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Cancer
Jun 3, 2015 8:42:52 GMT -5
Post by Master Kim on Jun 3, 2015 8:42:52 GMT -5
Chemotherapy: "Useless Poisonous Cure"? - www.healingcancernaturally.com/chemotherapy-useless.htmlWelcome to page 30 of “Why Choose Alternative Cancer Treatment?” featuring Dr. Ralph W. Moss’ review and partial translation of an article on chemotherapy published in Germany's Der Spiegel in October 2004. Titled "Useless Poisonous Cure" (Giftkur ohne Nutzen), it discusses among other things the manipulation of reports on the results of chemotherapeutic drugs. Ralph W. Moss, Ph.D., is one of the foremost authorities in the field of alternative cancer treatment. He is the author of "Questioning Chemotherapy: A Critique of the Use of Toxic Drugs in the Treatment of Cancer", and "Cancer Therapy: The Independent Consumer's Guide to Non-Toxic Treatment and Prevention" (more details at Books on Healing Cancer).German Magazine Der Spiegel Blasts Chemotherapyby Ralph Moss, PhDWhile I was in Germany last October an article on chemotherapy appeared in Der Spiegel, which is Germany's - in fact Europe's - highest-circulating news magazine. On average, over one million copies are sold every week, making it the German equivalent of Time or Newsweek [with the major distinction that Der Spiegel has always been a left-leaning magazine]. The article, highly critical of chemotherapy, created quite a stir. Der Spiegel, which has a history of being iconoclastic, has criticized the cancer establishment before. In the early 1990s it gave ample coverage to a critical report from Heidelberg epidemiologist Ulrich Abel, PhD, showing that chemotherapy was ineffective in the treatment of advanced carcinomas. (It was Abel's book that first inspired me to write Questioning Chemotherapy.) The latest article shows that for patients in the advanced stages of the major forms of cancer, chemotherapy has no appreciable effect on survival. This will come as no surprise to long-time readers of this newsletter. But the Spiegel article comes at a time when the pharmaceutical industry is already reeling from revelations of price gouging and the suppression of research data that indicated life- threatening side effects from some of its best-selling drugs. It follows a similarly hard-hitting exposé last spring in the American news magazine, Fortune. Perhaps such widely circulated articles will lead to a public outcry or at least to a changed perception of the value of chemotherapy—a treatment method that normally goes unquestioned in the mainstream media. Poisonous CuresThe title of the article is " Useless Poisonous Cures" (Giftkur ohne Nutzen). Unfortunately, Der Spiegel's website provides no English translation of the article. I have therefore summarized the contents for English-speaking readers. The article reads as follows: Increasingly sophisticated and expensive cellular poisons are being given to seriously ill patients with colon, breast, lung and prostate cancer. Now an epidemiologist has analyzed the actual rate of life extension in such patients. His findings are that despite all the alleged progress, patients do not actually live a day longer. On Christmas eve, Erika Meyer (fictitious name) was taken to ProsperHospital in Recklinghausen. Her doctors removed a malignant tumor from her colon and also removed her spleen. At the beginning of August, however, they discovered that her tumor had metastasized (spread). On Tuesday of the past week the 64-year-old homemaker began her first round of chemotherapy. "This is a complete nightmare for me," said Frau Meyer. "I never thought that I would one day develop cancer. But I hope that I will become better. One’s chances are always better with chemotherapy." (Die sind ja immer weiter mit der Chemotherapie.) At the Clinical Center of the University of Munich one scientist does not share her optimism. Epidemiologist Dieter Hoelzel, 62, says that "as far as survival with metastatic cancer of the colon, breast, lung and prostate goes, there has been no progress in the past 25 years." He has documented the outcome of patients treated since 1978 in and around Munich, according to the standard methods of oncology. These are people suffering from the advanced stages of one of the four major internal cancers, which annually claim about 100,000 victims in Germany alone. These tumors are the big killers. If a tumor has metastasized, and can no longer be reached by surgery or X rays, then chemotherapy is considered the treatment of last resort. For decades, a series of new cellular poisons have been used. Often drug manufacturers have also demanded astronomically high prices. In exchange, they promise a longer life. "A chance at life!" say large billboards, each about 9 feet high, for the drug Taxotere. The manufacturer of a competing product recruits patients using the slogan "Taxol give yourself a future!" (Taxol - dem Leben eine Zukunft geben!) Erika Meyer's physician in Recklinghausen speaks with confidence. Chemotherapy has clearly improved over the past 20 years, says conventional oncologist Friedrich Overkamp, MD, 47. "A considerable extension of lifespan" can be attained, he says. However, the latest figures from the cancer registry of the University of Munich do not confirm that view. Survival rates have not improved over the past decades. Today's patients die just as fast of their cancer as their fellow sufferers did 25 years ago. While the statistical curve for colon cancer shows a slight improvement, the survival rate for breast cancer actually fell over the course of the years. These fluctuations probably mean nothing, said Dr. Hoelzel, except the accidental ups-and-downs of statistics without any real significance. However, he fears that the systematic expansion of chemotherapy for cancer of the breast could be responsible for the decline of the survival rate. These statements from the Munich epidemiologist explicitly do not apply to the chemotherapy of Hodgkin's and non-Hodgkin's lymphoma, leukemia, sarcoma, and testicular cancer. These diseases can be cured in some cases in an almost spectacular way. Hoelzel's verdict also does not apply to chemotherapy that is used to shrink tumors before surgical intervention (neoadjuvant chemotherapy, ed.) or to destroy stray tumor cells after an operation (adjuvant chemotherapy, ed.) But experienced clinicians agree that the balance tips against chemotherapy when it comes to treating solid tumors in advanced stages. Gerhard Schaller, MD, 52, a gynecologist at the University of Bochum, states: "For the survival of women with advanced breast cancer, chemotherapy previously brought them practically no benefit - a lot of noise about nothing." Wolfram Jaeger, MD, 49, Director of Gynecology at the State Clinics of Düsseldorf, has had similar experiences. "Chemotherapy gave, and gives, no successes. Enormous numbers of women are treated, without proven benefit (ohne dass ein Nutzen tatsächlich bewiesen wäre). If we told this to the patients, however, they would totally despair." Millions of PatientsMillions of patients over the past 50 years have undergone chemotherapy. The first patient with an advanced lymphosarcoma (non- Hodgkin's lymphoma, ed.) was treated with mustard gas by US physicians in 1942. The tumor shrank in an almost miraculous way. This effect disappeared after three months and the patient died. Nevertheless, this temporary success rang in the era of chemotherapy against cancer suffering. Cytotoxic drugs are cellular poisons that intervene in a different way in the proliferation of cells. Because tumor cells divide more frequently than most other body cells, tumors and metastases are particularly susceptible to such drugs. Tumors can shrink, and, every now and then, they disappear even completely. However healthy cells, which divide rapidly, can also be damaged, including cells of the hair follicles and the blood forming cells of the bone marrow. The question [of whether or not chemotherapy really extends life, ed.] can probably no longer be answered. In clinical studies the manufacturers always compare their new drugs with older cellular poisons. There are no control groups that are given no treatment at all. In order to be allowed onto the market, it suffices to achieve a "statistically significant" advantage in one small group of hand- picked test subjects vs. those treated with some already approved cellular poison. Some of the early chemotherapeutic drugs led to the premature death of patients and were removed from the market. Other patients were put through hell. They lost their hair and appetite or were plagued by serious systemic infection. The late Klaus Thomsen, MD, long-time director of gynecology of the University Clinic Hamburg-Eppendorf, explained in September 1985, at an international congress in Berlin: "Upon reflection, we should not be surprised if an increasing number of doctors would say that they will abandon such an undistinguished form of treatment." Ten years later, the epidemiologist Ulrich Abel, PhD, of the University of Heidelberg, put the entire usefulness of chemotherapy in doubt. For over a year, this scientist reviewed several thousand publications on chemotherapy. He concluded that "for most internal cancers no proof exists that chemotherapy, especially the increasingly high dose variety, increases life expectancy or improves quality of life." Notable oncologists agreed: the expansion of chemotherapy could not stop that. But because physicians did not want to admit to their patients that they were completely defenselessly against cancer, this poisonous cure became one of the dogmas of medicine. That `benefits' all participants: "The physicians are happy that they have something they can offer, the patients are happy, that they can take something, and the industry is happy," say the Düsseldorf gynecologist Jaeger. Progress mainly consists in reducing the side effects that are caused by the drugs themselves. Earlier, these cellular poisons weakened patients to such an extent that they had to be supervised in the hospital. Now, however, methods of reducing hair loss, appetite loss, diarrhea and blood clots lie at hand. Many chemotherapies can even be carried out on an outpatient basis. Each quarter, oncologist Friedrich Overkamp uses 1.5 million Euro worth of medicines on his 1,100 cancer patients. Nationwide (in Germany) the use of the cytotoxic drugs between August 2003 and July 2004 added up to 1.8 billion Euro an increase of 14 per cent compared to the previous year. (Note: the Euro is currently worth around $1.30). Monoclonal antibodies, which can recognize cancer cells more specifically, are the latest market drivers. Again, the drug manufacturers envision a breakthrough. Nevertheless, in this situation as well, clear proof is lacking that the lifespan of incurably ill cancer patients is truly extended. Meanwhile, competition from the new monoclonal antibodies leads to a situation in which cellular poisons are pushed more aggressively in the market. For decades pharmaceutical manufacturers brought more new cytotoxic drugs to market; in the seventies there were just five, but in the nineties approximately 25 new drugs were approved. "If each of these signified some small progress," said Munich epidemiologist Hoelzel, "then this should have led to remarkable improvements over the past decades. However, we do not see that reflected in our cancer register." It is also difficult to find proof of a survival advantage in the thousands of reports from the drug industry. For metastatic breast cancer there are only about ten studies that suggest that a cytotoxic drug 'cocktail' extends life, when compared to another such mixture. Because, however, thousands such comparative studies have been performed, Heidelberg epidemiologist Abel argues that "statistically remarkable differences in a substantial number of studies are simply due to an expected coincidence." The proponents of chemotherapy refer particularly to two influential works. In the first of these, French researchers studied 724 female patients who had metastatic breast cancer. The three-year survival rate after diagnosis increased from 27 per cent (for those treated between 1987 and 1993) to 43 per cent (1994 to 2000). However, the epidemiologist Hoelzel attributes this apparent improvement to a shortcoming in sampling methodology. In the period 1994 to 2000, metastasized breast cancer tended to be more promptly recognized than it was in the earlier cases (1987-1993). Because the illness had not progressed so far at first diagnosis, life expectancy was much greater. This gave the illusion of an apparent increase in survival time, although of course the apparent improvement in survival rates was not the result of any therapy. Defenders of chemotherapy also cite a study from the University of Texas, Houston, published in August 2003. In this study, the five- year survival rate of women with metastasized breast cancer improved continuously over the years 1974 to 2000, from 10 per cent to 44 per cent. This article also contained an overview of all the cytostatic drugs, which the authors claimed had made this alleged progress possible. However, in the study in question women both with and without metastases were mixed together for comparison. The groups from more recent time were distorted by the inclusion of more female patients who had more favorable prognoses. The authors of this celebratory article actually admit that in a hidden sentence (in einem versteckten Satz). "There is no systematic documentation at all," says Hoelzel of such "trick research" (Trickforschung). "That is the great deficiency of cancer medicine," complains Dr. Hoelzel. Meanwhile, with his demand for clean scientific proof, critic Hoelzel will hardly be allowed to shake up the industry. Because the industry already manages very well without any proof of the utility of drugs for patients with advanced cancer.
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Cancer
Jun 3, 2015 21:43:49 GMT -5
Post by Master Kim on Jun 3, 2015 21:43:49 GMT -5
Why We’re Losing The War on Cancer [and How to Win It] - www.healingcancernaturally.com/conventional-cancer-treatment.htmlby Clifton Leaf, Fortune Magazine, March 22, 2004 Intro by Healing Cancer Naturally
Welcome to page 27 of “Why Choose Alternative Cancer Treatment?” featuring the front-page article Why We’re Losing The War on Cancer [and How to Win It] published in Fortune Magazine of March, 22, 2004. E. Yudenfriend who cured himself of lymphoma (considered incurable by mainstream medicine) comments, “the man who wrote this article is unbiased against or for any particular cancer treatment. He conclusively proves in this article that the cancer establishment [conventional cancer treatment] has made virtually NO significant strides toward curing cancer since the 1950s! Getting someone newly diagnosed with cancer to read this is a first step toward opening up their eyes ...”
And a second very important step is reading the following testimonial: Rushed into conventional breast cancer treatment: a woman’s horror story of manipulation, dishonesty, callousness, lack of integrity & ethics and the trauma, pain, shock, disfigurement and regret she experienced, complemented by the notes on Cancer “Overdiagnosing” and “Overtreatment: Do be aware!. And now over to Clifton Leaf.Avastin, Erbitux, Gleevec … The new wonder drugs might make you think we’re finally beating this dreaded scourge. We’re not. Here’s how to turn the fight around. It’s strange to think that I can still remember the smell after all this time. The year was 1978, not long after my 15th birthday, and I’d sneaked into my brother’s bedroom. There, on a wall of shelves that stretched to the ceiling, were the heaviest books we had in our house—24 volumes of the Encyclopedia Britannica. The maroon spines were coated in a film of dust, I remember. The pages smelled as if a musty old pillow had been covered in mint. I carefully pulled out the volume marked HALICARNASSUS TO IMMINGHAM and turned to the entry for Hodgkin’s disease. It took forever to read the half-dozen paragraphs, the weighty book spread open on my lap like a Bible. There was talk of a mysterious “lymphatic system,” of “granulomas” and “gamma rays,” as though this disease—the one the doctor had just told me I had—was something out of science fiction. But the last line I understood all too well: Seventy-five percent of the people who got it would die within five years. As it turns out, I did not die from Hodgkin’s, though the cancer had already spread from my neck to my lungs and spleen. I lost my spleen to surgery and most of my hair to chemotherapy and radiation. But I was lucky enough to get into a clinical trial at the National Cancer Institute that was testing a new combination therapy— four toxic chemicals, together called MOPP, plus those invisible gamma rays, which flowed from an enormous cobalt 60 machine three stories below ground. The nurses who stuck needles in my arm were so kind I fell in love with them. The brilliant doctor who tattooed the borders of an imaginary box on my chest, then zapped me with radiation for four weeks, had warm pudgy hands and a comic look of inspiration, as though he’d thought of something funny just before entering the exam room. The American taxpayer even footed the bill. Most of all, of course, I was lucky to survive. So it makes the question I am about to ask sound particularly ungrateful: Why have we made so little progress in the War on Cancer? The question may come as a shock to anyone who has witnessed a loved one survive the dread disease—or marveled at Lance Armstrong powering to his fifth Tour de France victory after beating back testicular cancer, or received a fundraising letter saying that a cure is within our grasp. Most recently, with media reports celebrating such revolutionary cancer medicines as Gleevec, Herceptin, Iressa, Erbitux, and the just-approved Avastin, the cure has seemed closer than ever. But it’s not. Hope and optimism, so essential to this fight, have masked some very real systemic problems that have made this complex, elusive, relentless foe even harder to defeat. The result is that while there have been substantial achievements since the crusade began with the National Cancer Act in 1971, we are far from winning the war. So far away, in fact, that it looks like losing. Just count the bodies on the battlefield. In 2004, cancer will claim some 563,700 of your family, friends, co-workers, and countrymen. More Americans will die of cancer in the next 14 months than have perished in every war the nation has ever fought … combined. Even as research and treatment efforts have intensified over the past three decades and funding has soared dramatically, the annual death toll has risen 73%—over one and a half times as fast as the growth of the U.S. population. Within the next decade, cancer is likely to replace heart disease as the leading cause of U.S. deaths, according to forecasts by the NCI and the Centers for Disease Control and Prevention. It is already the biggest killer of those under 75. Among those ages 45 to 64, cancer is responsible for more deaths than the next three causes (heart disease, accidents, and stroke) put together. It is also the leading disease killer of children, thirtysomethings—and everyone in between. Researchers point out that people live a lot longer than they used to, and since cancer becomes more prevalent with age, it’s unfair to look just at the raw numbers when assessing progress. So when they calculate the mortality rate, they adjust it to compare cancer fatalities by age group over time. But even using this analysis [], the percentage of Americans dying from cancer is about the same as in 1970 … and in 1950. The figures are all the more jarring when compared with those for heart disease and stroke []. Age-adjusted death rates for those diseases have been slashed by an extraordinary 59% and 69%, respectively, during the same half-century. Researchers also say more people are surviving longer with cancer than ever. Yet here, too, the complete picture is more disappointing. Survival gains for the more common forms of cancer are measured in additional months of life, not years. The few dramatic increases in cure rates and patient longevity have come in a handful of less common malignancies—including Hodgkin’s, some leukemias, carcinomas of the thyroid and testes, and most childhood cancers. (It’s worth noting that many of these successes came in the early days of the War on Cancer.) Thirty-three years ago, fully half of cancer patients survived five years or more after diagnosis. The figure has crept up to about 63% today. Optimism is essential, but the percentage of Americans dying from cancer is still what it was in 1970 … and in 1950. Yet very little of this modest gain is the result of exciting new compounds discovered by the NCI labs or the big cancer research centers—where nearly all the public’s money goes. Instead, simple behavioral changes such as quitting smoking have helped lower the incidence of deadly lung cancer. More important, with the help of breast self-exams and mammography, PSA tests for prostate cancer, and other testing, we’re catching more tumors earlier. Compare On Cancer Statistics, On Mammography, Prostate test 'all but useless' and Stanford researcher declares 'PSA era is over' in predicting prostate cancer risk. Ruth Etzioni, a biostatistician at Seattle’s Fred Hutchinson CancerResearchCenter, points out that when you break down the Big Four cancers (lung, colon and rectal, breast, and prostate) by stage—that is, how far the malignant cells have spread—long-term survival for advanced cancer has barely budged since the 1970s. Fortune Chart / Source: CDC And the new cases keep coming. Even with a dip in the mid-1990s, incidence rate has skyrocketed since the War on Cancer began. This year an additional 1.4 million Americans will have that most frightening of conversations with their doctor. One in two men and one in three women will get the disease during their lifetime. As a veteran Dana-Farber researcher sums up, “It is as if one World Trade Center tower were collapsing on our society every single day.” So why aren’t we winning this decades-old war on terror—and what can we do now to turn it around? That was the question I asked dozens of researchers, physicians, and epidemiologists at leading cancer hospitals around the country; pharmacologists, biologists, and geneticists at drug companies and research centers; officials at the FDA, NCI, and NIH; fundraisers, activists, and patients. During three months of interviews in Houston, Boston, New York, San Francisco, Washington, D.C., and other cancer hubs, I met many of the smartest and most deeply committed people I’ve ever known. The great majority, it should be said, were optimistic about the progress we’re making, believing that the grim statistics belie the wealth of knowledge we’ve gained—knowledge, they say, that will someday lead to viable treatments for the 100-plus diseases we group as cancer. Most felt, despite their often profound misgivings about the way research is done, that we’re on the right path. Yet virtually all these experts offered testimony that, when taken together, describes a dysfunctional “cancer culture”—a groupthink that pushes tens of thousands of physicians and scientists toward the goal of finding the tiniest improvements in treatment rather than genuine breakthroughs; that fosters isolated (and redundant) problem solving instead of cooperation; and rewards academic achievement and publication over all else. At each step along the way from basic science to patient bedside, investigators rely on models that are consistently lousy at predicting success—to the point where hundreds of cancer drugs are thrust into the pipeline, and many are approved by the FDA, even though their proven “activity” has little to do with curing cancer. “It’s like a Greek tragedy,” observes Andy Grove, the chairman of Intel and a prostate-cancer survivor, who for years has tried to shake this cultural mindset as a member of several cancer advisory groups. “Everybody plays his individual part to perfection, everybody does what’s right by his own life, and the total just doesn’t work.” Tragedy, unfortunately, is the perfect word for it. Heroic figures battling forces greater than themselves. Needless death and destruction. But unlike Greek tragedy, where the Fates predetermine the outcome, the nation’s cancer crusade didn’t have to play out this way. And it doesn’t have to stay this way. “A VERY TOUGH SET OF PROBLEMS”NUCLEAR FISSION WAS A MERE eight months old when the Panzers rolled into Poland in September 1939, beginning the Second World War. Niels Bohr had announced the discovery at a conference on theoretical physics at George Washington University. Three years later the crash program to build an atomic device from a uranium isotope began in earnest. And within three years of that— Aug. 6, 1945—a bomb named Little Boy exploded over Hiroshima. NASA came into existence on Oct. 1, 1958. Eleven years later, two men were dancing on the moon. Sequencing the entire human genome took just 18 years from the time the idea was born at a small gathering of scientists in Santa Cruz, Calif. Go back as far as Watson and Crick, to the discovery of the structure of DNA, and the feat was still achieved in a mere half-century. Cancer researchers hate such comparisons. Good science, say many, can’t be managed. (Well, sure, maybe easy stuff like nuclear physics, rocket science, and genetics—but not cancer.) And to be sure, cancer is a challenge like no other. The reason is that