Antioxidant Can Modify Fat Oxidation in the brain

Brain Training Program

We all face a gradual loss in mental sharpness as we age. Cognitive decline — a gradual weakening of understanding, thinking and remembering— is a natural and expected part of aging. This has been confirmed by numerous studies on memory, response time, attentiveness, the ability to speak and to understand what others are saying, and even IQ.. This type of decline is not the same as Alzheimer's disease, which is a pathological condition. People experience cognitive decline because of slowing in brain processing speed, a weakening of brain signals from the senses, A decrease in the production of key brain chemicals (neuromodulators).

To accelerate brain functioning we have used two approach by :

1.      providing important nutrients which replenish the shortage of neurotransmitter.

2.       encouraging the patient to work on brain training program developed by posit science to improve the cognitive functions.

Age-related changes in the brain include:

• Brain shrinkage: Throughout adulthood, there is a gradual reduction in the weight and volume of the brain. This decline is about 2% per decade. Contrary to previously held beliefs, the decline does not accelerate after the age of 50, but continues at about the same pace from early adulthood on. The accumulative effects of this are generally not noticed until older age.

• Lost connections: The complexity of the brain is due in part to the intricate system of interconnections between neurons in the different parts of the brain. Neurons communicate with one another via specialized chemicals called neurotransmitters, of which there are several. Changes in this network of communication may account for some of the cognitive changes seen with age. Some of the connections may be lost, and new connections may not be made as readily. In addition, levels of two neurotransmitters (acetylcholine and dopamine) are thought to decline with age.

• Plasticity: On the bright side, the brain has a great capacity for adaptation, modification, and repair. The term plasticity refers to the ability of the brain to modify its structure and function. This capability continues throughout life. For one thing, there is a certain amount of redundancy in the brain. If one network of neurons is damaged or dies, another network can take over the function. The death of neurons can also be compensated for by surrounding neurons sprouting new connections to take the place of the lost ones.The brain is a dynamic, not a static, system. The neurons respond to mental stimulation and environmental factors.  And there is the capacity to respond to age-related changes. It appears likely that cognitive changes are noticed at a point when the compensatory mechanisms of the brain are unable to overcome physical changes taking place. There may be strategies, either with medications, mental exercises, or something else, to enhance the brain's natural capacity for plasticity and thus forestall cognitive declines associated with aging.                                                                                                                                                                                                                                                                                                                                                     
• Pathological changes: Tangles of tau protein in the brain, a hallmark of Alzheimer's disease, can also be responsible for mild cognitive impairment in older individuals. Postmortem examinations of the brains of non-demented older adults have found a correlation between the number of neurofibrillary tau tangles in memory-related areas of the brain and memory impairment during life. Other changes associated with Alzheimer's disease and other forms of deventia include plaques of a protein called beta amyloid, and loss of synapses and neurons. Most researchers now believe that mild cognitive impairment represents an early stage of Alzheimer's disease.
  

Antioxidants Can Modify Fat Oxidation in the Brain

 The addition of vitamin E (20mg of a -tocopherol per 100 gm of finished diet) significantly improved performance in discrimination studies and capacity to deal with the operant situation. The results of these studies are compatible with the possibility that enhancing the level of lipid peroxidation has an adverse effect on the CNS out of proportion to its effect on the body as a whole, as measured by mortality rate. It also suggests that variation in the amount or degree of unsaturation of dietary fat and modifying factors such as high doses of antioxidant nutrients that can modify lipid oxidation rates may contribute to the variability in age of onset of evident degradative CNS changes such as senility above and beyond the variations expected from differences in mortality rates [Harman 1976].

The manner in which increases in the amount, or degree of unsaturation of fat alters CNS function is hypothesized on numerous mechanisms. It appears the brain has a high affinity for highly unsaturated fatty acids, particularly docosahexaenoic acid (22:6 w 3). The brain readily absorbs linolenic acid by coverting it to 22:6 w 3 and then binds it tightly. It is in the synaptic areas of the brain where this special affinity takes place [Marwick 1985; Galli 1973; Heikkila 1919; Quimby 1974]. These are the specific areas in humans where the first adverse changes are found-the formation of neuritic plaque which is characteristic of senile dementia.

