TREATMENT EXTENDS SURVIVAL IN MOUSE MODEL OF SPINAL MUSCULAR ATROPHY

TREATMENT EXTENDS SURVIVAL IN MOUSE MODEL OF SPINAL MUSCULAR ATROPHY

Drug therapy can extend survival and improve movement in a mouse model of spinal muscular atrophy (SMA), New research shows. The study, carried out at the NIH's National Institute of Neurological Disorders and Stroke (NINDS), suggests that similar drugs might one day be useful for treating human SMA.

"This study shows that treatment can be effective when started after the disease appears," says Kenneth H. Fischbeck, M.D., of the NINDS, who helped lead the New study. The finding is important because most children with SMA are diagnosed after symptoms of the disease become obvious, he adds. The report appears in the February 22, 2007, advance online publication of "The Journal of Clinical Investigation".[1]

SMA is the most common severe hereditary neurological disease of childhood, affecting one in every 8,000-10,000 children. Babies with the most common form of the disease, called SMA type I, develop symptoms before birth or in the first few months of life and have severe muscle weakness that makes it difficult for them to breathe, eat, and move. They usually die by age two. Other forms of SMA are not as severe, but still cause significant disability. While some symptoms of SMA can be alleviated, there is currently no treatment that can change the course of the disease.

SMA is caused by mutations in a gene called SMN1. Investigators studying the genetics of SMA have found that there is another gene, called SMN2, on the same chromosome. While the normal form of SMN1 produces a full-length functional protein, most of the protein produced by SMN2 is truncated and unable to function. The relatively small amount of normal SMN protein produced by the SMN2 gene can reduce the severity of the disease. Therefore, investigators are searching for drugs that can increase the amount of normal protein produced by this gene.

The New study, directed by Dr. Fischbeck's colleague Charlotte J. Sumner, M.D., at NINDS, tested a drug called trichostatin A (TSA) that is in a class of drugs called histone deacetylase (HDAC) inhibitors. These drugs increase the activity of certain genes in the body.

Previous studies have shown that HDAC inhibitors can increase the amount of SMN2 expression in cultured cells and that treating pregnant mice with an HDAC inhibitor can increase the survival of their babies with SMA. Preliminary clinical trials are now underway to test several HDAC inhibitors in children who have SMA. However, the drugs in those clinical trials are weak HDAC inhibitors with other biological effects that may limit their usefulness for treating this disease. More importantly, none of the previous studies has demonstrated that HDAC inhibitors can extend survival when delivered after symptoms appeared.

In the New study, the investigators tested TSA, which is a potent HDAC inhibitor, in cells from SMA patients and in a mouse model of SMA. They found that the drug increased the amount of SMN2 gene activity in both the cultured cells and the mouse model.

Next, the researchers gave daily injections of TSA to the SMA mice, starting when the mice were 5 days old. By that time, the mice showed clear symptoms of disease: they were significantly underweight and they had a markedly impaired righting reflex, or ability to get on their feet after being placed on their backs. The treated mice lived 19 percent longer, on average, than mice that did not receive TSA. About three-fourths of the treated mice had improved survival compared to control mice. The other fourth showed no improvement.

The treated mice had less weight loss and better righting reflexes, walking ability, and forelimb grip strength than mice that did not receive TSA. Examination showed that the TSA-treated mice also had larger neurons in the spinal cord, thicker muscle fibers, and more muscle mass than untreated mice.

"This is a proof-of-concept experiment," says Dr. Sumner. "It clearly demonstrates that this treatment can ameliorate the disease in mice." While the results are exciting, there are still no studies that have proven the effectiveness of HDAC inhibitors in humans, she cautions.

The investigators are now testing whether treatment with TSA earlier in the disease process will work better than the delayed treatment in this study. They also plan to test other HDAC inhibitors in mice and to study exactly how the drugs influence the disease process. While TSA is expensive to produce and it is not approved for clinical use, similar drugs being developed to treat cancer and other diseases may be useful for treating SMA, Dr. Sumner says.