this killer has a truly uncanny ability to change its identity. “The hallmark of a cancer cell is its genetic instability,” says Isaiah “Josh” Fidler, professor and chair of the department of cancer biology at Houston’s M.D. Anderson Cancer Center. The cell’s DNA is not fixed the way a normal cell’s is. A normal cell passes on pristine copies of its three-billion-letter code to every next-generation cell. But when a cancer cell divides, it may pass along to its daughters an altered copy of its DNA instructions—and even the slightest change can have giant effects on cell behavior. The consequence, says Fidler, is that while cancer is thought to begin with a single cell that has mutated, the tumors eventually formed are made up of countless cellular cousins, with a variety of quirky traits, living side by side. “That heterogeneity of tumors is the major, major obstacle to easy therapy,” he says. Harold Varmus, president of Memorial Sloan-Kettering Cancer Center in New York City, agrees. “I just think this is a very tough set of problems,” says Varmus, who has seen those problems from more angles than just about anybody. He shared a Nobel Prize for discovering the first oncogene (a normal gene that when mutated can cause cancer) in 1976. That crucial finding, five years into the War on Cancer, helped establish that cancers are caused by mutated genes. Later Varmus served as NIH director under Bill Clinton, presiding over a period of huge funding increases. “Time always looks shorter in retrospect,” he says. “I think, hey, in 30 years mankind went from being almost completely ignorant about how cancer arises to being pretty damn knowledgeable.” Yet all that knowledge has come at a price. And there’s a strong argument to be made that maybe that price has been too high. President Nixon devoted exactly 100 words of his 1971 State of the Union speech to proposing “an intensive campaign to find a cure for cancer.” The word “war” was never mentioned in the text, yet one would flare up in the months that followed—a lobbying war over how much centralized control the proposed national cancer authority would exert. Between the speech and the signing of the National Cancer Act that December, there was a “battle line between ‘creative research’ and ‘structured research,’ ” as a news report headlined it. A massive alliance of virtually all the medical societies, the medical schools, the then–Big Three cancer hospitals (Memorial Sloan-Kettering, M.D. Anderson, and Roswell Park in Buffalo) said yes to federal money but wanted very little direction and only loose coordination from Uncle Sam. On the other side was Sidney Farber, the Boston physician known as the godfather of cancer research. He wanted public backing for a massive, coordinated assault. “We cannot wait for full understanding; the 325,000 patients with cancer who are going to die this year cannot wait; nor is it necessary, in order to make great progress in the cure of cancer, for us to have the full solution of all the problems of basic research,” Farber testified in congressional hearings that fall. “The history of medicine is replete with examples of cures obtained years, decades, and even centuries before the mechanism of action was understood for these cures—from vaccination, to digitalis, to aspirin.” Farber lost. Today the cancer effort is utterly fragmented—so much so that it’s nearly impossible to track down where the money to pay for all this research is coming from. But let’s try anyway. We begin with the NCI budget. Set by Congress, this year’s outlay for fighting cancer is $4.74 billion. Critics have complained that is a mere 3.3% over last year’s budget, but Uncle Sam gives prodigiously in other ways too—a fact few seem to realize. The NIH, technically the NCI’s parent, will provide an additional $909 million this year for cancer research through the National Institute of Environmental Health Sciences and other little-noticed grant mechanisms. The Department of Veterans Affairs will likely spend just over the $457 million it spent in 2003 for research and prevention programs. The CDC will chip in around $314 million for outreach and education. Even the Pentagon pays for cancer research—offering $249 million this year for nearly 500 peer-reviewed grants to study breast, prostate, and ovarian cancer. Now throw state treasuries into the mix—governors signed 89 cancer-related appropriations from 1997 to 2003—plus the fundraising muscle of cancer charities, cancer centers, and research hospitals, which together will raise some $2 billion this year from generous donors, based on recent tax forms. And finally, that huge spender Big Pharma. The TuftsCenter for the Study of Drug Development estimates that drug companies will devote about $7.4 billion, or roughly a quarter of their annual R&D spending, to products for cancer and metabolic and endocrine diseases. CANCER’S BIG FOUR KILLERS In 1971, when the war on cancer began, 50% of people diagnosed with the disease went on to live at least five years. Today, 33 years and some $200 billion later, the five-year survival rate is 63%, a modest 13-point gain. But a look behind the numbers for the four biggest killers—lung, colon and rectal, breast, and prostate cancer—reveals that progress isn’t being made where you might think it is. With the help of early detection and treatment, more patients are living longer. Once a cancer has spread, however, chances of survival are scarcely better now than they were three decades ago. Cancer that has spread beyond the primary site region. FORTUNE CHARTS / SOURCE: SURVEILLANCE, EPIDEMIOLOGY AND END RESULTS (SEER) When you add it all up, Americans have spent, through taxes, donations, and private R&D, close to $200 billion, in inflation-adjusted dollars, since 1971. What has that national investment netted so far? Without question, the money has bought us an enormous amount of knowledge, just as Varmus says. Researchers have mapped the human cell’s intricate inner circuitry in extraordinary detail, identifying dozens of molecular chains of communication, or “signaling pathways,” among various proteins, phosphates, and lipids made by the body. In short, scientists now know (or think they know) nearly all the biochemical steps that a healthy cell uses to multiply, to shut down its growth, and to sense internal damage and die at the right time—as well as many of the genes that encode for these processes. What’s more, by extension, they know how these same gene-induced mechanisms go haywire in a cancer cell. According to PubMed, the NCI’s online database, the cancer research community has published 1.56 million papers—that’s right: 1.56 million!—largely on this circuitry and its related genes in hundreds of journals over the years. Many of the findings are shared at the 100-plus international congresses, symposiums, and conventions held each year. Yet somehow, along the way, something important has gotten lost. The search for knowledge has become an end unto itself rather than the means to an end. And the research has become increasingly narrow, so much so that physician-scientists who want to think systemically about cancer or the organism as a whole—or who might have completely new approaches—often can’t get funding. Take, for instance, the NCI’s chief funding mechanism, something called an RO1 grant. The grants are generous, averaging $338,000 apiece in 2003. And they are one of the easiest sweepstakes to win: One in three applications is accepted. But the money goes almost entirely to researchers who focus on very specific genetic or molecular mechanisms within the cancer cell or other tissue. The narrower the research niche, it sometimes seems, the greater the rewards the researcher is likely to attain. “The incentives are not aligned with the goals,” says Leonard Zwelling, vice president for research administration at M.D. Anderson, voicing the feeling of many. “If the goal is to cure cancer, you don’t incentivize people to have little publications.” Jean-Pierre Issa, a colleague of Zwelling’s who studies leukemias, is equally frustrated by the community’s mindset. Still, he admits, the system’s lure is powerful. “You get a paper where you change one gene ever so slightly and you have a drastic effect of cancer in the mouse, and that paper gets published in Science or Nature, and in your best journals. That makes your reputation. Then you start getting grants based on that,” he says. “Open any major journal and 80% of it is mice or drosophila [fruit flies] or nematodes [worms]. When do you get human studies in there? FUNDING APLENTY The National Cancer Institute isn’t the half of it. Major bucks for cancer R&D come from many sources—some you’d never expect (like the Pentagon). FORTUNE CHART / SOURCES: Totals derive from data for the most recent year available. Other federal funding includes cancer spending by NIH (except NCI) and the VA (excluding treatment), CDC, and Pentagon. Data on charities and cancer centers are from federal tax forms; state figures are not included. Pharma total is fromTuftsCenter for the Study of Drug Development and Fortune estimates. Indeed, the cancer community has published an extraordinary 150,855 experimental studies on mice, according to a search of the PubMed database. Guess how many of them have led to treatments for cancer? Very, very few. In fact, if you want to understand where the War on Cancer has gone wrong, the mouse is a pretty good place to start.THE MODELS OF CANCER STINKOUTSIDE ERIC LANDER’S OFFICE is a narrow, six-foot-high poster. It is an org chart of sorts, a taxonomy, with black lines connecting animal species. The poster’s lessons feel almost biblical—it shows, for example, that the zebrafish has much in common with the chicken; that hedgehog and shrew are practically kissing cousins; and that while a human might look more like a macaque than a platypus or a mouse, it ain’t that big of a leap, really. The connection, of course, is DNA. Our genomes share much of the same wondrous code of life. And therein lie both the temptation and the frustration inherent in cancer research today. Certain mutated genes cause cells to proliferate uncontrollably, to spread to new tissues where they don’t belong, and to refuse to end their lives when they should. That’s cancer. So research, as we’ve said, now revolves around finding first, the molecular mechanisms to which these mutated genes give rise, and second, drugs that can stop them. The strategy sounds obvious—and nobody makes it sound more so than Lander, the charismatic founding director of the Whitehead Institute’s Center for Genome Research in Cambridge, Mass., and a leader of the Human Genome Project. The “Prince of Nucleotides,” as FORTUNE once called him, sketches the biological route to cancer cures as if he were directing you to the nearest Starbucks: “There are only, pick a number, say, 30,000 genes. They do only a finite number of things. There are only a finite number of mechanisms that cancers have. It’s a large number; when I say finite, I don’t mean to trivialize it. There may be 100 mechanisms that cancers are using, but 100 is only 100.” So, he continues, we need to orchestrate an attack that isolates these mechanisms by knocking out cancer-promoting genes one by one in mice, then test drugs that kill the mutant cells. “These are doable experiments,” he says. “Cancers by virtue of having mutations also acquire Achilles’ heels. Rational cancer therapies are about finding the Achilles’ heel associated with each new mutation in a cancer.” The principle is, in all likelihood, dead-on. The process itself, on the other hand, has one heck of an Achilles’ heel. And that takes us back to the six-foot poster showing the taxonomy of genomes. A mouse gene may be very similar to a human gene, but the rest of the mouse is very different. The fact that so many cancer researchers seem to forget or ignore this observation when working with “mouse models” in the lab clearly irks Robert Weinberg. A professor of biology at MIT and winner of the National Medal of Science for his discovery of both the first human oncogene and the first tumor-suppressor gene, Weinberg is as no-nonsense as Lander is avuncular. Small and mustachioed, with Hobbit-like fingers, he plops into a brown leather La-Z-Boy that is somehow wedged into the middle of his cramped office, and launches into a lecture: “One of the most frequently used experimental models of human cancer is to take human cancer cells that are grown in a petri dish, put them in a mouse—in an immunocompromised mouse—allow them to form a tumor, and then expose the resulting xenograft to different kinds of drugs that might be useful in treating people. These are called preclinical models,” Weinberg explains. “And it’s been well known for more than a decade, maybe two decades, that many of these preclinical human cancer models have very little predictive power in terms of how actual human beings—actual human tumors inside patients— will respond.” Despite the genetic and organ-system similarities between a nude mouse and a man in a hospital gown, he says, the two species have key differences in physiology, tissue architecture, metabolic rate, immune system function, molecular signaling, you name it. So the tumors that arise in each, with the same flip of a genetic switch, are vastly different. Says Weinberg: “A fundamental problem which remains to be solved in the whole cancer research effort, in terms of therapies, is that the preclinical models of human cancer, in large part, stink.” A few miles away, Bruce Chabner also finds the models lacking. A professor of medicine at Harvard and clinical director at the Massachusetts General Hospital Cancer Center, he explains that for a variety of biological reasons the “instant tumors” that researchers cause in mice simply can’t mimic human cancer’s most critical and maddening trait, its quick-changing DNA. That characteristic, as we’ve said, leads to staggering complexity in the most deadly tumors. “If you find a compound that cures hypertension in a mouse, it’s going to work in people. We don’t know how toxic it will be, but it will probably work,” says Chabner, who for many years ran the cancer-treatment division at the NCI. So researchers routinely try the same approach with cancer, “knocking out” (neutralizing) this gene or knocking in that one in a mouse and causing a tumor to appear. “Then they say, ‘I’ve got a model for lung cancer!’ Well, it ain’t a model for lung cancer, because lung cancer in humans has a hundred mutations,” he says. “It looks like the most complicated thing you’ve ever seen, genetically.” Homer Pearce, who once ran cancer research and clinical investigation at Eli Lilly and is now research fellow at the drug company, agrees that mouse models are “woefully inadequate” for determining whether a drug will work in humans. “If you look at the millions and millions and millions of mice that have been cured, and you compare that to the relative success, or lack thereof, that we’ve achieved in the treatment of metastatic disease clinically,” he says, “you realize that there just has to be something wrong with those models.” Vishva Dixit, a vice president for research in molecular oncology at Genentech in South San Francisco, is even more horrified that “99% of investigators in industry and in academia use xenografts.” Why is the mouse model so heavily used? Simple. “It is very convenient, easily manipulated,” Dixit explains. “You can assess tumor size just by looking at it.” Although drug companies clearly recognize the problem, they haven’t fixed it. And they’d better, says Weinberg, “if for no other reason than [that] hundreds of millions of dollars are being wasted every year by drug companies using these models.” Even more depressing is the very real possibility that reliance on this flawed model has caused researchers to pass over drugs that would work in humans. After all, if so many promising drugs that clobbered mouse cancers failed in man, the reverse is also likely: More than a few of the hundreds of thousands of compounds discarded over the past 20 years might have been truly effective agents. Roy Herbst, who divides his time between bench and bedside at M.D. Anderson and who has run big trials on Iressa and other targeted therapies for lung cancer, is sure that happens often. “It’s something that bothers me a lot,” he says. “We probably lose a lot of things that either don’t have activity on their own, or we haven’t tried in the right setting, or you don’t identify the right target.” If everyone understands there’s a problem, why isn’t anything being done? Two reasons, says Weinberg. First, there’s no other model with which to replace that poor mouse. Second, he says, “is that the FDA has created inertia because it continues to recognize these [models] as the gold standard for predicting the utility of drugs.” Compare Cancer Research & Animal Experimentation: an Unholy Union?, particularly 1999 Cancer Research Review (good overview), Better Science: Limitations of Animal Tests, On Differences Between Species: Animal Experiment Results Often Not Transferable to Humans, The Harms to Humans from Animal Experimentation, Better Science: Benefits of Using Non-Animal Tests, Cancer: Why We're Losing the War, Cancer Research - A Super Fraud?, What The Vested Interest Groups Say About Animal Models of Human Disease in Cancer Research, Cancer Research Without Animals: Improved Cell Culture Methods for Anti-Cancer Drug Development, Better Science: Alternatives to Animal Research.
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Cancer
Jun 17, 2015 15:33:19 GMT -5
Post by Master Kim on Jun 17, 2015 15:33:19 GMT -5
'Stop Googling your symptoms', teenage cancer victim told before death - www.telegraph.co.uk/news/nhs/11677561/Stop-Googling-your-symptoms-teenage-cancer-victim-told-before-death.htmlBy Agency, video source SWNS 11:12AM BST 16 Jun 2015 Hospital admits it 'did not listen with sufficient attention' to fears of teenager whose online research of symptoms was dismissed by doctors before death A teenager who begged doctors to take her health fears seriously in the months before she died from a rare cancer was told by medics to "stop Googling your symptoms". Bronte Doyne died on March 23, 2013, aged 19 - just 16 months after she first complained of severe stomach pains. In text messages, tweets and personal diary entries, the student expressed her worries that medics were not acting as her health deteriorated. Doctors dismissed her concerns, leaving her desperate for someone to take her seriously. In one tweet in July 2012, Miss Doyne made a cry for help. Finally, after pleading to be taken seriously, she was admitted to hospital where she passed away 10 days later. Now bosses at the Nottingham University Hospitals NHS Trust have admitted they "did not listen with sufficient attention" and that they must embrace the "internet age". Miss Doyne, of West Bridgford, Nottingham, was first admitted to hospital in September 2011 with suspected appendicitis. But she was eventually told she had fibrolamellar hepatocellular carcinoma, which affects only 200 people globally each year. The family found information about the cancer on a website endorsed by the US government and discovered it had a high chance of recurrence but, when they raised the issue, doctors told them to stop searching the internet for information. Now Miss Doyne's mother Lorraine, 50, has criticised "a woeful lack of care and empathy" from doctors. She said: "Bronte was denied pain relief, referrals were hugely delayed and efforts by her family to gather information and understand Bronte's prognosis were handled in an evasive and aloof manner. "Her fears that her symptoms over the preceding months before she died were cancer-related were proved right. The messages from Bronte are all her own words and I believe that's more powerful for people to understand what she went through. I want to see changes and action now." Bronte Doyne (R) with her sister Kerrie and mother Lorraine (Newsteam) Miss Doyne had just celebrated her 18th birthday when she was diagnosed with the cancer, which attacks the liver, almost four years ago. Over a 16-month period, she was told by doctors she would survive and had nothing to worry about following surgery. But Miss Doyne and her family knew through their own online research that there was a high chance the cancer would return and eventually claim her life - which it did within months. Mrs Doyne, of Edwalton, Nottinghamshire, said: "We had no information forthcoming and the only sources we found were through our own research. We found a website for the Fibrolamellar Cancer Foundation, which is based in the United States, and it included an international forum. "It's not just some pathetic website on Google, it's been endorsed by the White House in publications, and was the only contact we had to get some awareness about this disease. "But that information was dismissed here. I told the clinician that I knew what was happening to my daughter and something needed to be done but I was just told to 'stop Googling'." Mrs Doyne said they were led to believe the surgery would cure the cancer but the online information suggested otherwise. She added: "We asked after the surgery if they were suspicious the cancer could come back but their response was 'how will that help Bronte?' We were told they will be seeing her over the next 20 years - it made her feel relieved but she still didn't feel quite right. "We weren't given any information by the hospital about this but we did know it had a really poor outcome, yet they did nothing and just left us to wait and dismissed her concerns." The text messages, tweets and diary entries written by Bronte during her illness were passed to NUH as part of the family's complaint after her death. They show how her fears grew as her health deteriorated and the disillusionment that no one, outside her family, would listen to her. After she was told the truth, Miss Doyne wrote in diary entries: "I have cancer. I'm scared. Mum rang keyworker. Need to know what this is. He doesn't know much. Help me." She underwent liver resection surgery in December 2011. But 11 months later, after doctors had told her she was fine, she wrote in her diary In November 2012: "Feeling sick for months now. Tired of this feeling crap. Hospital not worried so trying to get on with it." Six weeks before her death, she was advised by her GP to go to hospital as an emergency case if her symptoms worsened. But when she got to Nottingham's Queen's Medical Centre, Miss Doyne was told by a doctor that she did not need to be seen. She wrote: "I got so angry because the doctor was so rude and just shrugged his shoulders. He gave me a sarcastic comment like you can sleep here if you want but they won't do anything. So I just have to wait for another hospital appointment." • Woman diagnoses own ovarian cancer with Google search • 'When I googled breast pain, it came up with 8 million pages' Her concerns about feeling like "something's not right" continued to be ignored. Doctors put her weight loss down to being "part of a skinny family". It was only after Miss Doyne "chased results" from a six-monthly MRI scan that she found she had an abdominal growth and was transferred to the oncology department. In one diary entry less than a month before her death, Bronte wrote: "Mum tried to talk to my consultant but he didn't give her much help. "She even had to ask him when I was going to get my appointment for the oncologist. Really don't think he likes my mum asking questions." Her growing desperation in the weeks leading to her death was evident, as she wrote: "I feel things aren't good but no news from hospital. Need answers. Want to know what's going on. Something's not right. I'm sick of this." Patients are increasingly turning to the internet to self-diagnose Miss Doyne was eventually referred to the Hogarth ward, a Teenage Cancer Trust unit, where she stayed for 10 days before she died . Now her mother is working alongside health chiefs to improve how medics deal with patients and the hospital board has promised to learn from her daughter's case. NUH medical director Dr Stephen Fowlie said: "We explored all potential treatments, including participation in trials at other centres when her cancer returned. "Sadly, there were no further surgical, chemotherapy or radiotherapy treatment options for Bronte's very aggressive cancer. "We apologise that our communication with Bronte and her family fell short. We did not listen with sufficient attention. We should have referred Bronte to the expert support available from the Teenage Cancer Trust much sooner. "We are sharing the learning from Bronte's experience. Lorraine is assisting us to improve how we help patients." • Online self-diagnosis can cause sufferers to fear the worst Keith Girling, deputy medical director at Nottingham University Hospitals NHS Trust, said: "This has put the spotlight on how the internet age and the availability of information can challenge the way we respond to patients who may be very well informed, but can remain frightened and vulnerable. "Through the internet, patients and families now have access to worldwide information about health conditions and possible treatments as they seek the best for themselves and their loved ones. "The best information is helpful and accurate, based on evidence of what works. These sites help patients make choices, as they become experts in their condition. "But some sites are inaccurate or misleading, and may give false hope or cause distress. They may not be relevant to the unique clinical and other circumstances of the patient."
