~Parkinson's Disease

~Parkinson's Disease
Parkinson's Disease is a degenerative central nervous system disorder. In the United States about 1% of individuals over the age of 60 are affected.

Characteristic symptoms are tremors or shaking of one or both arms and sometimes of other muscles. Generally muscles are weak and rigid, movements slow and the face expressionless, also the voice becomes weak. Typically the walk is with slow, short, shuffling steps, the arms held stiffly at the sides and the trunk slightly bent forward, the patient may spontaneously break into a shuffling run.

The symptoms of Parkinson's disease are attributed to a loss of brain cells in the substantia nigra that produce the neurotransmitter dopamine. There also seem to be abnormalities in other parts of the brain and in the availability of other neurotransmitters such as serotonin and norepinephrine.

The onset of the disease is gradual and progression of symptoms usually slow. It may start with a mild shaking of the hands or involuntary nodding of the head. The mental abilities usually remain unimpaired, however, as the disease progresses there may be frequent mood changes, withdrawal and depression. The disease commonly starts in middle-aged and elderly individuals and seems to affect a somewhat higher percentage of males. However, while it used to be a disease of old people, now there is even juvenile-onset Parkinson's disease.

A high exposure to environmental chemicals and drugs, such as certain tranquilizers and antihypertensives, the designer drug MPTP (methylphenyl-tetrahydropyridine), inorganic iron, aluminum and carbon monoxide can induce an early onset of Parkinson-like symptoms in both sexes. Parkinsonism can also result from brain arteriosclerosis, stroke, head injury and after encephalitis or influenza. However, no such causative factors are known for the classical Parkinson's disease that is, therefore, called idiopathic (without apparent cause). Parkinson's disease apparently did not exist before the industrial revolution and this may be seen as an indication that toxic chemicals play a major role in its causation.

Chemicals and Endotoxins

Evidence is now accumulating to support the view that Parkinson's disease can originate from long-term subclinical damage to the nervous system from environmental chemicals. Initial reports linked the development of Parkinsonism mainly to medical drugs and to industrial workers exposed to chemicals, especially to industrial solvents.

More recently pesticides and herbicides used on farms and in households are increasingly linked to this disease. Development of symptoms due to low-level chronic exposure is gradual. It has been suggested by researchers that long-term exposure to sub-toxic levels of chemicals is much more likely to lead to neurological disorders, such as Parkinsonism than to physically based diseases. Betarbet reported in Nature Neuroscience (2000) that chronic systemic pesticide exposure reproduces the features of Parkinson's disease.

People who used pesticides in their homes were twice as likely to develop Parkinson's disease as people not exposed to pesticides. Also a combination of different pesticides is more likely to cause greater toxicity problems than individual chemicals.

Thiruchelvam reported this disturbing but not unexpected finding in Neuroscience (2000). Paraquat, a common herbicide and maneb, a common fungicide did not affect mice that were exposed to either one of them. However, when both chemicals were used together, dopamine neurons began to die at rather low exposure levels or at only a fraction of what is normally being regarded as toxic. Ongoing exposure lead to progressive neurotoxicity. There are countless combinations of low-level toxic residues in our food and water and no one knows what health effects they produce.

Furthermore, individuals with Parkinson's disease have much lower levels of detoxifying enzymes than healthy individuals, possibly only about 30% of normal levels. This means that toxic chemicals in such individuals accumulate much more than in those with normal liver functions. These chemicals are commonly fat-soluble and, therefore, stored in lipid structures such as the brain.

Aluminum greatly facilitates the passage of toxic chemicals into the brain. The brain is normally protected from undesirable chemicals in the bloodstream by a filter barrier. High aluminum levels have been shown to allow toxic chemicals that would otherwise be kept out to cross the blood-brain barrier. In addition, aluminum itself has neurotoxic properties. Aluminum inhibits the synthesis of important brain chemicals, it has the potential to block nucleic acid metabolism within nerve cells and to interfere with magnesium in the regulation of neurotransmitter receptors.

The injection of aluminum salts into the fluid surrounding the brain initiates degenerative brain changes. There is an unusually high rate of motorneurone disease and Parkinson's disease in the indigenous population of Guam in the Western Pacific. The soil and drinking water in this area is unusually high in aluminum and low in magnesium and calcium.

Our main intake of aluminum comes from cooking utensils, antacids, some baking powders, municipal water supplies and aerosol sprays. Encephalopathy has been clinically induced in dialysis patients through aluminum overload with mental deterioration and the EEG suggesting movement disorders.

