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Letters to the Editor Issue 228

by Letters(more info)

listed in letters to the editor, originally published in issue 228 - February 2016

Zika Virus in Brazil Raises Mosquito and Vaccine Questions

Reprinted from:

by Melanie Grimes


The Zika virus outbreak in Brazil has been blamed on mosquito bites, but the real cause of the children born with a brain defect called microcephaly may not be the Zika virus. The Zika virus is transmitted by mosquitoes. However, sources report that only a FEW of the infants born with this condition had ANY evidence of the Zika virus in their brains. Brazil had fewer than 150 cases of microcephaly in all of 2014, but there have been more than 3,500 reported cases since October 2015. At the same time, in 2015, Brazil instituted a mandatory vaccine policy for pregnant women. Could vaccines be causing the brain defect in infants in Brazil?

The WHO Website States…

“The link with Zika has not been confirmed. But some babies who died had the virus in their brain and it has been detected in placenta and amniotic fluid too.”

Are Vaccines a Cause of the Microcephaly Brain Deformity Occurring in Brazil?

It has been shown that vaccine injection can cross the blood brain barrier in utero, if the blood brain barrier has not been fully formed. In Brazil, mandatory vaccination of expectant mothers was instituted in early 2015. Brazil’s Minister of Health required a new TDAP vaccine be given to all expectant mothers. TDAP is a new type of DPT vaccine, which contains vaccines for diphtheria, pertussis and tetanus. Pertussis vaccines have been given to pregnant women in England since 2012 and have not been known to cause risk to the pregnancies or the infants.

About the TDAP Vaccine

The TDAP vaccine is a reduced-dose acellular pertussis vaccine that also includes tetanus and diphtheria vaccines. Since 2011, The TDAP shot has been recommended by the Center for Disease Control (CDC) for women at 20 weeks of gestation. The FDA classifies the TDAP as a Class C drug, which means that is it NOT SAFE to be given during pregnancy, and there have been no test to see if the TDAP is safe for pregnant women. Research is underway at Vanderbilt University, where the hope is that vaccinating the pregnant mothers will pass along the immunity in utero to the children but this research has not yet been published.

What the World Health Organization says about the Zika Virus

On Jan 21, 2016, the World Health Organization (WHO) stated “The Brazilian authorities believe the increase (in brain deformities) is caused by an outbreak of Zika virus.” The WHO has previously stated, “Zika is generally mild and only causes symptoms in one in five people”. On Jan 28, 2016, the WHO director general Dr Margaret Chan declared that Zika has escalated “from a mild threat to one of alarming proportions”. WHO has established a Zika “emergency team” because there has been what is called an “explosive” spread of the virus.

What are Symptoms of the Zika virus?

Most people who have the Zika virus have little or no symptoms. Some people experience a fever or get a rash. Other symptoms include headaches, joint pain, or eye redness (conjunctivitis).

How does Zika spread?

The carriers of the Zika virus are a mosquito with the scientific name of Aedes aegypti and Aedes albopictus. The same mosquito also spreads dengue fever and chikungunya fever. These mosquitoes are active in the daytime, unlike the mosquitoes that spread malaria which are only active at night. The mosquito bites a person who is infected with the virus and then spreads the infection when they bite another person.

Could GMO Mosquitoes be Causing the Outbreak of Zika Virus?

Beginning in 2011, the British biotech company Oxitec has released GMO mosquitoes in Brazil. This strain of Aedes mosquitoes has been genetically modified to help eliminate dengue fever, which is spread by the Aedes mosquito. Up to 2 million GMO mosquitoes are produced each week in the Brazilian factory.

There is not yet a sure link between the Zika virus and brain deformities seen in Brazil. This link needs to be further established. Research on the efficacy of the Tdap vaccine also needs to be quickly published and brought to light. Further information about the GMO mosquitoes also needs further elucidation.

