Articles

Useful Information - One True Cause of Disease #

THE ONE TRUE CAUSE OF DISEASE

In the early 1800s Isaac Jennings, M.D. quietly started a revolution in health care when he noticed that changes in lifestyle produced EXCELLENT RESULTS.

Dr. Jennings, after practicing as a traditional medical doctor for 20 years without getting any significant results, one day he faced a shortage of drugs during a fever outbreak in the summer of 1815, so people in town came to see him with all kinds of symptoms. But he didn't treat them because there weren't any drugs available.

All he could tell them was to go home, rest, and drink lots of fluids.

And what happened? Surprise, surprise these people got well, WITHOUT ANY MEDICINE!

Based on this, he decided to carry out an experiment: he was going to treat people using only placebos (dummy pills) and some common sense instructions that is, he would advise his patients to correct their lifestyle and diet to a more natural approach.

The results were excellent: his patients recovered in absolute record time compared to patients who had been medicated.

In 1822 he gave up medical pills, plasters, powders and potions and treated patients with pills made from bread and coloured water.

He then practised for a further 20 years the - "do nothing mode of treating disease." - Yale University conferred an honorary degree upon him in recognition of his great success substituting pills with placebos.

NOW WE KNOW THAT OUR BODY IS INHERENTLY HEALTHY AND SELF-HEALING AND ALWAYS STRIVES TO MAINTAIN OR RE-ESTABLISH OPTIMAL HEALTHFUL CONDITIONS.

There is no healing force outside the body. Dr. Isaac Jennings

Dr. Jennings is also the founder of the Natural Hygiene Philosophy. Natural Hygiene is a set of principles that people throughout human history have practiced to achieve and MAINTAIN optimum health. Natural Hygiene principles are based upon meeting the body's inherent, natural needs.

Remember, you can never poison your body into being healthy.

Twenty-five years in which I used prescribed drugs, and 33 years in which I have not used prescribed drugs, should make my belief that drugs are unnecessary and in most cases injurious, worth something to those who care to know the truth.

John H. Tilden, M.D. (1940)

Useful Information - The Dangers of Toxic Metals #

 

The Dangers Of Toxic Metals

http://www.lifedynamix.com/articles/Medicine/Toxic_Metals.html

By Lawrence Wilson M.D.

Toxic metals comprise a group of minerals that have no known function in the body and in fact are harmful. Today mankind is exposed to the highest levels of these metals in recorded history, thanks to their industrial use and burning of coal, petroleum and incineration of waste material. They affect everyone and are a major cause of illness, aging and even genetic defects.

The study of toxic metals is part of nutrition and toxicology, areas not emphasized in medical schools. For this reason, these important causes of disease are accorded little attention in conventional mainstream medicine. This article focuses on the extent of toxic metal problems sources of toxic metals, symptoms and how to remove them.

 

INTRODUCTION TO THE MINERALS

Minerals are the building blocks of our bodies. They are required for body structure, fluid balance, protein structures and to produce hormones. They are a key for the health of every body system and function. They act as co-factors, catalysts or inhibitors of all enzymes in the body. Copper and iron, for example, along with other minerals are required for the electron transport system, and thus needed for all cellular energy production.

Minerals are classified into four groups: The macrominerals, or those needed in large quantity, include calcium, magnesium, sodium, potassium, phosphorus, sulphur, iron, copper and zinc. Required trace minerals include manganese, chromium, selenium, boron, bromine, silicon, iodine, vanadium, lithium, molybdenum, cobalt, germanium and others. Possibly required trace minerals include fluorine, arsenic, rubidium, tin, niobium, strontium, gold, silver and nickel. Toxic metals include beryllium, mercury, lead, cadmium, aluminum, antimony, bismuth, barium, uranium and others.

These categories overlap slightly because assessing minerals that are required by humans is problematic. Some may be needed in minuscule amounts. Clinical studies to prove this by depriving people of vital minerals would be cruel and possibly disastrous.

Also, note that minerals needed in lesser quantities are usually toxic in greater amounts. Examples are copper, iron, manganese, selenium and vanadium. Even calcium and sodium are quite toxic in excess.

 

TOXIC METAL DANGERS

Today mankind is exposed to the highest levels in recorded history of lead, mercury, arsenic, aluminum, copper, tin, antimony, bromine, bismuth and vanadium. Levels are up to several thousand times higher than in primitive man. In my clinical experience, everyone has excessive amounts of some or all of the toxic metals.

Toxic metals are also persistent and cumulative. The late Dr. Henry Schroeder, MD, who was a world authority on trace elements, wrote:

Most organic substances are degradable by natural processes. (However), no metal is degradable, they are here to stay for a long time.

Toxic metals replace nutrient minerals in enzyme binding sites. When this occurs, the metals inhibit, overstimulate or otherwise alter thousands of enzymes. An affected enzyme may operate at 5% of normal activity. This may contribute to many health conditions. Toxic metals may also replace other substances in other tissue structures. These tissues, such as the arteries, joints, bones and muscles, are weakened by the replacement process. Toxic metals may also simply deposit in many sites, causing local irritation and other toxic effects. They may also support development of fungal, bacterial and viral infections that are difficult or impossible to eradicate until this cause is removed.

The mineral replacement process often involves the idea of preferred minerals. For example, the body prefers zinc for over 50 critical enzymes . However, if zinc becomes deficient - and our soil and food are very low in zinc today - or exposure to cadmium, lead or mercury is sufficiently high, the body will use these in place of zinc. Cadmium, in particular, is located just below zinc in the periodic table of the elements, so its atomic structure is very similar to that of zinc. It almost fits perfectly in the zinc binding sites of critical enzymes such as RNA transferase, carboxypeptidase, alcohol dehydrogenase and many others or great importance in the body.

The ability to replace a vital mineral means, however, that toxic metals are not completely harmful. Indeed, they can extend life. They keep bodies functioning when vital minerals are deficient.

An analogy is to imagine taking an automobile journey. If one is far away from a repair shop when a key part like the fan belt breaks, if one had a spare piece of rope, one could tie it around the pulleys and continue the trip slowly. The rope would not function nearly as well as the original part, but would allow one to keep going. This is how toxic metals can function positively in the body. Many people limp along on grossly deficient diets, and are even born deficient and toxic. They do not realize their fatigue and other symptoms are due to the presence of incorrect replacement parts in their biological engine compartments. Depending on where toxic metals accumulate, the resulting effects may be given names such as hypothyroidism, diabetes or cancer.

 

MODERN DIETS AND TOXIC METALS

The danger of toxic metals is greatly aggravated today by the low mineral content of most of our food supply. An abundance of vital minerals protects against toxic metals. Vital minerals compete with toxic metals for absorption and utilization in enzymes and other tissue structures. However, when food is low in essential minerals, the body absorbs and makes use of more toxic metals. To continue the previous analogy, we are not stocking up sufficiently on factory parts, so we must use the greatly inferior replacement parts ≠ toxic metals. Causes for the low mineral content of almost all agricultural products are primarily:

Hybrid crops are bred for production or disease resistance, rather than superior nutrition.

Superphosphate fertilizers produce higher yields by stimulating growth, but do not provide all the trace elements.

Monoculture, the growing of just one crop over and over on the same piece of land, eventually depletes the soil.

Toxic sprays damage soil microorganisms needed to help plants absorb minerals from the soil.

Food refining and processing almost always reduce the mineral content of our food. Whole wheat flour, when milled to make white flour, loses 40% of its chromium, 86% of its manganese, 89% of its cobalt, 78% of its zinc and 48% of its molybdenum. Refining cane into sugar causes even greater losses. EDTA may be added to frozen foods to retain their color. However, this chelating agent removes minerals that otherwise would cause the surface minerals to ?tarnishπ, discoloring the vegetables.

According to Dr. Weston Price, author of Nutrition and Physical Degeneration, primitive man ate 5 to 11 times the amount of the essential minerals in his diet as modern man . The term 'empty calories' aptly describes most of our food today.

 

SOURCES AND DETECTION OF TOXIC METALS

For a more complete list of sources for each of the major toxic metals organized by the metal, see the Reference Guide at the end of this article.

Food Sources. Food grown near highways or downwind of industrial plants may contain lead and other toxic amounts of metals. Even organic home gardens may be contaminated if, for example, old house paint containing lead leaches lead into the soil.

Lead is considered the most widely distributed toxic metal due to its many uses in industry. However, mercury, arsenic, cadmium and particularly aluminum are just as widespread if not more, but are less well-studied.

Pesticides used on fruits, vegetables and many other foods may contain arsenic, lead, copper, mercury and other toxic metals.

Fish, especially those caught near the coast or in contaminated streams or lakes, are universally contaminated. Shellfish and bottom feeders in particular contain excessive cadmium, mercury and other toxic metals. Large fish concentrate mercury a million times or more. The federal government recently issued a warning that pregnant and lactating women should avoid tuna, shark, king mackerel and other large fish. I recommend everyone avoid these fish!

Table salt has aluminum added as an anti-caking agent. Sea salt is much better. Beverages in aluminum cans or food cooked in aluminum may contain elevated levels of aluminum. Ceramic plates and cookware from other nations often contain leaded glazes that come off onto the food.

Hydrogenated oils found in commercial peanut butter, margarines including soy margarine and vegetable shortening may contain nickel and cadmium used as catalysts.

Drinking Water. This is the most important source of toxic metals for most people. Aluminum, copper, toxic chlorides and fluorides are added to many municipal water supplies. Aluminum allows dirt to settle out of the water, while copper kills algae that grows in reservoirs. Chlorine is used to disinfect water, although ozone works very well and is a far more healthful treatment. Wells and even municipal water may also contain some lead, arsenic and other undesirable metals. Galvanized and black plastic pipes can be an important source of cadmium. Lead-soldered pipes and copper pipes may increase these metals in the drinking water if the water is soft. It is an uncommon problem in hard water areas.

Fluoride compounds added to drinking water are extremely toxic. They have found their way into ground water supplies, and thus into the food chain. Fluoride levels in foods processed with water may be very high, especially baby foods and reconstituted fruit juices. Health authorities who recommend fluoridating the water rarely if ever take into account fluorides already found in natural foods, foods processed with fluoridated water and fluoridated toothpaste. The combination adds up to overload in all cases.

Hydrofluosilicic acid, the chemical often used to fluoridate drinking water, is a smokestack waste that contains lead, mercury, cadmium, arsenic, aluminum, benzene and radioactive waste material .

Note that carbon and carbon block filters do not remove most toxic metals from water. Only distillation and reverse osmosis remove most toxic metals. Good quality spring water is probably best way to avoid the most common source of toxic metals and at the same time obtain vital minerals.

Airborne Sources of Toxic Metals. Most toxic metals are effectively absorbed by inhalation. Auto and particularly aircraft exhaust, industrial smoke and products from incinerators are among the airborne sources of toxic metals and other chemicals. Burned high in the atmosphere, aircraft fuel deposits everywhere and affects everyone on earth.

Burning coal can release mercury, lead and cadmium among other metals . Iranian and Venezuelan oil are high in vanadium. Other oil is excessive in toxic sulphur compounds. Tetraethyl lead was added to gasoline for many years. Residues are present on pavement and may settle on buildings, cropland and elsewhere. Today, manganese is added to gasoline. Uranium exposure is largely from airborne sources such as nuclear tests and accidental nuclear releases.

Older methods of incineration of electronic parts, plastics, treated fabrics, batteries and even diapers release all the toxic metals into the air. The use of scrubbers and newer methods of very high temperature incineration are much better.