Further brain deterioration can be caused by accumulations of the heavy metals cadmium, lead and mercury. Of these, mercury is generally the greatest brain hazard, coming mainly from amalgam tooth fillings. Organic mercury compounds are strong nerve poisons that may kill nerve cells and cause tremors. The problem is worse with two or more different kinds of metal in the mouth which cause micro-currents that interfere with nerve functions, and also the presence of different toxic metals in the brain greatly potentises their harmful effects.

Finally, iron overload, especially in inorganic form, can intensify Parkinson problems. Not only have PD patients low levels of natural antioxidants (glutathione and superoxide dismutase) but also high levels of iron in the substantia nigra areas of their brains. Iron tends to catalyze free radical reactions that destroy dopamine-producing cells.

Hidden food allergies and chemical sensitivities contribute to most degenerative diseases. However, in Parkinson's disease the body generally is insensitive and does not readily react even when specifically testing for hidden allergies. Nevertheless, it has been shown that the intestinal barrier becomes increasingly inefficient with advancing age and degenerative diseases. This allows only partly digested protein fragments or peptides to enter the bloodstream and reach the brain, causing chronic inflammation and long-term degeneration of brain cells.

Instead of reacting directly, food allergies and chemical sensitivities may be noticed as higher L-dopa requirements, gradual worsening of symptoms or increase of dysfunctional periods. After many years on levodopa, I noticed one patient being sensitive to the blue coloring of the standard Sinemet tablets with pronounced improvement when tablets with a different color were used. I suspect that many patients of all kinds of diseases deteriorate because of unbiological colors and preservatives used in tablet making.

Copper levels are significantly higher in the cerebrospinal fluid of patients with idiopathic Parkinson's disease than in a control group. While the specific reason for the elevated copper levels are not known, these are generally high when there is a chronic inflammation as caused by autoimmune and hidden allergy reactions. Furthermore, a copper enzyme is required to convert tyrosine into levodopa and elevated brain copper levels may be an attempt to stimulate levodopa production. However, high copper levels in the presence of antioxidant deficiencies tend to cause increased free-radical damage to the DNA of nerve cells.

Endotoxins are toxic chemicals produced by pathogenic intestinal bacteria. Undesirable changes in the composition of the intestinal flora and resulting overgrowth of the small intestine with pathogenic bacteria and fungi commonly results from antibiotic therapy and other immuno-suppressive drugs, from low gastric acidity and from frequently drinking alcohol.

Furthermore, drugs, such as aspirin, alcohol as well as allergic inflammations of the intestinal walls allow not only partly digested food fragments to be absorbed but also bacterial endotoxins. These eventually reach the brain where they act as neurotoxins. If the body is still sufficiently sensitive as in younger individuals neurotoxins tend to produce acute psychotic symptoms while with advancing age neurotoxins more commonly cause chronic nerve and brain degeneration.

Another common source of endotoxins is from root canal filled or otherwise dead teeth or from the jawbone cavitations after extracting infected teeth.

Normally, the liver acts as an additional filter and barrier against the invasion of internal organs by endotoxins. However, a persistently high influx of endotoxins combined with either food and chemical allergies or deficiencies of protective nutrients cause the liver to degenerate, thereby losing its detoxifying abilities.

Nutritional Factors

Some supplements with reported benefits in Parkinson's disease are acetyl-L-carnitine, octacosanol and evening primrose oil. Carnitine helps to increase energy production by channeling fatty acids into cells, it is especially brain active as acetyl-L-carnitine and helps to improve memory and possibly other brain functions. Octacosanol is a long-chain lipid concentrated from wheat-germ oil. It generally increases endurance and some Parkinson patients responded with improvement in their daily living activities and mood. Evening primrose oil, on the other hand, may help to reduce tremors. Involuntary movements may be reduced with antioxidants, lecithin and manganese.

Amino acids: The neurotransmitter dopamine is formed in the brain from the amino acid tyrosine with L-dopa as an intermediary stage. Tyrosine can be obtained from food or synthesized from another amino acid, phenylalanine. Therefore, tyrosine and phenylalanine can be used as nutritional supplements to ensure that the brain has sufficient raw material for the synthesis of dopamine.

Growdon in an experimental study reported in Life Sciences in 1982 showed that supplementation with 100 mg /kg /day or about 6-7g of tyrosine increased the dopamine formation in the brain of patients with Parkinson' s disease.

L-dopa treatment tends to create a brain deficiency of the amino acid tryptophan resulting in depression and other side effects. Several studies show that patients benefit with mood improvement and functional abilities when given tryptophan in addition to L-dopa. Tryptophan is a precursor of the neurotransmitter serotonin. Serotonin has a sedating effect and may be helpful in improving or lessening uncontrolled movements caused by an oversupply of levodopa. It also improves the sleeping ability. Bananas (especially the skins) and milk are high in tryptophan. Recent reports of a Parkinson patient regaining mobility with the illegal drug ecstasy revealed that this drug did not increase dopamine but rather serotonin production.