About the Author:

Melanie Grimes CCH, is a writer, health educator and homeopath. She is a member of the Association of Health Care Journalists. She has taught at Bastyr University and lectured internationally. Follow her blog at To order professional quality vitamins, visit her online vitamin shop at

Keywords: birth defects, Dengue, DPT, DPT vaccine, FDA, GMO, GMO mosquito, microcephaly, mosquito, pertussis vaccine, pregnacy, vaccination, vaccine, WHO, Zika, Zika fever, Zika virus

Sources Include


Novel RNA Delivery System May Treat Incurable Blood Cancers  

TAU (Tel Aviv University) researchers develop unique system to deliver therapy at site of Mantle Cell Lymphoma

With a median survival rate of just five to seven years, Mantle Cell Lymphoma (MCL) is considered the most aggressive known blood cancer; and available therapies are scarce. Three thousand Americans are diagnosed with MCL every year, and despite progress in personalized therapies to treat metastases elsewhere in the body, systemic therapeutic drug delivery to cancerous blood cells continues to challenge the world of cancer research.

Mantle Cell Lymphoma Exosomes Transmission Electron Microscopy

A new study by Tel Aviv University researchers offers tangible hope of curing the currently incurable blood cancer - and others like it. The revolutionary system was found to successfully halt the proliferation of a cancer-related protein in white blood cells in both animal models and samples taken from MCL patients.

The research was led by Prof. Dan Peer of TAU's Department of Cell Research and Immunology and conducted by TAU PhD students Shiri Weinstein and Itai Toker, in collaboration with Prof. Pia Raanani of Rabin Medical Center and Prof. Arnon Nagler of Sheba Medical Center. The study was published in the early edition of the Proceedings of the National Academy of Sciences USA (PNAS).

A "Zip Code Identifier" System for Cancer Drug Delivery

"MCL has a genetic hallmark," said Dr Peer. "In 85 percent of cases, the characteristic that defines this aggressive and prototypic B-cell lymphoma is the heightened activity of the gene CCND1, which leads to the extreme overexpression - a 3,000- to 15,000-fold increase - of Cyclin D1, a protein that controls the proliferation of cells. Downregulation of Cyclin D1 using siRNAs is a potential therapeutic approach to this malignancy."

The research validates a novel strategy developed two years ago in Dr Peer's lab that involved small interfering RNAs (siRNAs). The radical new delivery system harnesses nanoparticles coated with "GPS" antibodies that navigate toward the location of the cancerous cells, where they then offload Cyclin D1-blockers in the form of siRNAs.

For the purpose of the research, the scientists designed lipid-based nanoparticles (LNPs) coated with anti-CD38 monoclonal antibodies that were taken up by human MCL cells in the bone marrow of affected mice. When loaded with siRNAs against Cyclin D1, the targeting LNPs induced gene silencing in MCL cells and prolonged the survival of tumor-bearing mice with no observed adverse effects.

"In MCL, Cyclin D1 is the exclusive cause of the over-production of B Lymphocytes, the cells responsible for generating antibodies," said Dr Peer. "This makes the protein a perfect target for RNA therapy by siRNAs. Normal, healthy cells don't express the gene, so therapies that destroy the gene will only attack cancer cells. The RNA interference we have developed targets the faulty Cyclin D1 within the cancerous cells. And when the cells are inhibited from proliferating, they sense they are being targeted and begin to die off."

The new research highlights the therapeutic potential of Cyclin D1 therapy in MCL and presents a novel RNA delivery system that opens new therapeutic opportunities for treating MCL and other similar B-cell malignancies.

Making Cancer Personal

"This research makes a definite contribution to the revolution of personalized medicine, whereby you tailor the drug based on the genetic profile of patient," said Dr Peer. "In this case, MCL is a disease with a specific genetic hallmark, so you can sequence the patient to identify the mutation(s), and design RNA blockers to be placed inside a nanovehicle.

"While the targeting antibodies - the 'GPS' - can be used to target many different B-cell malignancies, the drug itself is designed to silence this specific disease. However, the delivery system can be used to accommodate any disease with a genetic profile. This could be the future. We are seeing it happen before our very eyes."

The research was supported in part by the National Institutes of Health, The Israel Cancer Association, The Leona M and Harry B Helmsley Charitable Trust, the Lewis Trust and the Dotan Center for Haematological Research at TAU. The researchers intend to take the study further and translate these findings into clinical trials pending additional funding.

