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 PubMed 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
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.
Mr. CA, a 68-year-old salesman from Ohio was infected with hepatitis C, following
a blood transfusion in the hospital. Soon afterwards, he became ill and was
found to have hepatitis C. He was sent to a hepatologist who immediately
put him on interferon and ribaviron, which made him feel as if he had influenza
for several months, and the drugs ultimately damaged his bone marrow. After
the failure of interferon/ribaviron, Mr. CA was told that nothing could be
done other than liver transplantation.
Mr. CA presented to my office suffering from fatigue, anxiety, abdominal pain,
and anemia, and his abdomen was distended with fluid (ascites). I treated him
with my triple antioxidant therapy. Within a short time he began to feel normal
and was free of the signs and symptoms of liver disease. Some of his results
may be seen in figures 1,
2, 3, and 4. (33KB .pdf)
Mr. EA, a 54-year-old man from California was infected with hepatitis C during
a blood transfusion following surgery. He did not feel well for several years
following surgery, and his physician did some laboratory tests that demonstrated
hepatitis C. A liver biopsy showed moderate cirrhosis with active inflammation.
Mr. EA presented to my office with fatigue, anxiety, abdominal pain, and some
ascites. His ALT was elevated, and his viral load was elevated by the Chiron
PCR method. I treated him with my Triple Antioxidant Therapy (ALA, selenium,
and silymarin), and within a few months, he started to feel normal. Some of
his results are illustrated in figures 5,
6, 7, and 8.(31KB .pdf)
Mrs. KVP is a 40-year-old woman in excellent health who developed hepatitis
C from a blood transfusion following surgery. Her family doctor sent her
to a liver expert who told her that she was seriously ill and must be treated
immediately with interferon and ribaviron. KVP had no complaints and had
heard that the standard treatment often made people much sicker than doing
KVP presented to my office, and her blood tests were all normal, except her
ALT liver enzyme was elevated at about 300 mg/dL. This indicated that there
was viral activity and inflammation in her liver. KVP's original laboratory
tests and her progress after being treated with my triple antioxidant therapy
over three years are demonstrated in figures 9,
10, 11, 12, and 13. (41KB .pdf)
After three years, she once again visited her hepatologist who told her that
actually that she was getting sicker because her viral load had increased dramatically
(Figure 12 in
above .pdf). Again, he said that she should be put on interferon and ribaviron
and be evaluated
for a liver transplant. Incidentally, she had great health
Mrs. KVP is a health professional and questioned her hepatologist. She asked
him if the original viral load was acceptable. He said, yes, however, it had
increased from 600,000 to 6,000,000 units, and that showed progression of her
disease. She asked him if he knew that the first viral load tests were done
by the Chiron method and the second tests were done by the Quantasure method.
He did not know that. Then, she told him that viral load is an artificial exaggeration
(amplification) of the amount of viruses by millions, and the Quantasure method
appears to amplify the amount of viruses by ten times more than the Chiron
method. After hearing this reasonable explanation, he answered that viral load
was not a very important test anyway.
The three people described in this study continued to stay on the triple antioxidant
therapy, and I still see two of them as patients today (Fall 2007). The two
continue to improve. In addition to ALA, I added silymarin and selenium to
my triple antioxidant therapy, because these agents also protect the liver
from free radical damage, regenerate the other fundamental antioxidants, and
interfere with viral replication. Although my first acute hepatic necrosis
patients were treated with ALA alone and did exceedingly well, all the patients
presented in this paper followed the triple antioxidant program and recovered
quickly from their illness.
The standard-of-care treatments for severe liver damage, especially liver transplant
surgery, can be painful, disabling, and extremely costly. From my experience
in my practice, interferon and antivirals have less than a 30% improvement
rate, and this response is usually not permanent. Liver transplant surgery
in a few cases can be lifesaving and necessary, but is uncertain and tentative,
partly due to the residual viremia that ultimately infects the newly transplanted
liver. I have found that the highest viral loads are seen following liver transplant
surgery, since the residual viruses in the bloodstream and tissues have a new
healthy liver on which to feed.
The triple antioxidant therapy offers a more conservative approach to the treatment
of hepatitis C that is much less expensive. One year of antioxidant therapies
described in this paper costs only a few thousand dollars, whereas liver transplant
surgery costs more than $400,000 a year, and in five years, the person will
probably require a new transplant. And, in addition, the transplant patient
will require anti-rejection drugs and many doctor and hospital visits. It appears
reasonable to me that prior to transplant evaluation or during the transplant
evaluation process, this conservative triple antioxidant treatment program
should be considered. If there is a significant improvement in the patient's
condition, liver transplant surgery may be avoided.
Not too long ago, I was invited by the Internal Medicine Society of Saxony
to present my triple antioxidant protocol to the group in Dresden, Germany.
I was asked why viral loads did not always fall to very low levels with my
treatment program. I answered that from a microbiologist's point of view
that I did not believe that one could ever completely eradicate a viral disease
without killing the patient. I added that we could only hope to support and "teach" the
immune system how to recognize and control a virus. Normally, viruses remain
part of our biology for the rest of our lives. And this does not necessarily
make a person sick. We are all filled with billions of dormant viruses. As
long as we have a healthy lifestyle and avoid unnecessary emotional and physical
stress, the viruses should remain dormant. I believe that one can live to 100
years old with hepatitis C and still be a healthy person.
Burton M. Berkson MD, MS, PhD
1155 Commerce Drive, Suite C, Las Cruces, New Mexico 88011
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