Cigarette and marijuana smoke are high in cadmium, found in cigarette paper. Pesticides used on these crops may contain lead, arsenic and other toxic metals.

Medications. Many patented prescription and over-the-counter drugs contain toxic metals. Cipro (fluoquinolones) and Prozac (fluoxetine) are fluoride-containing chemicals, for example. Thimerisol, a mercury-containing preservative, is used in some vaccines, including all flu shots. Independent evaluation of a large study that is part of the Centers For Disease Control Vaccine Safety Datalink concluded that children are 27 times as likely to develop autism after exposure to three thimerisol-containing vaccines than those who receive thimerisol-free versions.

Thiazide diuretics contain mercury. These include Maxzide, Diazide and many others. Antacids such as Ryopan, Gaviscon, Maalox, Mylanta and many others are very high in aluminum. Antibiotics may also contain toxic substances including metals.

Direct Skin Contact. Almost all anti-perspirants and many cosmetics contain aluminum. Dental amalgams contain mercury, copper and other metals. Dental bridges and other appliances often contain nickel. Prostheses and pins used to hold bones together may contain nickel and other toxic metals. Copper intra-uterine devices, if left in place for years, release a tremendous amount of copper into the body. Soaps, body lotions and creams often contain toxic compounds. A few hair dyes contain lead. Selsun Blue shampoo contains selenium that is quite toxic in high doses.

Household lawn and garden chemicals may contain lead, arsenic and other compounds. Mercury treated seeds and arsenic-treated wood are other common sources of toxic metals.

Occupational exposure is important for plumbers, electricians, auto mechanics, printers, ironworkers, office workers and many other occupations. Workers need to wear gloves, masks and take other precautions when handling inks, metals and other toxic materials.

Congenital Toxic Metals. Today, all children are born with some toxic metals acquired in utero. All the toxic metals pass through the placenta from mother to child. This is seen clearly when reviewing mineral analyses of infants, such as that of Chloe, age 4 months, shown in the figure.

 

DETECTING TOXIC METALS

Toxic metals are not easy to detect as they lodge deep within tissues and organs. Serum tests are helpful at times, and not helpful for most chronic exposure. Toxic metals are removed from the blood rapidly and deposited in storage organs and tissues where they will do less damage.

Tissue tests such as hair mineral analysis are therefore more often helpful. The United States Environmental Protection Agency reviewed over 400 reviews of the use of hair for toxic metal detection and concluded that:

Hair is a meaningful and representative tissue for (biological monitoring for) antimony, arsenic, cadmium, chromium, copper, lead, mercury, nickel, vanadium and perhaps selenium and tin.

The author of a study of lead toxicity in Massachusetts school children, Dr. R. Tuthill, concluded:

Scalp hair should be considered a useful clinical and epidemiological approach for the measurement of chronic low-level lead exposure in children.

Skilled interpretation of the hair analysis is required. For example, when aluminum is elevated in the hair, iron and manganese are almost always elevated, but hidden as they do not accumulate in the hair.

Another method of detection is a challenge test in which one takes an injection of a chelating agent such as EDTA or DMPS. Then a 24-hour urine sample is analyzed for toxic metals. This will reveal some metals that are in the arteries, veins and kidneys, but misses most of the others.

No test can detect anywhere near all the toxic metals in the body. Often they are sequestered in hard-to-reach places such as the bones or poorly-perfused fatty tissues. They will be revealed, however, as they are excreted through the hair if one performs repeat hair mineral tests. As a clinician, I must assume everyone has toxic metals and any sound health program needs to be designed to remove them.

 

SYMPTOMS ASSOCIATED WITH TOXIC METALS

For a complete list of symptoms for each toxic metal, see the Reference Guide at the end of this article.

Toxic metals can contribute to any imaginable illness. For example, lead that replaces calcium in the bones can contribute to weakened bones and osteoporosis. Cadmium that replaces zinc in the arteries causes inflammation and hardening of the arteries. Iron that replaces zinc and other minerals in the pancreas, adrenals and elsewhere can contribute to impaired blood sugar tolerance and diabetes. Copper that replaces zinc in the brain is associated with migraine headaches, premenstrual syndrome, depression, anxiety, panic attacks and much more. Mercury and copper that replace selenium in various tissues impairs the conversion of T4 to T3, contributing to thyroid imbalances.

Toxic Metals and Aging. The slow, or not so slow, replacement of vital minerals with toxic metals is an important and neglected cause of aging due to deactivation of enzyme systems and the loss of organ and tissue integrity.

Toxic metal accumulation also feeds on itself. As one's energy production decreases with age, the body is less able to eliminate toxic metals, causing more metal accumulation.

Toxic Metals and Gene Expression. Genetic birth defects may be caused by faulty DNA or by faulty gene expression. Even if one's DNA is perfect, the synthesis of proteins from that DNA can be faulty. For example, zinc is required for a key enzyme in gene expression, RNA transferase. Not surprisingly, zinc deficiency is associated with conditions such as neural tube defects. A recent article in the American Journal of Clinical Nutrition discussed this hidden cause of genetic defects.

"An alternate form of a gene present in greater than 1% of the population is called a polymorphism".

While the article mainly discusses vitamin deficiencies as a cause for genetic defects, it gives the example that "mutations in Cu/Zn superoxide dismutase cause 25% of amyotrophic lateral sclerosis."

 

SOLUTIONS TO TOXIC METAL OVERLOAD

One should not fear toxic metals. They cannot be completely avoided, but one can minimize exposure with careful eating and a healthful lifestyle. Also, our bodies have a lot of evolutionary experience with them and effective mechanisms to eliminate them. These can be supported and enhanced by nutritional and other therapies. The following program, when followed faithfully, will lead to the safe removal of toxic metals.

1. Eat a varied, excellent-quality diet of mineralized foods. The body will absorb and utilize less toxic metals if it receives more preferred minerals. In a 1994 study in the Journal of Clinical Nutrition, food labelled "organic" selected randomly from Chicago food markets had an average of twice the mineral content of standard supermarket food. The famed people of Hunza who lived to 120 years or longer in excellent health drank glacial runoff that was so mineral-rich the water was cloudy.

Especially mineral-rich foods include kelp, sea salt, other sea vegetables, small fish and all root vegetables except potatoes and yams. Root vegetables must be cooked at least 45 minutes for their minerals to be most bio-available.

Adequate protein, especially animal protein, supplies sulphur-containing amino acids which help chelate toxic metals and support liver detoxification pathways.

Other high-sulphur foods include egg yolks and vegetables in the cabbage, radish, garlic and onion families. Sulphur is very helpful for detoxification in general, and for mercury and copper in particular.

Fibre is also helpful to reduce some toxic metals. It reduces bowel transit time, which can limit absorption of toxic metals. Certain fibres such as modified citrus pectin bind some toxic metals that reduces their absorption.

2. Improve Your Lifestyle and Habits of Living. Eat regular, sit-down meals. Also, eat quietly and slowly, and chew thoroughly. This can greatly enhance digestion and absorption of vital minerals. Most everyone needs to take digestive enzymes at least for a while to improve digestion. A relaxed and positive outlook also greatly facilitates digestion.

Sleeping 9 or 10 hours per night is most helpful to eliminate toxic metals. Most people do not sleep nearly enough. Six or seven hours per night is not sufficient for healing and detoxification. These are parasympathetic activities that occur mainly during the hours of sleep and rest.

3. Avoid all extreme or deficient diets. Strict vegetarian diets, for example, are always deficient in zinc and usually in many other essential nutrients. Raw food diets, while higher in some vitamins and other nutrients, are usually much lower in vital minerals. Cooking does not reduce the mineral content of food and usually makes minerals much more bio-available by breaking down fibre. Cooking also concentrates the food so that one ends up ingesting many more vital minerals.

Skipping meals or snacking on the run, eating the same foods every day or living on protein drinks also induce mineral deficiencies. For example, egg or whey protein powder is not a substitute for eating eggs or fresh goat milk. The latter are whole foods that are much richer in many minerals. Food supplements are never a substitute for an excellent diet.

Avoid refined foods such as white sugar, white flour, table salt and white rice. These are almost devoid of vital minerals and will cause the body to absorb and utilize more toxic metals.

4. Take Nutritional Supplements. Supplements can help reduce the absorption of toxic metals and facilitate their removal. Kelp supplements are one of the best. Kelp contains a wide range of vital minerals. It also contains some toxic metals, as do all products from the sea. However, they are tightly bound. Alginates found in kelp also help bind and remove radioactive minerals, another hidden and important health concern related to toxic metals.

One can use antagonists to help eliminate toxic metals. These compete specifically with toxic metals for absorption, transport and utilization in enzyme binding sites and in other tissue structures. For example, zinc and calcium are cadmium antagonists. Selenium and zinc are mercury antagonists.

I worked for a time at the National Institute of Occupational Safety and Heath. We investigated a factory in which workers were fed milk to help avoid lead poisoning. While a bit crude, the principle was sound, as calcium is a lead antagonist.

Specific minerals that most people need to add to their daily diet are more zinc, chromium, selenium and manganese. Most multivitamins do not contain enough. Other supplements that are helpful for toxic metals are N-acetyl cysteine, garlic, chlorella, cilantro extract and other sulphur-containing amino acid supplements. Chlorella, raw garlic, cilantro and NAC have a disadvantage in that they are extremely yin in Chinese medical terminology. This is not helpful for most people. The Life Extension Foundation offers a number of excellent mineral supplements, as well as Only Minerals and Phyto-food.

5. Reduce Airborne Exposure and Skin Contact. Avoid contaminated air as much as possible. City dwellers should use air filters in their homes and offices that can trap toxic metals. Unfortunately, even rural areas can experience pesticide drift, and auto and industrial fumes. If you must handle toxic materials at home or at work, wear gloves, masks and other protective gear.

Read labels carefully on skin care products. Most cosmetics and skin care products are somewhat toxic.

6. Improve your energy. This greatly enhances the body's ability to eliminate toxic metals. Nutritional balancing science using hair analysis is the key to this. It can assess metabolic rate, metabolic type, and exactly which supplements and how much of each are needed. Random supplementation does not work well.

Also, a combination of adequate rest and sleep, excellent diet and a healthful lifestyle are important. When needed, other natural therapies such as chiropractic, body work, energy work and others are also most helpful to restore and maintain an optimum energy level.

7. Improve your eliminative organs. In almost everyone, these do not function optimally. They are congested or sluggish due to glandular imbalances and the burden of toxic substances everyone must cope with. Nutritional support includes milk thistle and dandelion root for the liver, uva ursi and parsley for the kidneys, and fibre, digestive enzymes and other products for the bowel. Other excellent therapies include saunas, coffee enemas, colonic irrigation, massage, skin brushing and others.

Excessive sympathetic nervous system activity inhibits detoxification. Supplementary nutrients that inhibit excessive sympathetic activity include calcium, magnesium, zinc, choline, inositol, GABA, taurine and calming herbs. Other helpful therapies for this purpose include saunas, meditation, tai chi and biofeedback.

Saunas (hot air baths) have been used for thousands of years by many cultures. They are quite safe and very effective for detoxification. The New York Times recently reported on the success of saunas when nothing else was effective for the firemen who became ill at the World Trade Center disaster. Saunas draw blood to the surface, powerfully stimulate circulation and decongest the internal organs. Infrared saunas penetrate more deeply and are often more comfortable as they work at lower temperatures. Note that sweating during exercise is not as effective for detoxification as sweating when one is relaxed in a sauna. The best saunas I have experienced are those powered by infrared heat lamps.

