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586 lines
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<html>
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<head><title>Breast Cancer</title></head>
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<body>
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<h1>
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Breast Cancer
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</h1>
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<article class="posted">
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<p>
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It’s important to know the realities of cancer in the population, the death rate from cancer, and the
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effects of its aggressive diagnosis and treatment. Appreciating those, I think the need for a new
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attitude toward cancer can be seen.
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</p>
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<p>
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Official US data for the years 1990 to 1993 showed 505,300 cancer deaths in 1990, and 529,900 cancer
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deaths in 1993. This was an increase of roughly 1.3% per year (which was faster than the population
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growth) during the time in which Rodu and Cole (1996) and agencies of the U.S. government claimed the
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death rate was <strong><em>decreasing</em></strong> one half percent (0.5%) per year.
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</p>
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<p>
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This increase happened despite the abnormal population bulge in the number of people between the ages of
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35 and 50, resulting from the postwar baby boom. Cancer incidence is about ten times higher among the
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older population than in this younger age range, so in this abnormally structured population, the death
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rate from cancer is much lower than it would be if the population composition were the same as before
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the war, and it is lower than it will be in ten or twenty years, when the population bulge reaches the
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prime cancer years.
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</p>
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<p>
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In 1994, total cancer deaths increased to 536,900 (an increase of 1.32% over 1993). The crude death rate
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per 100,000 population was 203.2 in 1990, in 1993 it was 205.6, in 1994 it had increased to 206. <strong
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>This, despite the population distortion caused by the baby boom,</strong> causing a scarcity of people
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in the age groups with the highest rates of cancer mortality.
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</p>
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<p>
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In the U.S. in 1994 there were altogether 2,286,000 deaths. In a population of about 260 million, this
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was a death rate of less than 1% per year (about 0.88%). The chance of dying that year for any person
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was less than one in a hundred. That doesn’t mean that life expectancy is over 100 years, but that would
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be implied if we ignored the population bulge of the baby boomers, as the cancer statisticians are
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doing.
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</p>
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<p>
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When the U.S. Department of Health and Human Services, and every major medical journal in the United
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States lies about the simple statistics of cancer death rates, it’s clear that very powerful and
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dangerous social forces are operating. Anyone who knows about the baby boom that started right after the
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second world war must also realize that in 1940, at the end of the great depression, when infant and
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childhood mortality was very high and people postponed having children, the population had a
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disproportionate number of old people, and that it would be outrageous to use the rate of cancer in the
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pre-war population to evaluate the rate of cancer in the post-war population. But that is what is being
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done, and the mass media are helping to prevent the public from questioning the official story about
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cancer.
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</p>
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<p>
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If the health of the population in 1940 is to be compared to that of a very differently constituted
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later population, the appropriate method is to compare the rate of death among people of a certain age.
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The death rate from leukemia, especially among children, was greatly increased in the post-war years,
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when people were being exposed to radiation from atomic bomb tests. The death rates among adults of
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various ages, from breast cancer, prostate cancer, and melanoma have steadily increased. Rodu and Cole,
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who declared victory in the war against cancer, said the decline in total cancer mortality began in
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1991. (Cole and Rodu, 1996) If lung cancer is excluded, <strong>they say mortality from other cancers
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has been declining since 1950! (“The fifty-year decline of cancer in America,”</strong> Rodu and
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Cole, 2001.) The first time I saw this bizarre use of “age restandardization” was when Professor Bruce
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Ames was on a lecture tour for the American Cancer Society, and was speaking to the biology department
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at the University of Oregon. He showed a graph indicating that the mortality curves for most types of
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cancer in the U.S. had begun their downward curve in the late 1940s just after the A.C.S. came onto the
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scene. Even though I think the A.C.S. probably initiated the practice of age-standardizing with
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reference to the 1940 population, they don’t always find that date suitable for their purposes. In
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fund-raising literature showing their past success in curing childhood leukemia, they restandardized
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mortality with reference to the postwar year when the leukemia death rate was at its highest, with the
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result that their cures appeared to be steadily lowering the death rate. But the incidence rate varied
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according to the intensity of the radioactive intensity that pregnant women were exposed to, and so both
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the incidence and the mortality fell after atmospheric testing was stopped.