The polyunsaturated fats derived from precursors of linolenic and linoleic acids have been found to be important functional components of the photoreceptor cell membrane in the eye. The position and number of unsaturated bonds appears to control the electrical response of the photoreceptor cell membrane. A low-fat, low-cholesterol diet can partially ameliorate senile maculopathy, a degenerative retinal disorder [Haddad 1984]. The "hair cells" of the cochlea, the sound-sensing nerves of the human ear, also require these highly unsaturated fatty acids. Similarly, the olfactory bulb in the human is surrounded by a deep layer of myelinated (highly subject to peroxidation) nerve fibers passing to and from the olfactory tract. Taste is so closely related in experience to olfactory sensibility that in speaking it is customary not to distinguish them from one another. This may explain why so many elderly people report loss of taste.

Zinc deficiency is known to play a role in the loss of taste and odor reception. Zinc helps protect lipids from peroxidation as part of the antioxidant enzyme superoxide dismutase (SOD). So it is entirely likely that the decline in sensory perception associated with aging may be partially die to uncontrolled free-radical damage in the brain related to the relative increase in polyunsaturated fat consumption, and deficiencies in absorption or availability of other essential nutrients in diets of the elderly (Ca, Fe, folic acid, B₁₂, intrinsic factor, vitamin B complex, C, zinc, selenium, vitamin D, lack of dark-green leafy vegetables, fiber, lactose intolerance, achlorohydria, protein deficiency, trace minerals) which are essential factors in internal defenses against damage from "internal radiation."

The above neuronal dysfunction may be mediated in part by the deleterious effect of dietary fat on the glial cells (the supporting structure of the nervous tissue). The rate of peroxidation of serum and vessel wall constituents may be increased, leading to a more rapid development of arteriocapillary fibrosis [Marwick 1985]. Increased lipid peroxidation in the synaptic areas, areas rich in polyunsaturated fatty acids [Galli 1973] (such as 22:5 w 6 and 22:6 w 3) could cause damage in a manner similar to that caused by b -hydroxydopamine [Heikkila 1973], or by the anesthetic halothane [Quimby 1974; Van 1975].

A peroxidative autoimmune attack is thought to initiate the autoxidation of L-Dopa and its metabolic product dopamine to b -hydroxydopamine. Thus reaction further autoxidizes to produce free radicals, hydrogen peroxide and hydroxyl radicals. The resultant damage to dopaminergic nerve cells is likely to be the cause of Parkinson’s disease. L-Dopa is the amino acid precursor to the neurotransmitter dopamine and is generally effective in improving the symptoms of Parkinsonism.  Liquid Deprenyl (Selegiline), a monoamine oxidase inhibitor, protects brain cell membranes from free radical attacks, such as described above. 

Also, the intake of nutritional supplements rich in antioxidants and brain chemical building blocks is vital. 

L--Dopa crosses the blood brain barrier, but dopamine does not. Administration of vitamin B₆, which helps convert L-Dopa to dopamine peripherally as well as centrally has been shown to temporarily worsen the symptoms of Parkinson’s disease when not enough L-Dopa is available to elevate the dopamine levels in the brain. Interestingly, when L-Dopa is used for its other CNS effects such as stimulation of growth hormone  release, the precaution against use of vitamin B₆ has not been found necessary.

There is some evidence that the antioxidant bromocriptine can facilitate L-Dopa by lowering the usual effective dose to half. This has sometimes been found to result in less long-term degeneration and sometimes seems to lead to repairs of damage to dopaminergic nerve cell layers [Teychenne 1983; Vance 1984]. (It should be noted that bromocriptine is structurally related to Ergoloid Mesylates, which may explain its antioxidant effects.)

Vitamin C has been shown to prevent autoxidation of L-Dopa. Vitamin C is an essential membrane stabilizing agent. The concentration of Vitamin C in cerebrospinal fluid (CSF) is about ten times the concentration in the blood. The interior of each nerve cell contains about ten times the concentrations of vitamin C in the CSF. This is one of the CNS’s most important defense mechanisms in protecting highly susceptible, but vitally important polysaturated lipid membranes in the brain, and spinal cord from free-radical destruction [Spector 1977]                         

 Brain Training Program:

 Your self-confidence will soar as you think faster, focus better, and remember more. For more information on brain training program visit

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