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Brain, spinal cord & nerve disorders

Introduction

Dementia is the fourth leading cause of death in those over sixty, while Alzheimer's disease (AD) alone kills 100,000 people per year in the United States. However, AD does not affect elderly people only, but may strike when a person is in his or her forties.

Once considered a psychological phenomenon, AD is now known to be a degenerative disorder that is characterized by a specific set of physiological changes in the brain. Nerve fibers surrounding the hippocampus, the brain's memory center, become tangled, and information is no longer carried properly to or from the brain. New memories cannot be formed, and memories formed earlier cannot be retrieved. Characteristic plaques accumulate in the brain as well. These plaques are composed largely of a protein-containing substance called beta-amyloid. Scientists believe that the plaques build up in and damage nerve cells (Balch and Balch, 1997).

Alzheimer’s disease and oxidative stress

AD and vascular dementia are the two most common types of dementia with the former being the most predominant. It is evident that oxidative stress, an environment where pro-oxidant (free radicals) species overwhelm antioxidant species, is involved in the pathogenesis of both forms of dementia. An increased level of reactive oxygen species in the vasculature, reduced nitric oxide bioavailability, and endothelial dysfunction leading to vascular disease is associated with vascular dementia. In AD, an increased amount of amyloid-beta peptide induces elevated reactive oxygen species production thereby causing neuronal cell death and damage.

Other disorders can cause symptoms similar to those of AD. Dementia may result from arteriosclerosis (hardening of the arteries) and high levels of homocysteine that slowly cuts off the supply of blood to the brain. The death of brain tissue from a series of minor strokes, or from pressure exerted by an accumulation of fluid in the brain, may also cause dementia.

There is no known cure for AD and dementia; there are however certain medication which offer some encouragement in that they slow the progression of the disease. Alternative medicine, a good healthy lifestyle and exercise also offer some benefit. The medical approach to dementia should include an assessment of the aspects of life style somewhat unique to the elderly. Therefore, one should consider the following as possible contributory causes of dementia: oxidative stress, lack of exercise, poor diet, nutritional deficiencies, cardiovascular disease, and the need for nutritional supplements.

Alzheimer’s disease and nutritional supplements

Numerous research studies have shown certain antioxidant supplements to be of benefit in reducing the risk of AD. The most commonly recommended is folic acid at a dosage of 2.5 to 10 mg per day. The herb ginkgo biloba is also commonly used and is a good antioxidant for the brain and entire body. Other supplements including vitamins B12, B6, C, E, zinc, beta-carotene and phosphatidyl choline are also beneficial.

Since most dementia patients are elderly, there probably isn't too much we can do to realistically alter the lifestyle. However, there is one thing, albeit it controversial, that should be addressed. That is the matter of aluminum which has been shown in some studies to be a causative factor in Alzheimer's disease. The main sources of aluminum in our environment are cookware, cigarette filters, and antiperspirants. These sources of aluminum should definitely be eliminated from the environment. If there has been excessive exposure to aluminum in the patient's life, it would be a good idea to have a hair analysis for toxic metals.

The second concern for most senior citizens is good nutrition. The Center for Disease Control says we all should eat 5 servings of fruits and vegetables, preferably raw, a day. Very few of us do that, let alone seniors. Fruits and vegetables are nature's source of antioxidants - our antioxidant status deteriorates with age and the need is compounded in patents with Alzheimer's.

Cellfood®

In a clinical trial on athletes at the University of Pretoria (2001) 35 drops of Cellfood® increased the oxygen uptake by 5%, and the ferritin levels by 31%, amongst others.

  • An oxygen mineral supplement like Cellfood® is rapidly absorbed by the body, assists with oxygenation and increases the oxygen saturation in the blood;
  • The increased ferritin levels can assist with the production of more red blood cells that are needed to transport oxygen to the different organs (including the brain) and cells;
  • Cellfood® is a powerful antioxidant that assists the immune system; it also assists the body in producing glutathione, a powerful antioxidant that will help negate the negative effects of free radicals, and
  • It provides essential nutrients including amino acids directly at cellular level.

In 2011 Benedetti and co-workers investigated the antioxidant properties of Cellfood® in vitro in different model systems:

  • Three pathophysiologically relevant oxidants were chosen to evaluate Cellfood’s protection against oxidative stress: hydrogen peroxide, peroxyl radicals and hypochlorous acid;
  • Both biomolecules (GSH and plasmidDNA) and circulating cells (erythrocytes and lymphocytes) were used as targets of oxidation;
  • Cellfood® protected, in a dose-dependent manner, both GSH and DNA from oxidation by preserving reduced GSH thiol groups and supercoiled DNA integrity, respectively;
  • At the same time, Cellfood® protected erythrocytes from oxidative damage by reducing cell lysis and GSH intracellular depletion after exposure to the oxidant agents;
  • In lymphocytes. Cellfood® reduced the intracellular oxidative stress inducedby the three oxidants in a dose-dependent manner; and
  • The overall in vitro protection of biomolecules and cells against free radical attacks suggests that Cellfood® might be a valuable coadjuvant in the prevention and treatment of various physiological and pathological conditions related to oxidative stress, from aging to atherosclerosis, from neurodegeneration to cancer.

Vitamin and mineral supplementation and homocysteine

The correlation between homocysteine, an intermediate in methionine metabolism, and vascular disease has recently become a popular topic and the possibility that elevated homocysteine levels might contribute to the development of coronary heart disease (CHD) and stroke, has been investigated to a large extent.

For efficient homocysteine metabolism, an adequate supply of vitamin B12, vitamin B6, folic acid, zinc and trimethylglycine (betaine) is required.

From scientific research it is clear that the vitamin and mineral status is an important determinant of circulating homocysteine levels. Kruger and co-worker (2009) for example studied the efficacy of Cellfood Longevity (containing all the co-factors for effective homocysteine metabolism) on physical performance and selected markers of health status in males.

Twenty healthy sedentary volunteers between the ages of 30 and 60 years with a homocysteine level higher than 10 mmol/l were included in the study. Some of the findings were as follow:

  • Statistically significant increase in serum folate (proving the bio-availability of the liquid supplement)
  • Statistically significant reduction in homocysteine (15%) 
  • No change in urate levels (will not cause gout)

References

Balch J.F. and Balch P.A. 1997. Prescription for nutritional healing. Avery Publishing Group.

Benedetti S., Catalani S., Palma F., and Canestrari F. 2011. The antioxidant protection of CellfoodŌ against oxidative damage in vitro. Food and Chemical Toxicology 49: 2292-2298.

Kruger P.E., Wood P.S., Grant R. and Clark J. 2009. Efficacy of NCODE (Cellfood Longevity) on physical performance and selected markers of health status in males. Research report, Institute for Sports Research, University of Pretoria.


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