Essay on Cancer: Types, Causes and Treatment.
Alpha Lipoic Acid (ALA, thioctic acid, pyruvate oxidation factor) was first discovered by bacteriologist Irwin C. Gunsalus in 1948 when he observed that aerobic (oxygen-requiring) bacteria could not grow without it. Later, Gunsalus and Lester Reed determined the true structure and named it ALA (1951). ALA is a natural substance, produced in every higher-type cell, and it has many functions. Probably most importantly, ALA is the rate-limiting factor for the production of energy from carbohydrates (pyruvate). Without ALA, you could not obtain energy from the food you eat, and you could not stay alive.
ALA is also an excellent antioxidant and recycles other nutrients such as co-enzyme Q-10, vitamin C, and vitamin E. In addition, ALA chelates heavy metals such as mercury, lead, and arsenic, and it stabilizes NF kappa B transcription factor so that it helps to inactivate deleterious genes. It can also help people with diabetes mellitus by increasing the sensitivity of their cells to insulin, and it helps reverse diabetic neuropathies.
The first large human clinical studies using ALA in the United States were carried out by Drs. Fredrick C. Bartter, myself, and associates from the National Institutes of Health (NIH) in the 1970s. We administered ALA to 79 people with severe and acute liver damage at various hospitals around the United States, and 75 recovered full liver function.
Dr. Bartter and I were appointed by the FDA as principal ALA investigators, and I went on to use it successfully for the treatment of chronic liver disease. In combination with low-dose naltrexone, I have used ALA to treat various cancers for which no other treatment exists. (For more information, readers might want to go to and type in "liver, Berkson.")
My first experience using antioxidant therapy was in 1977, when I was an internal medicine resident. A man was poisoned and suffering from acute liver failure. His liver function tests were in the thousands of mg/dL, and he had propulsive diarrhea, projectile vomiting, and dreadfully painful muscle spasms throughout his body. He was the sickest person that I had ever seen. Due to the relentless muscle cramping and pain, he could not find a comfortable resting position. One of the department chiefs told me that nothing could be done to save his life except for an immediate liver transplant, however, a donor liver was not available. I was ordered to administer medical support and to just observe the patient as he went though the phases of death. I was told to take notes and prepare a report for grand rounds at the hospital.
Death from liver necrosis usually involves four separate stages: (1) ingestion of a poison, such as acetaminophen, a poisonous mushroom, hepatotoxic hydrocarbon solvent, etc.; (2) development of acute and difficult gastroenteritis with dehydration, pain, and electrolyte depletion; (3) a noticeable recovery phase in which the patient is often released from the hospital in a weakened state; and (4) increased weakness followed by coma and death. Because I did not want to see this happen to my patient, I began a search for a way to reverse his condition.
Fortunately, I remembered reading an article about a new drug that had been shown to be helpful in the treatment of severe liver damage. The drug, alpha-lipoic acid (ALA) was stocked at the NIH by Fred Bartter, MD, the chief of endocrinology. Dr Bartter was interested in this agent because he thought that because it lowered blood sugar levels, ALA might be used as a drug for diabetes mellitus and its complications.
About 30 hours after my patient had ingested the deadly toxins, the intravenous (IV) ALA was started. Within a few hours, the patient began to feel better. We were all surprised that he continued to improve, and he was soon discharged from the hospital with nearly normal laboratory values and feeling a little tired, but normal. He is still well and free of liver disease, 30 years later.
After I treated three more patients with severe liver damage with ALA and obtained the same remarkable results, most of the hospital chiefs were still skeptical, however, Dr. Bartter and I were delighted. NIH sent a team of doctors to Cleveland to examine my patients, and I was eventually awarded the FDA investigational drug permit for the use of IV ALA. Dr. Bartter and I published three papers describing our successes with IV ALA, and we expected a certain amount of interest in this remarkable organ regenerative protocol. We were disturbed by the lack of attention from the American medical community. Dr. Bartter died in 1985, and I continued to study ALA as a therapeutic agent and as a nutraceutical.
Since my work with Dr. Bartter, I have treated hundreds of patients with IV and oral ALA for acute and chronic liver damage, autoimmune disease, cancer, etc., along with other interesting agents with promising results. Below are a few case studies of Hepatitis C taken from my office practice.
In my opinion, there are four laboratory tests that really tell a doctor what is going on in the liver. The first is the platelet count. It is important because as liver inflammation and scarring progress, the platelet count goes down. So, the platelet count is a very helpful indirect indication of liver health, and a rise in platelet count is an indication of a healing liver.
I believe that the albumin level is the most important liver function test. A diseased liver can only produce a small amount of albumin. So a person with severe liver disease has a low albumin level, and as the liver improves, the albumin level rises.
The ALT is a liver enzyme that results from damage to the liver. It normally goes up and down from day to day, however, a downward trend may suggest an improvement of liver function. Interestingly enough, in cases of severe liver disease, the ALT is very low because most liver cells have been killed off.
The prothrombin time is a very important tool for measuring liver health, because a sick liver cannot produce much of the clotting factors, and thus the prothrombin time (a time it takes the blood to clot) is elongated in severe liver disease. As the liver regenerates, the prothrombin time shortens.
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