It would be nice if we all had a healthy liver to begin with, but an alcoholic liver is just one cause of excess ammonia, and excess glutamate.
A non-alcoholic fatty liver is also a sick liver....drugs are a cause, viruses, hepatitis, parasites/plugged up bile ducts, chemicals. Lots of causes of a sick liver. It would be nice if we all had healthy, functioning livers, but most people here know they have some sort of liver and/or kidney problems.
>>So why didnt this last? was it because i got back on the alcohol after the few week break>>
Exactly, sick liver, sick kidneys can not process ammonia. I don't have to tell you what alcohol does to the liver. So, where exactly does it go when it's not processed out and more is being made? It's a neurotoxin.
>>>Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver before toxins are removed. As a result, toxins such as ammonia and manganese can accumulate in the blood and enter the brain, where they can damage nerve cells and supporting cells called astrocytes. Positron emission tomography analyses have determined that ammonia levels are elevated in the brains of HE patients; ammonia accumulation can alter the expression of various important brain genes.
The liver and the brain interact in numerous ways to ensure normal brain functioning. For example, the liver plays a key role in supplying nutrients to the brain, which cannot produce these compounds itself. The liver also removes toxic substances from the blood, including substances that have been generated in the brain and must be eliminated from the body, as well as compounds produced in other tissues that are harmful to the brain’s nerve cells (i.e., are neurotoxic). Thus, liver dysfunction can cause disturbances of brain function and even contribute to brain damage.
Liver dysfunction of varying severity is a frequent complication of chronic alcohol abuse. The most common and least severe form of alcoholic liver disease—fatty liver (steatosis)—is characterized by fat deposits in the primary liver cells (i.e., the hepatocytes). More serious stages of alcoholic liver disease include inflammation of liver tissue (hepatitis), scar tissue formation (fibrosis), and destruction of the normal liver architecture (cirrhosis). When the liver becomes fibrotic and cirrhotic, the number of functional hepatocytes decreases, and the liver loses its capacity to remove toxic substances from the blood. Moreover, during these disease stages some of the blood entering the liver through the portal vein cannot penetrate the diseased liver and is diverted directly into the general circulation; this phenomenon is known as portal–systemic shunting. Blood that bypasses the liver is not detoxified, and blood levels of toxic substances increase. Researchers have identified several toxins that normally are removed in the liver but are found in the circulation of patients with alcoholic cirrhosis, including ammonia, manganese, and chemicals called mercaptans, all of which readily enter the brain and are neurotoxic. Consequently, brain function in patients with severe alcoholic liver disease is compromised, resulting in a condition known as hepatic encephalopathy (HE) or portal–systemic encephalopathy.
Excess ammonia is a crucial factor in the development of neurodegenerative diseases, since ammonia interferes with the oxidative metabolism of neurons and thus reduces the production of ATP, our "energy molecule." In addition, ammonia gives rise to very harmful nitrogen-based free radicals.
In the brain, glutamine is a substrate for the production of both excitatory and inhibitory neurotransmitters (glutamate and gamma-aminobutyric acid, popularly known as GABA).
Ammonia normally is removed from the blood in the liver by a series of chemical reactions called the urea cycle. During these sequential reactions, ammonia is converted into urea, which is excreted in the urine. The brain, however, lacks an effective urea cycle and therefore has only a limited capacity to remove any ammonia that enters the tissue from the blood because of the increased PS. The only way to eliminate any ammonia that has reached the brain cells is through a reaction mediated by an enzyme called glutamine synthetase, which combines a molecule of the amino acid glutamate with a molecule of ammonia to form the amino acid glutamine. The relevance of this reaction was confirmed in neuroimaging analyses measuring glutamine levels in the brains of alcoholic patients with HE. These studies found that the amounts of glutamine formed in the brain correlated with the severity of HE, confirming that the brain is exposed to elevated levels of ammonia (Lockwood et al. 1997). However, glutamine synthetase is present only in astrocytes, not in neurons, and cannot remove all the ammonia that enters the brain. As a result, neurons are virtually defenseless against increased ammonia concentrations and therefore are most likely to exhibit impaired function indicative of ammonia–related damage.
Glutamate, in excess, is suspected of causing oxidative stress and leading to the destruction of neurons in Parkinson’s disease, amyotrophic lateral sclerosis and other autoimmune disorders.
Excess glutamate has also been suspected of destroying myelin and contributing to the disease process in multiple sclerosis.
Read more: http://autoimmunedisease.suite101.com/article.cfm/glutamate_excess_in_multipl...
Glutamate transporters are found in neuronal and glial membranes. They rapidly remove glutamate from the extracellular space. In brain injury or disease, they can work in reverse and excess glutamate can accumulate outside cells. This process causes calcium ions to enter cells via NMDA receptor channels, leading to neuronal damage and eventual cell death, and is called excitotoxicity
Excitotoxicity due to glutamate occurs as part of the ischemic cascade and is associated with stroke and diseases like amyotrophic lateral sclerosis, lathyrism, autism, some forms of mental retardation and Alzheimer's disease.
Maybe the Mayo Clinic doesn't know what they are talking about either??
Excess Glutamate, Lyme Disease and Multiple Sclerosis:
In the Mayo Clinic Study published in October 2008, Dr. Vanna Lennon and her team have demonstrated that glutamate accumulates in the brain of patients with neuromyelitis optica. They propose that this is a result of NMO antiboides leading to glutamate excess. Dr. Lennon's study suggests that glutamate is responsible for the myelin destruction in this disorder.
Dr. Hong has previously shown the destructive role of glutamate in Parkinson’s disease. Dr. Yash Agrawal has explained how glutamate toxicity causes symptoms in both Lyme disease and multiple sclerosis. Dr. Agrawal explains that the ability of the beta-lactam antibiotic cefrixatone to reduce glutamate accumulations accounts for its effectiveness in Lyme disease. He proposes that both cefrixatone and low dose naltrexone, by having the potential to reduce glutamate accumulations, have therapeutic value in Lyme disease, MS, and other neurological disorders.
Thus, while the Mayo researchers propose finding ways to block glutamate, the benefits of low dose naltrexone and beta lactam antibiotics lie in their ability to reduce glutamate excess
The Mayo team, lead by Dr. Vanda Lennon, now show that NMO-IgG sets off a chain of events that leads to a toxic build-up of a neurotransmitter called glutamate. NMO-IgG binds to a protein that normally sops up excess glutamate from the space between brain cells. When NMO-IgG is around, this sponge-like action is blocked, allowing glutamate to accumulate. And too much glutamate can kill the cells that produce myelin - the protein that coats and protects neurons. The authors suggest that glutamate-induced damage to nerve cells and their insulating myelin coats might account for the neurological symptoms associated with Devic's disease.
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