Excitoxicity And How It Creates Neurological Diseases, Fibromyalgia, ADHD, Etc

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Excitoxicity is the damaging and killing of nerves by the excessive stimulation of nerve cells by neurotransmitters such as glutamate and similar substances. Glutamate or a like substance overactive the receptors for the excitatory neurotransmitter glutamate (known as a glutamate receptor); these are also called the NMDA receptor and AMPA receptor. Pathologically high levels of glutamate (and other excitotoxins like NMDA and kainic acid) bind themselves to these receptors; this causes excitoxicity by opening or widening an otherwise closed or limited pathway allowing high levels of calcium ions to enter the interior of the cell.


The influx of calcium ions activates a number of enzymes in higher than normal quantities including phospholipases, endonucleases, and proteases. These enzymes damage the structural components of the cell like the cytoskeleton, membrane and DNA.


In ALS (amyotrophic lateral sclerosis), damage to the mitochondrial DNA of the motor neuron cell triggers the production of reactive oxygen species (ROS) leading to a further increase in the glutamate concentration, leading to higher calcium ion levels and a cascading serious of damaging events to the motor neurons. In ALS, the motor neurons are highly susceptible to excitoxicity.


Glutamate is a normal excitatory neurotransmitter in the human central nervous system. IN a normally functioning central nervous system, the glutamate concentrate can increase briefly in the synaptic cleft between neurons, but then rapidly decreases. It is when the concentration cannot be decreased or reaches higher levels that the neuron kills itself in a process called apoptosis.


Many neurological diseases are associated within the breakdown in communication between neurons, either because they have been damaged, have died, or have been encumbered internally by abnormal fibrous growths or accumulations of proteins that inhibit function and communication. As such, any progression of damage results in a progression of symptoms. While the presence of glutamate has not been cited as a direct cause of Alzheimer’s Disease or Multiple Sclerosis, the damage it does to neurons can mimic the symptoms of these diseases and may, in the end, be an actual contributor to the progression of these diseases.


Parkinson’s disease is identified by the death of dopamine-generating cells in the substantia nigra, a region of the midbrain. The exact cause of the cell death is unknown, therefore giving glutamate excitoxicity a possible role in this neurodegenerative disease. However, the excitoxicity may just as possibly be related to dopamine itself, either not enough or too much of it leading to an imbalance causing damage to the neuron receptors.


Fibromyalgia is a recognized central nervous system disorder caused by neurological abnormalities. Studies are still underway to fully understand the myriad array of symptoms and causes of the disorder, one of the theories centers on the main cause of fibromyalgia to be a disruption of normal dopamine-related neurotransmission.


Huntington’s disease is another neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and dementia. It is a genetically inherited disorder, but is theorized to be aggravated by even normal amounts of glutamate in the system causing excitoxicity in a cascading effect, combining with the Huntingtin protein in accelerating motor neuron damage.


Attention deficit hyperactive disorder (ADHD) is a developmental disorder primarily characterized by the co-existence of attention problems and hyperactivity. Several studies have established a strong link with scientific data that ADHD is connected to abnormalities with the neurochemical dopamine. Other studies have indicated possible links to pesticides and artificial food colorings as being contributing factors to the development of the disorder in utero and early childhood.

There is a clear link between excitotoxins and other chemicals disrupting the normal function of the brain and even damaging it, leading or contributing to many of these disorders and diseases.

Hirudin Evolution

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The evolution of Hirudin in Medical Science

A Natural Blood Cleanser For Optimal Health
and Anti-Aging.

While the word HIRUDIN is not often heard in everyday language the medical value of HIRUDIN has long been recognized by the medical profession. Hirudin has long been used in the practice of Chinese medicine dating back to several thousand years . .

Leeching was also practiced as an art in ancient Egypt. It reached its

zenith in the late 18th and early 19th centuries. The antithrombotic quality of leech saliva was first noted by Haycraft in 1884 and the active anticoagulant ingredient isolated in 1904 by Jacoby. He gave this agent the name ‘hirudin’. Hirudin was isolated in pure crystalline form by Markwardt in 1957 and first produced in quantity by genetic engineering in 1986. The salivary glands of several species of leech also contain other biologically active substances which are currently undergoing investigation.

The following article is from Lab Lines, March/April 2001 Volume 11 A publication of the Department of Pathology and Laboratory Medicine at the University of Cincinnati

Hirudin and Its Derivatives as Thrombin Inhibitors

Thrombosis is a major cause of death and disability from myocardial infarction, stroke, peripheral ischemia, and pulmonary embolism. Standard heparin has been used successfully for the prevention and treatment of thrombotic disorders. However, its use has several limitations, including a variable anticoagulant effect, an inability to inhibit clot-bound thrombin, and the potential to cause thrombocytopenia. Direct thrombin inhibitors such as hirudin do not share these limitations.

Hirudin is the most potent non-covalent inhibitor of thrombin. It is a single peptide chain of 65 amino acids with molecular weight of ~7000. It is isolated from the salivary gland of the medicinal leech, Hirudo medicinalis. It selectively binds thrombin in a 1:1 fashion at each of two sites on the enzyme: 1) the domain that recognizes fibrinogen, and 2) the catalytic domain. Because of the specificity of binding, hirudin does not inhibit other enzymes in the coagulation or fibrinolytic pathways, such as factor Xa, factor IXa, kallikrein, activated protein C, plasmin or tissue-type plasminogen activator.

