Alpha Lipoic Acid Protects Beta Cell Function

June 10, 2009
By Wayne Kuznar

A small clinical study shows improvements in insulin secretion and insulin sensitivity and prevention of oxidative stress with the use of alpha-lipoic acid in obese persons with impaired glucose tolerance (IGT), according to Chinese researchers.

Obese patients often have elevated levels of free fatty acids, which may increase the formation of reactive oxygen species, says Ping Han, MD, department of endocrinology, Shengjing Hospital, Liaoning, China. Oxidative stress plays an important role in insulin resistance, leading to beta-cell dysfunction.

Alpha-lipoic acid is a powerful antioxidant and a scavenger of reactive oxygen species and has been prescribed in Germany for more than 30 years for the treatment of diabetes complications, mostly diabetic polyneuropathy, notes Dr. Han.

In this study, alpha-lipoic acid was investigated in a dosage of 600 mg daily, given intravenously for 14 days, in 10 obese patients with IGT. Six obese patients with normal fasting glucose served as controls.

First-phase insulin secretion and second-phase insulin secretion were evaluated with a 2-hour hyperglycemic clamp before and after the completion of therapy in the obese IGT patients. First-phase insulin secretion increased by 42% (p<0.01) and second-phase insulin secretion increased by 33% (p<0.01) after the 14 days of therapy.

The insulin sensitivity index and glucose disposition index also increased significantly (p<0.05 for both) after treatment. Alpha-lipoic acid also prevented oxidative stress and inflammation, as evidenced by decreases in levels of interleukin-6 and tumor necrosis factor-alpha.


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OnJune 10, 2009, posted in: Alpha Lipoic Acid, Articles by admin

Oxidative stress

Medical Research News
Dr. Marcus Conrad of the Institute of Clinical Molecular Biology and Tumor Genetics at the Helmholtz Zentrum Munchen has decrypted the molecular mechanism through which the death of cells is caused by oxidative stress.
This knowledge opens novel perspectives to systematically explore the benefit of targeted therapeutic interventions in the cure of ageing and stress-related degenerative diseases.
Life processes in cells require a reducing environment that needs to be sustained with the help of a large number of antioxidative enzymes. This may sound abstract and incomprehensible, but everyone knows the phenomenon that a piece of cut apple or a piece of cut meat changes colour quickly and deteriorates, because the oxygen in the air produces chemical reactions in the tissues (oxidation of biomolecules).
If the equilibrium in the organism moves towards oxidative processes, then this is known as oxidative stress. Oxidative stress, for instance, is associated with the aging of body cells. Furthermore, a strong accumulation of reactive oxygen species (ROS) along with drops in cellular concentrations of glutathione, (GSH), the major antioxidant produced by the body, is well known as a common cause of acute and chronic degenerative diseases, such as, arteriosclerosis, diabetes, stroke, Alzheimer’s and Parkinson’s diseases.
“To investigate the molecular function of the cellular reducing agent GSH in the metabolic pathway of cell death triggered by oxidative stress, mice and cells were generated that specifically lack glutathione peroxidase 4 (GPx4), which is emerging as one of the most important GSH dependent enzymes”, explains Marcus Conrad. The induced inactivation of GPx4 caused massive oxidation of lipids and eventually cell death. A similar phenotype could be observed when intracellular GSH was removed from wild-type cells by a chemical inhibitor of GSH biosynthesis.
Interestingly enough, this cell death could be completely prevented by Vitamin E, but not by water-soluble antioxidants. Since the oxidation of fatty acids in this cell death pathway, was of paramount importance, multiple studies were performed to describe, in greater detail, the source and nature of lipid peroxides.

Pharmacological and reverse genetic analyses showed that lipid peroxides in GPx4-depleted cells do not appear by coincidence, but accumulate due to increased activity of a specific enzyme of the arachidonic acid metabolism, the 12/15-lipoxygenase. Activation of apoptosis inducing factor (AIF), evidenced by its relocation from mitochondria to the cell nucleus, was identified as another important event in this signaling cascade.

The fact that oxidative stress is a major inducer of cell death is a well accepted current model. Until now however, the source and nature of the reactive oxygen species has remained obscure, as have questions concerning the way they act. Marcus Conrad: “So far, it was assumed that oxidative stress is detrimental to cells by unspecific oxidation of many essential biomolecules, such as proteins and lipids. That is why we were amazed to find that in cells lacking either glutathione or glutathione peroxidase 4, a distinctive signaling pathway is engaged, which causes cell death. The data represent the first molecular analyses of a redox-regulated signaling pathway, describing how oxidative stress is recognized in the body and translated into cell death”.