Melatonin, a hormone produced by the pineal gland only when we sleep in total darkness, stimulates serotonin synthesis as well. However, melatonin production is blocked if we do not get sufficient sunlight or other full-spectrum light into our eyes during the daytime, including the ultraviolet fractions. These are filtered out by windows or when wearing glasses.

Antioxidants: Ascorbic acid helps to counteract the severe side effects of L-dopa. Sacks reported a double-blind study in the Lancet (1975) of a patient who could not tolerate L-dopa because of severe nausea. If the drug was supplemented with ascorbic acid his condition greatly improved while every time he received a placebo instead of vitamin C his condition rapidly deteriorated.

There are now studies showing the benefits of high-level supplementation with antioxidants, especially vitamin C. Best results are usually achieved by combining several antioxidants. The time until levodopa treatment becomes necessary may be delayed for several years in newly diagnosed patients receiving 3000 mg per day each of vitamin C and E as compared to a group without supplementation. Even stronger antioxidants than vitamin C are the various bioflavonoids that provide the red, pink and purple colors in flowers, fruits and vegetables. Most of these are water-soluble and easily cross the blood-brain barrier. Some suggested antioxidant supplements are proanthocyandins from grape seed extract and tocotrienols extracted from palm oil.

While the level of dopamine in the brain of aging individuals and especially with Parkinson's disease declines to about half its normal level, the colored oxidation products of dopamine and of other neurotransmitters increasingly accumulate. Very high amounts of such colored deposits were found in a specific area of the brain after L-dopa treatment as compared to Parkinson patients without L-dopa treatment.

In addition, other oxidized substances, especially lipids and proteins, accumulate in cells, including nerve cells. These accumulations of oxidation products in the skin are known as 'age spots' or 'liver spots'. Such age pigments are composed of lipofuscin, ceroid and amyloid and begin filling up the nerve cells until they are killed when residue levels reach up to 70%. An additional factor may be the autoxidation of dopamine yielding hydrogen peroxide and free radicals that damage dopamine receptors. All of these harmful oxidation effects can be prevented and partially reversed by long-term supplementation with high amounts of antioxidants, preferably combined with periodic cleansing diets.

Vitamin B6 is essential for the synthesis of dopamine. Therefore, this vitamin, together with its cofactor zinc, should be provided in high amounts to overcome long-term deficiency symptoms and stimulate the production of dopamine. While there is also a negative report, various other studies show varying degrees of benefits from vitamin B6 supplements. Supplementation of 10 - 100 mg of vitamin B6 daily resulted in decreased cramps, rigidity and tremors as well as in better walking and bladder control. Improvement generally was more frequent in cases of shorter duration and least pronounced in long-standing conditions.

Of course, improvements from vitamin B6 supplementation would be limited by existing deficiencies in zinc and tyrosine or phenylalanine as well as other cofactors in dopamine synthesis. The same applies to magnesium the classical relaxation mineral. It helps to relieve tremors, trembling, twitching, muscle rigidity and cramps.

In addition, it should be noted that when taken together with L-dopa, vitamin B6 stimulates production of dopamine from the provided L-dopa in other parts of the body with less L-dopa reaching the brain and a decreased effectiveness. This may be a factor causing negative findings in some experimental studies. However, this is not so much of a problem if L-dopa is used together with a decarboxylase inhibitor. Nevertheless, with higher doses of vitamin B6 it is advisable to take the vitamin either at the end of the day after the last levodopa or during the day in smaller amounts about an hour after taking levodopa and several hours before the next lot.

Dietary Factors: For patients on L-dopa the meal composition is important. With meals high in protein, absorption is delayed and also less L-dopa reaches the brain through the blood-brain barrier and the condition may deteriorate. After a meal high in carbohydrates, on the other hand, more L-dopa reaches the brain and dyskinesia (uncontrolled movements) may develop. Therefore, drug intake should be adjusted to the type of the meal. The best way is to eat only one protein meal daily and have this in the evening after the last daily dose of levodopa.

Detrimental dietary effects can be seen with a high intake of sugar and fat. A high sugar diet increases the risk of developing Parkinson's disease three-fold (Hellenbrand in Neurology 1996) while a high intake of animal fats is associated with a five-fold increase (Logroscino in Annals of Neurology1996). Conversely diets high in vitamin C and beta-carotene are highly protective. The way in which a high-fat diet is detrimental may simply be by reducing the blood flow to the brain and thereby causing oxygen deficiency. Sugar, on the other hand, induces an excessive release of insulin which causes hypoglycemia and with this a shortage of brain fuel. Both of these factors would make brain cells susceptible to chemical toxicity.

