Alzheimer's Disease is usually diagnosed by a process of exclusion. (Doc rules out simple senility, hardening of arteries, etc,) It effects between 5 - 10% of people over the age of 65 years. But the Baby Boomers seem to have it at ten times the normal rate, so that means it is not genetic. It is environmental. ALZHEIMER'S DISEASE
A.D is associated with loss of memory and cognitive functions and inability to carry out activities of daily life. The person affected is usually not aware of the memory loss. On autopsy these individuals have brains that show atrophy, senile plaques and neurofibrillary tangles particularly in the cerebrocortex and hippocarpal formation. The clinical features of Alzheimer's disease are believed to be related to cholinergic dysfunction due to appreciable reductions in the activity of the enzyme choline acetyl transferase, the enzyme that synthesises acetyl choline and the neuronal transfer of choline. The cholinergic nerve destruction is caused by excitatory amino acid (glutamate or aspartate), excitotoxicity. This excito toxicity causes the tangles associated with Alzheimer's disease.
Alzheimer's Disease patients are prone to B12, folate and essential fatty acid deficiency. As one might expect, many demented individuals are at high risk of malnutrition which, in its own right, may be associated with apathy, disorientation, poor concentration and memory deficits.
Alzheimer's Disease patients tend to have low vitamin B1, B3, B12, Folic Acid, Linoleic and linolenic acid and Zinc (each of which can cause dementia ). Heavy metals such as Aluminium, Cadmium and Lead may also play a role.
Furthermore, many Alzheimer's patients are gluten/alpha gliadin sensitive as well as being low in thyroxine. If they have a palma crease or Sydney line, this increases sensitivity to food fractions such as milk, gluten and alpha gliadin. Dehydration in the elderly can mimic Alzheimers disease.
THE ALUMINIUM CONNECTION
Aluminium (Al3+) inhibits the second messenger system, causing neuronal malfunctions and cell death. It also inhibits the incorporation of inositol into phospholipids. Aluminium competes with iron (Fe2+), binds with silicic acid to form the aluminosilicate. Aluminosilicate does not form in the extracellular environment in which Al3+ is bound strongly to transferrin nor in the intracellular environment in which phosphate binding is favoured, but will form in an environment in which the pH is increased. These silicates can be a significant causal agent in cell-derived generation of free radicals and consequent nerve cell damage. (NOTE: AVOID TOOTHPASTE. ALWAYS made with ALUMINUM as 99% of its bulk. Read ARTICLE.Furthermore, Aluminium competes effectively for Magnesium (Mg2+) binding sites in biological systems. Al3+ initiates tubular polymerisation. Mg2+ blocks the N-methyl-D-aspartate receptor (NMDA) channel in CNS neurons. The NMDA receptor complex provides a recognition site for the neurotransmitter glutamate that is coupled to a Calcium (Ca2+) selective ion channel. Mg2+ blocks this channel, thus Al3+ allows unrestrained Ca2+ influx at the NMDA receptor, followed by neuronal death and Alzheimer's or other neurodegenerative disease. Adenosine can reduce this toxic over stimulation.
Increasing the level of transferrin,(a natural aluminium chelator), increases the synthesis of tetrahydrobiopterin. This enzymatic cofactor is inhibited by Al3+. Zinc and magnesium deficiency enhances brain aluminium accumulation. Aluminium can be removed from the body by taking desferrioxamine, a trivalent ion chelator. Calcium and magnesium supplementation also reduces body burden of aluminium.
GLUTAMIC ACID
Recently the neurotoxicity of the excitatory amino acid glutamic acid has been suggested as being involved in the development of senile dementia. The neurotoxicity of glutamate is strongly potentiated by neuronal hypoxia (metabolic hypoxia is associated with B1 deficiency). The potentiating hypoxia can be of cardiovascular or cerebrovascular origin. Glutamine and Taurine have been found to have a protective role against neuronal hypoxia. The minerals Zinc and Magnesium modify the neurotoxicity of glutamate. Glutamate's excito toxicity can also be eliminated by branch chain amino acids, threonine, glycine and carnitine.IMMUNE SYSTEM AND ALZHEIMERS
The nerve cell death of Alzheimers patients is linked to the build up of plaques in their brain, which consists mostly of insoluble protein called beta amyloid. Unfortunately, although the b amyloid is non toxic, the microglia (the brain immune system) interacts with it to produce a number of cytokines - gamma interferon and tumour necrosing factor, which are toxic to nerve cells. Free radicals are also produced during this interaction which further contributes to the destruction of nerve cells. The use of free radical scavengers may therefore be of some benefit to Alzheimers patients.NUTRITIONAL TREATMENT
Filter all water through reverse osmosis filter. Drink 2 litres of fluid per day. Avoid all antacids that contain aluminium. Avoid cooking in aluminium pots or drinking fruit juice or soft drinks from aluminium containers. Avoid citrate containing fluids in aluminium containers as they increase the availability of aluminium. 3 - 4 dessertspoons of Lecithin granules should be sprinkled over food per day. Check for thyroid disease and treat appropriately. Check medication, eg. barbiturate and psychotropic drugs, diuretics. Check for vitamin B1, B3, folate, B-group and essential fatty acid deficiency. Check for heavy metal toxicity - through hair analysis. Metals that need to be tested are Aluminium, Copper, Lead and Iron levels. Check for food sensitivities, particularly wheat and milk. GLA/EFA which is a mixture of essential fatty acid should be taken regularly, it has been suggested that Alzheimer's may be due to EFA deficiency. It also decreases inflammation. Increase antioxidant intake to reduce free radical damage. Supplement with histidine, vitamin E, vitamin C and zinc. Increase intake of onion and ginger. Be careful of neuroleptics that have anti cholinergic and anti histamine effects eg. chlorpromazine as they aggravate Alzheimers. NUTRITIONAL SUPPLEMENT OPTIONS
The nutritient supplements mentioned above reflect the major nutrients that may help the condition. Please do remember however that nutritional supplementation is an adjunct to medical treament and in no way replaces medical treatment.Mineral Matrix 3/day. (Helps detoxify Al) Heme 100 3 - 4/day. (B12/folate supplement) Parachol 5/day. (Acetyl choline synthesis/B1 supplement) Inhibin 2 3/day. (Improve release of Acetylcholine from nerve terminals, neuroinhibitor, threonine supplement) SFM 3/day. (Improve noradrenaline/ dopamine/thyroid function) Hydrozyme 1 with meals. (Improves digestion) BACE 3/day. (Anti-oxidant/zinc supplement) Kelamin 3/day. (Multi-B complex) Taurine 500 4/day. (Decrease neuronal hypoxic damage) Zinc C Lozenge 3 - 4/day. (Zinc supplement/decrease glutamate toxicity) GLA/EFA 3 tspn/day. (Improves blood viscosity status EFA supplement and decreases inflammation.) Adenosine 2/day (suck sublingually) (Regulates Neurve over excitability) Glycoamines 3tsp/day (Reduces glutamate toxicity, Branch chain amino acid supplement) Zymin 10 - 20mls/day (Magnesium and Zinc supplement) D alpha tocopheryl succinate 632mg 1/day (Inhibits neuronal lipid peroxidation) Vitamin C with Bioflavonoids 3 tsp/day (Decreases lipid peroxidation, antioxidant) Selenium 200 - 400 mg/day (Antioxidant) Carnitine 2 g/day divided dose (Depresses glutamate, increase sensitivity of cortical neurones to acetyl choline) Super Lecithin 3 - 4 dstspn/day (Choline supplement) Taurine 3 - 6/day (Reduces glutamate neurotoxicity)