Prevent the initiators of disease from getting started by preparing the body for free radical war.
Among modern hypotheses, the free radical theory of aging has the most support among researchers and gerontologists.
Its fundamental presumption is that free radicals are products of normal metabolic processes and are an inevitable destructive consequence of time.
Aging at the molecular speed of life.
The free radical theory of disease provides the best molecular explanation for the interaction between aging and disease. It argues that nature provided humans with foods and a well-balanced synergistic defense system to protect it from oxidative threats.
The mechanism depends on the highly efficient scavenging activity of nutrients and sophisticated antioxidant enzyme systems that monitor hotspots.
During an athlete's youth when conditions are more ideal, these systems counterbalance and limit cellular damage by intercepting and quenching free radicals.
When antioxidants levels decrease as they do with aging or free radical generation increases, as it does with exercise, oxidative damage occurs.
The oxidized macromolecules progressively accumulate in cells and lead to premature death.
A corollary of the free radical theory is the assumption that the human life span can be prolonged by minimizing free radical generation or neutralizing them.
Oxidative stress represents an accumulation of free radicals.
Three classes of free radicals are implicated in the aging process.
Mitochondria activity generates free radicals from the aerobic metabolism that requires molecular oxygen to burn biological fuel. The peroxidation of lipids in membranes produces aldehyde radicals. Nitric Oxide System
The free radical nitric oxide is synthesized from amino acids in the brain. Nitric oxide is a recently discovered chemical messenger and free radical gas. Nitric oxide is not to be confused with the dental anesthetic, nitrous oxide or “laughing gas”.
Nitric oxide ia an uncharged chemical messenger. Nitric oxide generation appears to be beneficial to the brain. Due to its lack of charge, nitric oxide freely crosses the blood-brain barrier and rapidly diffuses through nerve cell membranes. Nitric oxide is formed from the amino acid arginine. This reaction is catalyzed by the enzyme nitric oxide synthase.
Within the central nervous system, nitric oxide is involved with appetite control, memory, and the perception of pain. Nitric oxide acts on smooth muscle to cause relaxation and dilation of target blood vessels at the sites of injury. Nitric oxide acts indirectly by stimulating production of the second messenger, cyclic GMP (guanine monophosphate).
Increased cyclic GMP levels cause vasodilation of arterioles and capillaries, along with reducing platelet adhesion. It is interesting to note that the effect of relaxing smooth muscle is believed to account for the mechanism of initiating a male’s erection and underlies the pharmacological effect of Pfizer’s erectile dysfunction drug Viagra ™.
This probably explains some of the cerebral effects that users of Viagra ™ claim.
There is a direct association between free radical generation and the process of aging.
Although they are not commonly thought of as chronic diseases, brain diseases as well as stroke can be considered as a chronic disease because it results from a dysfunction in nerve cells and a breakdown in nerve transmissions over time. It also means they can be prevented or delayed.
Brain diseases are considered neuro-degenerative diseases. Neurogenerative diseases can be initiated by free radical attack.
Free radical propagation anywhere in the body leads to cell membrane damage if they are not neutraliaed before they can attack cell membranes. The attacks themselves causes a decrease in membrane permeability and an increase in cell stiffness.
in the brain, it is neurons that are attacked and that results in a damged nerve network that eventually loses function.
Aging is better viewed as another chronic disease; best prevented rather that treated.
Aging is distinguished from those other chronic diseases by its universality and unavoidability.
According to the oxidative stress theory of disease, the chronic diseases associated with aging are associated with specific accumulations of malformed compounds. These altered compounds are the result of continual attack on membrane lipids by free radicals.
Chronic brain disease is the result of excessive free radical activity and a lack of antioxidants in the brain.
The accumulation of altered compounds is not unique to the brain. When accumulations occur in muscles, joints, and blood vessels, arthritis and heart disease follows.
Oxidative stress is the prevailing theory regarding brain cell death.