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</p>
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<p>
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Government officials, editors of the big medical journals, professors and broadcasters, have been able
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to get away with this huge statistical fraud. I suspect that they will soon feel encouraged to simply
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make up the data that they want, because eventually “age standardization” isn’t going to work to hide
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the actual increases in mortality. Since people with cancer usually die of something else, such as a
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stroke or heart failure, it will be no trick at all to make cancer mortality decline to be replaced by
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other causes of death. The precedent for such fabulizing of data exists in the FDA’s approval of AZT,
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and other less notorious drugs.
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</p>
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<p>
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Radiation, estrogen, and a variety of chemical pollutants are known to be the major causes of breast
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cancer, but the efforts of the cancer establishment have been directed toward denying that these
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avoidable agents are the cause of the great increase in breast cancer during the last several decades.
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The cancer industry, including major producers of chemotherapy drugs, subsidizes the American Cancer
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Society and “Breast Cancer Awareness Week,” and it is in their interest to convince the public that
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early detection and conventional treatment with surgery, chemotherapy, and radiation are winning the war
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against cancer. There is always light at the end of the tunnel, in the war against cancer, just as there
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was in the Vietnam war. Their consistent effort to dissuade the government from acting to reduce the
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public’s exposure to the known causes of cancer should make it clear that they are in the business of
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treating cancer, not eliminating it.
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</p>
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<p>
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In the 1960s I read some articles in a small town newspaper about Leonell Strong’s cancer research, and
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his treatment by the American Cancer Society and the Salk Institute. Leonell Strong had developed
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strains of mice for use in cancer research. In some of the strains, 100% of the females developed
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mammary cancer. Strong had demonstrated that these strains had very high levels of estrogen. He showed
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me mice that he had treated with simple extracts of liver, that were free of cancer, and whose
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descendants remained free of cancer for several generations.
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</p>
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<p>
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Strong had received his PhD in genetics under T. H. Morgan. For a person trained in classical genetics,
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and who had spent his career developing the supposedly genetically determined cancer trait, the
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elimination of the trait by a few injections must have been hard to understand, but at least he tried to
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understand it.
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</p>
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<p>
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When he had earlier demonstrated the presence of a virus in the milk of cancer-prone mice, and when he
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showed the role of heredity in cancer, he was popular with the cancer business, but when he showed that
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“genetic” cancer could be eradicated with a simple treatment, he became the object of official abuse. He
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said that the Salk institute had offered him a position to induce him to move with his large colony of
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mice from New York to San Diego, but when he arrived he found that he had no job, and his records of
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decades of research had been lost. He said that a memo which was discovered in a lawsuit revealed that
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the institute had just wanted his mice, and never intended to give him the promised job. For the cancer
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establishment, his discovery of a way to prevent cancer was not welcome.
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</p>
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<p>
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In 1969, two years before the war against cancer had begun pouring public money into the pockets of the
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cancer establishment, Harry Rubin gave a lecture that criticized the cancer establishment’s claim that
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it was curing cancer. He cited a study by a pathologist who had looked for cancer in the tissues of
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people who had been killed in accidents. He found identifiable cancers in the tissues of everyone over
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the age of fifty that he examined. If everyone over 50 has histologically detectable cancer, <strong
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>then the use of biopsy specimens as the basis for determining whether a person needs treatment has no
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scientific basis.</strong>
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</p>
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<p>
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The definition of a disease, and the recognition of its presence, has an important place in medicine,
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but understanding its cause or causes is essential for both treatment and prevention. The dominant
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belief in medicine is that diseases are significantly caused by “genes,” including diseases such as
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cancer, diabetes, psychoses, and neurological diseases. In Israel, ethnic groups that had never had much
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diabetes before immigrating, within a single generation had diabetes as often as other Israelis. Shortly
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after insulin became available for the treatment of diabetes, the incidence of the disease in the U.S.
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began to increase. The simple death rate from diabetes per 100,000 population is now higher than it was
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in 1920, before insulin treatment became available. Neurological diseases and autoimmune diseases, along
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with diabetes and cancer, have increased greatly in recent generations. These simply aren’t genetic
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diseases, and there should be a shift of resources away from useless or harmful treatments toward their
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prevention.