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Cancer
Jun 24, 2015 14:31:03 GMT -5
Post by Master Kim on Jun 24, 2015 14:31:03 GMT -5
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Cancer
Jul 10, 2015 19:33:00 GMT -5
Post by Master Kim on Jul 10, 2015 19:33:00 GMT -5
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Cancer
Jul 13, 2015 9:34:10 GMT -5
Post by Master Kim on Jul 13, 2015 9:34:10 GMT -5
Dr. Michael Farley (Forensic Pathology Consultant, N.D.) shares a story about an cancer director at a major hospital that he worked with. You won't believe the doctors response to what Dr. Farley tried to help him with. Watch and learn for yourself what so many doctors aren't!
He Nails A Problem With Many Traditional Oncologists at 2:28 of This Video!
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Cancer
Jul 17, 2015 13:45:17 GMT -5
Post by Master Kim on Jul 17, 2015 13:45:17 GMT -5
Using Oxygen to Treat Cancer? Watch This! Interview with Mark Rosenberg, M.D.
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Cancer
Jul 28, 2015 13:35:24 GMT -5
Post by Master Kim on Jul 28, 2015 13:35:24 GMT -5
THYROID HORMONE THERAPY APPEARS TO CAUSE BREAST CANCER - www.newswithviews.com/Howenstine/james47.htmBy Dr. James Howenstine, MD. July 27, 2006 NewsWithViews.com Medical journals and textbooks typically portray iodine as an unimportant substance which should be taken in small amounts[1] because of it's dangers. Actually approximately one third of humanity has iodine deficiency. When humans lack iodine the thyroid gland enlarges (goiter), nodules appear in the thyroid gland and over a period of time cancer may appear in a thyroid nodule. Conventional medicine treats thyroid gland enlargement with thyroid hormone without considering the possibility that the hypothyroidism and goiter may be due to lack of iodine. This failure to diagnose and treat iodine deficiency can lead to an increased risk of breast cancer and the longer the diagnosis is missed the greater the chance that breast cancer will occur. Women taking thyroid hormone appear to be twice (12.1%) as likely to develop breast cancer as women not using thyroid hormone (6..2%). Women who had taken thyroid hormone for 15 years had a 19.5% incidence of breast cancer whereas women who have only taken thyroid hormone for 5 years had only a 10% incidence of breast cancer. Why is this? The essential trace element iodine may be the most important least publicized mineral in existence. Iodine is the only element needed in hormones and in the production of hormones. The iodine containing hormones are involved in the creation of embryos, development of brain function, growth, metabolism and maintenance of body temperature. This means that proper amounts of thyroid hormone, estrogen, progesterone, testosterone, insulin, growth hormone etc. can not be made when iodine is lacking from the body. One third of all individuals on Earth are functioning with subnormal levels of iodine. Low intake of iodine is the leading cause for intellectual deficiency in the world. There is strong evidence that iodine lack predisposes to breast cancer. One out of seven women in the U.S. has deficiency of iodine proven by urine iodine screening tests (urine I less than 50 ug/L). This is the same incidence for breast cancer seen in U.S. women. Without bothering to check urine for iodine, physicians visited by a woman with a goiter or symptoms of hypothyroidism are routinely prescribing thyroid hormone therapy. Hintze et al[2] compared the results of 400ug/L of Iodine with 150ug of T4 (synthyroid) for 8 months and then four months after stopping therapy. The results clearly favored iodine therapy. Both treatments led to similar suppression in the size of the goiter. However, four months later the size of the thyroid had returned to pre-treatment levels in the group treated with T4 hormone. The group who had received iodine therapy continued to have normal sized thyroid glands four months after therapy was stopped. Several investigators have concluded that iodine lack is a probable cause for breast cancer in women.[3] [4] [5] [6] [7] Demographic studies in Japan and Iceland revealed that both countries have a high intake of iodine and low incidences of goiter and breast cancer. In Mexico and Thailand where iodine intake is low there is a high incidence of goiter and breast cancer.[8] Thyroid gland size measured by ultrasound is significantly larger[9] in Irish women with breast cancer than control women. Administration of thyroid hormone to iodine deficient women appears to increase the risk of developing breast cancer. In a group of women undergoing screening mammograms the incidence of breast cancer[10] was twice as high in the women taking thyroid hormone. for hypothyroidism (probably caused by iodine lack) than in women not taking thyroid supplements. The mean incidence was 6.2% in controls and 12.1% in women on thyroid hormones. The incidence of breast cancer was twice as high in women taking thyroid hormone for more than 15 years (19.5%) compared to those on thyroid hormones for only 5 years (10%). In the state of Michigan, during a period of iodine supplementation in bread (1924-1951) the prevalence of goiter diminished from 38.6% to 1.4%. Of interest the incidence of breast cancer remained unchanged during this time frame. This information was used to suggest that iodine supplementation had no effect on the incidence of breast cancer. However, Ghent and Eskin were able to show in women and female rats that the amount of iodine needed to protect against fibrocystic disease of the breast and breast cancer was at least 20 to 40 times greater[11] than the iodine needed to control goiter. In the 1960s mandated iodine containing dough was equivalent to the RDA of 150 ug per slice of bread. At that time the incidence of breast cancer was only 1 in 20.[12] In the past 20 years the use of iodine supplementation in bread was eliminated and a goiter producing substance toxic to the thyroid gland (bromine) was introduced as replacement for iodine. The risk for breast cancer is now 1 in 8 and this risk is increasing by one percent[13] each year. The decision to replace iodine in an iodine deficient population with a goitrogen was illogical lacking in common sense. The damaging effects of bromine on thyroid tissue also appears to contribute to the development of auto-immune diseases in the thyroid gland (Hashimoto's thyroiditis). The mammary glands have a trapping system for iodine similar to that of the thyroid gland. The breasts effectively compete with the thyroid gland for ingested iodine. This distribution of iodine to both breast and thyroid gland in pubertal girls explains why goiter is 6 times more common in girls than pubertal boys. The disappearance of iodine into breast tissue in women leads to decreased ability to supply the thyroid gland with an adequate amount of iodine. The development of a goiter in young girls indicates deficient distribution of iodine to both breast and thyroid tissue. Treating such a patient with thyroid hormone is not sensible and appears to increase the risk of breast cancer. Study of radioiodine uptake in normals and women with fibrocystic breast disease FDB reveals that the FDB breasts were able to take in 12.5% of the iodine dosage compared to only 6.9% in normal breasts. This proves the existence of considerable iodine depletion in the breasts of women with FDB. There is considerable evidence for an increased risk of thyroid cancer as well as breast cancer in persons with iodine deficiency. Untreated iodine deficiency leads to goiter, thyroid nodules and eventually some of these nodules become malignant. The decreasing intake of iodine has resulted in an increase in thyroid nodules and increase in thyroid cancer. In 2001 there were 19,500 new cases of thyroid cancer in the U.S. with 14,900 of these cases occurring in women. Iodine has a role in promoting general well being as well as protecting against infections, degenerative diseases and cancer. Iodine promotes the normal killing of defective and abnormal cells (apoptosis). Thus, iodine helps the body's surveillance system to detect and remove abnormal cells. Additionally, the presence of iodine triggers differentiation away from the more dangerous undifferentiated type of cell toward normal cells. The presence of adequate levels of iodine in the body (Japanese diet with lots of sea vegetables and fish) reduces reactive oxygen species (ROS). in the body which decreases the oxidative burden in the body This results in slowing of degeneration disease processes and decreasing the risk of cancer. Nearly every physician in the United States will reach for a prescription pad to order thyroid hormone when he sees a patient with goiter or symptoms of hypothyroidism. This can be exactly the wrong thing to do if the patient has deficient stores of iodine. Insist on obtaining a 24 hour urine collection for iodine to eliminate iodine lack as the cause for your symptoms (values below 50 ug/liter are abnormal). Thyroid hormone therapy in the presence of iodine deficiency increases the risk of breast cancer and probably thyroid cancer as well. Endocrinologist, Dr. Guy Abraham, formerly of the U.C.L.A. Department of Endocrinology, is convinced that everyone needs to be on iodine therapy until their iodine stores have been fully restored. After this time frame periodic intake of iodine will help insure that the many body functions requiring iodine run smoothly. A dosage of two tablets of Iodoral twice daily for three months followed by one Iodoral tablet daily for a year will restore iodine stores for most persons. At that point periodic taking of an Iodoral tablet daily one month out of 4 to 6 months etc. will be adequate to maintain iodine stores. Iodine stores can be easily monitored by taking 4 Iodoral tablets (50 mg iodine) and collecting a 24 hour urine sample for iodine content. If 80% of the ingested iodine is found in the urine collection the iodine stores are normal. Iodoral can be obtained from Optimox Corp. Torrance, Cal. To purchase a referral from a health care practitioner is needed. Footnotes: 1, Abraham, Guy F. et al Orthoiodosupplementaion: Iodine Sufficiency Of The Whole Body pg 1 2, Hintze, G. et al treatment of Endemic goiter due to iodine deficiency with iodine, levothyroxine or both:results of a multicentre trial. European Journal of Clinical Investigation, 19:527-534, 1989 3, Eskin B et al Mammary Gland Dysplasia in Iodine Deficiency JAMA , 200:115-119. 1967 4, Eskin B Iodine and Mammary Gland Cancer Adv. Exp. Med. Biol., 91:293-304, 1977 5, Ghent, W. et al Iodine Replacement in Fibrocystic disease of the Breast Can. J. Surg. , 36:453-460, 1993 6, Eskin B. et al Different Tissue Responses for Iodine and Iodidein Rat Thyroid and mammary Glands Biol. Trace Element Research 49:9-19, 1995 7, Derry , D Breast Cancer and Iodine Trafford Publishing, Victoria B.C. , 92, 2001 8, Finley JW., Bogardus, G.M., Breast Cancer and Thyroid Disease Quart. Review Surg. Obstet. Gyn. 17:139-147, 1960 9, Smtyhe, P. , Thyroid Disease and Breast Cancer J. Endo. Int. , 16:396-401, 1993 10, Ghandrakant, C. et al Breast Cancer Relationship to Thyroid Supplements for hypothyroidism JAMA, 238:1124, 1976 11, Backwinkel, K., Jackson, A.S. Some Fearures of breast Cancer and Thyroid Deficiency Cancer17:1174-1176 , 1964 12, Epstein, S.S., Sherman, D. Breast Cancer Prevention Program Macmillan , NY. 1998 pg 5 13, Ibid Dr. James A. Howenstine is a board certified specialist in internal medicine who spent 34 years caring for office and hospital patients. After 4 years of personal study he became convinced that natural products are safer, more effective, and less expensive than pharmaceutical drugs. This research led to the publication of his book A Physicians Guide To Natural Health Products That Work. Information about these products and his book can be obtained from amazon.com and at www.naturalhealthteam.com and phone 1-800-416-2806 U.S. Dr. Howenstine can be reached by mail at Dr. James Howenstine, C/O Remarsa USA SB 37, P.O. Box 25292, Miami, Fl. 33102-5292. E-Mail: dr.jimhow@gmail.com
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Cancer
Jul 28, 2015 13:39:18 GMT -5
Post by Master Kim on Jul 28, 2015 13:39:18 GMT -5
More BAD news if you are on T4-only like Synthroid??: it can cause Lung Cancer, says a study! - www.stopthethyroidmadness.com/2013/08/12/t4-only-lung-cancer/August 12, 2013 By Janie BowthorpeAfter worldwide patient experience has revealed that T4-only treatment results in a slew of continuing hypothyroid symptoms, now we have a study which implies that T4-only treatment could be raising your risk of LUNG CANCER. This complete study came out just last Thursday, August 8, 2013, in the Reproductive Biology and Endocrinology journal and it’s certainly not good news, if true, on top of what thyroid patients already know has been a failure in so many ways. The Italian authors said the correlation between lung cancer and T4-only treatment was “significant“! In other words, says the study, as hypothyroid patients raise their T4-only levothyroxine medication to chase continuing symptoms of hypothyroidism, it can lead to medication-induced hyperthyroid state, which in turns leads to an overproduction of oxidative stress. The latter oxidative stress is a known cause of cancer and other chronic diseases. But with T4-use, it’s specifically problematic for lung cancer, implies the study. Oxidative stress can be defined as a that which results in “significant decrease in the effectiveness of your iinherent antioxidant defenses, such as glutathione” (Wikipedia). And there are two main consequences: your body doesn’t detoxify itself well, nor does it repair any damage well because of free radicals. The study states:The prevalence of breast, colorectal, gastric and lung cancer in 18 Italian Regions during 2010 was correlated with the sales of LT4 in 2009. The cancer prevalence was analyzed in women aged 30–84. This age range corresponds to more than 80% of the consumers of the drug and to about 99% of all malignant cancers. The correlation between sales of LT4 and cancers was determined with the technique of Density Ellipses. The age and smoking contribution for lung cancer was determined with the Sequential test. It also adds:Lung cancer was the only tumor found directly correlated with LT4 supplementation. It’s particularly interesting to note that simply being hypothyroid results in increased oxidative stress, but the use of T4-only medications creates the same problem via a different route, explains the study. “LT4 can alter the oxidative balance in lungs and behave as a negative factor because of oxidative stress….” The authors conclude that “hypothyroidism might also be involved in the development of lung cancer”, but the study does send an alarming message about the correlation between T4 use and lung cancer, as well. The website Green Med Info, which promotes natural and integrative modalities, goes further into the discussion about the problematic nature of treating hypothyroidism with T4-only, stating And they conclude: “There is also compelling research indicating that desiccated thyroid extract (Armour thyroid) results in superior clinical outcomes versus the synthetic hormone, especially as concerns improved body weight.” And of course, patients who have switched to natural desiccated thyroid (NDT) have reported FAR better results repeatedly! Brands are not limited to Armour. Other brands which patients like include Erfa, Acella (NP Thyroid), Naturethroid, Westhroid-P and more. Message to those still using T4-only Millions of hypothyroid patients have reported millions of prices in their own degree and kind thanks to their use of T4-only medications. Now we have a study that implies your risk of getting lung cancer is increased. What’s next?? It’s not a pretty picture, if the correlation turns out be accurate for some. Time to take a strong and open-minded look at what patients have learned. ADDENDUM FROM JANIE: Please note that this study doesn’t say that every single T4 user is going to get lung cancer. My mother was on Synthroid her entire life, and though she had many miserable symptoms from it being a poor treatment for her, she never got lung cancer. It just seems to say that the researchers noted increased oxidative stress with T4 use, and they saw a correlation between that and lung cancer in some. Read the entire study information here and decide for yourself.
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Cancer
Aug 2, 2015 15:49:32 GMT -5
Post by Master Kim on Aug 2, 2015 15:49:32 GMT -5
Chemotherapy kills cancer patients faster than no treatment at all - www.naturalnews.com/048827_chemotherapy_cancer_treatment_patient_survival.html#Monday, March 02, 2015 by: Ethan Huff (NaturalNews) Wishful thinking simply won't deter from the fact that the cancer industry is just that: an industry. Doctors, drug companies, hospitals and other key stakeholders profit heavily each time a cancer patient submits to the conventional treatment model, which typically involves injecting chemotherapy poisons into the body, blasting it with ionizing radiation or cutting off body parts -- or some barbaric combination of all three. It might rub some people the wrong way to state this, especially those who've had to watch a loved one die from conventional cancer treatment, but each of these supposed treatments don't actually work, in many cases. Little-known science, which the medical-industrial complex has made it a practice to ignore or cover up, reveals that, despite what the medical industry often claims, chemotherapy in particular just isn't an effective cancer treatment. Dr. Hardin B. Jones, a former professor of medical physics and physiology at the University of California, Berkeley, had been studying the lifespans of cancer patients for more than 25 years when he came to the conclusion that, despite popular belief, chemotherapy doesn't work. He witnessed a multitude of cancer patients treated with the poison die horrific deaths, many of them meeting their fate much earlier than other patients who chose no treatment at all. After investigating this further, Dr. Jones found that cancer patients who underwent chemotherapy actually died more quickly, in most cases, than those who followed their doctors' recommendations by getting the treatment. A few number-crunching efforts later and Dr. Jones exposed a fact that the conventional cancer industry doesn't want the world to know about its multi-billion-dollar cash cow. "People who refused treatment lived for an average of 12 and a half years," stated Dr. Jones about his study's findings, which were published in the journal Transactions of the New York Academy of Sciences. "Those who accepted other kinds of treatment lived on an average of only 3 years." Breast cancer patients who reject all conventional therapies live four times longer than those who follow the systemDid you catch that? Refusing conventional cancer treatments and doing nothing resulted in cancer patients living more than four times longer than their more compliant counterparts. This is something you'll never hear about from the mainstream media, which continues to peddle the myth that cancer patients somehow need poison injected into their bodies in order to survive and reach "cure" status. Dr. Jones' study also found that the same is true concerning conventional treatments for breast cancer. Women with breast cancer who refused chemotherapy, radiation and surgery -- and remained untreated -- likewise lived four times longer than women who went under the knife or agreed to be poisoned with chemicals. As admitted in a more recent study published in the journal Clinical Oncology back in 2004, chemotherapy is really only effective about 2 percent of the time for all cancers. And this is based on the standard five-year survival rate criteria, which isn't technically indicative of a cure -- even though health authorities often like to claim it is. More on this is available here: EndAllDisease.com [PDF] A separate study published in the Journal of the American Medical Association back in 1979 found that many of the most common procedures for diagnosing and treating breast cancer, nearly all of which are still used today, have done nothing to lower breast cancer rates or increase survival for breast cancer patients. Two other studies, one of out Israel that was published in 1978 and another out of the UK that was published in The Lancet in 1980, came to similar findings. "Overall survival of patients with primary breast cancer has not improved in the past 10 years, despite increasing use of multiple-drug chemotherapy for treatment of metastasis," explains the Lancet study, entitled "Failure of Chemotherapy to Prolong Survival in a Group of Patients with Metastatic Breast Cancer." "Furthermore, there has been no improvement in survival from first metastasis, and survival may even have been shortened in some patients given chemotherapy." Natural cancer treatments are your best bet should you develop this horrible diseaseThere are solutions to treating cancer naturally, though, that don't involve just doing nothing -- which is still clearly better than going the conventional route. An abundance of natural cancer treatment options are outlined over at EndAllDisease.com, a free resource containing an abundance of information about health, disease, the environment and more: E ndAllDisease.com.The section of the site on natural cancer cures is available here: EndAllDisease.com.You can also learn more about how to treat and cure cancer naturally by visiting CancerTutor.com: CancerTutor.com.Sources: www.researchgate.netwww.thetruthseeker.co.ukwww.endalldisease.com[PDF] www.ncbi.nlm.nih.govwww.thelancet.comwww.cancertutor.comAbout the author:Ethan Huff is a freelance writer and health enthusiast who loves exploring the vast world of natural foods and health, digging deep to get to the truth. He runs an online health publication of his own at wholesomeherald.blogspot.com.