Hirudin produces a dose-dependent increase in the activated partial thromboplastin time (aPTT), prothrombin time and thrombin time. Unlike heparin, after which wide fluctuations in the aPTT are common, hirudin maintains a stable aPTT during its infusion period. The ability to achieve a more stable aPTT may be an important benefit because it avoids periods of inadequate anticoagulation. In addition to a dose-dependent increase in the aPTT, hirudin achieves a very consistent level of anticoagulation. In contrast to heparin, hirudin: 1) does not require antithrombin as a cofactor, 2) is not inactivated by anti-heparin protein, 3) has no direct effect on platelets, and 4) may also inactivate thrombin bound to clots or to subendothelium. Hirudin also appears to improve indices of coronary reperfusion and patency. Initial results with clinical end points, including death or myocardial infarction, appear to favor hirudin over heparin.

The hirudin-thrombin complex circulates in the blood for 4 to 6 hours after which it is cleared by the reticuloendothelial system. Circulating free hirudin is excreted by the kidneys and, thus, dose adjustment must be made in the setting of renal dysfunction. The dose-dependent elimination half-life is 1-2 hours. Because it is a foreign polypeptide, hirudin may elicit an immunological response.

Today, hirudin and synthetic analogues of hirudin are being developed using recombinant DNA technology. These drugs are alternatives to heparin for the treatment of: 1) unstable angina, 2) abrupt closure and restenosis following coronary angioplasty, and 3) prevention of deep vein thrombosis after major orthopedic surgery. They are also used as adjunct to fibrinolytic therapy. They are fast becoming the drugs of choice for the anticoagulant treatment of patients with heparin-induced thrombocytopenia with thromboembolic complications.

The aPTT has been used to monitor hirudin treatment. Chromogenic assays for accurate determination of plasma levels of hirudin are commercially available in Europe. However, in a recently published multicenter study on hirudin treatment of HIT patients, hirudin plasma levels did not correlate with bleeding complications. The ecarin-clotting time is also used in Europe to monitor hirudin levels. In the United States, no FDA-approved methods are yet available to monitor hirudin.

The primary adverse effect of hirudin is bleeding. The majority of bleeding events occur at invasive sites. An antidote is not yet available.

Lab Lines Authors: Irena Sheyn, MD, Cytopathology Fellow, and Gregory S. Retzinger, MD, PhD, Deparment of Pathology and Laboratory Medicine, Universtiy of Cincinnati. References: Cannon CP et al. Hirudin: initial results in acute myoc­ Cardial infarction, unstable angina and angioplasty. JACC, 1995; 25: 30S-37S Fischer KG et al. Recombinant hirudin (lepirudin) as Anticoagulant in Intensive care patients treated with continuous hemodialysis. Kidney Internat, 1999; 56: S46- S50 5. Greinacher A et al. Lepirudin (recombinant hirudin) for parenteral anticoagulation in patients with heparin-in duced thrombocytopenia. Circulation 1999, 100: 587-593 6. Johnson PH. Hirudin: clinical potential of a thrombin in hibitor. Annu Rev. Med 1994; 45: 165-177 7: Steuer S et al. Anticoagulation with r-hirudin in a patient with acute renal failure and heparin-induced thrombocy topenia. Nephrol Dial Transplant 1999; 14: 45-47

Cleansing The Body

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Why Is Blood Cleansing So Important?


Demi Moore recently used blood-sucking leeches to “cleanse” and “detoxify,” she said during an appearance Monday on “The Late Show With David Letterman.”

“I’ve always been somebody looking for the cutting edge of things that are for optimizing your health and healing, so just a week ago I was in Austria doing a cleanse and part of the treatment was leech therapy,” she told Letterman.

“These aren’t just swamp leeches, these are highly trained medical leeches,” she said. “These are not just some low-level scavengers; we’re talking high-level blood-suckers.”

Moore said they tested a leech on her belly button before putting several others on different areas of her body. She also said the worms are a fan of a certain type of grooming.

“Leeches don’t like hair, they much prefer a Brazilian,” she said.

Moore said she came away from the treatment feeling good.

“It detoxifies your blood,” she told Letterman. “And they have a little enzyme that when they’re biting down on you, gets released into your blood and generally you bleed for quite a bit. And your health is optimized. It detoxified the blood and I’m feeling detoxified right now.”

MSNBC, Acess Hollywood, March 25, 2008

There are primarily 3 sources where toxic elements come from?

Food: It comes from the food we eat such as a chicken that gets roasted even though it is rotten, melamine milk powder, pork with lean meat powder, agricultural products with pesticide residue, food with chemical dyes and other substandard food.
Air: It comes from the air we breathe. Everyday we breathe the toxic auto emissions, industrial exhaust, second hand smoking, cooking fume, air dust, formaldehyde hidden in certain construction materials etc. The toxic air and fume make it to our blood system through the respiratory system. Our Body: We ourselves produce toxin in the metabolic process such as lipofuscin, lactic acid and other toxic waste in our blood. While our body is supposed to detoxify itself through the metabolic process the toxins will invade and build up in every corner of our body including the blood circulation system, viscera and respiratory system if the metabolism does not function effectively .

Countless Medical research demonstrates that all toxin that go into the blood system eventually turn into blood poison. The free radicals, the chemical residue, the excess cholesterol and fat, blood rust, endogenous waste in the blood all constitute the formation of blood poison.
1000 Toxins: There are more than 1,000 toxins in the human blood system. 70 different types of human diseases can be traced directly to blood poisoin. The blood toxins accumulate over the years and become more damaging to the health of the middle aged population. The most common blood related problems that threaten the health of the middle aged are: high blood viscosity , dyslipidemia (high fat content on blood), hyper tension (high blood pressure) and hyperglycemia ( high blood sugar) . All such health problems are directly caused by an unclean contaminated blood system.

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