Reporters: for more information, call 301-496-5924 or go to . Information about SMA is available at . A photo of mice used in this study is available at .

The National Institute of Neurological Disorders and Stroke is the nation's primary funder of research on the brain and nervous system. More information about SMA and other neurological disorders can be found on the NINDS web site, .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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[1]Avila AA, Burnett BG, Taye AA, Gabanella F, Knight MA, Hartenstein P, Cizman Z, Di Prospero NA, Pellizzoni L, Fischbeck KH, Sumner CJ. "Trichostatin A increases SMN expression and survival in a mouse model of spinal muscular atrophy." "The Journal of Clinical Investigation", Advance Online Publication, February 22, 2007, doi: 10.1172/JCI29562.

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This NIH News Release is available online at:

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Saludos Cordiales

Dr. José Manuel Ferrer Guerra

Cholesterol's role in heart attacks probed

EAST LANSING, Mich., -- A Michigan State University study has focused on the role cholesterol plays in causing heart attacks, strokes and other cardiovascular events in humans. The work by cardiologist Dr. George Abela found cholesterol built up along an artery's wall and crystallized from a liquid to a solid state can expand and then burst, sending material into the bloodstream. It is such a chain of events -- the expansion of the liquid cholesterol as it crystallizes into a solid -- that kickstarts the body's natural clotting process, which, unfortunately in such a case, works against the body, essentially shutting down the artery. "As the cholesterol crystallizes, two things can happen," Abela said. "If it's a big pool of cholesterol, it will expand and just tear the cap off the deposit in the arterial wall. Or the crystals, which are sharp, needle-like structures, poke their way through the membrane covering the cholesterol deposit, like nails through wood. Once a rupture or erosion of the surface of the artery occurs, then the clotting system is activated to do its job." The study is published in the September edition of Clinical Cardiology.

LARGEST-EVER SEARCH FOR AUTISM GENES REVEALS NEW CLUES

LARGEST-EVER SEARCH FOR AUTISM GENES REVEALS NEW CLUES

The largest search for autism genes to date, funded in part by the National Institutes of Health (NIH), has implicated components of the brain's glutamate chemical messenger system and a previously overlooked site on chromosome 11. Based on 1,168 families with at least two affected members, the genome scan also adds to evidence that tiny, rare variations in genes may heighten risk for autism spectrum disorders (ASD)*.

The study is the first to emerge from the Autism Genome Project (AGP) Consortium, a public-private collaboration involving more than 120 scientists and 50 institutions in l9 countries. Their report is published online in the February 18, 2007 issue of "Nature Genetics".

With NIH support, the AGP is pursuing studies to identify specific genes and gene variants that contribute to vulnerability to autism. These include explorations of interactions of genes with other genes and with environmental factors, and laboratory research aimed at understanding how candidate susceptibility genes might work in the brain to produce the disorders.

"This is the most ambitious effort yet to find the locations of genes that may confer vulnerability to autism," said NIH Director Elias A. Zerhouni, M.D. "The AGP is revealing clues that will likely influence the direction of autism research for years to come."

"Although we know autism is highly heritable, complex gene interactions and submicroscopic anomalies create a din of statistical noise that drowns out detection of signals from linked sites in the genome," explained Dr. Bernie Devlin, University of Pittsburgh, who served as a corresponding author on the project along with the University of Toronto's Dr. Stephen Scherer. "To amplify these signals, we brought to bear gene chip technology with a huge sample, and also screened for these fine-level anomalies, factoring them into the analysis."

Clues emerged adding to evidence that implicates components of the brain's glutamate neurotransmitter system in autism. Glutamate increases neuronal activity and plays an important role in wiring up the brain during early development. Since autism likely stems from faulty wiring, a genetic blueprint gone awry in this pivotal neurotransmitter system is a prime suspect. Some key genes associated with the glutamate system are located in chromosome regions previously associated with autism, note the researchers.

Previous studies have also linked abnormal glutamate functioning to disorders such as Fragile X syndrome and tuberous sclerosis, which share some symptoms with autism. It's not unusual for individuals with either syndrome to be diagnosed with autism.