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</p>
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<p>
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Even when a disease’s cause isn’t clearly understood, it is essential to use logical thinking in
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diagnosing its presence. The presence of a certain gene or “genetic marker” is often thought to have
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great diagnostic significance, which it rarely has. But even gross “signs” of a disease can be used
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diagnostically <strong>only if we know that similar signs aren’t present in perfectly healthy
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people.</strong> When pains are thought to be the result of a herniated intervertebral disk, x-ray
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pictures may be produced as confirmation of the diagnosis. But when people without pains are just as
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likely to have herniated disks (about 2/3 of normal people have them), the diagnosis fails to be
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convincing. When x-rays or MRIs show “plaques” in the head, multiple sclerosis is often “confirmed,” but
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when normal medical students show just as many brain plaques, the diagnosis must be questioned.
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Similarly, when mature people who were perfectly healthy until they were killed by an accident are found
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to always have identifiable cancers, any diagnosis of cancer that is based on a similar histological
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specimen must be reconsidered.
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</p>
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<p>
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By diagnosing something that is as common and trivial as dandruff as “cancer,” physicians can get a very
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high rate of cures, whether they use surgery, radiation, or chemotherapy. Abnormal cellular
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proliferation is usually harmless, but it has become an important part of a business that makes several
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billion dollars per year, with no definite benefits except the financial benefits for those in the
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business.
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</p>
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<p>
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Before cancer treatment became culturally practically obligatory, and when fewer people died of cancer,
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some people lived into old age with clearly “malignant” cancers, and died of some other cause. The
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policy of leaving a cancer alone is now established for prostate cancer in old men. Until there is clear
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evidence to the contrary, a similar policy might be appropriate for many kinds of cancer.
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</p>
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<p>
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If every year more people are treated for cancer, and every year more people die of cancer, one simply
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wonders whether fewer people would die if few were treated.
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</p>
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<p>
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If the first rule of medicine is to do no harm, then the second rule, growing out of the first, would
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have to be to give no treatment without knowing what is being treated, and to have a valid basis for
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believing that the damage done by the treatment is not worse than the damage that the disease would
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cause. If cancer specialists haven’t demonstrated that their treatments improve their patients’
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situation, then their professional activities aren’t justified; the statistics suggest that they aren’t.
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</p>
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<p>
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There simply isn’t a valid base of knowledge about the natural history of cancer development in humans
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to permit a valid judgment to be made about the meaning of particular signs or indicators or
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histological structures. The extensive use of mammograms has increased the diagnosis of “ductal
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carcinoma <strong><em>in situ</em></strong>” by more than 1000% (a 16- or 18-fold increase in some
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hospitals, and expected to double in the next decade), increasing the number of mastectomies and other
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treatments, <strong><em>but the increased treatments and early diagnosis haven’t produced any visible
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change in the death rate.
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</em></strong>
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</p>
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<p>
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The pathologists talk knowingly of “pre-neoplastic” conditions that indicate an increased risk of
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malignancy, but instead of data, what they have is an ideology about the nature of cancer. When they say
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that a growth pattern is premalignant or that a cell has a malignant structure, they might as well be
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talking about goblins, because the scientific basis for what they are saying is nothing but a belief in
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the ideology that cancer is “clonal,” that a particular cancer derives from a <strong>single defective
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cell.</strong> They are so self-assured, and have so many sources to cite about the “clonal nature
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of cancer,” that it seems impolite to suggest that they might simply be misusing language and logic.
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</p>
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<p>
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Isn’t a person derived from a single cell, and so, in that sense, “clonal”? As organs differentiate in
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the development of the organism, can’t organs be traced back to the cells from which they developed?
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Isn’t every tissue “a clone” in that sense? What is it that makes the “clonal” nature of cancer tissue
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so special? Isn’t it just that a nasty, mean, malignant tissue is, mentally, traced back to a
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“malignant” cell, by analogy with the way good tissues are traced back to good cells? If the tumor is
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odious, it must derive from an odious cell, and what could make that cell so hateful if it is
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genetically identical to the good cells? Therefore, the goblin reasoning goes, a genetic mutation must
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have produced the evil cell.
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</p>
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<p>
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The actual evidence is that there are broad changes in tissues preceding the appearance of cancer. The
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goblin theory explains this by saying that a multitude of “precancerous” mutations occurred before the
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mutant cancer cell appeared. Harry Rubin has carefully shown experimentally and logically that cancer
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precedes the genetic changes that occur in tumors. But the ideology that cancer is the result of a
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genetic mutation forces its devotees to say that the genetic changes that can be found in a mature tumor
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must have occurred in one cell that was previously not malignant. An effect is identified as a cause.
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</p>
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<p>
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The clonal-goblin theory of cancer leads logically to the conclusion that the cancer clone must be
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exorcised by surgery, chemotherapy, and/or radiation.