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Cancer
Aug 12, 2015 22:52:08 GMT -5
Post by Master Kim on Aug 12, 2015 22:52:08 GMT -5
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Cancer
Aug 21, 2015 16:44:26 GMT -5
Post by Master Kim on Aug 21, 2015 16:44:26 GMT -5
Doubt Is Raised Over Value of Surgery for Breast Lesion at Earliest Stage - www.nytimes.com/2015/08/21/health/breast-cancer-ductal-carcinoma-in-situ-study.html?ref=health&_r=0By GINA KOLATAAUG. 20, 2015 - New York Times Therese Taylor of Mississauga, Ontario, had a mastectomy four years ago after a diagnosis of ductal carcinoma in situ. She now believes it was unnecessary. Credit Michelle Siu for The New York TimesAs many as 60,000 American women each year are told they have a very early stage of breast cancer — Stage 0, as it is commonly known — a possible precursor to what could be a deadly tumor. And almost every one of the women has either a lumpectomy or a mastectomy, and often a double mastectomy, removing a healthy breast as well. Yet it now appears that treatment may make no difference in their outcomes. Patients with this condition had close to the same likelihood of dying of breast cancer as women in the general population, and the few who died did so despite treatment, not for lack of it, researchers reported Thursday in JAMA Oncology. Their conclusions were based on the most extensive collection of data ever analyzed on the condition, known as ductal carcinoma in situ, or D.C.I.S.: 100,000 women followed for 20 years. The findings are likely to fan debate about whether tens of thousands of patients are undergoing unnecessary and sometimes disfiguring treatments for premalignant conditions that are unlikely to develop into life-threatening cancers. Diagnoses of D.C.I.S., involving abnormal cells confined to the milk ducts of the breast, have soared in recent decades. They now account for as much as a quarter of cancer diagnoses made with mammography, as radiologists find smaller and smaller lesions. But the new data on outcomes raises provocative questions: Is D.C.I.S. cancer, a precursor to the disease or just a risk factor for some women? Is there any reason for most patients with the diagnosis to receive brutal therapies? If treatment does not make a difference, should women even be told they have the condition? Such questions are unlikely to be resolved by the new study. Some doctors, including the chief breast cancer surgeon at Memorial Sloan Kettering Cancer Center, said they did not see reason to change the current approach. The new data are helpful, said Dr. Barnett S. Kramer, director of the division of cancer prevention at the National Cancer Institute, and are consistent with other data pointing in the same direction. The new study, he added, provides, “the type of evidence that builds the justification for less morbid treatment.” Dr. Otis W. Brawley, chief medical officer at the American Cancer Society, said he was not ready to abandon treatment until a large clinical trial is done that randomly assigns women to receive mastectomies, lumpectomies or no treatment for D.C.I.S., and that shows treatment is unnecessary for most patients. But Dr. Brawley, who was not involved in the study, also said he had no doubt that treatment had been excessive. “In medicine, we have a tendency to get too enthusiastic about a technique and overuse it,” Dr. Brawley said. “This has happened with the treatment of D.C.I.S.” Continue reading the main story Featured Comment gemini3 Oregon To me the 'disfigurement' of the surgery was my scar of having survived a battle for my life. 586 Comments Write a comment A majority of the 100,000 patients in the database the researchers used, from a national cancer registry, had lumpectomies, and nearly all the rest had mastectomies, the new study found. Their chance of dying of breast cancer in the two decades after treatment was 3.3 percent, no matter which procedure they had, about the same as an average woman’s chance of dying of breast cancer, said Dr. Laura J. Esserman, a breast cancer surgeon and researcher at the University of California, San Francisco, who wrote an editorial accompanying the study. Advertisement Continue reading the main story The data showed that some patients were at higher risk: those younger than 40, black women and those whose abnormal cells had molecular markers found in advanced cancers with poorer prognoses. D.C.I.S. has long been regarded as a precursor to potentially deadly invasive cancers, analogous to colon polyps that can turn into colon cancer, said Dr. Steven A. Narod, the lead author of the paper and a researcher at Women’s College Research Institute in Toronto. The treatment strategy has been to get rid of the tiny specks of abnormal breast cells, just as doctors get rid of colon polyps when they see them in a colonoscopy. But if that understanding of the condition had played out as expected, women who had an entire breast removed, or even both breasts as a sort of double precaution, should have been protected from invasive breast cancer. Instead, the findings showed, they had the same risk as those who had a lumpectomy. Almost no women went untreated, so it is not clear if as a group they did worse. But some women who died of breast cancer ended up with the disease throughout their body without ever having it recur in their breast — many, in fact, had no breast because they had had a mastectomy. Those very rare fatal cases of D.C.I.S. followed by fatal breast cancer, Dr. Narod concluded, had most likely already spread at the time of detection. As for the rest, he said, they were never going to spread anyway. Dr. Esserman said that if deadly breast cancers started out as D.C.I.S., the incidence of invasive breast cancers should have plummeted with rising detection rates. That has not happened, even though in the pre-mammography era, before about 1980, the number of women found to have D.C.I.S. was only in the hundreds. Nearly 240,000 women receive diagnoses of invasive breast cancer each year. Those facts lead Dr. Narod to a blunt view. After a surgeon has removed the aberrant cells for the biopsy, he said, “I think the best way to treat D.C.I.S. is to do nothing.” Others drew back from that advice. Dr. Monica Morrow, chief breast cancer surgeon at Memorial Sloan Kettering Cancer Center, said it made more sense to view D.C.I.S. as a cancer precursor that should be treated the way it is now, with a lumpectomy or mastectomy. She questioned whether those women who were treated and ended up dying of breast cancer anyway had been misdiagnosed. In some cases, pathologists look at only a small amount of tumor, Dr. Morrow said, and could have missed areas of invasive cancer. Even the best mastectomy leaves cells behind, she added, which could explain why a small number of women with D.C.I.S. who had mastectomies, even double mastectomies, died of breast cancer. Continue reading the main story Recent Comments Therese Taylor 45 minutes ago Unbeknownst to me in 2011 when I was told I needed surgery, it had been reported, (though scantly) by our local media that milk duct tumours... mommyjam 1 hour ago This question is misleading. Lumpectomy is standard treatment for DCIS and mastectomy is recommended if there are large areas of DCIS... Lael Weyenberg 1 hour ago I had a double mastectomy with reconstruction in 2011 after an LCIS diagnosis (Lobular instead of Ductal Carcinoma In Situ). My quality of... See All Comments Write a comment Dr. Brawley said the new study, by showing which D.C.I.S. patients were at highest risk, would help enormously in defining who might benefit from treatment. It could not show that the high-risk women — young, black or with tumors with ominous molecular markers — were helped by treatment because there were too few of them, and pretty much every one of them was treated. But Dr. Brawley said he would like to see clinical trials that addressed that question, as well as whether the rest of the women with D.C.I.S., 80 percent of them, would be fine without treatment or with anti-estrogen drugs like tamoxifen or raloxifene that can reduce overall breast cancer risk. Advertisement Continue reading the main story Advertisement Continue reading the main story The notion that most women with D.C.I.S. might not need mastectomies or lumpectomies can be agonizing for those, like Therese Taylor of Mississauga, Ontario, who have already gone through such treatment. Four years ago, when she was 51, a doctor sent her for a mammogram, telling her he felt a lump in her right breast. That breast was fine, but it turned out she had D.C.I.S. in her left breast. A surgeon, she said, told her that “it was consistent with cancer” and that she should have a mastectomy. “I went into a state of shock and fear,” Ms. Taylor said. She had the surgery. She regrets it. “It takes away your feeling of attractiveness,” she said. “Compared to women who really have cancer, it is nothing. But the mastectomy was for no reason, and that’s why it bothers me.” But if D.C.I.S. is actually a risk factor for invasive cancer, rather than a precursor, it might be possible to help women reduce their risk, perhaps with hormonal or immunological therapies to change the breast environment, making it less hospitable to cancer cells, Dr. Esserman said. “As we learn more, that gives us the courage to try something different,” she said. The stakes in this debate are high. Karuna Jaggar, executive director of Breast Cancer Action, an education and activist organization, said women tended not to appreciate the harms of overtreatment and often overestimated their risk of dying of cancer, making them react with terror. “Treatment comes with short- and long-term impacts,” Ms. Jaggar said, noting that women who get cancer treatment are less likely to be employed several years later and tend to earn less than before. There are emotional tolls and strains on relationships. And there can be complications from breast cancer surgery, including lymphedema, a permanent pooling of lymphatic fluid in the arm. “These are not theoretical harms,” Ms. Jaggar said.
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Cancer
Sept 2, 2015 21:20:24 GMT -5
Post by Master Kim on Sept 2, 2015 21:20:24 GMT -5
Apigenin flavonoid health benefit and research Use in cancer and leukemia by Ray Sahelian, M.D. - www.raysahelian.com/apigenin.htmlJanuary 8 2015, Ray Sahelian, M.D. Apigenin is one of the flavonoids - more precisely one of the citrus bioflavonoids. Just like most flavonoids, it has antioxidant, anti-inflammatory, and anti-tumor properties. Perhaps apigenin can even block the formation of uric acid leading to beneficial effects in gout. Apigenin is found in high amounts in several herbs including parsley, thyme, and peppermint. It is is also found in a number of other herbs, including chamomile herb, Horsetail herb, lemon balm herb, perilla herb, vervain herb, and yarrow. Red wine and tomato sauce contain this flavonoid, also. Apigenin supplementYou can purchase chamomile extract herbal supplement online. Which supplement would you recommend to get the highest concentration of apigenin and/or hesperetin? Chamomile and thyme appear to be good sources. Benefits of apigeninAs with many flavonoids, it has potential to reduce the risk of cancer since it has anti-tumor activity. Apigenin also could potentially be useful in allergy conditions since it can have anti-inflammatory properties. Anti-inflammatoryIbuprofen and apigenin induce apoptosis and cell cycle arrest in activated microglia. Neurosci Lett. 2005. In case of injury or disease, microglia are recruited to the site of the pathology and become activated as evidenced by morphological changes and expression of pro-inflammatory cytokines. Evidence suggests that microglia proliferate by cell division to create gliosis at the site of pathological conditions such as the amyloid plaques in Alzheimer's disease and the substantia nigra of Parkinson's disease patients. The hyperactivation of microglia contributes to neurotoxicity. In the present study we tested the hypothesis that anti-inflammatory compounds modulate the progression of cell cycle and induce apoptosis of the activated cells. We investigated the effects of ibuprofen (non-steroidal anti-inflammatory drug) and apigenin (a flavonoid with anti-inflammatory and anti-proliferative properties) on the cell cycle of the murine microglial cell line BV-2. The findings indicate that apigenin-induced cell cycle arrest preferentially in the G2/M phase and ibuprofen caused S phase arrest. The binding of annexin V-FITC to the membranes of cells which indicates the apoptotic process were examined, whereas the DNA was stained with propidium iodide. Both apigenin and ibuprofen induced apoptosis significantly in early and late stages. The induction of apoptosis by ibuprofen and apigenin was confirmed using TUNEL assay, revealing that apigenin and ibuprofen significantly increased apoptosis in BV-2 cells. The results from the present study suggest that anti-inflammatory compounds might inhibit microglial proliferation by modulating the cell cycle progression and apoptosis. DepressionAntidepressant-like effects of apigenin and 2,4,5-trimethoxycinnamic acid from Perilla frutescens plant in the forced swimming test. Biol Pharm Bull. 2003. We studied the effects of apigenin and 2,4,5-trimethoxycinnamic acid on the behavioral despair test (forced swimming test), and the central noradrenergic, dopaminergic and serotonergic activities in mice. Behavioral and biochemical results indicate its antidepressant properties which may be mediated by the dopamine effects in the mouse brain. CancerApigenin inhibits VEGF and HIF-1 expression via PI3K/AKT/p70S6K1 and HDM2/p53 pathways. FASEB J. 2005. The Mary Babb Randolph Cancer Center, Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia Apigenin is a nontoxic dietary flavonoid that has been shown to possess anti-tumor properties and therefore poses special interest for the development of a novel chemopreventive and/or chemotherapeutic agent for cancer. Our findings reveal a novel role of apigenin in inhibiting HIF-1 and VEGF expression that is important for tumor angiogenesis and growth, identifying new signaling molecules that mediate this regulation. Flavonoid apigenin inhibits motility and invasiveness of carcinoma cells in vitro. Int J Cancer. 2005. Investigations of the mechanisms of the cancer-preventive activity of apigenin (4',5,7,-trihydroxyflavone), a plant-derived, anti-carcinogenic flavonoid, showed its interference with cell proliferation, survival, and gap junctional coupling. We used a model based on non-invasive HeLa wild-type cells and their connexin43 (Cx43) transfected counterparts to correlate the effect of apigenin on tumour cell invasiveness with its influence on cell motility. Both cell lines displayed similar motile properties in control conditions. Apigenin treatment resulted in a significant and reversible inhibition of translocation of both HeLa wild-type cells and HeLa Cx43 transfectants. The effect of apigenin on cell proliferation was less pronounced especially at low apigenin concentration, whereas its influence on cell motility correlated with the reduction of the invasive potential of HeLa Cx43 cells as shown by an invasion assay based on the confrontation of tumour cell spheroids with chick embryo heart fragments. HeLa Cx43 cells were highly invasive in controls, but did not invade the heart tissue at tumour cell aggregate-fibroblast capsule interfaces in the presence of apigenin and failed to fully engulf these heart fragments. Because the motility of chick heart fibroblasts was only slightly affected by apigenin, these observations indicate that apigenin exerts its anti-invasive effect on HeLa cells predominantly via a specific inhibition of tumour cell motility. This inhibitory effect of apigenin on tumour cell invasiveness in vitro demonstrates that apigenin may exert its anti-tumorigenic effect in vivo via inhibition of tumour cell penetration of the healthy tissue. CervicalApigenin induced apoptosis through p53-dependent pathway in human cervical cancer cells. Life Sci. 2005. Apigenin is a widely distributed plant flavonoid and was proposed as an antitumor agent. In this study, we reported for the first time that apigenin inhibited the growth of human cervical carcinoma cells (HeLa) and through apoptotic pathway. The results showed that apigenin significantly decreased the viability of HeLa cells. Apigenin-induced apoptosis in HeLa cells was confirmed by DNA fragmentation assay and induction of sub-G1 phase by flow cytometry. Apigenin-treated HeLa cells were arrested at G1 phase, which was associated with a marked increment of the expression of p21/WAF1 protein. The induction of p21/WAF1 appeared to be transcriptionally upregulated and was p53-dependent. In addition, apigenin induced Fas/APO-1 and caspase-3 expression which were also correlated with apoptosis. Apigenin decreased in the protein expression of Bcl-2 protein, which is an anti-apoptotic factor. The conclusion of this study is the apigenin induced p53 expression which caused cell cycle arrest and apoptosis. These findings suggest that apigenin has strong potential for development as an agent for preventing cervical cancer. GastrointestinalApigenin and its impact on gastrointestinal cancers. Mol Nutr Food Res. 2013. Department of Pathology, Dalhousie University, Halifax, Nova Scotia, Canada. Apigenin is a flavonoid found in many fruits, vegetables, and herbs, the most abundant sources being the leafy herb parsley and dried flowers of chamomile. Present in dietary sources as a glycoside, it is cleaved in the gastrointestinal lumen to be absorbed and distributed as apigenin itself. For this reason, the epithelium of the gastrointestinal tract is exposed to higher concentrations of apigenin than tissues at other locations. This would also be true for epithelial cancers of the gastrointestinal tract. We consider the evidence for actions of apigenin that might hinder the ability of gastrointestinal cancers to progress and spread. It has been shown to inhibit cell growth, sensitize cancer cells to elimination by apoptosis, and hinder the development of blood vessels to serve the growing tumor. It also has actions that alter the relationship of the cancer cells with their microenvironment. Apigenin is able to reduce cancer cell glucose uptake, inhibit remodeling of the extracellular matrix, inhibit cell adhesion molecules that participate in cancer progression, and oppose chemokine signaling pathways that direct the course of metastasis into other locations. Heart benefitChem Biol Interact. 2014 Dec 31. Apigenin attenuates heart injury in lipopolysaccharide-induced endotoxemic model by suppressing sphingosine kinase 1/sphingosine 1-phosphate signaling pathway. Ovarian cancerDr. Margaret A. Gates, of Brigham and Women's Hospital and Harvard Medical School, in Boston, Massachusetts, reviewed the foods commonly eaten over a one-week period by 1,140 women with ovarian cancer and 1,180 women without. From this information Dr. Margaret A. Gates and her team calculated the women's intake of 5 common flavonoids -- myricetin, kaempferol, quercetin, luteolin, and apigenin -- frequently obtained by drinking tea or red wine, or eating apples, romaine or leaf lettuce, kale, blueberries, oranges, celery, or tomato sauce. There was no connection between total flavonoid intake and ovarian cancer risk. Only apigenin intake was associated with a suggestive decrease in ovarian cancer risk. International Journal of Cancer, 2009. Leukemia preventionConsuming foods like celery and parsley which contain the naturally occurring flavonoid apigenin may reduce the risk for leukemia. Maikel Peppelenbosch of the University of Groningen in the Netherlands said in January 2010 that apigenin was able to slow the development of two kinds of cells in leukemia and cut their survival chances. The findings suggest apigenin could hold promise for preventing leukamia. Maikel Peppelenbosch cautioned that his study had also found the compound has chemotherapy resistance properties, suggesting it might interfere with standard treatments for people already diagnosed with leukemia so it should not be taken at the same time as chemotherapy for established disease as it could interfere with the positive effects of treatment. Dietary flavonoids as proteasome inhibitors and apoptosis inducers in human leukemia cells. Biochem Pharmacol. 2005 . Barbara Ann Karmanos Cancer Institute, and Department of Pathology, School of Medicine, Wayne State University, Detroit, MI It has been shown that proteasome activity is required for cancer cell survival and consumption of fruits and vegetables is associated with decreased cancer risk. Previously, we reported that grape extract could inhibit proteasome activity and induce apoptosis in tumor cells. In this study, we examined the flavonoids apigenin, quercetin, kaempferol and myricetin for their proteasome-inhibitory and apoptosis-inducing abilities in human tumor cells. Our results suggested that the proteasome may be a target of these dietary flavonoids in human tumor cells and that inhibition of the proteasome by flavonoids may be one of the mechanisms responsible for their cancer-preventive effects. Osteoporosis, bone healthCytotechnology. 2014 Feb 6. Apigenin inhibits osteoblastogenesis and osteoclastogenesis and prevents bone loss in ovariectomized mice. StudiesSynergistic interaction between hesperidin, a natural flavonoid, and diazepam. Eur J Pharmacol. 2005. It has been recently reported the presence in Valeriana of the flavone 6-methylapigenin and the flavanone glycoside hesperidin. The apigenin derivative is a ligand for the benzodiazepine binding site in the gamma-aminobutyric acid receptor type A (GABA(A)) and has anxiolytic properties. Hesperidin has sedative and sleep-enhancing properties but is not a ligand for the benzodiazepine binding site. 6-Methylapigenin is able to potentiate the sleep-enhancing effect of hesperidin. In this work we demonstrate that this property is shared with various GABA(A) receptor ligands, among them the agonist diazepam, which was used to study the potentiation as measured in the hole board test. Isobolar analysis of the results showed the interaction being synergistic. We discarded pharmacokinetic effects or a direct action of hesperidin on the benzodiazepine binding site. A possible use of hesperidin properties to decrease the effective therapeutic doses of benzodiazepines is suggested. Decreased pro-inflammatory cytokine production by LPS-stimulated PBMC upon in vitro incubation with the flavonoids apigenin, luteolin or chrysin, due to selective elimination of monocytes / macrophages. Biochem Pharmacol. 