Further Information

Further information regarding this research is available online at:


Breast Cancer Survivors Vulnerable To Common Viral And Bacterial Infections

Breast cancer survivors treated with chemotherapy could be lacking sufficient antibodies to protect against common illnesses, as chemotherapy reduces the body’s immune response, according to research published in the open access journal Breast Cancer Research.[1] This work raises the possibility that these survivors could benefit from additional post-treatment monitoring. Further work is required to assess if revaccination would be beneficial.

Chemotherapy is used to treat 30% of breast cancer patients. Although an effective treatment, delivering an increase in survivorship, post-treatment welfare may deserve additional attention. Many studies have investigated the effects of chemotherapy on our immune system during the therapy itself and up to a short period after the last treatment, but little is known about the long-term impact on immunity.

Measuring the levels of lymphocytes (a group of white blood cells involved in our body’s immune response) and antibodies researchers from University of Leeds and Leeds Teaching Hospitals NHS Trust found that chemotherapy reduced levels of some components of the immune system of breast cancer survivors for at least nine months after treatment. These changes may leave patients vulnerable to some infections, despite having had routine vaccinations for such infections years before.

The researchers investigated the immune system of 88 women with breast cancer. Levels of lymphocytes were measured before and at intervals between two weeks and nine months after chemotherapy. However, there was no pre-chemotherapy data for 26 of these participants.   

Levels of all the major types of lymphocytes dropped significantly after chemotherapy. This included T and B cells and natural killer cells, which together defend the body against viral and bacterial infection. The impact of chemotherapy on most lymphocytes was found to be only short term, with recovery to pre-chemotherapy levels by nine months. However, chemotherapy had a long term effect on B cells (cells that ultimately produce antibodies) and helper T cells (cells that are responsible for helping antibody production), both of which only partially recovered to around 65% of initial levels in the first six months and did not continue to recover after a further three months. Levels of antibodies against tetanus and pneumococcus (the bacterium that can lead to pneumonia) also were reduced and stayed low even after nine months.

Chemotherapy uses different chemical agents. The researchers compared an anthracycline only regime with anthracyclines followed by taxane cycle. The anthracyclines regime was more damaging to B cells and helper T cells initially, but a relatively full recovery was made afterwards. On the other hand, anthracyclines followed by taxanes was associated with sustained reductions in levels of immune cells with poor recovery. 

Smoking also appeared to slow down the recovery of some immune cells with levels in smokers reaching only half pre-chemotherapy levels after nine months compared to 80% in non-smokers.

Researcher, Thomas Hughes, from the School of Medicine at the University of Leeds says: “We were surprised that the impact of chemotherapy is so long lived. We were also surprised that smoking and choice of chemotherapy agent influenced the dynamics of the recovery of the immune system. We might need to take into account the future immune health of breast cancer patients when planning treatments, but more research is needed to determine whether this would improve patient outcomes.”

This was an observational longitudinal study which means that although it can increase our understanding of the links between chemotherapy, smoking and immune defence, it cannot show cause and effect because other factors may play a role.

References and Notes

  1. Rashmi Verma; Ruth E Foster; Kieran Horgan; Katherine Mounsey; Helen Nixon; Natuley Smalle; Thomas A Hughes, MA DPhil; Clive RD Carter Lymphocyte depletion and repopulation after chemotherapy for primary breast cancer Breast Cancer Research. 2015

During embargo article available here:

After embargo article available at journal website here:  

  1. Breast Cancer Research is an international, peer-reviewed online journal, publishing original research, reviews, editorials and reports. Open access research articles of exceptional interest are published in all areas of biology and medicine relevant to breast cancer, including normal mammary gland biology, with special emphasis on the genetic, biochemical, and cellular basis of breast cancer. In addition to basic research, the journal publishes preclinical, translational and clinical studies with a biological basis, including Phase I and Phase II trials.
  2. BioMed Central is an STM (Science, Technology and Medicine) publisher which has pioneered the open access publishing model. All peer-reviewed research articles published by BioMed Central are made immediately and freely accessible online, and are licensed to allow redistribution and reuse. BioMed Central is part of Springer Science+Business Media, a leading global publisher in the STM sector.