Among the New clues is stronger evidence for an association between autism and sites of genes for neurexins, molecules that build glutamate synapses -- the connection machinery by which brain cells communicate.

A site on chromosome 11 most strongly linked to autism in this study harbors genes for proteins that shuttle glutamate across the synapse. Although detected previously, the linkage signal at this site was regarded as less important until now.

Submicroscopic anomalies -- tiny deletions, or the doubling, tripling or even multiplying of stretches of genetic material -- are relatively common in the human genome and aren't necessarily harmful. However, recent evidence suggests that these anomalies may contribute to risk for -- or rarely even cause -- autism if they affect certain sites associated with the disorder. The AGP researchers found a number of these variations in such suspect chromosomal locations in affected individuals, including deletion of a neurexin gene.

These anomalies can also make it more difficult to detect the genes that more commonly account for autism risk, say the researchers. Since each major autism candidate gene likely contributes to risk for a relatively small percentage of families, its linkage signal can easily be lost in the statistical noise generated by those of the anomalies -- just as a high level of static can drown out a weak radio signal.

To amplify the power of possible linkages detected, the researchers analyzed many subsets of data, variously excluding from the sample factors like the submicroscopic anomalies, female sex, and ethnicity. These analyses unmasked several suggestive linkages that would otherwise have eluded detection.

Researchers last Fall reported discovery of a gene version linked to autism and how it likely works at the molecular level to increase risk. The AGP researchers propose that multiple such gene variants, perhaps interacting with each other and with the tiny anomalies, contribute to risk. As more such genes are identified, studies of how they work in the brain -- in mice and other model systems -- will help to sort out the genetic and proposed environmental influences on autism spectrum disorders, say researchers.

A second phase of AGP studies will follow up on leads suggested in this first phase.

Gene typing and data analysis was funded by Autism Speaks (formerly NAAR). NIH Institutes, led by NIMH, funded the recruitment and assessment of U.S. Families.

The AGP Consortium is comprised of four existing consortia: Autism Genetics Cooperative (AGC), Autism Genetic Resource Exchange (AGRE) Consortium, Collaborative Programs of Excellence (CPEA), International Molecular Genetic Study of Autism Consortium (IMGSAC). Dr. Andy Shih of Autism Speaks served as scientific manager of the project.

Principal investigators of NIH-funded components of the study were: Joseph Buxbaum, Susan Folstein, Neil Risch, James Sutcliffe, Daniel Geschwind, Bernie Devlin, Edwin Cook, Catherine Lord, NIMH; Joachim Hallmayer, Margaret Pericak-Vance, James Sutcliffe, Thomas Wassink, NINDS; Geraldine Dawson, Gerard Schellenberg, William McMahon, Fred Volkmar, NICHD. The research was also supported by General Clinical Research Centers at Yale University and the University of Utah, both funded by the NCRR.

Information about Autism Spectrum Disorders:

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The National Institute of Mental Health (NIMH) mission is to reduce the burden of mental and behavioral disorders through research on mind, brain, and behavior. More information is available at the NIMH website .

The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Web site at .

The National Institute of Neurological Disorders and Stroke is the nation's primary supporter of research on the brain and nervous system. More information about stroke and other neurological disorders can be found on the NINDS web site, .

The National Center for Research Resources (NCRR) provides laboratory scientists and clinical researchers with environments and tools that they can use to prevent, detect, and treat a wide range of diseases. This support enables discoveries that begin at the molecular and cellular level, move to animal-based studies, and then are translated to patient-oriented clinical research, resulting in cures and treatments for both common and rare diseases. NCRR connects researchers with patients and communities across the nation to bring the power of shared resources and research to improve human health. For more information, visit .

The National Institutes of Health (NIH) -- The Nation's Medical Research Agency -- includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit .

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Saludos Cordiales

Dr. José Manuel Ferrer Guerra

Treatment of Kawasaki Disease

Treatment of Kawasaki Disease

These data do not support adding IV steroids to routine treatment.