2005. Apigenin and its structural analogues chrysin and luteolin were used to evaluate their capacity to inhibit the production of pro-inflammatory cytokines by lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells (PBMC). Furthermore, flowcytometric analysis was performed to compare the effects of apigenin, chrysin, luteolin, quercetin and naringenin on the different cell types present in PBMC. LPS-stimulated PBMC were cultured in the presence of the flavonoids and TNFalpha, IL-1beta and IL-6 were measured in the supernatants. In parallel, metabolic activity of the PBMC was determined by measuring succinate dehydrogenase activity. Apigenin, chrysin and luteolin dose-dependently inhibited both pro-inflammatory cytokine production and metabolic activity of LPS-stimulated PBMC. With increasing concentration of apigenin, chrysin or luteolin the monocytes/macrophages disappeared as measured by flowcytometry. This also appeared to occur in the non-LPS-stimulated PBMC. At the same time there was an increase in dead cells. T- and B-lymphocytes were not affected. Quercetin and naringenin had virtually no effects on cytokines, metabolic activity or on the number of cells in the studied cell populations. In conclusion, monocytes were specifically eliminated in PBMC by apigenin, chrysin or luteolin treatment in vitro at low concentrations (around 8 microM), in which apigenin appeared to be the most potent. The flavones luteolin and apigenin inhibit in vitro antigen-specific proliferation and interferon-gamma production by murine and human autoimmune T cells. Biochem Pharmacol. 2004. Flavonoids such as luteolin, fisetin and apigenin are inhibitors of interleukin-4 and interleukin-13 production by activated human basophils. Int Arch Allergy Immunol. 2004. Molecular modeling of flavonoids that inhibits xanthine oxidase. Biochem Biophys Res Commun. 2002. The inhibition of xanthine oxidase activity by various flavonoids was assessed. All of the tested flavonoids were competitive inhibitors, and from the kinetic analysis suggested that flavonoids bind to the reactive site. To further understand the stereochemistry between these flavonoids and xanthine oxidase, structure-based molecular modeling was performed. Apigenin was the most potent inhibitor. questionsQ. Can a flavonoid supplement such as apigenin be used with tongkat ali LJ100? A. Probably, but keep dosages low. Q. Excellent review of the pathways associated with apigenin, Luteolin- flavones etc. Briefly, I find apigenin in combination with the other flavonoids to be an exciting treatment for prostate cancer patients, specific to inhibiton of fatty acids synthase activity /angiogenesis. However, can we get enough of the flavonoids in the olive leaf product to mount a successful campaign? I believe, with synergy, we will need at least 1gram of apigenin alone. A. It is difficult to know at this time with hardly any research done with apigenin and prostate cancer. Perhaps many types of flavonoids would help beside apigenin. Please see the prostate cancer page for updates. Q. There is a great deal of very promising information about the potential value of apigenin at doses of about 150 mg/day in animal models of prostate cancer, and there are no apparent toxicities. However, I cannot find a source for apigenin in anything but trivial quantities. Do you know of such a source? A. I am not aware of any particular supplement companies that make an apigenin supplement product by itself. Q. The U.S.D.A says that apigenin is an aromatase Inhibitor. Do you have any info on that. A. I have not come across human studies regarding the in vivo effect of apigenin supplements in terms of aromatase inhibition. There have been some in vitro and animal studies that indicate apigenin and other flavonoids to have aromatase inhibiting activity, but whether these flavonoids, when ingested as supplements, have a significant effect in humans has yet to be fully elucidated. On your apigenin page, a reader asked where to find this supplement in non-trivial quantities. I have had this same problem, since the most common formulation is chamomile extract standardized to 1.5% Apigenin. That's better than nothing but probably not much more than can be obtained dietarily through chamomile tea or broccoli. I, and probably others, would like to find a more potent form in case it would work therapeutically in ways similar to lab and animal studies reported recently. (Of course I realize that there are many questions of bioavailability and delivery that have not been addressed yet.) Recently I have seen advertising for 50-mg Apigenin capsules from Swanson. Their standard supplement label lists Apigenin 50 mg and no other measureable ingredients so I assume it is fairly pure. However theirs is extracted from grapefruit. Does it make any difference what food product it comes from? Probably not, as long as the quality of the product is good and the capsules do contain the actual ingredient, it should not matter where it is derived from. Q. I wanted to let you know that it is currently available from Swanson in 50 mg capsules. It may be available from other sources now but I ran into it on amazon dot com. Is there any research you know of that would suggest the minimum oral intake of apigenin to have an appreciable effect on, for example, residual OvCa cells present during post-chemotherapy remission? I have found several interesting mouse studies but I have no idea whether a daily dose of 50 or 100 mg would be likely to produce any effect in a human subject. Please understand I am not asking for medical advice, just looking for existing information that might be useful for reaching our own conclusions. I am not aware of such research as of December 2009.
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Cancer
Sept 3, 2015 15:00:29 GMT -5
Post by Master Kim on Sept 3, 2015 15:00:29 GMT -5
Dr Pam Popper: Man Who Discovered PSA Says the Test is Useless
Published on Aug 28, 2014
According to the researcher who discovered Prostate Specific Antigen (PSA), PSA screening for the general population is a terrible idea; the false positive rate is 78%! This is information that all men should have access to!!
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Cancer
Sept 3, 2015 17:32:30 GMT -5
Post by Master Kim on Sept 3, 2015 17:32:30 GMT -5
False Positive Screening For Cancer Found To Be Frequent And Costly - www.sciencedaily.com/releases/2004/12/041220002224.htmDate: December 30, 2004 Source: American Association For Cancer Research Summary: Cancer screening tests can frequently produce false positive outcomes that may result not only in anxiety but also additional economic costs as well, according to research conducted by scientists at the Henry Ford Health System, Detroit, Mich., and published in the December issue of Cancer Epidemiology, Biomarkers & Prevention. PHILADELPHIA -- Cancer screening tests can frequently produce false positive outcomes that may result not only in anxiety but also additional economic costs as well, according to research conducted by scientists at the Henry Ford Health System, Detroit, Mich., and published in the December issue of Cancer Epidemiology, Biomarkers & Prevention. Among 1,087 individuals participating in a cancer screening trial who received a battery of tests for prostate, ovarian, colorectal and lung cancer, 43 percent had at least one false positive test result, according to Jennifer Elston Lafata, Ph.D., director of the Center for Health Services Research at the Henry Ford Health System and the lead author on the study. "As new cancer screening tests are developed it is important to consider not only their potential clinical benefits, but also their potential for adverse effects," said Lafata, director of the Center for Health Services Research at the Henry Ford Health System. "One such adverse effect is the medical care costs associated with false positive cancer screening test results. Although such costs are often overlooked, we've shown they can be quite substantial." Specifically, men who incurred a false positive result for either prostate, lung or colorectal cancer averaged $1,171 in additional medical care expenditures compared to men with all negative screens. More than half, 51 percent, of the men in the study had at least one false positive test. For women, 36 percent had false positive screening results. Women with a false positive screen for ovarian, colorectal or lung cancer experienced $1,024 more in follow-up medical care expenses compared to women with all negative results. The study was funded by the National Cancer Institute and is part of a larger trial of the effectiveness of screening for prostate, lung, colorectal and ovarian cancers. "The results of this smaller study add to the growing body of evidence highlighting the importance of understanding not only the likely benefits of cancer screening, but also how the accuracy of screening tests impacts patients and medical care expenditures, and thus the overall cost-effectiveness of different screening alternatives," Lafata said. "Although the clinical evidence for the use of these and many other new screening tests is still being developed, many such screening tests are already widely used in practice thereby resulting in what can be substantial additional medical care costs without known benefits." Henry Ford Medical Group researchers who collaborated with Lafata in the study included Janine Simpkins, M.A., Lois Lamerato, Ph.D., Laila Poisson, M.S., George Divine, Ph.D., and Christine Cole Johnson, Ph.D. ### Founded in 1907, the American Association for Cancer Research is a professional society of more than 24,000 laboratory, translational, and clinical scientists engaged in all areas of cancer research in the United States and in more than 60 other countries. AACR's mission is to accelerate the prevention and cure of cancer through research, education, communication, and advocacy. Its principal activities include the publication of five major peer-reviewed scientific journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. AACR's Annual Meetings attract more than 15,000 participants who share new and significant discoveries in the cancer field. Specialty meetings, held throughout the year, focus on the latest developments in all areas of cancer research. Story Source: The above post is reprinted from materials provided by American Association For Cancer Research. Note: Materials may be edited for content and length.
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Cancer
Sept 7, 2015 16:19:38 GMT -5
Post by Master Kim on Sept 7, 2015 16:19:38 GMT -5
Brazilian wasp venom kills cancer cells by opening them up - phys.org/news/2015-09-brazilian-wasp-venom-cancer-cells.htmlSeptember 1, 2015 Brazilain social wasp Polybia paulista. Credit: Prof. Mario Palma/Sao Paulo State University The social wasp Polybia paulista protects itself against predators by producing venom known to contain a powerful cancer-fighting ingredient. A Biophysical Journal study published September 1 reveals exactly how the venom's toxin—called MP1 (Polybia-MP1)—selectively kills cancer cells without harming normal cells. MP1 interacts with lipids that are abnormally distributed on the surface of cancer cells, creating gaping holes that allow molecules crucial for cell function to leak out. "Cancer therapies that attack the lipid composition of the cell membrane would be an entirely new class of anticancer drugs," says co-senior study author Paul Beales, of the University of Leeds in the UK. "This could be useful in developing new combination therapies, where multiple drugs are used simultaneously to treat a cancer by attacking different parts of the cancer cells at the same time." MP1 acts against microbial pathogens by disrupting the bacterial cell membrane. Serendipitously, the antimicrobial peptide shows promise for protecting humans from cancer; it can inhibit the growth of prostate and bladder cancer cells, as well as multi-drug resistant leukemic cells. However, until now, it was not clear how MP1 selectively destroys cancer cells without harming normal cells. Beales and co-senior study author João Ruggiero Neto of São Paulo State University in Brazil suspected that the reason might have something to do with the unique properties of cancer cell membranes. In healthy cell membranes, phospholipids called phosphatidylserine (PS) and phosphatidylethanolamine (PE) are located in the inner membrane leaflet facing the inside of the cell. But in cancer cells, PS and PE are embedded in the outer membrane leaflet facing the cell surroundings. The researchers tested their theory by creating model membranes, some of which contained PE and/or PS, and exposing them to MP1. They used a wide range of imaging and biophysical techniques to characterize MP1's destructive effects on the membranes. Strikingly, the presence of PS increased the binding of MP1 to the membrane by a factor of 7 to 8. On the other hand, the presence of PE enhanced MP1's ability to quickly disrupt the membrane, increasing the size of holes by a factor of 20 to 30. "Formed in only seconds, these large pores are big enough to allow critical molecules such as RNA and proteins to easily escape cells," Neto says. "The dramatic enhancement of the permeabilization induced by the peptide in the presence of PE and the dimensions of the pores in these membranes was surprising." In future studies, the researchers plan to alter MP1's amino acid sequence to examine how the peptide's structure relates to its function and further improve the peptide's selectivity and potency for clinical purposes. "Understanding the mechanism of action of this peptide will help in translational studies to further assess the potential for this peptide to be used in medicine," Beales says. "As it has been shown to be selective to cancer cells and non-toxic to normal cells in the lab, this peptide has the potential to be safe, but further work would be required to prove that." More information: Biophysical Journal, Leite et al.: "PE and PS Lipids Synergistically Enhance Membrane Poration by a Host-Defense Peptide with Anticancer Properties" dx.doi.org/10.1016/j.bpj.2015.07.033
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Cancer
Sept 28, 2015 21:04:11 GMT -5
Post by Master Kim on Sept 28, 2015 21:04:11 GMT -5
Tokyo Journal; When Doctor Won't Tell Cancer Patient the Truth - www.nytimes.com/1995/02/25/world/tokyo-journal-when-doctor-won-t-tell-cancer-patient-the-truth.htmlBy NICHOLAS D. KRISTOF, Published: February 25, 1995 - The New York Times Hirohito may have been a virtual god in the early part of his reign, but he was also a patient -- and doctors in Japan mostly lie to cancer patients, even former divinities. "I don't regret that I didn't tell him about his cancer," Akira Takagi, the Emperor's chief doctor, said at the time of Hirohito's death in 1989. But these days, a mild-mannered radiologist is crusading for the principle of telling patients the truth, even when that means breaking their hearts. The radiologist, Dr. Makoto Kondo, returned from a year in the United States determined to tell patients bad news, and his campaign for radical change -- for pulling doctors down a notch and injecting democracy into the Japanese medical system -- is provoking such outrage among fellow physicians that they refuse to refer patients to him. He is scarcely more polite about them. "The present system is like the medical experiments on prisoners during World War II," Dr. Kondo said as he took a break in his cluttered office, surrounded by books in Japanese and English. "It's a very awful thing. It's a shame." Dr. Kondo's latest book, "Side Effects of Anti-Cancer Drugs," has hit several best-seller lists since it arrived in bookstores late last year. Patients flock to his practice, and he has become about as much of a celebrity as a full-time radiologist can. Surveys suggest that only about a quarter of Japanese doctors always tell patients when they have cancer. People are especially unlikely to be told if they have inoperable cancers with a poor prognosis; patients with stomach cancer may be told they have nothing more than an ulcer. A 50-year-old woman named Kazuko Makino was told that she had gallstones, even though her doctor suspected gallbladder cancer. The doctor recommended surgery, but Mrs. Makino was a nurse and decided that she did not need an operation to remove her "gallstones." The cancer spread, and Mrs. Makino died. Her family sued the hospital for malpractice, but a court rejected the claim, ruling in a landmark case in 1989 that doctors need not tell cancer patients their true condition. Japanese doctors do not disclose bad news primarily because of fear that it would upset the patient and harm the prognosis. Neither side can cite statistics about whether patients live longer if they have been lied to, but even some of those who favor honesty worry about the psychological and physiological consequences if a doctor is seen as pronouncing a death sentence. Dr. Kondo acknowledges that he used to go along with this. "I didn't tell patients the truth," he said. "I lied to them. But it was a very bad experience." Dr. Kondo was also greatly affected by a year he spent in the United States, in 1979. "I realized that if a doctor could tell the truth to patients in the U.S.," he said, "then I could do the same to patients in Japan." The best gauge of what Dr. Kondo is up against is the popularity of an anti-cancer drug called Krestin. Its manufacturer says Krestin sales amount to about $100 million a year. It is said to be popular because doctors can prescribe it without telling patients that they have cancer. Krestin is taken orally, and does not have debilitating side effects that might give patients clues to the diagnosis. But critics assert that Krestin does not have much in the way of good effects either. The Japanese Hospital Association has condemned the drug, saying doctors wasted $10 billion on it and another anti-cancer drug. Sankyo Pharmaceuticals, which sells Krestin, takes a different view. "We consider it effective, in that the Ministry of Health and Welfare conducted a review and permitted its use," said a company spokesman. Dr. Masanori Fukushima, a cancer specialist who is critical of Krestin, said, "Things happen in this country which are ridiculous." Still, Dr. Fukushima and everyone else interviewed said the number of doctors who tell the truth to patients is greater than it was five years ago. "It's a process of democracy developing in the health system," Dr. Fukushima said. "We're about 20 or 30 years behind the United States." The authoritarian, paternalistic elements in the current Japanese health care system are evident even in a checkup. Japanese doctors are less likely than American ones to explain what they are doing and why, or to indicate what they have found. Moreover, Japanese prescription bottles do not state the medicine being taken. Instead, there are symbols that a patient can decipher by consulting a technical reference that has been a huge best seller in Japan. "The relationship between the physician and the patient is like that between God and the people," said Dr. Masao Miyamoto, a psychiatrist who earned his medical degree in Japan and later taught and practiced in the United States. "The problem then is that in Japan a patient can't get a second opinion. It becomes an insult." Underlying the dispute about telling patients the truth is a conflict among lay people about what the policy should be. A poll last year found that 64 percent of those interviewed would want to be told the truth if they had cancer. But when asked their opinion if the patient was another family member, 58 percent said they would not want the doctor to tell the truth to their loved ones. "A majority of family members are against telling the truth to the patient, at least initially," said Dr. Mitsuru Sasako, a professor of surgery at the National Cancer Center Hospital in Tokyo. Dr. Sasako said that he normally tells patients the truth anyway, but that it must be done with special care in Japan because there are none of the support organizations that exist in America to counsel terminally ill patients. Dr. Sasako argues that Dr. Kondo's advice to the public was initially useful in shaking up the medical establishment. But like most doctors, he said Dr. Kondo's pronouncements are now too sweeping and opinionated and leave patients skeptical and uncertain about their options. "If he makes people unable to believe doctors, that can make patients unhappy," he said. "If Dr. Kondo makes too many accusations, that causes confusion among patients." Photo: Dr. Makoto Kondo, a radiologist, is campaigning to inject some democracy into the Japanese medical system by telling patients the truth about their illnesses. He consulted with a patient this week in his office in Tokyo. (Fumiyo Asahi for The New York Times)
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Cancer
Sept 28, 2015 21:49:09 GMT -5
Post by Master Kim on Sept 28, 2015 21:49:09 GMT -5
How to treat pet cancer: Do nothing, says one doctor - www.japantoday.com/category/kuchikomi/view/how-to-treat-pet-cancer-do-nothing-says-one-doctorKuchikomi Jun. 24, 2014 - 06:25AM JST TOKYO — Dr Makoto Kondo’s aged pet beagle was sinking. What to do? The poor beast had breast cancer. That’s something new in dogs. They’re living longer and longer, afflicted in old age by once unheard-of diseases. Treatment was one option. It’s available. Pet aging has rejuvenated the veterinary business, as owners spare no expense to keep their beloved animal companions alive as long as possible. If you’ve heard of Dr Kondo – and you may have; he’s well-known – you’ll know he was having none of it. What, then? Euthanasia? As he mulled it over the dog solved the problem by dying quietly and naturally. Kondo’s public notoriety rests on a number of bestsellers he’s written whose shared theme is, “Say ‘no’ to cancer treatment.” No surgery, no radiation, no chemotherapy. Even if these procedures extend the lives of cancer patients – and they don’t necessarily – they are so painful, debilitating and invasive, he says, as to make the cure worse than the disease. Cancer is not necessarily fatal; sometimes it can be lived with. If it can’t be, his advice is to come to terms with death and dying; medical intervention should be limited to making the passage as easy as possible. The medical establishment excoriates him. The general public, judging by his books’ robust sales figures, is at least willing to give him a hearing. His main concern of course is human cancer, but Josei Jishin (July 1) sounds him out on the spreading scourge of pet cancer. Once upon a time, the average pet dog lived five, six years; now it’s 15. Ditto for cats. Half of all pet dogs, and one-third of cats, end up with cancer. Kondo himself is an animal lover and understands what owners go through. He went through it himself. But treatment? Never, he says. “I see what vets are offering in the way of cancer treatment, and it reads like a parody novel,” he says. “Parody” because it mimics human treatment – CT scans, MRIs, surgery – although “there is no evidence” any of this works on animals. Human treatment is at least subject to regulation. Pet treatment, he says, is not – neither the regime nor the costs, which easily run into the hundreds of thousands of yen. “It’s all baseless and meaningless,” he tells Josei Jishin – “but many of the owners are elderly; they say, ‘It’s my last pet;’ they’re very attached to them.” Unscrupulous vets find them willing listeners to promises of cures. If they shrink from the expense they feel guilty. Still, “Best do nothing,” Kondo advises. As for people, so for pets. He doesn’t use the phrase “death with dignity,” but it fits the point he’s making. “Whether for human cancer or pet cancer,” he says, “I wish society would learn to accept this as normal thinking.”