8. Add Chelating Agents. To chelate means to bind to a metal. Certain substances bind tightly to toxic metals and assist their removal. Natural chelators include vitamin C, sulphur-containing amino acids, and some herbs including yellow dock and bugleweed. Molybdenum complexes with copper and is excellent when used sparingly.

Synthetic chelating agents include penicillamine and BAL (British anti-lewisite) for copper and deferoxamine for iron and aluminum. EDTA (ethylene diamine tetra-acetic acid) is a synthetic amino acid that binds to many minerals, toxic and essential. DMPS (sodium salt of 2,3-dimercapto-1-propane sulphonic acid) and DMSA (meso-2,3-dimercaptosuccinic acid) are synthetic agents used for mercury toxicity. Synthetic chelators are drugs that have more side effects, among which is their tendency to remove more good minerals along with the toxic ones. They may also accumulate in the body, along with the toxic metals they bind.

Toxic metals are in a delicate balance with other nutrients. Aggressive use of any chelator can have adverse and sometimes devastating health effects for this reason. This applies to high dose vitamin C, which powerfully lowers copper, and even moreso to the synthetic agents. For example, DMPS can dislodge mercury from fairly safe storage sites. It may then redeposit in more vital organs. It must be used with utmost caution.

Though chelation is the best known method to eliminate toxic metals, in my experience, synthetic chelators are hardly ever needed if one will undertake a complete healing program.

 

CONCLUSION

Toxic metal exposure is higher than ever before and an important cause of ill health. I predict that removing them will become recognized as a great secret for healing many health conditions. Unfortunately, few doctors test for or even consider searching for toxic metals.

Reducing our exposure is the simplest and most cost-effective way to prevent toxic metal problems. Efforts to clean up the water, food and air have advanced greatly, but more needs to be done. Governments can do their part, but the public must also learn about the dangers of toxic metals and how to avoid them. It should be a top priority in the education of the children.

Young men and especially young women can do much to help the next generation and themselves to avoid toxic metals by improving their health before having children. Dr. Weston Price discovered that in many primitive cultures, prenatal care for young women began at puberty by feeding the women special foods designed to maximize their vital mineral intake.

One can greatly enhance the elimination toxic metals by reducing exposure, increasing vital minerals in the diet and avoiding mineral-deficient food. Assisting the eliminative organs, improving digestion, taking appropriate supplements, obtaining plenty of rest and using antagonists and perhaps chelators are also most helpful. The general use of inexpensive, infrared electric light saunas would be another excellent additional way to enhance toxic metal removal. These are excellent health insurance and well worth the effort.

 

SOURCES AND SYMPTOMS OF THE COMMON TOXIC METALS

SOURCES

Aluminum - cookware, beverages in aluminum cans, tap water, table salt, baking powders, antacids, processed cheese, anti-perspirants, bleached flour, antacids, vaccines and other medications and occupational exposure.

Arsenic - pesticides, beer, table salt, tap water, paints, pigments, cosmetics, glass and mirror manufacture, fungicides, insecticides, treated wood and contaminated food.

Beryllium - air pollution (burning fossil fuels), manufacture of plastics, electronics, steel alloys and volcanic ash.

Cadmium - cigarettes, (tobacco and marijuana), processed and refined foods, large fish, shellfish, tap water, auto exhaust, plated containers, galvanized pipes, air pollution from incineration and occupational exposure.

Copper - copper water pipes, copper added to tap water, pesticides, swimming in pools, intra-uterine devices, vegetarian diets, dental amalgams, nutritional supplements - especially prenatal vitamins, birth control pills, weak adrenal glands and occupational exposure.

Lead - tap water, cigarette smoke, hair dyes, paints, inks, glazes, pesticide residues and occupational exposure in battery manufacture and other industries.

Mercury - dental amalgams, large fish, shellfish, medications, air pollution, manufacture of paper, chlorine, adhesives, fabric softeners and waxes.

Nickel - hydrogenated oils (margarine, commercial peanut butter and shortening), shellfish, air pollution, cigarette smoke, plating and occupational exposure.

 

SYMPTOMS

Aluminum - Alzheimer's disease, amyotrophic lateral sclerosis, anaemia and other blood disorders, colic, fatigue, dental caries, dementia dialactica, hypoparathyroidism, kidney and liver dysfunctions, neuromuscular disorders, osteomalacia and Parkinson’s disease.

Arsenic - abdominal pain, abnormal ECG, anorexia, dermatitis, diarrhea, edema, enzyme inhibitor, fever, fluid loss, goiter, hair loss, headache, herpes, impaired healing, interferes with the uptake of folic acid, inhibition of sulphydryl enzyme systems, jaundice, keratosis, kidney and liver damage, muscle spasms, pallor, peripheral neuritis, sore throat, stomatitis, stupor, vasodilation, vertigo, vitiligo and weakness.

Beryllium - adrenal insufficiency, arthritis, bone spurs, bursitis, depression, fatigue, osteoporosis and symptoms of slow metabolism.

Cadmium - hypertension, arthritis, diabetes, anaemia, arteriosclerosis, impaired bone healing, cancer, cardiovascular disease, cirrhosis, reduced fertility, hyperlipidemia, hypoglycemia, headaches, osteoporosis, kidney disease, schizophrenia and strokes.

Copper - acne, adrenal hyperactivity and insufficiency, agorophobia, allergies, hair loss, anaemia, anxiety, arthritis, autism, cancer, chronic candida albicans infection, depression, elevated cholesterol, cystic fibrosis, depression, diabetes, dyslexia, elevated estrogen, failure to thrive, fatigue, fears, fractures of the bones, headaches, heart attacks, hyperactivity, hypertension, hypothyroidism, infections, inflammation, insomnia, iron storage diseases, kidney and liver dysfunctions, decreased libido, multiple sclerosis, nervousness, osteoporosis, panic attacks, premenstrual syndrome, schizophrenia, strokes, tooth decay and vitamin C and other vitamin deficiencies.

Lead - abdominal pain, adrenal insufficiency, anaemia, arthritis, arteriosclerosis, attention deficit, back problems, blindness, cancer, constipation, convulsions, deafness, depression, diabetes, dyslexia, epilepsy, fatigue, gout, impaired glycogen storage, hallucinations, hyperactivity, impotency, infertility, inflammation, kidney dysfunction, learning disabilities, diminished libido, migraine headaches, multiple sclerosis, psychosis, thyroid imbalances and tooth decay.

Mercury - adrenal gland dysfunction, alopecia, anorexia, ataxia, bipolar disorder, birth defects, blushing, depression, dermatitis, discouragement, dizziness, fatigue, headaches, hearing loss, hyperactivity, immune system dysfunction, insomnia, kidney damage, loss of self-control, memory loss, mood swings, nervousness, numbness and tingling, pain in limbs, rashes, excessive salivation, schizophrenia, thyroid dysfunction, timidity, tremors, peripheral vision loss and muscle weakness.

Nickel - cancer (oral and intestinal), depression, heart attacks, hemorrhages, kidney dysfunction, low blood pressure, malaise, muscle tremors and paralysis, nausea, skin problems, tetany and vomiting.

 

REFRENCES

[1] Schroeder, H., Trace elements and Man, The Devin-Adair Company, CT, 1975.

[1] Ibid, p. 154

[1] Braunwald, E. et al, editors, Harrisonπs Principles of Internal Medicine, McGraw-Hill, Professional, 15th edition, 2001.

[1] Pfeiffer, C., Zinc and Other Micronutrients, Keats Publishing, CT, 1978.

[1] Kutsky, R., Handbook of Vitamins, Minerals and Hormones, 2nd edition, Van Nostrand Reinhold Company, NY, 1981.

[1] Ibid., Schroeder, H., Trace Elements and Man.

[1] Hall, R.H., Food For Naught, The Decline in Nutrition, Vintage Books, NY, 1974.

[1] Anderson, M. and Jensen, B. Empty Harvest; Understanding the Link Between Our Food, Our Immunity and Our Planet, Avery Penguin Putnam, 1993.

[1] Price, W., Nutrition and Physical Degeneration, Price-Pottenger Nutrition Foundation, CA, 1949.

[1] Stannard, J., Shim, Y.S., Kritsineli, M., Labropoulo, P.,Tsamtsouris, A., Fluoride levels and fluoride contamination of fruit juices, J Clin Ped Dentistry, 1991;16(1).

[1] From the warning label on hydrofluosilicic acid, Cargill Corporation, FL.

[1] Casdorph, H.R. and Walker, M., Toxic Metal Syndrome, Avery Publishing, NY, 1995.

[1] National Autism Association, Press Release, Feb. 9, 2004.

[1] Eck, P. and Wilson, L., Toxic Metals in Human Health and Disease, Eck Institute of Applied Nutrition and Bioenergetics, Ltd., AZ, 1989, p. xiv.

[1] Shamberger, R.J., Validity of hair mineral testing, Bio Trace Element Res, 2002, 87:1-28.

[1] Muir, M., Current controversies in the diagnosis and treatment of heavy metal toxicity, Alternative and Comp Ther., June 1997:170-178.

[1] Environmental Protection Agency, Research and Development, Toxic Trace Metals in Human and Mammalian Hair, EPA-600, 4.79-049, August 1979, p. 3.

[1] Tuthill, R., Hair lead levels related to childrenπs classroom attention-deficit behavior, Arch Env Health, 1996, 51(3)214-220.

[1] Ames, BN, Elson-Schwab, I., Silver, EA, High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity: relevance to genetic disease and polymorphisms, Am J Clin Nut. April 2002;75(4):616-658.

[1] 1993, J Applied Nut, 45(1).

[1] Mortensen, M.E. and Watson, P., Chelation therapy for childhood lead poisoning: The changing scene in the 1990s, Clin Ped., 1993;32:284-291.

[1] Committee on Drugs, American Academy of Pediatrics Treatment guidelines for lead exposure in children, Pediatrics, 1995, 96:155-159.

Dr. Lawrence Wilson specializes in mineral analysis and the removal of toxic metals, and has done so for 23 years. He consults for Analytical Research Laboratories, a mineral testing facility, where he apprenticed for 14 years with a brilliant biochemist, Dr. Paul C. Eck. He wrote a text about his work, Nutritional Balancing and Hair Mineral Analysis.

He has reviewed some 15,000 hair mineral analyses and followed some 5000 patients as they removed their toxic metals and balanced their minerals. He has also experimented extensively with sauna therapy, an emerging treatment modality for toxic metal removal.

Dr. Lawrence Wilson

P.O. Box 54

Prescott, AZ 86302-0054

              (928) 445-7690      

 

Visit http://www.drlwilson.com/ for books, and audio tapes from Dr. Wilson.

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Causes of Parkinson's Disease - LRRK2 Gene

Genia Brin’s Double Parkinson’s Mutation

Copied from The Northwest Parkinson’s Foundation Weekly News Update

Nadine Epstein

Moment - Eugenia Brin was 48 when she first noticed that her left leg was dragging. It took two years for doctors finally to diagnose her with early onset Parkinson’s disease, because she didn’t have tremors or other easily identifiable symptoms. The diminutive Brin, trained as an applied mathematician in the Soviet Union and then working as a meteorological analyst at NASA’s Goddard Space Flight Center in Maryland, knew there was no cure for the degenerative disorder of the central nervous system, which affects about one in every 250 people over 40 and more than one in 100 in people over 65. All she could do was work with her physicians to find the right combination of drugs and dosages to help relieve the symptoms—at least temporarily.