Intravenous immune globulin (IVIG) plus aspirin reduces the risk for coronary artery disease in patients with uncomplicated, acute Kawasaki disease (KD). The use of steroids in patients with complicated disease has led to speculation that steroids should become part of routine therapy. In a U.S. Multisite, double-blind, clinical trial, researchers randomized 199 patients with KD and fever for 10 days to receive a single pulsed dose of IV methylprednisolone (30 mg/kg) or placebo added to conventional therapy with IVIG (2 g/kg) and aspirin (80–100 mg/kg/day).

At week 1 and week 5, no differences were noted between groups in any measure of coronary disease, including changes in dimensions of the left anterior descending and right coronary arteries. However, compared with placebo recipients, patients who received IV steroids had shorter periods of initial hospitalization and a lower median erythrocyte sedimentation rate at week 1 (69 vs. 57 mm/hr). The total number of hospital days (including readmissions), days of fever, patients requiring retreatment with IVIG, and adverse events was similar in both groups.

Comment: As noted by the authors and an editorialist, these data do not support the addition of a single dose of IV steroids for primary treatment of uncomplicated KD. However, the duration of follow-up was short. Steroids possibly might further prevent the long-term development of coronary artery disease, but because IVIG reduces the rate of coronary-artery aneurysms detectable by echocardiography to between 3% and 5%, a much larger study would be needed to detect any additional benefit from steroids. In contrast with the results of this study, a randomized study of Japanese children with KD reported improved outcomes using a different IVIG and steroid regimen.

— Howard Bauchner, MD

Published in Journal Watch Pediatrics and Adolescent Medicine February 14, 2007

Citation(s):

Newburger JW et al. Randomized trial of pulsed corticosteroid therapy for primary treatment of Kawasaki disease. N Engl J Med 2007 Feb 15; 356:663-75.

Original article (Subscription may be required)

Burns JC. The riddle of Kawasaki disease. N Engl J Med 2007 Feb 15; 356:659-61.

Original article (Subscription may be required)

Saludos Cordiales

Dr. José Manuel Ferrer Guerra

ASCO GI: Modest Gain With Avastin for Advanced Colorectal Cancer

ORLANDO, Jan. 22 -- Avastin (bevacizumab) added to Eloxatin (oxaliplatin)-based chemotherapy modestly extended progression-free survival in metastatic colorectal cancer, according to results of a randomized phase III trial.

But the improvement, although statistically significant (P=0.0023), only added a little over a month to progression-free survival, which was about 9.4 months, said Leonard Saltz, M.D., of the Memorial Sloan-Kettering Cancer Center in New York, at a gastrointestinal cancers symposium here. Action Points

Explain to interested patients that this report suggests that adding Avastin to standard chemotherapy for metastatic colorectal cancer can extend progression-free survival by a little more than a month.

Explain to interested patients that this study found no significant differences in efficacy of either chemotherapy regimen studied, which suggests that either regimen is an effective treatment option.

This report is based on abstracts presented at a meeting. These data and conclusions should be considered preliminary as they have not yet been reviewed and published in a peer-reviewed publication.

The benefit, said Dr. Saltz, was "more modest than we expected."

"Although previous studies have not examined its use in the first-line setting, oxaliplatin-based chemotherapy plus bevacizumab is nonetheless currently a widely used first-line treatment regimen in standard practice in the United States for advanced colorectal cancer," said Dr. Saltz.

The modest benefit notwithstanding, he added, "it shows that doctors who have been adding Avastin have been doing the right thing in treating patients."

In addition to a less than robust improvement in progression-free survival, Dr. Saltz said, it was also disappointing to learn that "the inclusion of Avastin did not improve the response rate in these patients."

Another finding of the trial, and one that has the potential for greater clinical impact than the Avastin benefit, was the observation that the XELOX chemotherapy regimen, which combined Xeloda (capecitabine) and Eloxatin, was as effective as the standard FOLFOX4 regimen, which contains 5FU (5 fluorouracil), Wellcovorin (leucovorin), and Eloxatin.