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Cancer
Oct 8, 2015 17:11:55 GMT -5
Post by Master Kim on Oct 8, 2015 17:11:55 GMT -5
Why Doctors Are Rethinking Breast-Cancer Treatment - time.com/4057310/breast-cancer-overtreatment/?utm_content=20852998Siobhan O’Connor @siobhannyc - Oct. 1, 2015 For the video clip, please click below link. ti.me/1LlZ03RToo much chemo. Too much radiation. And way too many mastectomies“What if I decide to just do nothing?” It was kind of a taunt, Desiree Basila admits. Not the sort of thing that usually comes out of the mouth of a woman who’s just been diagnosed with breast cancer. For 20 minutes she’d been grilling her breast surgeon. “Just one more question,” she kept saying, and her surgeon appeared to her to be growing weary. She was trying to figure out what to do about her ductal carcinoma in situ (DCIS), also known as Stage 0 breast cancer, and she was already on her second opinion. The first surgeon had slapped a photograph of her right breast onto a viewer, pointed to a spot about 5 cm long and 2.5 cm wide and told her there was a slot open the following week for a mastectomy. Basila’s first reaction to her diagnosis was an animal-instinct panic that she registered as “10,000 bricks” crushing into her chest when she woke up in the morning. After that, Basila, who is now 60 and teaches high school science in San Francisco, did a little research. She learned that there were a lot of unknowns about the progression of DCIS, which is noninvasive–it’s confined to the milk ducts–and is the earliest stage of breast cancer. She also learned there was some disagreement in the field about how to treat it. She knew she wasn’t ready to have one or both of her breasts cut off. And she wasn’t sure she wanted a lumpectomy either. That’s why when Dr. Shelley Hwang, then a surgeon at the University of California, San Francisco (UCSF), recommended a lumpectomy, Basila grew frustrated. She was coat in hand and ready to walk out the door when she issued that half taunt. And when she did, Hwang said this: “Well, some people are electing to do that.” Basila sat back down, and as their meeting reached the hour mark, she made a choice that humans are practically hardwired not to make in the face of a cancer diagnosis: she decided to do nothing. Well, not nothing, exactly. She would start taking a drug called tamoxifen that blocks estrogen, which can fuel tumor growth, and she would enroll in a clinical trial involving active surveillance: twice-a-year visits in which she would get mammograms alternating with MRIs. As long as there were no worrisome changes, Basila would be spared the standard arsenal in breast-cancer treatment: surgery, radiation and chemotherapy. That conversation took place eight years ago. And if it sounds radical today, it was all but heresy back then. This was before the U.S. Preventive Services Task Force said in 2009 that women should start mammograms at 50, not the previous guideline of 40, because there’s insufficient evidence that earlier screening does more good than harm. Before research showed that for some women with Stages 1 and 2 breast cancer, the absolute survival benefit from preventive double mastectomies is less than 1% after 20 years. Before the paper in August showing that no matter how a woman is treated for DCIS, the mortality risk is 3%–similar to the average for the general population. And before the news that some women with early-stage breast cancer don’t benefit from chemo and can skip it. In other words, that conversation took place before doctors and patients were faced with the evidence that in the U.S., many women with breast cancer are being massively overtreated. Thanks to advances in genomic testing and deeper insights into the biology of different kinds of breast cancer, doctors are learning that the one-size-fits-all approach isn’t working. They’re also learning that every woman brings with her a unique profile of biological risk–as well as a unique appetite for risk. That means that while some women require urgent and aggressive treatment, there are many who can slow down and take a more sparing approach. Now those at the vanguard of breast-cancer treatment are calling for a major shift in the way doctors treat–and talk about–the disease, from the first few millimeters of suspicious-looking cells in milk ducts to the invasive masses found outside of them. That’s making the tough conversations between a woman and her cancer doctor ever harder, but it also stands to make them more fruitful. Because as good as we have gotten at finding breast cancer–and we’ve gotten very good–all this new data suggests there may be better ways to treat some breast cancers, particularly those at the early stages. Evidence is mounting that aggressive treatments, designed in earnest to save women’s lives, can have unforeseen and sometimes devastating consequences. Call it collateral damage. It’s the multiple follow-up surgeries after a mastectomy and the subsequent infections; the radiation that doesn’t always improve survival and the cancer risk that can come with too much of it; the sometimes unnecessary chemotherapy and its life-sapping side effects. For some in the field, that collateral damage is getting harder and harder to justify. Now a small but influential chorus of leaders is calling for a radical–measured but still radical–shift in the way doctors are approaching the disease. “As a surgeon, to say we shouldn’t be operating as much as we are is a very big deal,” says Dr. Mehra Golshan, a surgical oncologist at the Dana-Farber/Brigham and Women’s Cancer Center. “And that’s what I’m saying.” Medicine is slow to move, and that’s especially true with breast cancer. Doctors are up against not only new data but also an accumulated mass of public opinion seeded by policymakers and advocacy groups with strong positions on how best to screen for and treat breast cancer. These measures were put into place for good reason, of course–because experts thought they would save lives. But they didn’t–or at least not as many as anticipated. This year more than 40,000 women in the U.S. will die of breast cancer. That’s the same, give or take, as last year, and the 13 years before that. At the same time, fear of the disease has led many to overestimate the risk it poses. The chance that a woman will die of breast cancer is 3%, and that’s been the case since the early 2000s, when a blockbuster report demonstrated that hormone-replacement therapy (HRT), which women took during menopause to help with side effects, could unwittingly fuel the development of breast cancer. Once HRT fell out of vogue, the number of deaths dropped, and it’s remained largely unchanged since. “I hear people say that medicine is so important that we can’t be too quick to change, and I would say the opposite: Because it’s so important, we need to innovate,” says Dr. Laura Esserman, a surgeon and the director of the Carol Franc Buck Breast Care Center at UCSF. “If we were doing so well and no one was dying, I would agree we don’t need to change. But patients don’t like the treatment options, and physicians don’t like the outcomes.” Esserman and Hwang, now chief of breast surgery at Duke University and Duke Cancer Institute in North Carolina, are leading a number of studies that they hope will fill in some of the knowledge gaps that make change such an uphill battle. DCIS now accounts for about 20% to 25% of breast cancers diagnosed through screening. Before routine screening, which went wide in the mid-1980s, it was 3%. “Our two greatest challenges,” says Dr. Eric Winer, director of breast oncology at Dana-Farber, “are figuring out better treatments for the 40,000 women who die of breast cancer every year, and at same time, figure out who, on the other end of the spectrum, is getting exposed to needless toxicity.” If only doctors could agree on how to do that. Everyone says surgeons and radiologists need to know more about how to do less. And doctors don’t want to be responsible for the patient who isn’t treated aggressively and dies on their watch. That’s where the two camps split: motivated by the same thing, some in the field are working to find even more proof the disease can be treated responsibly another way, while others say it’s just too risky to pivot without proof. It used to be accepted that tumors grow at a steady clip. Once they get big enough, they spread, and when they spread, you’re in trouble. That was the reasoning behind the “early detection saves lives” thinking and it did, in fact, help save many lives. But now experts know that many breast cancers are, in the apt medical term, indolent–slow-growing tumors that may never cause symptoms, let alone hasten a woman’s death. They also know there are a small number of breast cancers that spread very quickly, sometimes even before they are detected. They’re working to figure out which ones are which–and what to do in the meantime. “Many doctors still say that any breast cancer is a failure of a patient to get a mammogram or failure of a doctor to detect it,” says Dr. Otis Brawley, chief medical officer of the American Cancer Society. “If you look at the science, that is so clearly not the case.” Indeed, the 2009 guideline that most women start screening at 50, which caused a national uproar, is still controversial today–despite the fact that when mammograms went wide, the reduction in deaths didn’t match what experts say was expected. Screening presents doctors and patients with a modern conundrum. If you have the technology to detect something, you are without a doubt going to find more of it. One doctor puts it this way: In a beachside tragedy, a shark attacks a swimmer and the swimmer dies. In the past, that would have been seen, perhaps, as a freak accident. But today we have flying robots with cameras and sensors that can patrol the waters. When we discover the area is teeming with creatures that may also have an appetite for humans, though we can’t be sure, what do we do? Do we close the beach? No one is suggesting that women stop getting mammograms. But experts think it’s important to be honest that it’s an imperfect technology. “Mammograms are here to stay,” says Hwang, who has about 20 patients at any given time who have chosen to do active surveillance instead of surgery and the treatments that follow it. “It’s not the ‘finding more’ that we need to work on. It’s what are we going to do with the more that we find?” That’s what’s keeping cancer doctors up at night. That, and the growing concern that with all breast cancers being treated aggressively, some patients are getting hurt. With breast cancer, the burden of proof for not doing something is greater than it is for acting. And when doctors deviate from what’s called the standard of care, they can face malpractice lawsuits. Some experts note that with other diseases, insurers would be the bad cops, denying payment for treatments that may be unnecessary. But with breast cancer, otherwise hard-nosed insurers will often pay for many of the approved therapies as long as they’re in line with published guidelines. Since the guidelines for breast cancer tend to err on the side of caution, it means that regardless of the stage of her disease or her prognosis, a woman is likely to have insurance that will cover both mastectomy and reconstruction. “There is no check on what is a reasonable treatment for an anticipated outcome,” says Hwang. “If we are going to accept that everyone, even those who have a 1% chance of mortality improvement, can get a treatment, that is not biologically a good way to approach the problem. It’s also just incredibly expensive.” The increase in women opting for a contralateral prophylactic mastectomy–which doesn’t improve survival for most patients–worries a number of surgeons because it isn’t clinically indicated for most of the patients who get one. (One exception is women with rare BRCA1 and 2 mutations, which greatly increase a woman’s chance of developing breast and ovarian cancer. That’s why Angelina Jolie famously had the procedure and why doctors continue to recommend the surgery in such cases.) “We are talking about major surgery,” says Hwang. “It can involve revisions, prolonged pain, hernias. I think the best way to understand it is that it may require surgeries for the rest of your life. Some small, some major. But it’s not like you’re done and you can forget about it. It just doesn’t work that way.” There are psychological effects for some women, though not all. Some women say they struggle with feelings around femininity and sexuality after surgery. Some who have had nipple-sparing mastectomies–a reconstruction that preserves the woman’s own nipples–wonder when the sensation will return. (The answer is often, never.) They’re also at increased risk of depression and all that can come with it. “It’s not my job to say that their decision is wrong,” says the breast surgeon Golshan, who worries that patients are not adequately cautioned about–or at least not fully aware of–the potential risks. “Women may see end-result pictures, and it looks wonderful. But the vast majority of reconstruction requires multiple steps of revision.” Cancer has a language problem–not just in the way we speak about it, as a war that drafts soldiers who never signed up for it, who do battle and win, or do battle and lose. There’s also the problem of the word itself. A 57-year-old woman with low-grade DCIS that will almost certainly never become invasive hears the same word as the 34-year-old woman who has metastatic malignancies that will kill her. That’s confusing to patients conditioned to treat every cancer diagnosis as an emergency, in a world that still reacts to cancer as though it’s the beginning of the end and in a culture where we don’t talk about death until we have to. “We think that word means the most aggressive thing,” says Basila, recalling the shock when she first learned she had DCIS. “I’m not saying doctors should sugarcoat it. But we have to have the perspective that we can sometimes afford to not see it as a death sentence, de facto.” That is hard to do in an hour, let alone in a 10-minute appointment. Dr. Steven J. Katz, a professor at the University of Michigan who studies patient and physician decisionmaking, points out that the vast majority of women feel healthy when they’re diagnosed. And with most women diagnosed from ages 55 to 64, their own mortality is not, for good reason, top of mind. But now, inevitably, it will come up. This is not an easy conversation to have. “They’re well and told they’re sick,” says Katz. “And then they are told they will have to get really sick to get well.” Talk to women about what that’s like and you’ll hear things like: “I literally went into shock.” “I was blindsided.” “I got sort of dizzy.” You may also hear: “I don’t really remember what we spoke about, but I remember it said 4:01 on the clock.” That’s a difficult position from which to make a life-changing decision, and most women make a decision within weeks of diagnosis, says Katz. It’s not the right way to do things, says UCSF’s Esserman. “The time has come to ask, What happens if I do nothing right away.” The “right away” part of the question is important. “Let’s not make it a panic. There is no evidence to support getting surgery in two weeks.” Katz’s research has demonstrated that there’s a natural instinct in patients, when faced with the C word, to outsource the decision to their doctors. That’s why who your doctor is, what she tells you and how she tells it to you matter enormously. Because for many women, the strong inclination is to do whatever can be done–and as quickly as possible–to begin to feel like their normal selves again. That can get tricky when a patient’s attempt to get back to normal as quickly as possible is at odds with the science of how best to do that. Some new tools are pushing the field forward, though they’re not perfect. A genomic test called Oncotype DX, for instance, can help doctors determine whether or not some patients will respond to chemo. It was part of a landmark study in the New England Journal of Medicine in September showing that some women with early-stage disease could be treated with hormone therapy alone. Another gene test, the Oncotype DX DCIS, can help indicate who is at low, intermediate and high risk of recurrence of DCIS, helping inform whether a woman needs radiation therapy following a lumpectomy. And while there aren’t yet diagnostics to say precisely who is a good candidate for active surveillance, the doctors who partner with their patients on such a plan say they do so prudently. Many in the field still don’t think there’s enough evidence to support active surveillance for anyone, because the method hasn’t been tested in a randomized prospective trial–the gold standard for the widespread adoption of a medical treatment. That’s something Hwang and Esserman are hoping to address in the U.S. Hwang was awarded $1.8 million in September to perform a retrospective study comparing active surveillance with standard care, and she’s hoping she’ll soon have the green light to do a prospective study looking at the same thing. Esserman is creating a DCIS registry at the five University of California medical centers. Women diagnosed with DCIS at any of the facilities will be offered options–including active surveillance–and be tracked over time. The hope: that the data will refine doctors’ understanding of who, with DCIS, will go on to develop invasive breast cancers and who will not. Esserman has also launched something called the WISDOM study, which will randomize women to either annual screening or a more personalized screening approach. “We’ll learn over time what works,” says Esserman. “How wonderful if we can learn how to do less for women.” In the U.K., meanwhile, where bilateral prophylactic mastectomies are rarely performed unless a patient has a gene defect or is at a very high risk of invasive breast cancer, a first-of-its-kind investigation is under way. Called LORIS, it’s a 10-year randomized controlled prospective study, funded by the U.K.’s National Institute for Health Research, that will include 900 women. Half will get the standard care, and half will be actively monitored. “My personal view is that enough time has been spent arguing about screening, and we now should be addressing the issue through well-run clinical trials that are long overdue,” says Dr. Adele Francis, a breast surgeon at University Hospital Birmingham and the lead on the LORIS study. Some experts doubt that such a trial would fly in the U.S., given how risk-averse the field historically has been. There’s another important piece of the puzzle: the women with the diagnosis. “Change in medicine comes from patients,” says Esserman. “My patients don’t like the options we have. So I say, Get the facts. Find someone who will go through those options with you.” For some women, like Basila, that’s already happened. And just as some women choose to take a “get it out of me” approach, there are some–not many, but some–for whom the opposite is appropriate. As with all the hardest decisions we have to make about our health, it comes down to the impossible calculus of what level of uncertainty can I live with? “What I am doing is not foolproof,” says Basila. “I know that. I also know life is finite and that death is unavoidable. For me it came down to the quality of the life I want to live. I don’t want to be tired and bitchy if I can avoid it. And come what may, I think we really hurt ourselves by trying to just not be dead.” Correction: This piece has been updated to reflect the proper title of the Dana Farber/Brigham and Women’s Cancer Center. An earlier version of this story also misstated which patients would be involved in the WISDOM study. This appears in the October 12, 2015 issue of TIME.