Source: Alanna Orpen, PR Assistant

BioMed Central  T: +44 (0)20 3192 2054


Liver Recovery Difficult even with Improved Diet - But Faster if Sugar Intake is Low

by David Stauth

Liver damage caused by the typical ‘Western diet’ - one high in fat, sugar and cholesterol that’s common in developed countries such as the United States - may be difficult to reverse even if diet is generally improved, a new study shows.

The research, published 13 Jan  in PLOS ONE by scientists from Oregon State University, found that a diet with reduced fat and cholesterol helped, but did not fully resolve liver damage that had already been done - damage that in turn can lead to more serious health problems, such as cirrhosis or even cancer. This study, done with laboratory animals, showed that diets low in fat and cholesterol could in fact aid with weight loss, improved metabolism and health. But even then, if the diet was still high in sugar there was much less liver recovery, the scientists concluded. The findings are significant, scientists say, because liver problems such as non-alcoholic fatty liver disease are surging in the US, affecting 10-35 percent of adults and an increasing number of children. The incidence of this problem can reach more than 60 percent in obese and type-2 diabetic populations.

“Many people eating a common American diet are developing extensive hepatic fibrosis, or scarring of their liver, which can reduce its capacity to function, and sometimes lead to cancer,” said Donald Jump, a professor in the OSU College of Public Health and Human Sciences, principal investigator with the Linus Pauling Institute, and corresponding author on this research.

“There’s a lot of interest in finding ways to help the liver recover from this damage, but this research suggests that diets lower in fat and cholesterol, even if they help you lose weight, are not enough,” Jump said. “For more significant liver recovery, the intake of sugar has to come down, probably along with other improvements in diet and exercise.”

The issues are both serious and complex, the researchers said.

“Everyone recognizes this is a serious problem,” said Kelli Lytle, an OSU doctoral candidate and lead author on this study. “We’re trying to find out if some of the types of dietary manipulation that people use, such as weight loss based on a low fat diet, will help address it. However, a common concern is that many ‘low-fat’ food products have higher levels of sugar to help make them taste better.” Weight loss does appear to help address some of the problems associated with the Western diet, the research shows. But according to this study, a diet with continued high levels of sugar will significantly slow recovery of liver damage that has already been done.

Complications related to liver inflammation, scarring and damage are projected to be the leading cause of liver transplants by 2020, the researchers noted in their study. Such scarring was once thought to be irreversible, but more recent research has shown it can be at least partially reversed with optimal diet and when the stimulus for liver injury is removed.

In this report, scientists studied two groups of laboratory mice that had been fed a ‘Western diet’ and then switched to different, healthier diets, low in fat and cholesterol. Both of the improved diets caused health improvements and weight loss. But one group that was fed a diet still fairly high in sugar - an amount of sugar comparable to the Western diet - had significantly higher levels of inflammation, oxidative stress and liver fibrosis. More research is still needed to determine whether a comprehensive program of diet, weight maintenance, exercise and targeted drug therapies can fully resolve liver fibrosis, the study concluded.

This research was supported by the National Institutes of Health and the U.S. Department of Agriculture.

About the Linus Pauling Institute

The Linus Pauling Institute at OSU is a world leader in the study of micronutrients and their role in promoting optimum health or preventing and treating disease. Major areas of research include heart disease, cancer, ageing and neurodegenerative disease.

Further Information

David Stauth; Tel: +1 541-737-0787

Donald Jump  541-737-4007;

Kelli Lytle,

This story is available online:

The study this story is based on is available online:


Red Meat, Processed Meat, or No Meat?

by Ralph Campbell MD

Hullabaloo about the ‘new finding that bacon is bad for you might have found a reasonable level of attention but for the World Health Organization having entered the fray.[1,2] For several decades, we have known of the potential carcinogenicity of nitrates and nitrites used by the meat processing industry. Nitrites work as a meat preservative and, like rouge, make meat look ‘in the pink’ and appear far fresher than it really is. But WHO, adding an aura of science, went and created categories of carcinogenicity: 1) Firm link 2) Probable link 3) Possible link. Processed meats were put in the Type 1 category and red meat in Type 2. Any further distinction ends here, because they lumped together naturally red meat and processed meats in their statistical analysis. That makes about as much sense as studying polyunsaturated fats without separating out trans-fats.