Since this cell death cascade can be interrupted at any single stage with the help of drugs, this pathway harbors promising targets for therapeutic intervention to mitigate the deleterious effects of oxidative stress in complex degenerative human diseases.

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OnSeptember 3, 2008, posted in: Articles, Oxidative Stress by admin

Study of huge numbers of genetic mutations point to oxidative stress as underlying cause

CORVALLIS, Ore. – A study that tracked genetic mutations through the human equivalent of about 5,000 years has demonstrated for the first time that oxidative DNA damage is a primary cause of the process of mutation – the fuel for evolution but also a leading cause of aging, cancer and other diseases.
The research, just published in Proceedings of the National Academy of Sciences, also indicated that natural selection is affecting the parts of the genome that don’t contain genes – supposedly “junk” DNA that increasingly appears to have important roles in life processes that are very poorly understood.
The analysis was done by scientists at Oregon State University, Indiana University, the University of Florida and University of New Hampshire, in studies supported by the National Institutes of Health.
This research was unusual, scientists say, because the model animal used for the study, a type of roundworm called C. elegans, was tracked through 250 generations and in that period of time accumulated 391 genetic mutations through normal life processes. That’s more than 10 times as many mutations as have ever before been tracked in a study such as this.
Several Nobel Prizes have been awarded based on studies done with this roundworm, which was the first animal to have its entire genome sequenced. And despite their vast evolutionary separation as life forms, this tiny roundworm and humans still share comparable forms of DNA maintenance.
“Genetic mutations in animals are actually pretty rare, they don’t happen very often unless they are induced by something,” said Dee Denver, an assistant professor of zoology at OSU and principal investigator on the study. “The value of using this roundworm is that it reaches reproductive age in about four days, so we can study changes that happen through hundreds of generations, using advanced genome sequencing technology.”
Genetic mutations can take various forms, such as a disruption in the sequence of DNA bases, larger deletions of whole sections of DNA, or other events. They are a fundamental part of the biological process of life and the basis of evolution, allowing organisms to change – sometimes in ways that are good and lead to greater survival value, sometimes bad and leading to decline or death. But the process is difficult to study and a real understanding of the driving forces behind mutation, its frequency, and the types of mutation that happen most often has been elusive, researchers say.
A primary finding of the new study is that a predominant number of genetic mutations – most, but not all of them – are linked to guanine, one of the four basic nucleotides that make up DNA and form the genetic code of life. Guanine is known to be particularly sensitive to oxidative damage.
“Most life on Earth depends in some form on oxygen, which is great at the production of energy,” Denver said. “But we pay a high price for our dependence on oxygen, because the process of using it is not 100 percent efficient, and it can result in free oxygen radicals that can damage proteins, fats and DNA. And this process gets worse with age, as free radicals accumulate and begin to cause disease.”
This is one of the first studies, Denver said, that is clearly demonstrating the effects of oxidative damage at a genome-wide scale.
“The research showed that the majority of all DNA mutations bear the signature of oxidative stress,” Denver said. “That’s exactly what you would expect if you believe that oxidative stress is an underlying cause of aging and disease.”
Beyond that, however, the study also found that mutation and natural selection is also operating in the “junk DNA” parts of the roundworm, which actually comprises about 75 percent of its genome but traditionally was not thought to play any major role in life and genetic processes. This suggests that these poorly-understood and little appreciated parts of the genome may have important biological roles that are not yet known, Denver said.
Oxidative stress for decades has been suspected as a mechanism for some of the processes that lead to aging and disease, and it has been studied extensively for that reason. This research provides a better fundamental understanding of the genetic impacts of oxidative stress and its role in both genetic disease and evolution, researchers say.

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OnMarch 22, 2008, posted in: Articles, Oxidative Stress by admin

Alpha Lipoic Acid and Liver Disease

by Burton M. Berkson, MD, MS, PhD

December 2007

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 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 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.

Case 1
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)

Case 2
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)

Case 3
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 nothing.

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.

