OXYGEN, GENES, MEMORY, AND ALZHEIMER’S DISEASE
The incidence of Alzheimer’s disease (AD)—a problem of shrinking brain that robs the victim of memory and mentation—is rising worldwide at frightening rates. About 5.5 million Americans suffer from this dreaded disorder. According to the Alzheimer’s Association, one in eight people over age 65 have the disease. The annual cost to the nation is $183 billion. These figures, as disturbing as they are, do not adequately reveal the devastating problems of the dysfunction and death of brain cells. I am equally concerned about the problems of memory deficit among the young that is spreading like an epidemic.

Toxicities of foods, environment, and thoughts (disappointments, chronic anger, and mental health issues) impede or block the energetic, detergent, and developmental functions of oxygen. Dysfunctional oxygen metabolism (dysox) so produced causes injury and loss of brain cells and is the beginning of inflammation, deposition of amyloid proteins, and plaques formation that are the hallmarks of AD. This is the scientific basis of my Oxygen Model of Alzheimer’s Disease.

Oxygen Model of Alzheimer’s Disease Validated

Medical models are proposed to reduce complexities in biology to workable simplicities and to predict clinical characteristics of diseases. In the context of genetics, The Oxygen Model of Alzheimer’s Disease predicts that the genes to be linked with the disease will be primarily involved with oxystatic, inflammatory, and detoxification pathways in the brain. This prediction was proven correct in April 2011 with the publications of two large studies in the journal, Nature Genetics. A gene analysis of more than 50,000 people in the United States and Europe doubled the number of genes—from five to ten— that increase the risk of Alzheimer’s disease. All ten are involved with inflammation and cholesterol metabolism. Cholesterol, of course is an antioxidant and, like other antioxidants in physiologic ranges in human biology, serves anti-inflammatory roles and favorably influences molecular traffic across cell membranes.

The Oxygen Models of Memory Disorders and Alzheimer’s Disease

I put forth the oxygen models of memory disorders (dementia of various types and memory in the young) and Alzheimer’s disease to underscore the commonality of underlying energetic-molecular basis (add “and”???)a range of clinical, pathologic, and experimental observation concerning mental function. These unifying models meet the two essential characteristics of medical models mentioned above. In companion articles, I address problems of early and reversible memory loss in young people, memory loss associated with various forms of dementia, and AD to underscore the commonality of insults to brain cells and cellular dysfunction. Specifically, these models:

1.  Explains the scientific basis of memory lapses due to deranged oxygen signaling;
2.  Show how toxicities of foods, environments, and thoughts cause the loss of brain cells and plaques associated with clinical features of AD;
3. Reveal the mechanisms by which various direct and indirect oxygen therapies (including bowel and liver detox) work;
4. Compel clinicians to focus on all threats to oxygen homeostasis (balance) to restore the health of brain cells and mental functions;
5. Shed light on how all bodily functions improve when oxygen therapies are employed to improve the circulation and oxygen supply to the brain; and
6. Provide explanations of mechanisms by which time-honored natural remedies work to prevent or reduce the problems of memory and mentation.

Genetic Risks of Alzheimer’s

The main gene incriminated in AD is the gene for a protein called APO-E, which was discovered in 1995. It increases the risk for the disease by 400 percent if one copy is inherited from one parent and by 1,000 percent if from both parents. APO-E is involved with the metabolism of cholesterol. However, the genetic risk of a disease does not mean the presence of that disease. It is well established that genes respond to environmental changes (including the matters of foods and stress)—epigenomics, the field dealing with the phenomena is mushrooming—and we do not how many more genes carrying such risks will be discovered in the future.

In contrast, the newly discovered genes increase risk by about 10 to 15 percent. Researchers already believe it will not be reliable to use them to decide if a person is likely to develop Alzheimer’s. So, despite the front page story in The New York Times of April 4, 2011, the great jubilation about the recent discoveries do not signify much for people with AD.

While the new discoveries will undoubtedly open new venues for research in AD, they also underscore the importance of diligent and thoughtful examination of the issues of nutrition, environment, and stress that increase the risk of AD.

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