Of 190,000 adults studied for seven years, those eating the most processed meat such as deli meats and hot dogs had a 68 percent greater risk of pancreatic cancer than those who ate the least.[3]

Cancer-Causing Toxins

Soon after the scientific community first realized that exposure to toxins in our environment would prove to be carcinogenic, Dr Bruce Ames developed a test which determined whether a substance was mutagenic for some bacteria.[4] Many chemicals and heavy metals were found to be. More risk comes from the formation of carcinogenic polycyclic aromatic hydrocarbons in charred meat from grills and barbeques. The problem is compounded by chemicals in the meat and its fat. Did the animal graze on grass laden with herbicides and pesticides? Or did it consume antibiotics, furnished in the feed lot? In both animals and humans, fat-soluble pesticides are stored, predictably enough, in fat. Considering this, shouldn't the animals' environment and feed be carefully tested? And better yet, wouldn't true organic meat fill the bill? Would a pure vegetarian diet also work? Many would hope to be able to include some meat in their diet.

If bacon is not sick to begin with, it doesn't need to be cured.

Early Prevention

From the first mutagenic mishap until cancer is detectable may take years, even decades. What is currently called ‘preventive medicine’ is only early detection. The cat is already out of the bag. Instead, a group of participants should be followed on an organic or vegetarian diet for several decades, then checked carefully for cancer. True preventive medicine should begin early in life while still healthy. We know that a sufficient level of vitamin C may stop those first mutant cells.[5] Now there's a good cost effective preventive measure everyone can use.

Children who eat one hot dog a week double their risk of a brain tumor; two per week triples the risk. Kids eating more than twelve hot dogs a month (three a week) have nearly ten times the risk of leukemia as children who eat none.[6]

Hot dog eating children taking supplemental vitamins have been shown to have a reduced risk of cancer. [7]

We have to deal with the false notion that a single substance in the human diet causes cancer. There are many types of cancer. Some are influenced by hormones. Bowel cancer development depends, in part, on how long the carcinogen is in contact with the bowel, the concept of transit time developed by Dr Denis Parsons Burkitt.[8] By comparing the African diet with the British, he determined that dietary fibre was an important factor in decreasing transit time. We now know that fibre also creates a healthy intestinal flora or microbiome. I saw this information turn quite a few ‘meat and potato’ folks on to whole grains, yogurt and broccoli back in the '60s.

You Need the Team

Since many drugs are developed to have a specific target action of either inhibiting or enhancing the action of an enzyme or other biomolecule, their short-term effects are relatively easy to determine. Not so when testing a single element of the human diet. Nutrients work in concert, so testing for an adequate dose of just one alone will not determine its true effect. Laboratory studies on mice allow complete control of the mouse environment: food, temperature, noise level, time of exercise on their little Ferris wheels, or what have you. But with our human diet, we cannot find a test nutrient that can stand alone. Your internal nutritional chemistry program has many actors.

In studies of the effects of individual vitamins, we shouldn't always expect them individually to work miracles. We must also get beyond the mentality of a magic-bullet-drug cure for cancer. True prevention is boosting health by all possible means: diet, including adequate vitamin intake; healthy gut microbiome; exercise; minimizing mental stress; avoiding processed food and food chemicals. Orthomolecular medicine principles absolutely demand adequate intake of vitamins and essential nutrients. I find folks influenced by drug advertising thinking of vitamins as just more pills. They often question whether a dose of vitamin C that is just under the bowel tolerance level can be helpful. Well, it is.

But not Processed Meat

We know that processed meats are bad for us, especially when taken in large portions. Recently, I've seen ads for sandwiches containing huge servings of bacon as if to convey the idea that "It may be a bit bad for you, but it is sooooo good. Come, buy!" Is it better to be satiated than healthy? How much of a bit of unhealth is OK? The tricks for those eating meat are: 1) get organic and 2) don't eat a lot of it. I would suggest emulating the Mediterranean diet: make meat a condiment to go with your vegetables and other plant foods. Skip the half-pound bacon-burger. And maybe take a pass on that hot dog as well.

About the Author

Dr Ralph Campbell, a retired paediatrician, is getting close to 90 but you'd hardly know it. He is an active orchard farmer and still sets out his own irrigation pipelines. He is the author, along with Andrew Saul, of The Vitamin Cure for Children's Health Problems and also The Vitamin Cure for Infant and Toddler Health Problems.