Selected References
Bartter FC, Berkson B, Gallelli J, Hiranaka P. Thioctic acid in the treatment of poisoning with alpha-amanitin. In Amanita Toxins and Poisonings. Faulstich H., Kommerell B, Wieland T, Eds. Baden Baden: Wizstrock; 1980: 197-202.
Baur A, Harrer T. Alpha lipoic acid is an effective inhibitor of human immuno-deficiency virus (HIV-1) replication. Klin. Wochenzchr. 1991;69:722-724.
Berkson B. Thioctic acid in treatment of hepatotoxic mushroom poisoning. New England Journal of Medicine. 1979;300:371.
Berkson B. Treatment of four patients with thioctic acid. In Amanita Toxins and Poisonings. Faulstich H, Kommerell B, Wieland T, Eds. Baden-Baden: Wizstrock:1980;203-207.
Berkson BM. Alpha-lipoic acid (thioctic acid): my experience with this outstanding therapeutic agent. Journal of Orthomolecular Medicine. 1998;13:1:44-48



(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 insurance.

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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OnDecember 19, 2007, posted in: Articles, Hepatitis C, Liver Disease by admin

1 in 3 have fatty liver, study finds

Research uncovers disease that’s usually undetected, untreated
October 7, 2007
By SUE GOETINCK AMBROSE / The Dallas Morning News 


Although the Dallas Heart Study is primarily geared toward studying heart disease, the study has also included extensive analysis of the body’s fat distribution, including fat stored in the liver.
In a 2004 study published in the journal Hepatology, researchers led by UT Southwestern’s Dr. Jeffrey Browning reported that 31 percent of study volunteers have fatty liver disease, or abnormal accumulation of fat in their livers. The prevalence was highest in Hispanics and lowest in blacks.
Since the volunteers are representative of the county’s population, that means that about one-third of adults living in Dallas County are expected to have the condition.
And hardly any of those people know they have it, Dr. Browning said.
“If you look 15 to 20 years down the road, this may be a huge public health problem,” he said.
The UT Southwestern study is the first large survey of a population representative of the U.S., Dr. Browning said.
If the Dallas numbers apply to the U.S. population, Dr. Browning said, it means that as many as 71 million U.S. adults have the condition. Reports indicate that even obese children have the condition.
Fatty liver disease can progress over a decade or two to an inflamed liver and finally to cirrhosis, a condition where the liver becomes so scarred it can barely function and requires a transplant.
In the study, the scientists found that 45 percent of Hispanics, 33 percent of whites and 24 percent of blacks had fatty liver disease. In general, the disease went hand in hand with obesity and insulin resistance.
And almost 10 percent of lean people in the study had fatty liver disease, the researchers found. White men were more likely to have the condition than white women. Among Hispanics and blacks, the prevalence among men and women was similar. Too few people of Asian, Native American or other ethnicities had liver fat measured for the scientists to draw meaningful conclusions for those groups, Dr. Browning said.
There is no easy way to diagnose or treat the condition. Standard blood tests don’t pick up the condition reliably. And there are no magic pills known that can reverse or prevent the condition.

The best thing doctors can tell patients is to lose weight, advice that is notoriously difficult to follow.


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OnOctober 7, 2007, posted in: Articles, Liver Disease Articles by admin

Nutritional Supplements Improve Memory in Old Dogs (October 1, 2007

(CORVALLIS, Ore. ) – Nutritional supplements have successfully been used to improve the memory, ability to learn and cognitive function of old dogs – and might be able to do the same thing with humans.

These supplements, acetyl-l-carnitine and alpha lipoic acid, are continuing to be studied in work with humans, and scientists believe they may provide a new approach to the neurodegeneration and cognitive decline common with aging.

The newest study was just published in FASEB Journal, produced by the Federation of American Societies for Experimental Biology, by researchers from the Linus Pauling Institute at Oregon State University, the University of Toronto, University of California/Berkeley, Children’s Hospital Oakland Research Institute, and Juvenon, Inc.

It found that supplements of these two antioxidant compounds, which are believed to play a role in slowing mitochondrial decay in the cell, significantly increased the ability of “geriatric” beagle dogs to learn a new task.

The study builds on similar findings made several years ago, done with mice and published in Proceedings of the National Academy of Sciences.

In that research, the activity and energy level of old rats taking these same supplements almost doubled, and memory and cognitive function improved.

“The prospects for cognitive improvement from use of these supplements is both fascinating and exciting,” said Tory Hagen, an associate professor in OSU’s Linus Pauling Institute, and recognized expert on the biological processes of aging.

“This is the first time these two compounds, by themselves, have been tested in canines, which have brains that are more biologically similar to humans than some other animal models,” Hagen said. “The results should be relevant to what we could expect with humans, and are very encouraging.”

In this study, an inbred line of older, very similar beagle dogs were taught how to find a food treat by identifying certain markers, such as a yellow wooden peg.

Applied scents were used to control for any tip-off by sense of smell. Some dogs received short-term dietary supplementation with acetyl-l-carnitine and lipoic acid, and others did not.