"We found that the XELOX regimen resulted in progression-free survival that was basically the same as treatment with the FOLFOX4," he said.

Based on that finding, he added, "we think that XELOX is an acceptable alternative to FOLFOX and because XELOX included Xeloda which is an oral medication we believe that it should be offered to patients who are likely to be compliant with a complicated oral regimen."

Neal Meropol, M.D., of the Fox Chase Cancer Center in Philadelphia, commented that the results confirm that "Xeloda plus Eloxatin is an acceptable backbone of frontline treatment based on these results showing that the XELOX arm is equivalent to FOLFOX arm."

He also agreed that the "study validates the use of Avastin as a component of frontline therapy with Eloxatin-based chemotherapy for metastatic breast cancer."

Dr. Meropol, who was not involved in the study, chaired a press conference where the results of phase III trial were discussed.

The multicenter trial enrolled 1,401 patients who were receiving chemotherapy with either FOLFOX4 or XELOX regimens. The patients were randomized to regimen plus Avastin or placebo.

The complicated trial was designed to compare XELOX to FOLFOX4 in a non-inferiority trail that enrolled 317 patients in each arm from June 2003 to May 2004.

The trial was expanded in February 2004 to include the Avastin versus placebo arms.

That added 350 patients who received XELOX plus placebo, 350 Avastin plus XELOX, 351 who received FOLFOX4 plus placebo, and 349 randomized to FOLFOX4 plus Avastin.

Irrespective of chemotherapy regimen, the median progression-free survival for patients randomized to Avastin was 9.4 months versus eight months for the placebo groups.

The National Cancer Institute funded the trial with support from Roche. Dr. Saltz disclosed that he was a consultant or acted in an advisory capacity for Amgen, Genentech, Pfizer, Roche and Sanofi-Aventis; that he receives honoraria from Roche, and that he received research funding from Lilly Pharmaceuticals.

Dr. Meropol reported that he acted as a consultant or adviser to Amgen, Genomic Health, Genentech, Pfizer, Bristol-Myers Squibb, and also received research funding from Amgen and Genentech.

The American Society of Clinical Oncology, the American Society for Therapeutic Radiology and Oncology, the American Gastroenterological Association Institute, and the Society of Surgical Oncology, jointly sponsored the Gastrointestinal Cancer Symposium

Saludos Cordiales

Dr. José Manuel Ferrer Guerra

Carb control gains support

Fans of the Atkins weight-loss regimen can breathe a little easier -- contrary to what some believed, a low-carbohydrate, high-fat diet does not increase the risk of heart disease, a recent study suggests.

In 1973, a year after the book Dr. Atkins' Diet Revolution was published, the American Medical Association called the diet's emphasis on meat, eggs and cheese "potentially dangerous" and many in the Medical community agreed.

The study, conducted by researchers at Harvard University's Schools of Medicine and Public Health and published in the November 9, 2006, issue of the New England Journal of Medicine, claims otherwise. It found that low-carb, high-protein and high-fat diets do not increase the risk of heart disease in women and that when such diets primarily include vegetable sources of protein and fat, the risk of heart disease decreases by 30 per cent

Curbing carbs

The results don't surprise Elizabeth Frank, a dietitian in private practice in Lunenberg, N.S. "The fact is," she says, "when you reduce your carbohydrates, when you reduce your calories, you reduce your weight, and that helps fight heart disease." By reducing your intake of any food group, whether it's carbs, fat, protein or dairy, you'll lose weight -- it's the restriction of calories going in, not specifically the restriction of carbs, that makes you shed pounds. Further, low-carb diets appear to work in the short term because they help your body release water. Once you stop the diet, the water weight returns.

The study also showed that a low-fat diet that consists of lots of carbs in the form of refined sugars and highly processed foods increased blood sugar levels and the risk of heart disease. Study participants included almost 83,000 female nurses who, once a year, provided detailed reports of the food they ate for more than 20 years.

Resist extreme dieting

Researchers admit that any extreme diet, whether very low-fat or very low-carb, is not the best way to prevent cardiovascular disease -- especially because strict diets are hard to follow for long periods of time.