Alzheimer's disease, frontal-tropic dimentia, Parkinson's disease, multiple sclerosis, ALS and age-related senile dementia can be explained by this theory.
Free radical generation is higher in a hard driven metabolic system. This state is the normal result of intense exercise. Since exercise causes the body to flood all its tissues blood, having a high concentration of a spectrum of antioxidants following exerice during recovery is beneficial to brain chemistry since the rush of blood flushes out the army of free radicals.
Mitochondrion is the generator of all cell energy.
The responsibility of mitochondria is to oxidize glucose and convert its chemical bonds into useable energy. This takes place along its inner folds of membranes. These membranes are studded with enzymes and the various cofactors needed to carry out these reactions.
Mitochondria membranes are highly developed sections of lipid bilayers, which are continuously under free radical attack. The mitochondrion membrane is the organelle where damage occurs most often because it has the largest amount of membrane surface area exposed to free radicals.
The more membrane lipids that are exposed to free radical attack, the more damage free radicals can cause.
Mitochondria that are damaged then impair the oxidative phosphorylation (the formation of ATP) of the cell. As metabolic malfunctions accumulate over the course of a lifetime, millions of cells die.
Since nervous tissue demands enermous energy, there are many mitochondria present in the brain. Mitochondrion free radicals are therefore able to inflict serious damage, not because there are more free radicals produced but rather because there are fewer antioxidants present.
The high energy conversions that fuels brain activity releases enormous amounts of free radicals. Free radicals target the lipids embedded in the structure of nerves to cause cells to dysfunction. This program predicts a higher need for antioxidants to delay the aging process.
Only a few antioxidants are able to cross the blood-brain barrier. The scarcity of antioxidants leaves brain cells vulnerable to oxidative stress.
Bilberry, green tea polyphenols alpha-lipoic acid, beta-carotene, the oxidized form of ascorbic acid (Vitamin C) and to a lesser extent Vitamin E and the tocopherols are valuable scavengers that can reach the brain an neutralize the dangerous free radicals.
Alzheimer’s disease on the molecular level is characterized by abnormal deposits of the protein Amyloid-ß. Amyloid-ß induces the loss of ccmmunications between neurons that Alzheimer's disease is known for.
Preventing healthy synapses from become dysfunctional will delay the onset of the disease.
During the progression of Alzheimer's disease on a macro-level. an overall shrinkage of brain tissue takes place. The grooves or sulci are widened while the gyri, the well-developed folds of the outer layer, shrink. In addition, the chambers of the brain that contain cerebrospinal fluid become engorged.
In the early stages of the disease on a cognitive level, short-term memory begins to fade when the area of the brain known as the hippocampus, degenerates and its ability to perform routine tasks declines.
As Alzheimer's disease advances, the cerebral cortex becomes seriously impaired causing frequent emotional outbursts. As additional nerve cells die, changes in behavior lead to excessive wandering and intense agitation.
In the final stages of the disease, the ability to recognize faces, communicate and understand the world is lost as is the ability to control bodily functions.
Alzheimer's disease lasts from 8 to 10 years, with some unfortunate patients enduring it for up to 20 years.
Alzheimer's disease involves the formation of amyloid plaques and neurofibrillary tangles. This processs contributes to the degradation of nerve cells in the brain and the symptoms associated with the disease.
The signature hallmark of Alzheimer's disease is the accumulation of amyloid plaques between nerve cells in the brain. Amyloid are protein fragments the body normally produces.
Beta amyloid is a protein fragment snipped from an amyloid precursor protein.
In a healthy brain, these protein fragments are broken down and eliminated. In Alzheimer sufferers, the fragments accumulate to form hard, insoluble plaques.
Neurofibrillary tangles are insoluble twisted fibers found inside brain cells. These tangles consist primarily of a protein called tau. Tau is part of a structure called a microtubule that transports nutrients and other substances from one part of a nerve cell to another. In Alzheimer's disease, the tau protein is abnormal and the microtubule structures can't support themselves and consequently collapse.