In 2008, she was tested through 23andMe, a start-up launched by Anne Wojcicki, who is married to Brin’s eldest son, Sergey, a co-founder of Google. Among the variants the company’s basic consumer package tests for is a mutation on the LRRK2 gene that can lead to Parkinson’s, because, says Wojcicki, “our scientists recognized that LRRK2 was an important finding.” While visiting California, Brin, known to friends and family as Genia, provided a DNA sample. “Our family was one of the first to be tested,” she says. “We were trying it out.” The result was completely unexpected: She had the mutation on not one but both LRRK2 genes. “When I got the results I thought ‘that’s why,’” she recalls. “There was some sense of relief to know there was a reason behind the illness.”

Parknson’s doesn’t only strike Jews, but it does have a Jewish connection. Ashkenazi Jews such as Brin, says Susan Bressman, chair of the department of neurology at Beth Israel Medical Center in New York City and professor of neurology at Albert Einstein College of Medicine, do not develop Parkinson’s at a higher rate than any other group, but they are more likely to carry the LRRK2 mutation, the most common of the six or so mutations that cause increased incidence of the disease. “Two to five percent of Parkinson’s worldwide is due to LRRK2,” she says. “If you look at Ashkenazi Jews, 15 percent of Parkinson’s is due to LRRK2.” She stresses that the mutation does not necessarily mean someone will develop Parkinson’s; a variety of environmental factors are also thought to play a role. “All we can say for sure is that LRRK2 mutation as a cause is more prevalent in people who have Parkinson’s,” she says. “We don’t know why 30 percent of LRRK2 mutation carriers get the disease.” Nor does the absence of the mutation guarantee not developing the disease: The vast majority of the millions of people who suffer from Parkinson’s worldwide do not have a known mutation.

Everyone has two copies of the LRRK2 gene, but it is unlikely that one, let alone both, will have the mutation, says Neil Risch, director of the Institute for Human Genetics at the University of California, San Francisco. “It’s really rare, probably in the ballpark of one in 20,000 or 40,000.” While the double copy doesn’t make Brin’s symptoms worse or affect her treatment plan, “the big downside is that it means both of her kids have a copy,” Risch says. “Usually they’d have a 50-50 chance but if a parent has two mutations it is 100 percent.” As a result, both Sergey, 38, and Brin’s younger son Sam, 25, each have a single copy.

The Parkinson’s Institute in Sunnyvale, CA, asked the Brins to donate skin cells to a lab at Stanford University. Researchers there were most interested in Genia’s cells, which they used to create induced pluripotent stem cells that can reproduce themselves, says bioengineer and stem cell biologist Blake Byers, who directs this research at Stanford and wrote his doctoral dissertation on it. “This is the only homozygous mutant [double gene mutation] line that we have in our lab,” he says. “It is valuable because we know it contains a Parkinson’s-inducing factor unlike lines of other genetic backgrounds, where the initiation of Parkinson’s might require an environmental trigger.”

Byers and others then successfully grew the stem cells into mature neurons that secreted dopamine and generated normal neural signaling. They sped up the progression of Parkinson’s—which usually takes about 50 years in the human body—by subjecting the neurons to stress until they exhibited the telltale signs of the disease: the elevated levels of proteins that are thought to clog and kill the cells, halting necessary dopamine production. “It was the first time we were able to investigate what Parkinson’s neurons look like when they are alive for more than a few days, then watch them get sick and die,” says Byers. By comparing these neurons to healthy ones taken from a control group, the researchers were able to understand how the diseased cells behaved. “The paper we wrote on Genia’s genes shows increased accumulation of alpha-synuclein protein and increased oxidated stress levels and increased susceptibility to oxidated stress induced cell death,” says Byers. The next step is to bombard the neurons with drugs that may prevent or cure the disease, he says, adding that additional research results will be published in about six months.

“Genia’s genes were very instrumental for doing this work,” says Byers, explaining that usually researchers don’t know the identity of the person whose genes they are studying but that in this case, the family went public with the information. “I wanted to disclose it to put a face on a scientific finding for the reading audience to bring more attention to Parkinson’s,” explains Brin.

Brin’s Parkinson’s has progressed slowly but has begun to make everyday tasks more difficult, especially when she is tired or stressed. Nevertheless, she pushes herself to live normally, continuing to travel, ski and serve on the Michael J. Fox Foundation for Parkinson’s Research Patient Council. Meanwhile, her sons have shown no signs of developing the disease. Sam exercises regularly, and Sergey follows the regimen of others at increased risk: In addition to exercising, he drinks caffeine and takes good care of his immune system, says Byers, adding that he does not smoke, even though smoking has also been found to help stave off the development of the disease.

Sergey underwrote 23andMe’s Parkinson’s Disease Genetics Initiative, which provides free testing to people who suffer from Parkinson’s in the hopes of learning more about the disease and someday finding a cure. Says Byers: “The reality is, unfortunately, that most Parkinson’s patients don’t get tested,” adding that if Genia Brin’s homozygous cell line had not been discovered, it would have taken far longer for researchers to learn what they now know about the disease.


Causes of Parkinson's Disease - Dry Cleaning & Parkinson's Risk

 

Dry cleaning and Parkinson's risk

Copied from The Northwest Parkinson’s Foundation Weekly News Update

06/17/2010

Trichloroethylene (TCE), a chemical used in commercial may increase risk of getting Parkinson's disease. This population based study was presented at the American Academy of neurology Annual Meetin in Spring 2010.

Dr. Goldman from the Parkinson's Institute looked at 99 pairs of twins (half were identical twins) in which one of the pair had Parkinson's disease. Men exposed that worked with TCE for more than 2 years had over a 6 times increase in risk.

TCE is a chemical used in the dry cleaning industry. Fortunately it is being phased out of use. It is important to note that the increased of risk in the study above was associated with chronic occupational exposure (over 2 years) and not casual use of dry cleaning services.

Dry cleaning is not dry but uses solvents to clean clothes and dissolve stains. Organic dry cleaning options are available but consumer beware. Some dry cleaning store fronts that advertise organic or 'green' are still using organic solvents.

If you wish to find a different method for your dry clean only clothes, look for the 'wet method' or carbon dioxide method as an alternative method to clean your clothes.

Author: Monique Giroux, MD

 

 

 

Causes of Parkinson's Disease - Pesticides Can Trigger or Cause Pd

 

Pesticides can trigger Parkinson's disease

Copied from The Northwest Parkinson’s Foundation Weekly News Update

Researchers at Dresden's university clinic have found pesticides can trigger the degenerative nerve disorder Parkinson's disease.

thelocal.de - Publishing their findings in the journal "Nature Scientific Reports," the scientists showed how the poison rotenone caused and exacerbated Parkinson's.

The disease causes deterioration of a person's central nervous system, which results in rigid muscles, a mask-like facial expression and uncontrollable shaking. Primarily affecting the elderly, Parkinson's symptoms occur when the brain's nerve cells producing the neurotransmitter dopamine die.

Although it has long been suspected that external factors could cause Parkinson's, the latest research shows that agricultural workers frequently exposed to pesticides develop the disease more often than people with less experience of the chemicals.

The scientists also discovered that rotenone given to mice produced a protein in their intestinal tract that destroyed brain cells.

"If this can also be confirmed in Parkinson's patients, we will have taken an important step towards new strategies for diagnose and treatment," said Francisco Pan-Montojo, the director of the Dresden Institute for Anatomy


 

How Pesticides Can Cause Parkinson's

Copied from The Northwest Parkinson’s Foundation, Weekly News Update

Foreign chemicals may prevent the brain from disposing of its own toxic waste
Melinda Wenner Moyer

Scientific American - Many studies over the past decade have pointed to pesticides as a potential cause of Parkinson's disease, a neurodegenerative condition that impairs motor function and afflicts a million Americans. Yet scientists have not had a good idea of how these chemicals harm the brain. A recent study suggests a possible answer: pesticides may inhibit a biochemical pathway that normally protects dopaminergic neurons, the brain cells selectively attacked by the disease. Preliminary research also indicates that this pathway plays a role in Parkinson's even when pesticides are not involved, providing an exciting new target for drug development.

Past studies have shown that a pesticide called benomyl, which lingers in the environment despite having been banned in the U.S. in 2001 because of health concerns, inhibits the chemical activity of aldehyde dehydrogenase (ALDH) in the liver. Researchers at the University of California, Los Angeles, U.C. Berkeley, the California Institute of Technology and the Greater Los Angeles Veterans Affairs Medical Center wondered whether the pesticide might also affect levels of ALDH in the brain. ALDH's job is to break down DOPAL, a naturally forming toxic chemical, rendering it harmless.

To find out, the researchers exposed different types of human brain cells—and, later, whole zebra fish—to benomyl. They found that it “killed almost half of the dopamine neurons while leaving all other neurons tested intact,” according to lead author and U.C.L.A. neurologist Jeff Bronstein. When they zeroed in on the affected cells, they confirmed that the benomyl was indeed inhibiting the activity of ALDH, which in turn spurred the toxic accumulation of DOPAL. Interestingly, when the scientists lowered DOPAL levels using a different technique, benomyl did not harm the dopamine neurons, a finding that suggests that the pesticide kills these neurons specifically because it allows DOPAL to build up.

Because other pesticides also inhibit ALDH activity, Bronstein speculates that this pathway could help explain the link between Parkinson's and pesticides in general. What is more, research has identified high DOPAL activity in the brain of Parkinson's patients who have not been highly exposed to pesticides, so it is possible that this biochemical cascade is involved in the disease process regardless of its cause. If that is true, then drugs that block or clear DOPAL from the brain could prove to be promising treatments for Parkinson's.

 

Causes of Parkinson's Disease - Key Player in Pd Triggered Neuron Loss Pinpointed

 

Key player in Parkinson’s disease triggered neuron loss pinpointed

Copied from The Northwest Parkinson’s Foundation Weekly News Update


ZeeNews.com - London: By reprogramming skin cells from Parkinson’s patients with a known genetic mutation, researchers have identified the damage to neural stem cells as a powerful player in the disease.

The scientists from the Salk Institute for Biological Studies found that a common mutation to a gene that produce the enzyme LRRK2, which is responsible for both familial and sporadic cases of Parkinson’s disease, deforms the membrane surrounding the nucleus of a neural stem cell.

Damaging the nuclear architecture leads to destruction of these powerful cells, as well as their decreased ability to spawn functional neurons, such as the ones that respond to dopamine.

The researchers checked their laboratory findings with brain samples from Parkinson’s disease patients and found the same nuclear envelope impairment.

“This discovery helps explain how Parkinson’s disease, which has been traditionally associated with loss of neurons that produce dopamine and subsequent motor impairment, could lead to locomotor dysfunction and other common non-motor manifestations, such as depression and anxiety,” Juan Carlos Izpisua Belmonte, lead researcher of the study, said.

“Similarly, current clinical trials explore the possibility of neural stem cell transplantation to compensate for dopamine deficits. Our work provides the platform for similar trials by using patient-specific corrected cells. It identifies degeneration of the nucleus as a previously unknown player in Parkinson’s,” Belmonte said.

Although the researchers say that they don’t yet know whether these nuclear aberrations cause Parkinson’s disease or are a consequence of it, they say the discovery could offer clues about potential new therapeutic approaches.

For example, they were able to use targeted gene-editing technologies to correct the mutation in patient’s nuclear stem cells. This genetic correction repaired the disorganization of the nuclear envelope, and improved overall survival and functioning of the neural stem cells.

They were also able to chemically inhibit damage to the nucleus, producing the same results seen with genetic correction.

“This opens the door for drug treatment of Parkinson’s disease patients who have this genetic mutation,” Belmonte said.