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Cancer
Oct 16, 2015 14:00:54 GMT -5
Post by Master Kim on Oct 16, 2015 14:00:54 GMT -5
The Stink of Pink: Why Mammograms Are Vastly Oversold - articles.mercola.com/sites/articles/archive/2015/10/14/mammography-promotion.aspx?e_cid=20151014Z1_DNL_10OFF_art_1&utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20151014Z1_DNL_10OFF&et_cid=DM89809&et_rid=1168506431October 14, 2015 By Dr. Mercola Visit the Mercola Video LibraryEarly detection through mammography is the annual clarion call of pink-ribboned Breast Cancer Awareness campaigns. October 21 is National Mammography Day — a day during which women are barraged with reminders that getting a mammogram could save their life. However, little effort has been made to educate women about the crucial differences between non-malignant lesions and invasive or non-invasive cancers detected through this technology. Instead, the general idea that breast cancer is something you either have or don't have is perpetuated, without any distinctions of its relative risk for harm. Fortunately, there are rays of hope, as both researchers and journalists are starting to speak out against the overuse and risks of mammography. Ionizing Radiation Is a Cancer RISK — Why Is It Promoted as a Primary 'Prevention' Tool? First of all, it's important to realize that the ionizing radiation used to discern breast tumors is a risk factor for the development of breast cancer. Additionally, if you do have a malignant tumor, the crushing compression of your breast could potentially cause it to spread. Yet you won't see any information about these risks during these pinkwashing campaigns. Nor will you hear that these risks may be magnified if you are genetically predisposed to breast cancer. In fact, women with BRCA mutation are typically advised to get mammograms every six months or so, which is clearly a recommendation that will increase malignant transformation due to ionizing radiation exposure. Secondly, the identification of the word "prevention" with "early detection," is a disingenuous way of saying that "all we can do to prevent breast cancer is to detect its inevitable presence sooner than would be possible without this technology." This is absolute deceptive hogwash as nothing could be further from the truth. Detection is NOT prevention, and really should not be advertised as such. Pink-Washing Away Preventable Causes of Breast Cancer The Susan G. Komen Foundation has done a great deal of harm to women by obfuscating the authentic preventative measures available to combat breast cancer; downplaying the preventive role of a healthy diet rich in fruits and vegetables for example, while heavily promoting mammography. Another atrocious example of this conspiracy against identifying the obvious causes and cures for breast cancer is the National Breast Cancer Foundation's website. Type in "carcinogen" in their site wide search box and you will be rewarded with ZERO results. Not a single page addresses the role of carcinogenic chemicals in the development of breast cancer. On Susan G. Komen's website, the search term "carcinogen" yields just one study on an antidepressant ingredient. The word is not even listed in the breast cancer glossary. Meanwhile, researchers have identified a number of pervasive chemicals that increase your risk of breast cancer. Avoiding toxic exposures is one of the rational approaches to successful breast cancer prevention, along with healthy lifestyle strategies such as eating real food, exercising, and optimizing your vitamin D levels. By hiding the role that your lifestyle and exposure to carcinogenic chemicals play in the development of cancer, these massive organizations can continue to collect billions of dollars of donations every year in the name of "finding a cure." The Pink Ribbon ScamAs noted by Karuna Jaggar, executive director of Breast Cancer Action, in a Huffington Post article published last year: Breast Cancer Awareness Month Has Produced 'Reckless Misinformation' on Breast CancerAstraZeneca was in fact a by-product of one of the world's largest chemical (and carcinogen) producers, Imperial Chemical Industries (ICI). Before being acquired by AkzoNobel in 2008, ICI produced millions of pounds annually of known mammary carcinogens such as vinyl chloride. In 1993, ICI demerged its pharmaceutical bioscience businesses to form Zeneca Group, which later merged with Astra AB to form AstraZeneca in 1999. Over the years, a number of experts and organizations have pointed out this glaring conflict of interest: False Positives Create Pseudo-Survivors of 'Breast Cancer' Mammography can detect invasive breast cancer in women. This is not in dispute. What IS in dispute is whether or not routine mammograms are really the right tool to reduce breast cancer rates, and whether it might harm more women than it helps in the process. A growing body of evidence suggests that it does in fact, on the whole, do more harm than good by generating high rates of false positives. A woman receiving a false positive diagnosis undergoes the same emotional trauma as those with an accurate diagnosis, and this trauma cannot (and should not) be trivialized. According to a Swedish study, women who received a false positive before later being found to be cancer-free: 88 percent felt dejected, sad, or "unable to cope" 83 percent suffered anxiety 67 percent experienced behavioral changes, such as trouble dealing with work or spare time 53 percent had trouble sleeping Those who opt for aggressive treatment such as a mastectomy, radiation, and/or chemotherapy after a false positive diagnosis also undergo physical pain and suffering "for nothing." Yet women who believe their lives were saved by mammography are hard-pressed to buy into the idea that routine mammograms are more harmful than helpful. But as recently addressed by Forbes magazine in an article7 titled, "Has Mammography Created An Epidemic Of Pseudo-Survivorship?" many women who believe they're breast cancer survivors may not have had a life-threatening tumor at all... They're not survivors of breast cancer; they're survivors of breast cancer treatment. Ductal Carcinoma in Situ — Is it Actually Cancer? Forbes specifically addresses the issue of stage zero cancer known as ductal carcinoma in situ (DCIS), which refers to the abnormal growth of cells forming a lesion that is typically between 1 to 1.5 cm in diameter. About 25 percent (approximately 60,000 cases each year) of all new breast cancer diagnoses obtained through mammography fall in this category. Some experts have argued DCIS should be reclassified as a non-cancerous condition, yet proponents of mammography claim they're "saving lives" through the "early detection" and treatment of DCIS. They view DCIS as "pre-cancerous" and argue that, because it could eventually cause harm if left untreated it should be treated in the same aggressive manner as invasive cancer. The problem with this approach is that the weight of evidence indicates less than half of DCIS cases ever progress to invasive cancer, and in many cases, taking no action beyond "watchful waiting" is the best course of action. As reported by Time Magazine,10 a study published in August found that "no matter how a woman is treated for DCIS, the mortality risk is 3 percent – similar to the average for the general population. " The article also points out the problem with referring to non-invasive lesions like DCIS as "cancer:" Mammography Fuels Fear by Falsely Inflating Breast Cancer Rates One study found that at the 40-year follow-up period, 40 percent of DCIS lesions still had no signs of invasiveness. Adding even more uncertainty, another study showed that coexisting DCIS independently predicts lower tumor aggressiveness in node-positive luminal breast cancer, suggesting it may have a protective role. The irony is that while participation in X-ray mammography is considered a form of breast cancer prevention, it has become a very effective way of manufacturing false breast cancer diagnoses and justifying completely unnecessary treatment. As noted by Forbes,11 in which the harrowing story of a woman treated for DCIS is detailed: New Tools and Studies That May Improve Treatment Decisions New tools have emerged that may help in making treatment decisions following a diagnosis of breast cancer. These include genetic tests, such as: Oncotype DX, which may help determine how well your tumor might respond to chemotherapy Oncotype DX DCIS, which offers an indication of your risk for recurrence of DCIS, and whether radiation therapy following a lumpectomy might be beneficial A DCIS registry is also being created at five University of California medical centers. Women diagnosed with DCIS at these facilities will be given the option of active surveillance, and will be tracked over time to evaluate the outcomes of various treatment options for DCIS. Researchers have also launched a study aimed at learning more about screening. The WISDOM study, led by breast cancer surgeon Dr. Laura J. Esserman — an outspoken opponent of overdiagnosis and overtreatment — will randomly assign women with DCIS to receive either annual mammography screening or a personalized screening approach. As reported by The New York Times, which recently profiled Dr. Esserman's more cautious approach to breast cancer treatment: Adding Computer Analysis to Mammograms Doesn't Improve AccuracyEvery time we write a disparaging article on mammograms many women comment that they believe in them because they saved their life. While I am delighted they were able to avoid dying from breast cancer, that view fails to consider the broader picture that more and more studies confirm, which is that overall mammograms cause far more damage than good. Even newer mammogram revisions are proving to be poor at detecting cancer and improving outcomes. For example, computer-aided detection (CAD) for mammography, which is used in 90 percent of US mammograms at a cost of $400 million a year, does nothing to improve the accuracy of the test, according to a recent study. The study looked at more than 625,000 mammograms from nearly 324,000 women to determine whether CAD actually improves a radiologist's interpretation of a mammogram or not. As it turns out, CAD had no beneficial impact on mammography interpretation, leading the authors to conclude that: "These results suggest that insurers pay more for CAD with no established benefit to women." In fact, radiologists were more prone to miss cancer when using CAD compared to when not using it. Overall, radiologists correctly identified cancer 90 percent of the time when CAD was not used, and only 83 percent of the time when they used CAD. Two New Studies Refute the Value of Mammograms Last but certainly not least, I want to bring attention to two new studies that refute the validity of mammography as a primary tool against breast cancer. The first, published in JAMA Internal Medicine on July 6, 2015, confirmed previous findings showing mammography screenings lead to unnecessary treatments while having virtually no impact on the number of deaths from breast cancer. Previous research has shown that for every life saved by mammography screening, three women will be overdiagnosed and treated with surgery, radiation, or chemotherapy for a cancer that might never have given them trouble in their lifetimes. In the new JAMA study, a positive correlation between breast cancer screening and breast cancer incidence was again found, but there was no positive correlation with mortality. The second study published in the Journal of the Royal Society of Medicine declares its conclusion right in the title, which reads: "Mammography screening is harmful and should be abandoned." In short, decades of routine breast cancer screening using mammograms has done nothing to decrease deaths from breast cancer, while causing more than half (52 percent) of all women undergoing the test to be overdiagnosed and overtreated. According to lead author Peter C Gøtzsche, had mammograms been a drug, "it would have been withdrawn from the market long ago." Cancer Prevention Begins With Your Lifestyle ChoicesMammograms are portrayed as the best form of "prevention" a woman can get. But early diagnosis is not the same as prevention. And cancer screening that does more harm than good can hardly qualify as the best you can hope for... I believe the vast majority of all cancers could be prevented by strictly applying basic, common-sense, and healthy lifestyle strategies, such as the ones below: - Eat real food; avoid processed foods and sugars, especially processed fructose. All forms of sugar are detrimental to health in general and promote cancer. Fructose, however, is clearly one of the most harmful and should be avoided as much as possible.
- Stop eating AT LEAST three hours before going to bed. There is quite compelling evidence showing that when you supply fuel to the mitochondria in your cells at a time when they don't need it, they will leak a large number of electrons that will liberate reactive oxygen species (free radicals), which damage mitochondrial and eventually nuclear DNA. There is also evidence to indicate that cancer cells uniformly have damaged mitochondria, so the last thing you want to do is eat before you go to bed. Personally, I strive for six hours of fasting before bedtime.
- Optimize your vitamin D. Vitamin D influences virtually every cell in your body and is one of nature's most potent cancer fighters. Vitamin D is actually able to enter cancer cells and trigger apoptosis (cell death). If you have cancer, your vitamin D level should be between 70 and 100 ng/ml. Vitamin D works synergistically with every cancer treatment I'm aware of, with no adverse effects. I suggest you try watching my one-hour free lecture on vitamin D to learn more.
- Limit your protein. Newer research has emphasized the importance of the mTOR pathways. When these are active, cancer growth is accelerated. To quiet this pathway, I believe it may be wise to limit your protein to one gram of protein per kilogram of lean body mass, or roughly a bit less than half a gram of protein per every pound of lean body weight.
- Avoid unfermented soy products. Unfermented soy is high in plant estrogens, or phytoestrogens, also known as isoflavones. In some studies, soy appears to work in concert with human estrogen to increase breast cell proliferation, which increases the chances for mutations and cancerous cells.
- Improve your insulin and leptin receptor sensitivity. The best way to do this is by avoiding sugar and grains and restricting carbs to mostly fiber vegetables. Also making sure you are exercising, especially with high-intensity interval training.
- Exercise regularly. One of the primary reasons exercise works to lower your cancer risk is because it drives your insulin levels down, and controlling your insulin levels is one of the most powerful ways to reduce your cancer risks. It's also been suggested that apoptosis (programmed cell death) is triggered by exercise, causing cancer cells to die. Studies have also found that the number of tumors decrease along with body fat, which may be an additional factor. This is because exercise helps lower your estrogen levels, which explains why exercise appears to be particularly potent against breast cancer.
- Maintain a healthy body weight. This will come naturally when you begin eating right for your nutritional type and exercising. It's important to lose excess body fat because fat produces estrogen.
- Drink a pint to a quart of organic green vegetable juice daily. Please review my juicing instructions for more detailed information.
- Get plenty of high quality animal-based omega-3 fats, such as krill oil. Omega-3 deficiency is a common underlying factor for cancer.
- Use curcumin. This is the active ingredient in turmeric and in high concentrations can be very useful adjunct in the treatment of cancer. For example, it has demonstrated major therapeutic potential in preventing breast cancer metastasis. It's important to know that curcumin is generally not absorbed that well, so I've provided several absorption tips here.
- Avoid drinking alcohol, or at least limit your alcoholic drinks to one per day.
- Avoid electromagnetic fields as much as possible. Even electric blankets can increase your cancer risk.
- Avoid synthetic hormone replacement therapy, especially if you have risk factors for breast cancer. Breast cancer is an estrogen-related cancer, and according to a study published in the Journal of the National Cancer Institute, breast cancer rates for women dropped in tandem with decreased use of hormone replacement therapy. (There are similar risks for younger women who use oral contraceptives. Birth control pills, which are also comprised of synthetic hormones, have been linked to cervical and breast cancers.)
If you are experiencing excessive menopausal symptoms, you may want to consider bioidentical hormone replacement therapy instead, which uses hormones that are molecularly identical to the ones your body produces and do not wreak havoc on your system. This is a much safer alternative. - Avoid BPA, phthalates, and other xenoestrogens. These are estrogen-like compounds that have been linked to increased breast cancer risk
- Make sure you're not iodine deficient, as there's compelling evidence linking iodine deficiency with certain forms of cancer. Dr. David Brownstein, author of the book Iodine: Why You Need it, Why You Can't Live Without it, is a proponent of iodine for breast cancer. It actually has potent anticancer properties and has been shown to cause cell death in breast and thyroid cancer cells.
For more information, I recommend reading Dr. Brownstein's book. I have been researching iodine for some time ever since I interviewed Dr. Brownstein as I do believe that the bulk of what he states is spot on. However, I am not at all convinced that his dosage recommendations are correct. I believe they are too high. - Avoid charring your meats. Charcoal or flame broiled meat is linked with increased breast cancer risk. Acrylamide — a carcinogen created when starchy foods are baked, roasted, or fried — has been found to increase cancer risk as well.
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Cancer
Nov 8, 2015 10:06:35 GMT -5
Post by Master Kim on Nov 8, 2015 10:06:35 GMT -5
Killer T Cell: The Cancer Assassin - Published on May 19, 2015
How does a Killer T Cell Kill its target?
Our new film captures the behavior of cytotoxic T cells – the body’s ‘serial killers’ – as they hunt down and eliminate cancer cells before moving on to their next target.
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Cancer
Dec 12, 2015 19:52:54 GMT -5
Post by Master Kim on Dec 12, 2015 19:52:54 GMT -5
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Cancer
Feb 3, 2016 0:10:10 GMT -5
Post by Master Kim on Feb 3, 2016 0:10:10 GMT -5
REVEALED: Cancer industry profits 'locked in' by nagalase molecule injected into humans via vaccines... spurs tumor growth... explains aggressive vaccine push - www.naturalnews.com/050582_nagalase_GcMAF_cancer_industry_profits.html#ixzz3hRziMTZq Monday, July 27, 2015 by: Julie Wilson staff writer (NaturalNews) One of the world's most lucrative industries, spending on cancer drugs reached an all-time high last year, as it was valued at more than $100 billion. Spending on cancer drugs increased 6.5 percent annually over the past five years and is expected to continue growing at a rate of 8 percent each year through 2018, according to figures provided by the IMS Institute for Healthcare Informatics. That spending is highly concentrated, as the US and five of Europe's largest countries account for nearly two-thirds of the entire market. This means that billions and billions of dollars are secured by Americans being diagnosed with cancer. That's one profitable industry; however, it could all be completely dismantled by one thing: a cure. As Mike Adams recently reported, "A universal cancer cure would destroy the profitability of the highly lucrative cancer industry and collapse the American Cancer Society, hospitals, oncology clinics and pharmaceutical companies that depend on chemotherapy revenues to stay profitable." This means that anyone moving closer to developing a cure for cancer would be considered an extreme threat to the medical establishment and likely stopped at any cost. With that in mind, the mysterious deaths and disappearances of several natural health doctors throughout Florida is as suspicious as it is concerning. If anyone was close to finding a universal cure for cancer and would ensure the public had access to it, it would likely be natural health doctors, or naturopaths, as they're less likely to prescribe drugs and more likely to try and heal the body naturally using holistic medicine and nontoxic approaches. Breakthroughs using this type of medicine are extremely "controversial," as they threaten everything that the medical-industrial complex stands for, i.e. costly chemotherapy treatments and cancer drugs. Doctors leading this type of research are routinely raided and shut down by the U.S. Food and Drug Administration (FDA), after which they're treated like criminals and their reputations smeared. This is typically orchestrated against doctors who are considered a threat by the medical establishment. Renown holistic doctor found dead one week after FDA raids clinicThis seems to be the case with Dr. James Jeffrey Bradstreet, who was recently found dead after his body was discovered floating in a North Carolina river with a single gunshot wound to the chest. Bradstreet, a renowned physician known for his skepticism of immunizations (particularly the MMR vaccine), and his progressive autism research, was raided by the FDA one week before his mysterious death. The details of the raid remain largely unknown. Personally affected by autism, as both his son and stepson were diagnosed with the condition, a significant portion of Dr. Bradstreet's work was dedicated to this cause. He even testified twice before the U.S House of Representatives about the link between vaccines and autism. As Natural News' reported, leading up to his death, Dr. Bradstreet was working with a little-known molecule that occurs naturally in the human body. GcMAF (Globulin component Macrophage Activating Factor), which is the GC protein after it combines with vitamin D in the body, has the potential to be a universal cure for cancer. It's also believed to be capable of treating and reversing autism, HIV, liver/kidney disease and diabetes. Dr. Bradstreet was working with a naturally occurring compound that may be the single most effective thing in the immune system for killing cancer cellsIn an interview on the Hagmann and Hagmann Report, Dr. Ted Broer, an internationally recognized health and nutrition expert also based in Florida, describes how cutting edge Dr. Bradstreet's work was, as well as a discovery he made that very well may have placed him in great danger and could have been the motive for his suspected murder. The alternative doctors who went missing and/or were killed, were reportedly "interlocked" through Dr. Bradstreet and Dr. Gonzalez's extensive research on autism, and what's causing autism, according to Dr. Broer. Dr. Gonzalez, a renown holistic cancer treatment pioneer who helped thousands overcome the disease through alternative medicine, died of an apparent heart attack just one month after Dr. Bradstreet's body was discovered floating in a river. Internationally recognized health and nutrition doctor reveals possible motive for Bradstreet's deathDr. Broer stated in the interview: This information I'm about to give you right now is extremely controversial and a bunch of people have exited the planet who were working with it. This information has been around for awhile. They knew the information they were working with and they were basically being very, very careful, supposedly. And some of them were being accused of using GcMAF, and the FDA apparently raided several of their offices several weeks before they committed suicide or suddenly died. It's going to sound complicated, but I'm going to break this down for everybody super, super easy tonight. When you first hear these terms they're going to sound weird to you. GC protein is a protein in the body that's used by macrophages in the body. What it does is, macrophages in the body are the ones that kill cancer cells, they stop cytokines storms and can be involved in cytokines storms, we'll explain all these terms in a few minutes. After defining GcMAF and how it's formulated, Dr. Broer reiterates that it's "probably the single most effective thing in the immune system to kill cancer cells." However, what Dr. Bradstreet and his colleagues discovered is that the immune system is being compromised by a compound called "nagalase." Nagalase is an enzyme/protein that's made by cancer cells and viruses causing immunodeficiency syndromes and has also been linked to autism as well as a "host of other problems," Dr. Broer explains. Doctors found dead and/or went missing felt that nagalase was being introduced to the body through vaccines"What ends up happening is when the GC protein cannot be converted to McGAF, the entire immune system is compromised." Some of the doctors who wound up dead or missing believed that the nagalase protein/enzyme was being introduced intentionally into the body either virally or directly through vaccines. "This is such incredibly damning information to the entire medical profession and the immunological profession and those folks that [sic] are producing immunizations, that apparently they didn't want these guys around," Dr. Broer said. "I'm not saying what happened to these guys, I'm just saying they're not on this planet anymore." Doctor compares cancer-causing nagalase to stealth bomberNagalese blocks the GC protein from attaching itself to vitamin D, thus preventing the immune system from doing its job and therefore causing cancer and other serious diseases. Without an active immune system, cancer and viral infections can spread rapidly. Remarkably, there's a significant amount of research available on nagalase and the GcMAF protein. Citing a chapter from The GcMAF Book by Dr. Tim Smith, MD, Dr. Broer said: Nagalase is like a stealth bomber, the nagalase enzyme synthesized in or released from cancer cells or a virus particle pinpoints the GcMAF protein facilities on the surface of your T and B lymphocytes and simply wipes them out with an incredibly precise bomb. How precise? Nagalase locates and attacks one specific two-electron bond located only at the 420th amino acid position on a huge protein molecule, one of tens of thousands of proteins, each containing millions of electrons. This is like selectively taking out a park bench in a major city from 6,000 miles away. More astonishingly, if that is possible, nagalase never misses its target, so there is no collateral damage. Nagalase is being found in super high concentrations in autistic childrenDr. Bradstreet and his colleagues also learned that the nagalase protein was not present in children at birth but was somehow introduced into autistic children, they felt, during the immunization process. Before his death, Dr. Bradstreet treated 1,100 patients with GcMAF with an 85 percent response rate – something that was deemed impossible by the medical community. After reintroducing GcMAF (which had been blocked by nagalase), 15 percent of Bradstreet's autistic patients were no longer autistic, as all of their symptoms were completely eradicated. Since 1990, 59 research papers have been published on the healing effects of GcMAF, 20 of which pertain to the treatment of cancer. Research suggests that GcMAF can also cure or effectively treat Parkinson's and Alzheimer's disease and rheumatoid arthritis, as well as reduce cancerous breast, prostrate and kidney tumors. Stay tuned as Natural News continues to uncover more on this investigation. Sources: www.blogtalkradio.comfortune.comwww.naturalnews.comwww.naturalnews.comwww.washingtonpost.comwww.vaccinetruth.orgwww.naturalnews.comthefreethoughtproject.comwww.timsmithmd.com
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Cancer
Feb 8, 2016 13:15:14 GMT -5
Post by Master Kim on Feb 8, 2016 13:15:14 GMT -5
The Exploding Autoimmune Epidemic - Dr. Tent - It's Not Autoimmune, you have Viruses
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Cancer
Feb 8, 2016 21:56:09 GMT -5
Post by Master Kim on Feb 8, 2016 21:56:09 GMT -5
Cancer Prevention and Nutrition - Dr. Tent Published on Nov 20, 2012 Diverse Health Services presents Dr. Tent's August 2011 lecture; Cancer Prevention and Nutrition.