Coffee consumption has been found to be associated with a lower risk of developing Parkinson's disease (Benedetti in Neurology 2000 and Deleu in Neurology 2001). This may be due to the effect of caffeine in stimulating brain activity. Regardless whether this is a causal effect or not it should be beneficial to drink coffee in the morning in order to delay the time when the first levodopa is required.

Coenzyme Q10 is required for the oxidative energy production in the mitochondria of all cells and especially in the brain with its high energy requirement. It is specifically this impaired mitochondrial energy production that causes cells in the substantia nigra region of the brain to malfunction and die, creating a shortage of dopamine. Furthermore, coQ10 levels in Parkinson's patients were 35% lower than in age-matched controls. This deficit of coQ10 caused a significant reduction in the activity of enzyme complexes critical to the mitochondrial function of the brain cells affected by Parkinson's disease whereas supplementation preserves mitochondrial function.

CoQ10 levels decrease with aging. Depletion is caused by reduced synthesis of coQ10 in the body along with increased oxidation of in the mitochondria. In addition, coQ10 is a strong antioxidant. It is widely distributed in nature and available from food but only in rather small amounts. Therefore, supplementation can be of major benefit. The vitamin niacinamide has a similar beneficial effect on mitochondrial energy production. Furthermore, coQ10 and niacinamide are able to protect mitochondria from damage by toxins.

Other therapies that may provide some protection from the loss of cognitive function in certain patients include Acetyl-L-carnitine, Hydergine (a European medication), and phosphatidylserine (a phospholipid). Additional therapies that may be beneficial in treating the symptoms of PD include the hormones DHEA, NADH and melatonin.

Fish and other seafood are generally beneficial and a recommended food for Parkinson patients. Unfortunately, most species are now polluted with unacceptable levels of mercury, a brain poison. Dr Mercola (www.mercola.com) regards only the following as safe: Croaker, Haddock, Sardines, Summer Flounder and Wild Pacific Salmon. A more detailed selection is available from the Environmental Working Group (www.ewg.org).

Excitotoxins are taste or flavor enhancers that release glutamate and other brain-active amino acids such as aspartate and cysteine. The best known example is MSG or mono-sodium glutamate. High blood levels can cross the normally protective blood-brain barrier. Glutamate is a neurotransmitter that is present in the extracellular fluid only in very low concentration. If levels are inappropriately raised then neurons fire abnormally and at higher levels brain cells begin to die. Oxygen deficiency and lack of fuel (hypoglycemia) both interfere with the energy production of brain cells to make them susceptible to damage by these excitotoxins. This may be an important factor in the development of neurological diseases including Parkinson's disease as Blaylock pointed out in a review article in Medical Sentinel 1999.

Excitory amino acids cause problems mainly when they are used either in high concentrations or in free form while bound as in most natural foods they are slowly released and therefore harmless. Most processed foods contain excitotoxins especially any kind of commercial taste or flavor enhancers such as hydrolyzed vegetable protein, soy protein extract, yeast extract, beef stock, commercial soups, sauces and gravies, caseinate, aspartame. These may just be labeled as natural flavoring. Red meat, processed meat, cheeses and tomato puree have higher levels of free glutamate as well but fresh tomatoes are fine. All of these should be avoided with Parkinson's disease.

Liver Improvement: There are many studies showing the connection between intestinal bacteria, endotoxins, liver damage and finally diseases of the central nervous system. Therefore, a central medical feature of Parkinson's disease may well be liver damage caused either by environmental chemicals and drugs, by hidden allergies and endotoxins or by a combination of these factors.

This means that the treatment of Parkinson's disease should focus on improving liver functions by substituting the outlined negative factors for positive ones. This includes:

  • Living in an unpolluted environment
  • Eating low-allergy food free of unbiological chemicals
  • Minimizing alcohol and unnecessary drugs
  • Drinking chemical-free water
  • Normalizing the intestinal flora with a high intake of raw food and cultures of acidophilus and bifido-bacteria
  • Using a high level of antioxidants, MSM, chlorella, spirulina and other detoxifying nutrients in addition to specific therapies to regenerate the liver

A diet high in chlorinated water, sugar, fat and oxidized cholesterol encourages arteriosclerotic changes with reduced blood supply to the brain and even a single fatty meal can impair the blood flow to the brain for several hours.

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