1. Bouvard V, Loomis D, Guyton KZ et al. International Agency for Research on Cancer Monograph Working Group. Carcinogenicity of consumption of red and processed meat. Lancet Oncol. 16:1599-1600. doi: 10.1016/S1470-2045(15)00444-1. 2015.


3. Nothlings U, Wilkens LR, Murphy SP et al.  Meat and fat intake as risk factors for pancreatic cancer: The Multiethnic Cohort Study. J Nat Cancer Inst 97:1458-65. 2005.

4. Ames BN, Durston WE, Yamasaki E, Lee FD. Carcinogens are mutagens: a simple test system combining liver homogenates for activation and bacteria for detection. Proc Natl Acad Sci USA. 70:2281-22855. 1973.

5. Scanlan RA. Nitrosamines and cancer.  

6. Peters JM, Preston-Martin S, London SJ, Bowman JD, Buckley JD, Thomas DC. Processed meats and risk of childhood leukemia. Cancer Causes Control. Mar; 5(2):195-202. 1994.

7. Sarasua S, Savitz DA. Cured and broiled meat consumption in relation to childhood cancer: Denver, Colorado. Cancer Causes Control. Mar; 5(2):141-8. 1994.

8. Burkitt DP. (1971) Epidemiology of cancer of the colon and rectum. Cancer. 28:3-13. 1971.

Nutritional Medicine is Orthomolecular Medicine

Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: 

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The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:

Ian Brighthope, M.D. (Australia)

Ralph K. Campbell, M.D. (USA)

Carolyn Dean, M.D., N.D. (USA)

Damien Downing, M.D. (United Kingdom)

Michael Ellis, M.D. (Australia)

Martin P. Gallagher, M.D., D.C. (USA)

Michael Gonzalez, D.Sc., Ph.D. (Puerto Rico)

William B. Grant, Ph.D. (USA)

Michael Janson, M.D. (USA)

Robert E. Jenkins, D.C. (USA)

Bo H. Jonsson, M.D., Ph.D. (Sweden)

Peter H. Lauda, M.D. (Austria)

Thomas Levy, M.D., J.D. (USA)

Stuart Lindsey, Pharm.D. (USA)

Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)

Karin Munsterhjelm-Ahumada, M.D. (Finland)

Erik Paterson, M.D. (Canada)

W. Todd Penberthy, Ph.D. (USA)

Jeffrey A. Ruterbusch, D.O. (USA)

Gert E. Schuitemaker, Ph.D. (Netherlands)

Jagan Nathan Vamanan, M.D. (India)

Atsuo Yanagisawa, M.D., Ph.D. (Japan)


Robert G. Smith, Ph.D. (USA), Assistant Editor

Helen Saul Case, M.S. (USA), Assistant Editor

Michael S. Stewart, B.Sc.C.S. (USA), Technology Editor


Andrew W. Saul, Ph.D. (USA), Editor and contact person. Email:  This is a comments-only address; OMNS is unable to respond to individual reader emails. However, readers are encouraged to write in with their viewpoints. Reader comments become the property of OMNS and may or may not be used for publication.


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New Therapy Halts Progression of Lou Gehrig’s Disease in Mice 

by David Stauth

Researchers at Oregon State University announced today that they have essentially stopped the progression of amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, for nearly two years in one type of mouse model used to study the disease - allowing the mice to approach their normal lifespan. The findings, scientists indicate, are some of the most compelling ever produced in the search for a therapy for ALS, a debilitating and fatal disease, and were just published in Neurobiology of Disease.

“We are shocked at how well this treatment can stop the progression of ALS,” said Joseph Beckman, lead author on this study, a distinguished professor of biochemistry and biophysics in the College of Science at Oregon State University, and principal investigator and holder of the Burgess and Elizabeth Jamieson Chair in OSU’s Linus Pauling Institute.

In decades of work, no treatment has been discovered for ALS that can do anything but prolong human survival less than a month. The mouse model used in this study is one that scientists believe may more closely resemble the human reaction to this treatment, which consists of a compound called copper-ATSM. It’s not yet known if humans will have the same response, but researchers are moving as quickly as possible toward human clinical trials, testing first for safety and then efficacy of the new approach.