Belmonte added that the new finding may also help clinicians better diagnose this form of Parkinson’s disease.

“Due to the striking appearance in patient samples, nuclear deformation parameters could add to the pool of diagnostic features for Parkinson’s disease,” he added.

The study has been published online in Nature.


Causes of Parkinson's Disease - Head Injuriy, Pesticides Tied to Pd

 

Head injury, pesticides tied to Parkinson's disease

Copied from The Northwest Parkinson’s Foundation Weekly News Update

Genevra Pittman

reuters.com - The combination of a past serious head injury and pesticide exposure may be linked to an extra-high risk of developing Parkinson's disease, a new study suggests.

The findings don't prove being knocked unconscious or exposed to certain chemicals directly causes Parkinson's, a chronic movement and coordination disorder.

But they are in line with previous studies, which have linked head trauma and certain toxins - along with family history and other environmental exposures - to the disease.

"I think all of us are beginning to realize that there's not one smoking gun that causes Parkinson's disease," said Dr. James Bower, a neurologist from the Mayo Clinic in Rochester, Minnesota who wasn't involved in the new research.

"There might be many paths to the ultimate development of Parkinson's disease," he told Reuters Health.

For example, Bower said, some people who are genetically predisposed might need just one "environmental insult" - such as a blow to the head - to set them up for Parkinson's. Others who aren't naturally susceptible to the disorder could still develop it after multiple exposures.

Head trauma and contact with pesticides "may not be directly related, and may be two independent stresses," Columbia University neurologist David Sulzer, who also wasn't part of the study team, told Reuters Health in an email.

About 50,000 to 60,000 older adults in the U.S. are diagnosed with Parkinson's disease each year, according to the National Parkinson Foundation.

For the new study, researchers led by Pei-Chen Lee from the University of California at Los Angeles compared 357 people with a recent Parkinson's diagnosis to a representative sample of 754 people without the disease, all living in central California, which is a major agricultural region.

The study team asked all of them to report any past traumatic head injuries - in which people had been unconscious for at least five minutes - and used their home and work addresses to determine their proximity to pesticide sprayings since 1974.

Those surveys showed that close to 12 percent of people with Parkinson's had been knocked unconscious, and 47 percent had been exposed to an herbicide called paraquat near both their home and workplace.

That's in comparison to almost seven percent of control-group participants with a history of head injury and 39 percent with pesticide exposure.

On their own, traumatic brain injury as well as living and working near pesticide sprayings were each tied to a moderately increased risk of Parkinson's disease. Combined, they were linked to a tripling of that risk, the researchers reported Monday in the journal Neurology. That was after taking into account people's baseline risk based on their age, gender, race, education, smoking history and family history of Parkinson's.

Lee's team didn't know which came first in people who'd had both head trauma and paraquat exposure.

It makes sense, the researchers noted, that a head injury would increase inflammation in the brain and disrupt the barrier that separates circulating blood and brain fluid. Those changes could then make neurons in the brain more vulnerable to the effects of pesticides, ultimately increasing the risk of Parkinson's.

But that's just a theory.

"There are all kinds of hypotheses," Bower said. But the study "is more evidence that traumatic injury to the brain can lead to later problems that are usually neurodegenerative," he added. "We need to be increasingly careful about preventing these traumatic brain injuries."

SOURCE: bit.ly/TD3OA9 Neurology, online November 12, 2012.


 

Causes of Parkinson's Disease - Agent Orange

 

Despite knowing Agent Orange, Parkinson’s link some veterans still have questions

Copied from The Northwest Parkinson’s Foundation Weekly News Update

wuft news - Jon Anderson can’t run like he used to.

The 66-year-old Vietnam veteran has been running marathons since 1976 and ultra marathons since 2003.

But in 2008, Anderson stopped running, four years after he was diagnosed with Parkinson’s disease.

“Probably running one mile would be very difficult for me now,” he said.

Anderson said for the past eight years, he saw the disease slowly outrun his body and affecting the way he walks.

“I kind of do more of a shuffle and that’s really difficult because you have to will your legs to move,” he said. “Just moving your legs normally, you don’t think about it you just move your legs from point A to point B . . . but for me, and people with Parkinson’s disease it’s an arduous process just to walk sometimes.”

Anderson said he questioned why he had Parkinson’s disease and decided to check with doctors for help.

“I didn’t find out anything that linked it at the time,” he said.

Anderson said he called the Department of Veteran Affairs and asked what kind of treatment he should undergo following his diagnosis.

The department told him his diagnosis was not considered a service-connected disability, Anderson said.

In 2009, the department announced that veterans with Parkinson’s disease who were exposed to Agent Orange during military service may be eligible for disability compensation and health care.

Agent Orange is a herbicide used during the Vietnam War to kill plants in war zones, which made finding hidden enemy soldiers easier.

Although Agent Orange may have been useful in the war, the herbicide is said to be the cause of many health problems for veterans, which includes Parkinson’s disease.

“I’m not doing as well now,” Anderson said. “So now, I’m developing more of an attitude toward Agent Orange and Parkinson’s disease.”

Dr. Irene Malaty, a medical doctor from Shands at University of Florida, said the news brings a relief to veterans with the disease.

“In a sense, there’s a big victory for those who have Parkinson’s diesease because they no longer have to exactly prove that that exposure caused it, and that it’s probable that it did cause it,” she said.

Chris Alcantara wrote and edited this story online.

Note by John Pepper:

Phosphates and possibly other chemicals used in crop spraying have been linked in the past to Pd.

 

 

 

Causes of Parkiinson's Disease - Oxidative Stress

 

An underlying cause of Parkinson’s Disease

Copied from The Northwest Parkinson’s Foundation Weekly News Update

Oxidative stress is no longer a prime candidate for the development of Parkinson’s disease, suggests a recent study at the University of York Biology department.
Ashley Ferro

Theyourker.co.uk - Parkinson’s disease results from the progressive degeneration of specific neurons in the substantia nigra pars compacta, a region of the midbrain which modulates synaptic activity in the basal ganglion. The complex wiring between regions of the basal ganglion is essential for the regulation of motor activity. Disrupting this interaction through degeneration of the dopamine neurons which modulate this system consequently results in the characteristic motor impairments observed in Parkinson’s patients, predominantly resting tremor, rigidity, and bradykinesia (slow movement). The mechanisms underpinning this neuronal cell death in the substantia nigra have remained highly elusive, and oxidative stress has been a serious contender for this role for quite some time.

Undergraduate biology students at the University of York worked as part of the team to exploit the powerful model system of juvenile Drosophila melanogaster (fruit fly) and an understanding of Mendelian genetics to study the influence of knocking-out the Juvenile Parkinson’s-related gene parkin on neuronal characteristics, metabolism and movement.

The juvenile Drosophila system faithfully models progression of the disease in humans, thus allowing direct and highly translatable study of the neurophysiological defects which lead to locomotor impairment. Knocking-out (deactivating) the parkin gene in Drosophila influenced energy metabolism, neuronal resting potential, synaptic development, and kinesis. More specifically, ATP (the universal cellular energy currency) synthesis and oxygen consumption were significantly reduced, and elevated levels of reactive oxygen species were observed. These physiological and metabolic changes suggest that mutations in parkin results in a neuronal energy deficit which underpins bradykinesia.

Current concepts on the development and pathogenesis of Parkinson’s disease focus heavily on the involvement of oxidative stress in inducing cell death in the substantia nigra. Although experimental evidence exists to demonstrate the vulnerability of dopamine neurons to damage by reactive oxygen species, it has remained unclear as to whether the oxidative stress is a consequence of the disease or initially causes the disease. To definitively elucidate the role of oxidative stress in causing the neurophysiological defects observed by mutating the parkin gene, the parkin mutants were initially treated with ‘reactive oxygen species scavengers’, antioxidants which either donate an electron or remove an electron from the reactive species to neutralise their effects on the cell. Surprisingly, introducing scavengers did not restore the resting membrane potential of the neurons or affect the locomotor defects of the mutant juvenile Drosophila, thus suggesting that these defects derive from causes other than oxidative damage.

The wild-type parkin gene was then exploited as a ‘transgene’, and was over-expressed in a parkin mutant to confirm the energetic cause for bradykinesia. Introduction of the wild-type gene entirely restored wild-type functionality. The finding conclusively demonstrates that oxidative stress occurs downstream in the pathology of Parkinson’s disease and cannot therefore be the underlying cause, but simply a product of the neurodegenerative process.

This is the first time the interaction between central nervous system deficits and bradykinesia has been experimentally demonstrated, a relationship which has merely been inferred by previous studies within the field. This demonstration, and the conclusion that metabolic impairment of neurons rather than oxidative stress induces the neuronal damage leading to locomotor disorders, marks a considerable benchmark in our understanding of Parkinson’s disease . Dr Chris Elliott, who led the study, explains the next direction of Parkinson’s research in the deparment, "Our next step will be to test a range of drugs which are known to relieve oxidative stress in cells, to test if they - like the transgenes - don't rescue the parkin locomotion defects." Identification of drugs which can reduce oxidative stress in the neurons responsible for modulating interactions in the basal ganglion may have considerable implications for Parkinson’s treatments in the future. The quality and impact of this research pays tribute to the abilities of the students and academics at the York Biology department.

References Vincent, A., Briggs, L., Chatwin, G., Emery, E., Tomlins, R., Oswald, M., Middleton, A., Evans, G., Sweeney, S. and Elliott, C. (2012) parkin-induced defects in neurophysiology and locomotion are generated by metabolic dysfunction and not oxidative stress. Human Molecular Genetics, 1-10.

http://www.theyorker.co.uk/lifestyle/scienceand%20technology/12300

 

Causes of Parkinson's Disease - Roundup

 

Roundup, An Herbicide, Could Be Linked To Parkinson's, Cancer And Other Health Issues, Study Shows

 

Copied from The Northwest Parkinson’s Foundation Weekly Update


Huffington Post - Heavy use of the world's most popular herbicide, Roundup, could be linked to a range of health problems and diseases, including Parkinson's, infertility and cancers, according to a new study.

The peer-reviewed report, published last week in the scientific journal Entropy, said evidence indicates that residues of "glyphosate," the chief ingredient in Roundup weed killer, which is sprayed over millions of acres of crops, has been found in food.

Those residues enhance the damaging effects of other food-borne chemical residues and toxins in the environment to disrupt normal body functions and induce disease, according to the report, authored by Stephanie Seneff, a research scientist at the Massachusetts Institute of Technology, and Anthony Samsel, a retired science consultant from Arthur D. Little, Inc. Samsel is a former private environmental government contractor as well as a member of the Union of Concerned Scientists.

"Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body," the study says.

We "have hit upon something very important that needs to be taken seriously and further investigated," Seneff said.

Environmentalists, consumer groups and plant scientists from several countries have warned that heavy use of glyphosate is causing problems for plants, people and animals.

The EPA is conducting a standard registration review of glyphosate and has set a deadline of 2015 for determining if glyphosate use should be limited. The study is among many comments submitted to the agency.

Monsanto is the developer of both Roundup herbicide and a suite of crops that are genetically altered to withstand being sprayed with the Roundup weed killer.

These biotech crops, including corn, soybeans, canola and sugarbeets, are planted on millions of acres in the United States annually. Farmers like them because they can spray Roundup weed killer directly on the crops to kill weeds in the fields without harming the crops.

Roundup is also popularly used on lawns, gardens and golf courses.

Monsanto and other leading industry experts have said for years that glyphosate is proven safe, and has a less damaging impact on the environment than other commonly used chemicals.