Frank adds that you need carbohydrates for energy -- consume high-quality versions from fruits, vegetables and whole grains. Meanwhile, dietary fat is fine, as long as it's in the form of "good" fats, like olive and canola Oil, fish, nuts and seeds, rather than "bad" fats from tropical oils, marbled meats, lard and commercially prepared foods.

Don't diet alone

Whether you're dieting for heart health or weight loss, visit a doctor or dietitian for a good foundation. A recent survey found that 70 per cent of Americans try dieting on their own and turn to dietary supplements rather than their physicians. The first step, suggests Frank, is following Canada's Food Guide. Then:

• Avoid trans fats

• Watch your portions

• Don't give up any foods -- just eat in moderation

• Write down what, and when, you eat

• Get some exercise

When you want to lose weight, do it safely, persist and be patient. "You have to think of it as a permanent life change," explains Frank. "You didn't gain the weight in 10 days. Don't expect to lose it in 10 days. If you lose it slowly you keep it off."

Saludos Cordiales

Dr. José Manuel Ferrer Guerra

Cancer oral sore

Are Cancer Treatments Effective - The Real Story By Lena Sanchez

I do not wish this article to be discouraging and I do offer an alternative at the end, so do not despair half way through reading.

Let’s look at the 2000 sad stats on American Healthcare’s $1.3B industry. 1 out of 3 people get cancer, 1 out of 2 get heart disease, obesity is at epidemic levels, 70% of children are getting hardening deposits in their arteries as early as 12 years of age. And here is the worst one of all, 62% of accidental deaths are attributed to prescriptions. 2001 found prescription deaths greater than illegal drug deaths. In 2000 109,000 people died from prescription drugs another 2.2 million survive but have illnesses or severe debilitation caused by prescription use. So what does that tell you about how well we are doing as a westernized Medical society? The figures for 2001 & 2002 aren’t in yet but believed to be even more severe.

“Deadly Medicine? Every year over 500,000 people worldwide die from illness or organ diseased from the side effects of pharmaceutical products,” says the Journal of the American Medical Association (JAMA). These pharmaceuticals are used to treat the most deadly diseases known to Western Man: heart attack, cancer, and stroke.”

I shudder when reading reports like these, even though most are from a few years back, sadly the story is that the healing rate has not increased but actually decreased in some areas! I wonder how many people have lost their lives early because of money and the Medical mess that has been created by perpetuating cancer cures in the Medical community that aren’t really cures but money producers?

Harvard University’s published cancer mortality for 2,000 excluded non-melanoma skin cancer, non-Hodgkin’s Lymphoma, stomach cancers and other rare cancers. Their death figures from the top fourteen cancers were 216,700 men and 197,600 women, children were not reported. Aside from certain rare cancers, it is impossible to detect any sudden changes in the death rates for any of the major cancers that could be credited to chemotherapy.

Whether any of the common cancers can be cured by chemotherapy has yet to be established. In most common solid tumors-lung, colon, breast, etc. Chemotherapy is NOT curative.

Why the growth in chemotherapy in the face of such failure? A look at the financial intercourse between a large cancer Center such as Memorial Sloan-Kettering Cancer Center (MSKCC) and the companies that make billions selling chemotherapy drugs makes for revealing why.

James D. Robinson III, Honorary Chairman of the MSKCC Board of Overseers and Managers, is a director of Bristol-Myers Squibb, the world’s largest producer of chemotherapy drugs. Richard Gelb, Vice-Chairman of the MSKCC board is Chairman of the Board at Bristol-Myers. Richard Furlaud, another MSKCC board member, recently retired as Bristol Myers’ president. Paul Marks, MD, MSKCC’s President and CEO, is a director of Pfizer.

Very few know that chemotherapy drugs are not FDA approved. They are legally administered under the Rule of Probable Cause” states that experimental drugs may be used if the side effect of the drug is no worse than the end effect of the disease. In fact, every chemotherapy bottle is stamped “For Experimental Use Only” and the patient must sign a release before the doctor will prescribe or administer it.