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Cancer
Feb 19, 2016 15:28:29 GMT -5
Post by Master Kim on Feb 19, 2016 15:28:29 GMT -5
Dr. Mercola Discusses MammogramsUploaded on Jan 20, 2012 www.mercola.com/ Internationally renowned natural health physician and Mercola.com founder Dr. Joseph Mercola discusses the health risk of mammography.
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Cancer
Feb 19, 2016 15:53:44 GMT -5
Post by Master Kim on Feb 19, 2016 15:53:44 GMT -5
BEWARE MAMMOGRAMS
Uploaded on Feb 16, 2012
The gold standard life-saving tool for protecting women from the ravages of breast cancer by providing an early warning mammograms has been sold to us for years. It is a practice which is supposed to protect us from death as a result of malignancy. So powerful is the pro-mammogram lobby within the medical establishment that we have come to believe if we do not have regular scans we are being completely irresponsible. After all, mammograms save lives don?t they?
Researchers at Dartmouth in the United States decided to check out these assumptions. They wanted to find out how often lives actually are saved by mammography. They examined breast cancer data from The National Cancer Institute and the Centers for Disease Control and Prevention. They found out that the probability of a mammogram saving a life is well below 25%. They concluded that "Most women with screen-detected breast cancer have not had their life saved by screening. They are instead either diagnosed early (with no effect on their mortality) or over-diagnosed."
But, there's more: the annual mammograms which we are urged to have actually expose us to serious cancer-causing radiation that may shorten our lives. Take a look at Time Magazine October 25, 2011, and the Archives of Internal Medicine October 24, 2011, if you want more information.
Here's the gen: 50% of the breast cancer diagnoses doctors now make from mammograms are not in reality cancer at all. The physical and emotional damage of these "false positive" diagnoses fill people's lives with fear.
Personally I have never had a mammogram. Why? Because my gut feeling has always said ?no?. This was long before we had a growing accumulation of clinical evidence showing that the 30kVp range of low-energy radiation used in breast screenings is up to 400% more damaging to human DNA (read 400% more carcinogenic) than the so-called high-energy radiation which it is often compared to. Personally I would stay away from mammography in any shape or form.
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Cancer
Feb 23, 2016 15:58:09 GMT -5
Post by Master Kim on Feb 23, 2016 15:58:09 GMT -5
Oncology nurse quits after discovering nutrition heals cancerPublished on Dec 17, 2014 Show notes at www.chrisbeatcancer.com/oncolo... After 17 years as an oncology nurse, Valerie Warwick took a huge risk and walked away from a lucrative income because she could not be a part of the conventional cancer industry anymore. In our interview, Valerie shares insider information about the industry as well as vital resources and therapies that every cancer patient should consider.
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Cancer
Mar 18, 2016 22:12:04 GMT -5
Post by Master Kim on Mar 18, 2016 22:12:04 GMT -5
Iodine Treats Breast Cancer, Overwhelming Evidence - jeffreydachmd.com/iodine-treats-breast-cancer/by Jeffrey Dach MD This article is Part Two of a series. For Part One , Click Here. Spontaneous Regression of Breast CancerDavid Brownstein MD reports three cases of spontaneous regression of breast cancer after women take iodine supplementation. (This is reported on page 63 of the Iodine Book by David Brownstein MD.) Joan, an English TeacherThe first patient, Joan a 63 year old English teacher, was diagnosed with breast cancer in 1989, declined conventional treatment, and took 50 mg per day of Iodoral, (Iodine). Six weeks later, a PET scan (left image) showed, “all of the existing tumors were disintegrating”. Upper Left Image: Upper two frames is a PET scan showing breast cancer )(red arrows). Lower two frames is a CAT scan showing enhancing breast cancer mass, red arrow. Courtesy of Wikimedia Commons. DeloresThe second patient, 73 year old Delores, was diagnosed with breast cancer in 2003. She declined conventional treatment with radiation and chemotherapy. Instead, Dolores took 50 mg of Iodoral daily. A follow up ultrasound of the breast 18 months later showed,” It appears that these malignancies have diminished in size since the last examination. Interval improvement is definitely seen,” Two years later a follow up mammogram and ultrasound failed to show any abnormality and were read by the radiologist as normal. JoyceThe third patient, 52 year old Joyce was diagnosed with breast cancer two years prior (left image), and started on Iodoral 50 mg per day. Three years after starting Iodoral, her follow up mammograms and ultrasound exams show decreasing size of the tumor with no progression. Mammogram showing breast cancer courtesy of wikimedia commons. Iodine Deficiency Causes Breast Cancer – The Overwhelming EvidenceHuman Studies of Areas with Low IodineIodine deficiency is associated with a higher rate of goiter and breast cancer. Similarly, higher dietary Iodine intake is associated with less goiter and breast cancer. For example, Japan has the highest dietary intake of iodine (13 mg per day), and the lowest rates for goiter and breast cancer. However, when Japanese women immigrate and change dietary intake of Iodine to the lower 150 mcg/day in America, breast cancer rates increase. Iceland is another country with high Iodine intake and low rates for goiter and breast cancer. The high dietary iodine came from the fishing industry before WWI. In those days, the fish meal was fed to dairy cows providing milk with high iodine content. After WWI, the fish meal was eliminated from the dairy cows, and breast cancer rates soared ten-fold. Animal studiesIodine deficient diets in animals induces breast cancer and goiter. Iodine Research from Mexico, India and JapanIndiaThe Shrivastava group in India reported molecular iodine induces apoptosis (programmed cell death) in human breast cancer cell cultures. “Iodine showed cytotoxic effects in the cultured human breast cancer cells”. MexicoFrom Mexico, the Carmen Aceves Velasco Group reported Iodine to be safe, with no harmful effects on thyroid function, and an anti-proliferative effect on human breast cancer cell cultures. Their 2009 paper reported the mechanism by which Iodine works as an anti-cancer agent. Iodine binds to membrane lipids called lactones forming iodo-lactones which regulate apoptosis (programmed cell death). Iodine causes apoptosis which makes cancer cells undergo programmed cell death. Dr. Aceves concluded that continuous molecular iodine treatment has a “potent antineoplastic effect” on the progression of mammary cancer. JapanFrom Japan, Dr Funahashi reported a common seaweed food containing high iodine content is more beneficial than chemotherapy on breast cancer . “He found that administration of Lugol’s iodine or iodine-rich Wakame seaweed to rats treated with the carcinogen dimethyl benzanthracene suppressed the development of mammary tumors. The same group demonstrated that seaweed induced apoptosis in human breast cancer cells with greater potency than that of fluorouracil, a chemotherapeutic agent used to treat breast cancer." Fig 2 from Funahashi 2001. Breast cancer induced in rats with DMBA a carcinogenic chemical. Left column Images are rats pre-treated with Iodine (mekabu seaweed) showing no breast cancer tumors. Right column Images are untreated (Control) rats with large breast cancer tumors visible at the (red arrows) .. From Funahashi_2001_Jpn_Journal_Cancer_ResearchLung Cancer and IodineA 2003 study by Ling Zhang ahowed that molecular Iodine caused lung cancer cells to undergo programmed cell death (apoptosis). These lung cancer cells had been genetically modified to increase iodine uptake.(12) Interestingly, a 1993 case report describes spontaneous remission of lung cancer in a patient incidentally treated with Amiodorone which contains iodine (about 9 mg per day. In ConclusionCurrent Iodine research calls for use of molecular Iodine for all patients with breast cancer. (10)(11) Other cancers such as lung and prostate may also benefit. Further research on Iodine as cancer chemotherapy should receive top priority for NIH funding. How to Obtain Iodine TabletsIodine ( Iodoral) is available on the internet without a prescription. Financial Disclosure: The author has no financial interest in the Iodine Book mentioned above, or in any company that manufactures Iodine Supplements. Disclaimer: This article is not intended as medical advice. Make sure to discuss with your doctor and follow your own personal doctor’s recommendations when contemplating any changes to your diet, medications, or medical treatment programs. Click Here for WHO Iodine Testing Guidelines: Iodine Guidlines: WHO_Urinary Excretion 2013 World Health Organization
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Cancer
Mar 18, 2016 22:37:08 GMT -5
Post by Master Kim on Mar 18, 2016 22:37:08 GMT -5
Heal Yourself At Home - healyourselfathome.com/HEALTH_PROBLEMS/CANCER/TREATMENTS/1_NOT_ALLOWED/iodine_against_cancer.aspx1-2-3 CANCER PLAN(1) Cancer NOT Allowed Iodine against Cancer ♦ Iodine deficiency is strongly implicated in cancers of organs normally having a high iodine presence - including thyroid cancer, breast cancer, ovarian cancer, prostate cancer, stomach cancer, pancreatic cancer, colon cancer, and lung cancer. ● Iodine most important measure against reproductive and thyroid cancers ● Iodine involved in both development and multiplying phases of cancer ● How Does Iodine eliminate Abnormal Cells? ● The Overwhelming Evidence of Iodine against Cancer ● Estrogen / Iodine Connection ● Additional iodine roles in preventing cancer ● Mainstream medical breast cancer treatments are not effective Iodine sufficiency may be the most important preventative measure against reproductive organ cancers ♦ Iodine has been found effective against cancer of the breast, uterus, ovaries, endometrium, prostate and thyroid; Stadel B, Dietary iodine and risk of breast, endometrial, and ovarian cancer, The Lancet, 1976 Cancer is theorized to be roughly divided into two phases, and iodine plays a beneficial role in both phases (especially in organs usually having high iodine presence) This information sourced from thyroid.about.com/library/derry/bl1a.htm (1) The pre-cancerous phase (The development of abnormal, benign cells) ♦ The first, long-term, pre-cancerous phase, is when normal cells gradually become abnormal cells – E.g. the discovered breast cancer lump represents the end stage of a slow development over ~20-30 years. The pre-cancerous lesions (lumpy, tender breasts) are known as FDB (Fibrocystic Disease of the Breast). FDB - Link to breast cancer APOPTOSIS Appropriate and natural destruction of cells that represent a threat to the integrity of the organism – E.g. cancer cells and virus-infected cells. Essential to growth and development - E.g. Fingers form in the fetus by apoptosis of the tissue between them; ♦ When normal cells are damaged beyond repair, they are appropriately eliminated by apoptosis - the programmed or natural death of damaged, infected or malfunctioning cells. ♦ Cancer cells avoid apoptosis and continue to multiply in an unregulated manner ♦ Adequate Iodine stops and reverses the pre-cancerous stage of the cancer process by causing the natural death of abnormal cells (i.e apoptosis) – preventing them from becoming cancer cells. Sites of rapid apoptosis in the body are also sites with high iodine levels. Inadequate iodine in a tissue allows abnormal cells to persist, allows cysts to grow, and may eventually lead to cancer ♦ Dose to Prevent and Eliminate Pre-cancer cells? – An adequate dose of iodine to prevent pre-cancer phase (abnormal cells) may be defined as more than 3-4 mg / day. One drop of Lugol’s in water, juice or milk or ½ an Iodoral tablet (6.5 mg iodine/iodide) should both prevent cells from changing into cancer cells and gradually eliminate pre-cancer cells, so no new cancers can start. It will also kill abnormal cells floating around in the body at remote sites from the original cancer. Ghent W R et al, Iodine replacement in fibrocystic disease of the breast. Can J Surg 1993; Ghent WR et al, Iodine deficiency breast syndrome. Frontiers in Thyroidology, 1986 (2) The multiplying phase of cancer (a) Cancer cells can multiply and just stay where they are (carcinoma in situ) or (b) Cancer cells can multiply and spread (metastasis) On average, breast cancer cells double every 100 days, and it takes ~9 years before mammograms can pick them up. ♦ Adequate thyroid hormone (produced by a normal thyroid with sufficient iodine), prevents the spread of cancer cells to other organs - The amount of thyroid hormone present in tissues controls the strength of connective tissue, which forms a strong sieve-like barrier to the passage of cancer cells trying to spread. Clark WH, Tumour progression and the nature of cancer. J Cancer 1991; Smith,T.J. et al, Connective tissue, glycosaminoglycans, and diseases of the thyroid, Endocr.Rev, 1989 Iodine – Supplementation ♦ When there is sufficient thyroid hormone present, then the cancer cannot spread – Conversely . . . A low level of thyroid hormone in the tissues (especially connective tissues) allows cancer cells to spread ♦ Adequate Iodine Dose to Prevent Cancer Spread? – You should do your own research on this. However, this author has so far found that the available literature indicates a dose of about 50mg iodine/iodide (8 drops 5% Lugol’s Solution or 4 Iodoral ®) /day in split doses) according to tolerance, with the goal of achieving whole body iodine sufficiency (~1.5 g) in about 3-6 months. - Dr. Brownstein said he was using 200 to 300 mg with his prostate and breast cancer patients - with those who have metastases needing the highest dosages. ♦ There is some overlapping of the two iodine defense systems - in the pre-cancer and multiplying phases. How does iodine eliminate abnormal cells? 1. δ-Iodolactone is the main mediator for preventing cancer - this iodinated form of lactone (produced when iodide oxidizes polyunsaturated lipids) seems to be the main iodocompound which can inhibit growth and induce apoptosis in human thyroid carcinoma cell lines (B-CPAP cells, FTC-133 cells and 8505C cells) as well as on human breast cancer cells (MCF-7). Also, human lung cancer cells with genes spliced into them that enhance iodine uptake and utilization undergo apoptosis and shrink when given iodine, both in vitro and implanted in mice. Cann Stephen A., van Netten Johannes P., Glover David W. , Iodide Accumulation in Extrathyroidal Tissues, Journal of Clin. Endocrinology & Metabolism, 1999 ; Vol. 84, No. 2821 2. Iodine may also kill abnormal cells by the same method it destroys single-celled microbes – by reacting with exposed tyrosine. Once the thyroid gland has become iodine-saturated, most of the rest of the available iodine in the body then circulates throughout the body bathing the extracellular fluids found between body cells. If cell surface proteins have the amino acid tyrosine on the outside, the passing iodine reacts with this tyrosine. This reaction denatures the protein, and by disturbing the cell membrane, it thus kills the cell (This is the same chemical reaction by which iodine in dilute solutions causes the death of single-celled microbes – bacteria, viruses, fungi, and protozoa). Healthy vertebrate cell membranes do not have tyrosine on the portion of the protein sticking out into the extracellular fluid. However, the intra membrane proteins may have tyrosine which is only exposed when the membrane is distorted by abnormal cell development such as we see in the pre-cancerous forms of Fibrocystic Disease of the Breast (FDB). This would then expose the tyrosine to the iodine passing in the extracellular fluid, enabling the iodine to do its work and kill off the cell. Additional Iodine roles in preventing cancer ♦ Any excess iodine flows into the urine - preventing the development of abnormal cells in the bladder and kidney system, and thus also prevents cancers in those locations. ♦ The antioxidant properties of iodides have a role in cancer prevention – by their ability to markedly quench the high-energy, excited singlet oxygen to its less reactive triplet form, thus preventing singlet oxygen from causing oxidative damage to DNA. Kasha M, Collisional Perturbation of Spin-Orbital Coupling and the Mechanism of Fluorescence Quenching. A Visual Demonstration of the Perturbation. The Journal of Chemical Physics, 1952. Venturi S et al, Role of Iodine in Evolution and Carcinogenesis of Thyroid, Breast and Stomach, Adv. Clin. Path, 2000 ♦ Iodine is a powerful deactivator of environmental chemical toxins – cancer-causing suspects, E.g. xenoestrogens, pesticides, herbicides, industrial chemicals; The Overwhelming Evidence of Iodine against Cancer ♦ Spontaneous regression of breast cancer seen in 3 cases supplementing iodine Please visit the following site to read information on these cases where iodine supplementation has shrunk tumors in the breast: Jeffreydach.com ♦ Supporting evidence for iodine deficiency involvement in breast cancer, fibrosis and painful breasts in FDB patients Please see information at breastcancerchoices.org - Breastcancerchoices.org lists several of iodine’s impressive abilities against cancer: √ Desensitizes estrogen receptors in the breast; √ Reduces estrogen production in overactive ovaries; √ Reduces fibrocystic breast disease – which often precedes breast cancer; √ Causes more cell death than the chemo drug, Fluorouracil; √ Prevents rats from getting cancer when fed the breast cancer causing toxin DMBA. ♦ A deficiency of iodine is a known factor in the development of prostate cancer 1950’s article links deficient thyroid activity with cancer rates ♦ Data from 15 countries in four continents give support to the importance of local factors to account for the known local variations of cancer incidence - Iodine availability, traced by goiter incidence, appears to be one of such factors. Closer scrutiny of some of these countries corroborates these conclusions. ♦ Presence of thyroxine in the tissues has been amply demonstrated in animal experiments to bring about a tissue environment that is unfavorable to tumor growth and development - at least as long as tumors remain in the dependent phase. www.ncbi.nlm.nih.gov/pmc/articles/PMC2007963/pdf/brjcancer00388-0003.pdf Estrogen /Iodine Connection ♦ Iodine metabolizes carcinogenic estrone and estrogen metabolite 16-α-hydroxyestrone --► “anti-carcinogenic” estriol; ♦ Iodine desensitizes estrogen receptors in the breast; ♦ Iodine reduces estrogen production in overactive ovaries; Mainstream medical treatments are not working Breast cancer incidence worldwide has increased from 1 in 23 in the mid-1960s to currently 1 in 8, and is increasing by ~1% each year ♦ Mortality rates not improved with today’s technology – surgery, chemotherapy, mammography, and radiation have not altered the mortality rate since record-keeping began in the 1920’s. 85% of women who develop breast cancer will die of causes directly related to breast cancer. ♦ Radiation and chemotherapy to the breast can affect the thyroid gland – radiation to the breast for prevention of local recurrences can affect the thyroid gland. The thyroid gland in your neck is in close proximity to your breast and depending on the angle used by the radiation machine, the dosage used and also how good the machine is at preventing radiation scatter, the radiation can have both short and long term effect on your thyroid gland health. Chemotherapy (including Tamoxifen) delivers toxic compounds and can have side effects on many organs including the thyroid gland. The combination of chemotherapy and radiation can lead to clinically obvious low thyroid Links JM, Radiation physics (ch16) and Williams ED, Biologic effects of radiation on the thyroid (ch17), Werner and Ingbar's The Thyroid, 1991.
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