Jerry Steiner, Monsanto's executive vice president of sustainability, reiterated that in a recent interview when questioned about the study.

"We are very confident in the long track record that glyphosate has. It has been very, very extensively studied," he said.

Of the more than two dozen top herbicides on the market, glyphosate is the most popular. In 2007, as much as 185 million pounds of glyphosate was used by U.S. farmers, double the amount used six years ago, according to Environmental Protection Agency (EPA) data.

Causes of Parkinson's Disease - Clean-up Snafu

 

Scientists Identify 'Clean-Up' Snafu That Kills Brain Cells in Parkinson's Disease

Copied from The Northwest Parkinson’s Foundation Weekly News Update


sciencedaily.com - Researchers at Albert Einstein College of Medicine of Yeshiva University have discovered how the most common genetic mutations in familial Parkinson's disease damage brain cells. The study, which published online today in the journal Nature Neuroscience, could also open up treatment possibilities for both familial Parkinson's and the more common form of Parkinson's that is not inherited.

Parkinson's disease is a gradually progressing disorder of the nervous system that causes stiffness or slowing of movement. According to the Parkinson's Disease Foundation, as many as one million Americans are living with the disease.

The most common mutations responsible for the familial form of Parkinson's disease affect a gene called leucine-rich repeat kinase-2 (LRRK2). The mutations cause the LRRK2 gene to code for abnormal versions of the LRRK2 protein. But it hasn't been clear how LRRK2 mutations lead to the defining microscopic sign of Parkinson's: the formation of abnormal protein aggregates inside dopamine-producing nerve cells of the brain.

"Our study found that abnormal forms of LRRK2 protein disrupt an important garbage-disposal process in cells that normally digests and recycles unwanted proteins including one called alpha-synuclein -- the main component of those protein aggregates that gunk up nerve cells in Parkinson's patients," said study leader Ana Maria Cuervo, M.D., Ph.D., professor of developmental and molecular biology, of anatomy and structural biology, and of medicine and the Robert and Renee Belfer Chair for the Study of Neurodegenerative Diseases at Einstein.

The name for the disrupted disposal process is chaperone-mediated autophagy (the word "autophagy" literally means "self-eating"). It involves specialized molecules that "guide" old and damaged proteins to enzyme-filled structures called lysosomes; there the proteins are digested into amino acids, which are then recycled within the cell.

"We showed that when LRRK2 inhibits chaperone-mediated autophagy, alpha-synuclein doesn't get broken down and instead accumulates to toxic levels in nerve cells," said Dr. Cuervo.

The study involved mouse neurons in tissue culture from four different animal models, neurons from the brains of patients with Parkinson's with LRRK2 mutations, and neurons derived from the skin cells of Parkinson's patients via induced pluripotent stem (iPS) cell technology. All the lines of research confirmed the researchers' discovery.

"We're now looking at ways to enhance the activity of this recycling system to see if we can prevent or delay neuronal death and disease," said Dr. Cuervo. "We've started to analyze some chemical compounds that look very promising."

Dr. Cuervo hopes that such treatments could help patients with familial as well as nonfamilial Parkinson's -- the predominant form of the disease that also involves the buildup of alpha-synuclein.

Dr. Cuervo is credited with discovering chaperone-mediated autophagy. She has published extensively on autophagy and its role in numerous diseases, such as Huntington's disease, and its role in age-related conditions, including organ decline and weakened immunity. Dr. Cuervo is co-director of Einstein's Institute of Aging Research.

The paper is titled "Interplay of LRRK2 with chaperone-mediated autophagy." In addition to Dr. Cuervo, other Einstein contributors include Samantha J. Orenstein, a graduate student who performed most of this study as part of her Ph.D. thesis; Inmaculada Tasset, Ph.D.; Esperanza Arias, Ph.D.; and Hiroshi Koga, Ph.D., all members of Dr. Cuervo's group. Additional co-authors are: Sheng-Hang Kuo Ph.D., David Sulzer Ph.D., Etty Cortes, M.D., and Lawrence S. Honig, M.D. (Columbia University, NY); William Dauer, M.D., (University of Michigan, Ann Arbor, MI); Irene Fernandez-Carasa and Antonella Consiglio, Ph.D., (University of Barcelona, Barcelona Spain); and Angel Raya, M.D., Ph.D., (Institucio Catalana de Recerca I Estudies Avancas, Barcelona, Spain).

This work was supported by grants from the National Institute on Aging (AG031782 and AG08702), the National Institute of Neurological Disorders and Stroke Udall Center of Excellence both part of the National Institutes of Health; The Rainwaters Foundation, The Beatrice and Roy Backus Foundation, JPB Foundation; Parkinson's Disease Foundation; Fondazione Guido Berlucchi; Centers for Networked Biomedical Research; Ministry of Economy and Competitiveness; a Hirschl/Weill-Caulier Career Scientist Award; and a gift from Robert and Renee Belfer
.


 

Causes of Parkinson's Disease - Triggers?

 

What Triggers Parkinson's Disease?

Copied from The Northwest Parkinson’s Foundation Weekly News Update

 

Elaine Benton

Huffington Post - What causes Parkinson's? A frequently asked question, to which there is not yet a definitive answer. It is clear however, that some forms are hereditary, such as my case. Knowing your family medical history can be of great help, particularly when participating in clinical trials. In my family, several of us are unfortunate enough to have Gaucher disease AND Parkinson's - how lucky can you get?! A lot can be said for having good DNA! Other Parkinson's sufferers have no other members affected in their immediate family, so in these instances one would assume it is not hereditary. The question of environment has been raised many times, as to whether chemicals, pesticides, artificial additives in the food we eat - are contributing factors and ultimately responsible?

I have my own theory - call it a gut feeling or an inner voice, but invariably I follow my instincts. After having surgery on my right hip six years ago, I rapidly began to feel shaking in my left leg. Initially I thought it was merely weak leg muscles after being bedridden for many days, and barely able to walk, my thigh muscles were withered which did not aid a quick recovery. As the days went by, the shaking got worse, and spread to my left arm. It was at this point, that I had a gut feeling, knowing my family's medical history, that I may have the beginnings of Parkinson's. and it took just three months to confirm the diagnosis. Other indications quickly followed, and I was soon introduced to an array of unpleasant symptoms that manifest in this debilitating degenerative disease, and today I am not in the best of health.

Through my daily blog and writing for The Huffington Post UK I have come into contact with many fellow sufferers. There appears to be a common thread amongst some of us. Many with similar stories to my own, having had operations, found soon after surgery, that Parkinson's reared its ugly head. Knowing how stress and anxiety along with physical exhaustion can exacerbate Parkinson's at an alarming speed, this begs the question; if one was prone to get Parkinson's, could it be the extreme shock from the surgery itself to one's system, or the anaesthetic that "triggers" Parkinson's?

I'm not saying for one moment that I wouldn't have developed Parkinson's had I not had the hip surgery, for I am quite sure, that in my particular case, even without surgery, Parkinson's would have appeared at some point, just perhaps a little later on in my life. Maybe those who have the propensity towards Parkinson's could be prevented from suffering this disease if the trigger was determined. I don't know what or if any studies have been done regarding this train of thought. I would be interested to hear from any other patients who have similar stories, or from anyone who is doing research on this specific topic.

I'm all in favour of clinical trials, and have happily participated in quite a few. I view this involvement an important contribution that a patient can make. Hopefully someone somewhere will find what trigger's Parkinson's, solving the puzzle and a cure which millions around the world are waiting for will be found. I am the eternal optimist and wait in hope!

Website: http://www.elainebenton.net/


 

Causes of Parkinson's Disease - Alpha-synuclein

 

Overexpression of alpha-synuclein can cause Parkinson's

Copied from The Northwest Parkinson’s Foundation Weekly News Update


www.news-medical.net - Researchers at the University of California, San Diego School of Medicine say overexpression of a protein called alpha-synuclein appears to disrupt vital recycling processes in neurons, starting with the terminal extensions of neurons and working its way back to the cells' center, with the potential consequence of progressive degeneration and eventual cell death.

The findings, published in the February 6, 2013 issue of The Journal of Neuroscience, have major implications for more fully understanding the causes and mechanisms of Parkinson's disease (PD), a neurodegenerative movement disorder that affects an estimated one million Americans.

"This is an important new insight. I don't think anybody realized just how big a role alpha-synuclein played in managing the retrieval of worn-out proteins from synapses and the role of alterations in this process in development of PD," said principal investigator Mark H. Ellisman, PhD, professor of neurosciences and bioengineering and director of the National Center for Microscopy and Imaging Research (NCMIR), based at UC San Diego.

Parkinson's disease is characterized by the gradual destruction of select brain cells that produce dopamine, a neurotransmitter involved in regulating movement and emotion. Symptoms include increasing loss of muscle and movement control. While most cases are sporadic - that is, their causes are unknown - there are also inherited forms of PD linked to specific gene mutations and modifications.

The UC San Diego researchers, with colleagues at the University of Illinois, Urbana, focused upon one of those gene products: alpha-synuclein. Using a variety of leading-edge imaging technologies, including a new fluorescent tagging technique developed for electron microscopy by UC San Diego Nobel laureate Roger Tsien's lab and colleagues at NCMIR, the scientists created three-dimensional maps of alpha-synuclein distribution both in cultured neurons and in the neurons of mice engineered to over-express the human protein.

They found that excess levels of alpha-synuclein accumulated in the presynaptic terminal - part of the junction where axons and dendrites of brain cells meet to exchange chemical signals.

"The over-expression of alpha-synuclein caused hypertrophy in these terminals," said Daniela Boassa, PhD, a research scientist at NCMIR and the study's first author. "The terminals were enlarged, filled with structures we normally don't see."

Boassa said that as alpha-synuclein accumulates in the terminals, it appears to hinder normal degradation and recycling processes in neurons. This would progressively impair the release of neurotransmitters. In time, the neurons might simply stop functioning and die.

"Other studies have noted that PD is characterized by progressive loss of vesicle traffic, and neurotransmitter release," Boassa said. "Our study provides a structural and mechanistic explanation for why that happens."

Boassa said the findings shed greater light upon how PD is caused, at least in some heritable forms. Researchers plan to now probe more deeply into how the disease is propagated and how dysfunctional alpha-synuclein proteins spread from one neuron to another, hastening the advance of the disorder.

"The better we understand the mechanisms of PD, the easier it will be to develop clinical interventions," she said.

Source: University of California, San Diego School of Medicine



 

Causes of Parkinson's Disease - Pesticides?

 

More Evidence Links Pesticides to Parkinson’s

Copied from The Northwest Parkinson’s Foundation Weekly News Update

 

Rick Nauert

Psych Central - UCLA neurologists have discovered a link between the pesticide benomyl, a product whose toxicological effects still linger some 10 years after the chemical was banned, and Parkinson’ s disease.

The finding adds to the list of pesticides (paraquat, maneb and ziram) that have been tied to increases in Parkinson’s not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.

Researchers believe the association among benomyl and Parkinson’s disease is strong as the damaging series of events set in motion by benomyl may also occur in people with Parkinson’s disease who were never exposed to the pesticide, said Dr. Jeff Bronstein, senior author of the study and a professor of neurology at UCLA.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson’s. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain.

When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson’s patients.

Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Parkinson’s disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra.

This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease.

Often, symptoms of Parkinson’s become apparent after more than half of these neurons, known as dopaminergic neurons, have already been lost.

While researchers have identified certain genetic variations that cause an inherited form of Parkinson’s, only a small fraction of the disease can be blamed on genes, said the study’s first author, Arthur G. Fitzmaurice, M.D.