On one task, four of six dogs receiving supplements quickly learned to find the food treat by identifying the correct marker, while only two of six dogs on normal diet succeeded.

After 15 more weeks of training, more than 80 percent of supplemented dogs were successful, while only 50 percent of those not receiving supplements could learn the new task.

“We’ve shown in some previous animal work that these supplements could improve memory and energy level,” Hagen said. “Now we’re seeing that animals receiving supplements are much more readily able to learn new things as well, even at an advanced age.”

In these tests, the effects of supplementation with these compounds appeared to work fairly quickly, in a matter of days or weeks, the scientists said.

Some other studies, however, have required much longer periods of supplementation for various antioxidants to improve cognitive performance.

Humans also experience loss of the type of object and spatial discrimination that was improved by supplements in these animal tests – it’s often one of the early signs of human dementia.

The scientists suggested in the paper that long-term supplementation “may be effective in attenuating age-associated cognitive decline by slowing the rate of mitochondrial decay and cellular aging.”

Enhancing the function of mitochondria – which provide almost all of a cell’s energy – could literally be providing animals with more “mental energy,” leading to improved memory and learning, the study indicated.

The compounds may also cause increased synthesis of a neurotransmitter called acetylcholine.

An increasing body of research suggests that mitochondria may be an “Achilles heel” for absorbing age-related damage, as part of the natural process of oxidation in the body and the related “free radicals” that are produced and can cause cellular damage.

As the power plant of cells, mitochondria perform many of the roles critical to cell function, use up to 90 percent of the oxygen humans breathe, but are also among the first cellular components to be damaged by reactive radical oxygen species.

This study was funded by private industry, including companies that produce the compounds being studied.

Clinical experiments with humans using these supplements are already under way, scientists said.

Source: Oregon State University

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OnOctober 1, 2007, posted in: Alpha Lipoic Acid, Articles by admin

Exciting results against pancreatic cancer

March 2010

By Dr. Patrick Massey

Every once in a while, a piece of medical research crosses my desk that I feel has the potential to change how medicine is practiced.

Today is one of those days.

A recent medical article revealed that patients with end stage pancreatic cancer and treated with an antioxidant and narcotic-like medication lived longer than expected.

The pancreas is located in the abdomen, behind the stomach. It has multiple functions, including secreting enzymes that help digestion and regulating blood sugar levels by releasing insulin. Unfortunately, cancer can also begin in the pancreas. According to the National Institutes of Health, about 42,000 new cases of pancreatic cancer were diagnosed in 2009. Unfortunately, early stage pancreatic cancer rarely has symptoms and most cases are diagnosed at a late stage. As a result, the five-year survival rate is only 5 to 6 percent.

According to an article in the medical journal Integrative Cancer Therapies, a group of physicians in New Mexico used a powerful antioxidant (alpha-lipoic acid) and a medication used primarily for alcohol and drug dependence (naltrexone). Three patients with end-stage pancreatic cancer were treated intravenously and orally with alpha-lipoic acid and took naltrexone at night.

The patients improved significantly over the course of therapy. All had radiologic proof of the tumors getting smaller. All lived longer than expected.

Since most pancreatic cancers are found in a late stage, traditional medical approaches like surgery, chemotherapy and radiation therapy are less effective.

What is remarkable about the alpha-lipoic acid and naltrexone protocol is that it worked on patients with end-stage cancer. One patient is still alive 61/2 years after he was told that his “-prognosis was hopeless.”

In cancer cells, both alpha-lipoic acid and naltrexone suppress a specific cancer cell protein, NF KB. It is one of the proteins that allows cancer cells to grow rapidly.

In the test tube, suppression of NF KB results in cancer cell death. From the clinical results above, it is possible that the combination of alpha-lipoic acid and naltrexone results in cancer cell death.

Of note, suppressing production of NF KB is also a hot area of cancer drug research. A new anti-cancer drug, bortezomib, is showing promise.

Are these clinical results a breakthrough in cancer treatment? It may too early to tell and I must stress that there is a big difference between a positive result with a few patients and a real clinical trial. However, medical breakthroughs often start with a positive result in a few patients.

Overall, there do not seem to be significant side effects and few contraindications for the alpha-lipoic acid and naltrexone therapy.

It is worthy of more research.

Patrick B. Massey, M.D., Ph.D. is medical director for complementary and alternative medicine for the Alexian Brothers Hospital Network.

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OnJanuary 1, 1970, posted in: Alpha Lipoic Acid, Articles by admin