Multiple papers have been written stating that while some oncologists inform their patients of the lack of evidence that treatments work…others may well be misled by scientific papers that express unwarranted optimism about chemotherapy. Still others respond to an economic incentive. Physicians can earn much more money running active chemotherapy practices than they can providing solace and relief…to dying patients and their families.”

In my research to find cure rates they are knowningly and loudly unobtainable, saying more than numbers. You know if they exist or were good the pharmaceutical industry would be singing them loud and clear.

Alan C. Nixon, PhD, Past President of the American Chemical Society wrote that “As a chemist trained to interpret data, it is incomprehensible to me that physicians can ignore the clear evidence that chemotherapy does much, much more harm than good.”

In 1986, McGill Cancer Center scientists sent a questionnaire to 118 doctors who treated non-small-cell lung cancer. More than three-quarters of them recruited patients and carried out trials of toxic drugs for lung cancer.

They were asked to imagine that they themselves had cancer, and were asked which of six current trials they themselves would choose. Of the 79 respondents, 64 said they would not consent to be in a trial containing cisplatin, a common chemotherapy drug. Fifty-eight found all the trials unacceptable. Their reasons? The ineffectiveness of chemotherapy and its unacceptable degree of toxicity.

Famed German biostatistician Ulrich Abel, PhD, also found in a similar 1989 study that “the personal views of many oncologists seem to be in striking contrast to communications intended for the public.”

“Most cancer patients in this country die of chemotherapy. Chemotherapy does not eliminate breast, colon, or lung cancers. This fact has been documented for over a decade, yet doctors still use chemotherapy for these tumors.” Allen Levin, MD UCSF The Healing of Cancer, Marcus Books, 1990

Why so much use of chemotherapy if it does so little good? Well for one thing, drug companies provide huge economic incentives. In 1990, $3.53 billion was spent on chemotherapy. By 1994 that figure had more than doubled to $7.51 billion and tripled in 2002 when all other industries were struggling to stay afloat. This relentless increase in chemotherapy use is accompanied by a relentless increase in cancer deaths. Again death certificates state causes of death as cancer, when I personally know of some that were free of cancer but died from the ongoing chemotherapy prevention! This makes it impossible to know how many actually die from chemotherapy!

Oncologist Albert Braverman, MD, wrote in 1991 that “No disseminated neoplasm (cancer) incurable in 1975 is curable today…Many medical oncologists recommend chemotherapy for virtually any tumor, with a hopefulness undiscouraged by almost invariable failure.” Twelve years hasn’t changed that or the cancer death wouldn’t continue to rise.

If you or a loved one should have need of such medical treatment look long and hard before buying what you are being told. Take charge of your life and get to the bottom of the truth before being treated.

I do not get a cent from this recommendation for cancer treatment or second opinion. That is the “Oasis Cancer Center” with the largest cancer cure rate of any other treatment center and theirs is with natural cures and sometimes surgery where surgery is needed They are forced to practice medicine just across the border from the U.S. in order to practice without harassment For a free consultation online http://www.cancure.org/oasis_hospital.htm or call in the US (888) 500-4673 outside the US call 011 52 664 631 61 00

*** Lena Sanchez Author of “Handbook Of Herbs To Health & Other Secrets,” “Antibiotic Alternatives To Preventing Mega Bacteria,” & “Dangers & Secrets Doctors Refuse To Tell You.” Found online at http://www.antibiotic-alternatives.com and Editor of “Natural Environmental Health Facts & Your Home Business Coach” ezine subscribe at http://www.envirodocs.com/newsletter.htm

Author of “Handbook Of Herbs To Health & Other Secrets,” “Antibiotic Alternatives To
Preventing Mega Bacteria,” & “Dangers & Secrets Doctors Refuse To Tell You.” Found online at http://www.antibiotic-alternatives.com and Editor of “Natural Environmental Health Facts & Your Home Business Coach” ezine subscribe at http://www.envirodocs.com/newsletter

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Saludos Cordiales

Dr. José Manuel Ferrer Guerra