“As a result, environmental factors almost certainly play an important role in this disorder,” Fitzmaurice said.

“Understanding the relevant mechanisms — particularly what causes the selective loss of dopaminergic neurons — may provide important clues to explain how the disease develops.”

Benomyl was widely used in the U.S. for three decades until toxicological evidence revealed it could potentially lead to liver tumors, brain malformations, reproductive effects and carcinogenesis. It was banned in 2001.

The researchers wanted to explore whether there was a relationship between benomyl and Parkinson’s, which would demonstrate the possibility of long-lasting toxicological effects from pesticide use, even a decade after chronic exposure.

“We’ve known that in animal models and cell cultures, agricultural pesticides trigger a neurodegenerative process that leads to Parkinson’s,” said Bronstein, who directs the UCLA Movement Disorders Program.

“And epidemiologic studies have consistently shown the disease occurs at high rates among farmers and in rural populations. Our work reinforces the hypothesis that pesticides may be partially responsible, and the discovery of this new pathway may be a new avenue for developing therapeutic drugs.”

Source: UCLA



 

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Causes of Parkinson's Disease - Brain Damage #1

 

And what of football, the game we love?

Copied from The Northwest Parkinson’s Foundation Weekly News Update

 

It won't be changed easily, not with its public and personal histories.
Paul Zerby

Star Tribune - Is pro football about to go the way of the gladiators and the lions?

A new study of more than 3,400 National Football League players who played at least five seasons between 1959 and 1988 published in the journal "Neurology" reports a combined death rate from Alzheimer's, Parkinson's and Lou Gehrig's diseases in that cohort of about three times the rate for the general population of American men.

The study didn't deal with a disease known as CTE (for chronic traumatic encephalopathy), and of the 334 of the group who had died by the end of 2007, it is thought some may have died from CTE.

Now the NFL has pledged a $30 million grant to the National Institutes of Health to study the brain, specifically CTE, concussion management and treatment, and the relationship between traumatic brain injury and late-life neurodegenerative disorders, especially Alzheimer's.

The league's commissioner, Roger Goodell, has been quoted as saying, "We hope this grant will help accelerate the medical community's pursuit of pioneering research to enhance the health of athletes past, present and future," and observing that the NIH study is designed to help not only athletes but the general population, especially the military.

The Vikings' former great All-Pro defensive end, Carl Eller -- one of the anchors, along with Jim Marshall, of the Purple People Eaters, and now the board chair for the NFL Retired Players Association -- argues that the money will benefit current and future players and should be more focused on retired players.

One hopes that no generation of players will end up being compared to the tragic Tuskegee experiment. George Will, with whom I seldom agree, recently wrote: "Football is entertainment in which the audience is expected to delight in gladiatorial action that a growing portion of the audience knows may cause the players degenerative brain disease. Not even football fans, a tribe not known for savouring nuance, can forever block that fact from their excited brains."

All my life I've been a football guy, playing on grassy yards from Fargo to Duluth to St. Paul to Minneapolis and the suburbs, with no equipment at all other than a neighbourhood football. In late grade school, I weighed more than 100 pounds, but not more than 112, and played fullback for the Randolph-Snelling Midgets.

We wore shiny red-and-white jerseys furnished by a kindly drug store owner and won many of our games. We were scared to death of the Hallie Q. Brown team, reputed to be the super athletes that all black kids were, but managed to stumble to a tie with them. I even got my name in the paper for plunging for the extra point.

By the time I played offensive and defensive guard for the Cretin B-squad football team, I was up to around 125 pounds and stood over 5-foot-9. My B-squad football letter turned out to be the apex of my athletic career. Still, when years later my wife, unbeknownst to me, gave away my letter sweater, it was the nearly the end of a beautiful marriage.

I have also been an ardent fan since I can remember. I am often not so gently ridiculed at family gatherings when I share my memories of, as a small child held in my father's arms, watching the college all-stars play the Chicago Bears. I came close to death by appendicitis while listening to the Army-Notre Dame game when Army had Mr. Inside, Doc Blanchard, and Mr. Outside, Glen Davis, and clobbered my beloved Irish.

As a Boy Scout, I was privileged to usher for Gopher games at the old Memorial Stadium. (It was a lot like the TCF Bank Stadium, but with the seats farther from the field.) I got to watch Bud Grant, Leo Nomellini, Clayton Tonnemaker, Billy Bye and others who have faded into the obscurity of my failing memory.

Later, as a student at the U, I traveled down to Iowa City to watch some guy named Paul Giel, who eventually was instrumental in getting Memorial Stadium torn down in favor of the Metrodome, an awful baseball venue where I saw a couple of World Series, but a perfectly fine stadium for football.

A lot more comfortable than the old Met Stadium, where I purchased season tickets for the Vikings in 1962 that are still in my name, and where we bundled up in sleeping bags to watch Eller and Marshall and the Vikes play the game outdoors, where God intended.

Mr. Will doesn't seem to understand that watching football is an addiction; I will most likely continue to see some games as long as I can turn on the television and now and then get to a stadium. This week the competition wasn't only between the Cowboys and the Giants, but between the game and Bill Clinton at the Democratic National Convention. But I'm afraid Will is right about the heart of the matter.

Oh, well -- there's always politics, for those of us who love contact sports.

http://www.startribune.com/opinion/commentaries/168979886. html

 

 

Causes of Parkinson's Disease - Stress #1

 

An underlying cause of Parkinson’s Disease

Copied from The Northwest Parkinson’s Foundation Weekly News Update

 

Oxidative stress is no longer a prime candidate for the development of Parkinson’s disease, suggests a recent study at the University of York Biology department.
Ashley Ferro

Theyourker.co.uk - Parkinson’s disease results from the progressive degeneration of specific neurons in the substantia nigra pars compacta, a region of the midbrain which modulates synaptic activity in the basal ganglion. The complex wiring between regions of the basal ganglion is essential for the regulation of motor activity. Disrupting this interaction through degeneration of the dopamine neurons which modulate this system consequently results in the characteristic motor impairments observed in Parkinson’s patients, predominantly resting tremor, rigidity, and bradykinesia (slow movement). The mechanisms underpinning this neuronal cell death in the substantia nigra have remained highly elusive, and oxidative stress has been a serious contender for this role for quite some time.

Undergraduate biology students at the University of York worked as part of the team to exploit the powerful model system of juvenile Drosophila melanogaster (fruit fly) and an understanding of Mendelian genetics to study the influence of knocking-out the Juvenile Parkinson’s-related gene parkin on neuronal characteristics, metabolism and movement.

The juvenile Drosophila system faithfully models progression of the disease in humans, thus allowing direct and highly translatable study of the neurophysiological defects which lead to locomotor impairment. Knocking-out (deactivating) the parkin gene in Drosophila influenced energy metabolism, neuronal resting potential, synaptic development, and kinesis. More specifically, ATP (the universal cellular energy currency) synthesis and oxygen consumption were significantly reduced, and elevated levels of reactive oxygen species were observed. These physiological and metabolic changes suggest that mutations in parkin results in a neuronal energy deficit which underpins bradykinesia.

Current concepts on the development and pathogenesis of Parkinson’s disease focus heavily on the involvement of oxidative stress in inducing cell death in the substantia nigra. Although experimental evidence exists to demonstrate the vulnerability of dopamine neurons to damage by reactive oxygen species, it has remained unclear as to whether the oxidative stress is a consequence of the disease or initially causes the disease. To definitively elucidate the role of oxidative stress in causing the neurophysiological defects observed by mutating the parkin gene, the parkin mutants were initially treated with ‘reactive oxygen species scavengers’, antioxidants which either donate an electron or remove an electron from the reactive species to neutralise their effects on the cell. Surprisingly, introducing scavengers did not restore the resting membrane potential of the neurons or affect the locomotor defects of the mutant juvenile Drosophila, thus suggesting that these defects derive from causes other than oxidative damage.

The wild-type parkin gene was then exploited as a ‘transgene’, and was over-expressed in a parkin mutant to confirm the energetic cause for bradykinesia. Introduction of the wild-type gene entirely restored wild-type functionality. The finding conclusively demonstrates that oxidative stress occurs downstream in the pathology of Parkinson’s disease and cannot therefore be the underlying cause, but simply a product of the neurodegenerative process.

This is the first time the interaction between central nervous system deficits and bradykinesia has been experimentally demonstrated, a relationship which has merely been inferred by previous studies within the field. This demonstration, and the conclusion that metabolic impairment of neurons rather than oxidative stress induces the neuronal damage leading to locomotor disorders, marks a considerable benchmark in our understanding of Parkinson’s disease . Dr Chris Elliott, who led the study, explains the next direction of Parkinson’s research in the deparment, "Our next step will be to test a range of drugs which are known to relieve oxidative stress in cells, to test if they - like the transgenes - don't rescue the parkin locomotion defects." Identification of drugs which can reduce oxidative stress in the neurons responsible for modulating interactions in the basal ganglion may have considerable implications for Parkinson’s treatments in the future. The quality and impact of this research pays tribute to the abilities of the students and academics at the York Biology department.

References Vincent, A., Briggs, L., Chatwin, G., Emery, E., Tomlins, R., Oswald, M., Middleton, A., Evans, G., Sweeney, S. and Elliott, C. (2012) parkin-induced defects in neurophysiology and locomotion are generated by metabolic dysfunction and not oxidative stress. Human Molecular Genetics, 1-10.

http://www.theyorker.co.uk/lifestyle/scienceand%20technology/12300

 

 

Causes of Parkinson's Disease - Brain Damage #2

 

Head injury, pesticides tied to Parkinson's disease

Copied from The Northwest Parkinson’s Foundation Weekly News Update

 

Genevra Pittman

reuters.com - The combination of a past serious head injury and pesticide exposure may be linked to an extra-high risk of developing Parkinson's disease, a new study suggests.

The findings don't prove being knocked unconscious or exposed to certain chemicals directly causes Parkinson's, a chronic movement and coordination disorder.

But they are in line with previous studies, which have linked head trauma and certain toxins - along with family history and other environmental exposures - to the disease.

"I think all of us are beginning to realize that there's not one smoking gun that causes Parkinson's disease," said Dr. James Bower, a neurologist from the Mayo Clinic in Rochester, Minnesota who wasn't involved in the new research.

"There might be many paths to the ultimate development of Parkinson's disease," he told Reuters Health.

For example, Bower said, some people who are genetically predisposed might need just one "environmental insult" - such as a blow to the head - to set them up for Parkinson's. Others who aren't naturally susceptible to the disorder could still develop it after multiple exposures.

Head trauma and contact with pesticides "may not be directly related, and may be two independent stresses," Columbia University neurologist David Sulzer, who also wasn't part of the study team, told Reuters Health in an email.

About 50,000 to 60,000 older adults in the U.S. are diagnosed with Parkinson's disease each year, according to the National Parkinson Foundation.

For the new study, researchers led by Pei-Chen Lee from the University of California at Los Angeles compared 357 people with a recent Parkinson's diagnosis to a representative sample of 754 people without the disease, all living in central California, which is a major agricultural region.

The study team asked all of them to report any past traumatic head injuries - in which people had been unconscious for at least five minutes - and used their home and work addresses to determine their proximity to pesticide sprayings since 1974.

Those surveys showed that close to 12 percent of people with Parkinson's had been knocked unconscious, and 47 percent had been exposed to an herbicide called paraquat near both their home and workplace.

That's in comparison to almost seven percent of control-group participants with a history of head injury and 39 percent with pesticide exposure.