ALS was identified as a progressive and fatal neurodegenerative disease in the late 1800s, and gained international recognition in 1939 when it was diagnosed in American baseball legend Lou Gehrig. It’s known to be caused by the death and deterioration of motor neurons in the spinal cord, which in turn has been linked to mutations in copper, zinc superoxide dismutase.

Copper, zinc superoxide dismutase is essential to life, but when damaged can become toxic. Photo courtesy of Oregon State University

Copper, zinc superoxide dismutase is essential to life, but when damaged can become toxic. Photo courtesy of Oregon State University

Copper-ATSM is a known compound that helps deliver copper specifically to cells with damaged mitochondria, and reaches the spinal cord where it’s needed to treat ALS. This compound has low toxicity, easily penetrates the blood-brain barrier, is already used in human medicine at much lower doses for some purposes, and is well tolerated in laboratory animals at far higher levels. Any copper not needed after use of copper-ATSM is quickly flushed out of the body. Experts caution, however, that this approach is not as simple as taking a nutritional supplement of copper, which can be toxic at even moderate doses. Such supplements would be of no value to people with ALS, they said. The new findings were reported by scientists from OSU; the University of Melbourne in Australia; University of Texas Southwestern; University of Central Florida; and the Pasteur Institute of Montevideo in Uruguay. The study is available as open access in Neurobiology of Disease.

Using the new treatment, researchers were able to stop the progression of ALS in one type of transgenic mouse model, which ordinarily would die within two weeks without treatment. Some of these mice have survived for more than 650 days, 500 days longer than any previous research has been able to achieve.

In some experiments, the treatment was begun, and then withheld. In this circumstance the mice began to show ALS symptoms within two months after treatment was stopped, and would die within another month. But if treatment was resumed, the mice gained weight, progression of the disease once again was stopped, and the mice lived another 6-12 months.

In 2012, Beckman was recognized as the leading medical researcher in Oregon, with the Discovery Award from the Medical Research Foundation of Oregon. He is also director of OSU’s Environmental Health Sciences Center, funded by the National Institutes of Health to support research on the role of the environment in causing disease.

“We have a solid understanding of why the treatment works in the mice, and we predict it should work in both familial and possibly sporadic human patients,” Beckman said. “But we won’t know until we try.”

Familial ALS patients are those with more of a family history of the disease, while sporadic patients reflect the larger general population.

“We want people to understand that we are moving to human trials as quickly as we can,” Beckman said. “In humans who develop ALS, the average time from onset to death is only three to four years.”

The advances are based on substantial scientific progress in understanding the disease processes of ALS and basic research in biochemistry. The transgenic mice used in these studies have been engineered to carry the human gene for “copper chaperone for superoxide dismutase,” or CCS gene. CCS inserts copper into superoxide dismutase, or SOD, and transgenic mice carrying these human genes die rapidly without treatment.

After years of research, scientists have developed an approach to treating ALS that’s based on bringing copper into specific cells in the spinal cord and mitochondria weakened by copper deficiency. Copper is a metal that helps to stabilize SOD, an antioxidant protein whose proper function is essential to life. But when it lacks its metal co-factors, SOD can ‘unfold’ and become toxic, leading to the death of motor neurons. There’s some evidence that this approach, which works in part by improving mitochondrial function, may also have value in Parkinson’s disease and other conditions, researchers said. Research is progressing on those topics as well.

The treatment is unlikely to allow significant recovery from neuronal loss already caused by ALS, the scientists said, but could slow further disease progression when started after diagnosis. It could also potentially treat carriers of SOD mutant genes that cause ALS.

This work has been supported by the Department of Defence Congressionally Directed Medical Research Program, the U.S. National Institutes of Health, the Amyotrophic Lateral Sclerosis Association, the Australian National Health and Medical Research Association, and gifts by Michael Camillo and Burgess and Elizabeth Jamieson to the Linus Pauling Institute.

Further Information

Source: David Stauth <>

Tel: +1 541-737-0787

Contact: Joseph Beckman, 541-737-8867 or

This story is available online:

The study this story is based on is available online:


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