On their own, traumatic brain injury as well as living and working near pesticide sprayings were each tied to a moderately increased risk of Parkinson's disease. Combined, they were linked to a tripling of that risk, the researchers reported Monday in the journal Neurology. That was after taking into account people's baseline risk based on their age, gender, race, education, smoking history and family history of Parkinson's.

Lee's team didn't know which came first in people who'd had both head trauma and paraquat exposure.

It makes sense, the researchers noted, that a head injury would increase inflammation in the brain and disrupt the barrier that separates circulating blood and brain fluid. Those changes could then make neurons in the brain more vulnerable to the effects of pesticides, ultimately increasing the risk of Parkinson's.

But that's just a theory.

"There are all kinds of hypotheses," Bower said. But the study "is more evidence that traumatic injury to the brain can lead to later problems that are usually neurodegenerative," he added. "We need to be increasingly careful about preventing these traumatic brain injuries."

SOURCE: bit.ly/TD3OA9 Neurology, online November 12, 2012.



 

 

Causes of Parkinson's Disease - IL-13ra1 Gene?

 

Potential Cause of Parkinson's Disease Identified

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www.sciencedaily.com - Deciphering what causes the brain cell degeneration of Parkinson's disease has remained a perplexing challenge for scientists. But a team led by scientists from The Scripps Research Institute (TSRI) has pinpointed a key factor controlling damage to brain cells in a mouse model of Parkinson's disease. The discovery could lead to new targets for Parkinson's that may be useful in preventing the actual condition.

The team, led by TSRI neuroscientist Bruno Conti, describes the work in a paper published online ahead of print on November 19, 2012 by the Journal of Immunology.

Parkinson's disease plagues about one percent of people over 60 years old, as well as some younger patients. The disease is characterized by the loss of dopamine-producing neurons primarily in the substantia nigra pars compacta, a region of the brain regulating movements and coordination.

Among the known causes of Parkinson's disease are several genes and some toxins. However, the majority of Parkinson's disease cases remain of unknown origin, leading researchers to believe the disease may result from a combination of genetics and environmental factors.

Neuroinflammation and its mediators have recently been proposed to contribute to neuronal loss in Parkinson's, but how these factors could preferentially damage dopaminergic neurons has remained unclear until now.

Making Connections
Conti and his team were looking for biological pathways that could connect the immune system's inflammatory response to the damage seen in dopaminergic neurons. After searching human genomics databases, the team's attention was caught by a gene encoding a protein known as interleukin-13 receptor alpha 1 chain (IL-13Ra1), as it is located in the PARK12 locus, which has been linked to Parkinson's.

IL-13r
α1 is a receptor chain mediating the action of interleukin 13 (IL-13) and interleukin 4 (IL-4), two cytokines investigated for their role as mediators of allergic reactions and for their anti-inflammatory action.

With further study, the researchers made the startling discovery that in the mouse brain, IL-13Ra1 is found only on the surface of dopaminergic neurons. "This was a 'Wow!' moment," said Brad Morrison, then a TSRI postdoctoral fellow and now at University of California, San Diego, who was first author of the paper with Cecilia Marcondes, a neuroimmunologist at TSRI.

Conti agrees: "I thought that these were very interesting coincidences. So we set out to see if we could find any biological significance."

The scientists did -- but not in the way they were expecting.

'Something New Going On'
The scientists set up long-term experiments using a mouse model in which chronic peripheral inflammation causes both neuroinflammation and loss of dopaminergic neurons similar to that seen in Parkinson's disease. The team looked at mice having or lacking IL-13Ra1 and then compared the number of dopaminergic neurons in the brain region of interest.

The researchers expected that knocking out the IL-13 receptor would increase inflammation and cause neuronal loss to get even worse. Instead, neurons got better.

"We were very surprised at first," said Conti. "When we stopped to think, we got very excited because we understood that there was something new going on."

Given that cells fared better without the receptor, the team next explored whether damage occurred when dopaminergic neurons that express IL-13R
α1 were exposed to IL-13 or IL-4. But exposure to IL-13 or IL-4 alone did not induce damage.

However, when the scientists exposed the neurons to oxidative compounds, they found that both IL-13 and IL-4 greatly enhanced the cytotoxic effects of oxidative stress.
"This finally helps us understand a basic mechanism of the increased susceptibility and preferential loss of dopaminergic neurons to oxidative stress associated with neuroinflammation," said Marcondes.

The finding also demonstrated that anti-inflammatory cytokines could contribute to neuronal loss. In their article, the authors note they are not suggesting that inflammation is benign but that IL-13 and IL-4 may be harmful to neurons expressing the IL-13R
α1, despite their ability to ultimately reduce inflammation. "One could say that it is not the fall that hurts you, but how you stop," said Conti.

More Clues
Along with these results, additional clues suggest that the IL-13 receptor system could be a major player in Parkinson's. For instance, some studies show Parkinson's as more prevalent in males, and the gene for IL-13R
α1 is located on the X chromosome, where genetic variants are more likely to affect males.

And, though not definitive, other studies have suggested that Parkinson's disease might be more common among allergy sufferers. Since IL-13 plays a role in controlling allergic inflammation, Conti wonders if the IL-13 receptor system might explain this correlation.

If further research confirms the IL-13 receptor acts in a similar way in human dopaminergic neurons as in mice, the discovery could pave the way to addressing the underlying cause of Parkinson's disease. Researchers might, for instance, find that drugs that block IL-13 receptors are useful in preventing loss of dopaminergic cells during neuroinflammation. And, since the IL-13 receptor forms a complex with the IL-4 receptor alpha, this might also be a target of interest. With much exciting research ahead, Conti said, "This is just the beginning."

This research was funded by the Ellison Medical Foundation; National Institutes of Health grants AG028040 and DA030908; and the Ministry of Education, Culture, Sports, Science and Technology of Japan.

In addition to Morrison, Marcondes and Conti, the other authors on the paper, "IL-13R
α1 expression in dopaminergic neurons contributes to their oxidative stress-mediated loss following chronic systemic treatment with LPS," were Daniel Nomura, Manuel Sanchez-Alavez, Alejandro Sanchez-Gonzalez, Indrek Saar, and Tamas Bartfai, from TSRI, Kwang-Soo Kim from Harvard University, Pamela Maher from the Salk Research Institute, and Shuei Sugama from the Nippon Medical School in Tokyo.


 

Causes of Parkinson's Disease - Solvents?

 

Common Household Solvent Linked to Parkinson’s Disease

Copied from Northwest Parkinson’s Foundation Weekly News Update

 

STUART SILVERSTEIN

FairWarning - A chemical often found in groundwater and widely used in household products, including spot removers and carpet cleaning fluids, has been linked in a new study to Parkinson’s disease.

The study, which appeared in the Annals of Neurology medical journal, focused on 99 sets of twins. In each case one of the twins suffered from Parkinson’s and the other did not.

Researchers, led by scientists from The Parkinson’s Institute and Clinical Center in Sunnyvale, Calif., asked the twins about their job histories and hobbies, and determined what the twins’ exposure in those settings would have been to six common solvents.

Based on those evaluations, the researchers found a strong link between Parkinson’s and exposure to  or TCE. They concluded that people who worked with TCE had more than a six times greater risk of developing Parkinson’s, a neurodegenerative disease estimated to afflict as many as 500,000 Americans. Symptoms of Parkinson’s include limb tremors, slowed movement and speech impairment.

As a news release from the Annals of Neurology noted, researchers also found that people exposed to two other solvents — perchloroethylene, or PERC, and carbon tetrachloride, or CCI4 — “tended toward significant risk of developing the disease.”

“Our study confirms that:

 

common environmental contaminants may increase the risk of developing PD, which has considerable public health implications,”

 

said one of the leaders of the study, Dr. Samuel M. Goldman of The Parkinson’s Institute.

Goldman said his research team’s findings and previous reports “suggest a lag time of up to 40 years” between TCE exposure and the onset of Parkinson’s,

 

“providing a critical window of opportunity to potentially slow the disease process before clinical symptoms appear.”

Still, he warned that exposure to TCE is pervasive, and doesn’t just occur in the kinds of settings he and his colleagues examined.

According to the journal news release and a fact sheet from The Parkinson’s Institute, TCE still is commonly found in such substances as

 

dry-cleaning solutions, carpet cleaners, adhesives and paints, and as a grease-removing material in industry.

 

That wide use comes even though the Environmental Protection Agency declared it a human carcinogen in September, and despite the 1977 decision by the Food and Drug Administration to ban the use of TCE as a

 

general anaesthetic, skin disinfectant and coffee decaffeinating agent.



The researchers called TCE the most common organic contaminant found in groundwater, and said

 

it is detected in up to 30 percent of drinking water supplies in the country. It also is found in soil and in the air.”



 

 

Causes of Parkinson's Disease - Free Radicals?

What Causes Parkinson’s Disease?

 

 

It is now thought that Parkinson’s disease is caused by:

 

‘Free Radicals’.

 

We are yet to determine where these free radicals come from and how they get through the blood/brain barrier.

 

What is a free radical?

 

A free radical is a cell, which has one electron missing. Cells are made up of a number of atoms of various chemicals. Atoms consist of a nucleus, a varying number of protons and at least two electrons. The missing electron makes the cell unstable, and it has to find a replacement electron, from another cell.

 

In the case of Parkinson’s disease, free radicals have taken their required electrons from certain neurons (Brain cells), in a specific area of the brain,

 

which kills those neurons.

 

 

Normally, when body cells die, they get removed from the body and replaced by new cells. However, the damaged neurons, in the brain of a Parkinson’s patient,

 

remain in the brain in a ‘dormant’ condition.

 

Why? I think scientists have yet to discover the answer to this question.

 

It is possible for the ‘dormant’ cells to be repaired by:

 

glial derived neurotrophic factor (GDNF),

 

which is produced by the brain:

 

when it thinks the body is under attack.

 

(Glial cells are brain cells or neurons; Neurotrophic factor means something capable of repairing a brain cell.)

 

This GDNF is created, when we do

 

‘energetic’ exercise,

 

such as hard running or walking, which raises the rate of breathing and the pulse rate for a prolonged period of time. That is what makes the brain think that it is under attack, because when we are under attack, we would either fight, or run away. This is known as the, ‘Fight or Flight Syndrome’. When the GDNF finds a damaged brain cell it is capable of repairing it by replacing the missing electron. Thus we can repair our damaged brain cells, by doing some prolonged walking or running, and maintaining it for an optimal period of one hour.

 

Most of us are not capable of walking or running fast enough, in order to create this GDNF in our damaged brain. This does not mean that we cannot make use of this natural repair kit, it means that we have to slowly build up our bodily fitness to the point where

 

we can sustain this level of exertion.

 

 

All of us can walk fast enough to make us breathe heavily, for a short period of time, even if it is less than one minute. Then, if we do just that, three times a week, with one day’s break in between each exercise period, we are all capable of slowly building that time up to the point where we can sustain it for one hour. This assumes that we do not suffer from some other health problem, which would prevent us from doing this. Doctors recommend this for people who have had heart problems, because it improves the blood circulation, the lungs and the whole muscular system.

 

Reluctance to exercise is not an excuse for not exercising!

 

Perhaps the Free Radical is produced in the brain!

 

Every cell in the body, including brain cells, is regularly replaced by a new cell. This process is called:

 

Apoptosis

 

When this happens, the brain cell gains an electron, and becomes a

 

free radical.

 

What if that very same brain cell damages a healthy brain cell, which is what happens with Parkinson's Disease?

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