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</p>
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<p>
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The biological theory of cancer, on the other hand, is inclined to view the normal and abnormal
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development of cells in terms of the cells’ responses to conditions.
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</p>
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<p>
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Estrogen and ionizing radiation are the most clearly documented causes of breast cancer. Their
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excitatory effects lead to inflammation, edema, fibrosis, and interruption of intercellular regulatory
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processes. Radiation is estrogenic, and increased estrogenic stimulation produces growth and temporary
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loss of differentiated functions. Estrogen and radiation aren’t the only things that can cause these
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systematic changes in the structure of tissues--for example, vitamin A deficiencies, hypothyroidism,
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chlorinated hydrocarbons, irritation, and lack of oxygen can cause similar changes--but estrogen and
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irradiation have been studied enough to give us a fairly distinct picture of the real processes involved
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in the development of cancer.
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</p>
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<p>
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Polyunsaturated fats are another clearly identified cause of cancer, especially breast cancer. These
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fats synergize with estrogen, and sensitize to radiation. Their effects on the mother can be seen in the
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offspring, as an increased tendency to develop breast or prostate cancer.
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</p>
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<p>
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An individual’s hormone balance can be disrupted by exposure to radiation, estrogens, or unsaturated
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fats. The hormonal balance of the parent is imprinted upon the offspring, acting on the chromosomes, the
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liver, brain, genitals, pituitary, bones--in fact, the prenatal imprint can probably be found everywhere
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in the offspring.
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</p>
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<p>
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<strong>It’s easy to reduce our exposure to radiation, by avoiding mammograms, bone density scans, and
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other x-rays of all sorts. Ultrasound and MRI can produce good images of any tissue without the
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deadly effects of ionizing radiation.
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</strong>
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</p>
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<p>
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Polyunsaturated fats can be reduced by careful selection of foods, but the food industry is finding ways
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to contaminate traditionally safe foods, such as beef and milk, by using new kinds of animal feed.
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Still, milk, cheese, beef, and lamb are safe, considering their high nutritional content, and the
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remarkable purification that occurs in the rumen of cows, sheep, and goats. Some studies suggest a
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protective effect from saturated fat (Chajes, et al., 1999.)
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</p>
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<p>
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Estrogenic influences can be significantly reduced by avoiding foods such as soy products and
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unsaturated fats, by eating enough protein to optimize the liver’s elimination of estrogen, and by using
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things such as bulk-forming foods (raw carrots, potatoes, and milk, for example) that stimulate bowel
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action and prevent reabsorption of estrogens from the intestine. Avoiding hypothyroidism is essential
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for preventing chronic retention or formation of too much estrogen.
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</p>
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<p>
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Some studies show that dietary starch, rather than fat, is associated with breast cancer. Starch
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strongly stimulates insulin secretion, and insulin stimulates the formation of estrogen.
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</p>
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<p>
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Estrogen is formed in fat cells under the influence of cortisol, and this formation is suppressed by
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progesterone and thyroid. Postmenopausal obesity is associated with increased estrogen and breast
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cancer. The prevention of weight gain, and supplementation with thyroid and progesterone if necessary,
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should be protective against many types of cancer, especially breast, kidney, and uterine cancer.
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</p>
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<p>
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Prenatal or early life exposure to estrogens, including phytoestrogens, or to irradiation, or to
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polyunsaturated oils, increases the incidence of mammary cancers in adulthood.
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</p>
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<p>
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Protein deficiency prenatally or early in life causes a life-long excess of serotonin. Feeding an excess
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of tryptophan, the precursor of serotonin, during pregnancy produces pituitary and mammary tumors in the
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offspring. Serotonin, besides being closely associated with the effects of estrogen (e.g., mediating its
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stimulation of prolactin secretion) and polyunsaturated fats, can be metabolized into carcinogens.
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</p>
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<p>
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Prenatal protein deficiency and excess unsaturated oils predispose to a developmental pattern involving
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hypothyroidism and hyperestrogenism<strong>;</strong> puberty occurs at an earlier age, along with a
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tendency to gain weight. Inflammatory processes (e.g., “autoimmune diseases”) are usually intensified
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under those conditions. Inflammation itself increases the effects of estrogen and serotonin.
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</p>
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<p>
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Both preventively and therapeutically, the use of the antiinflammatory and antioxidative substances such
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as aspirin, caffeine, progesterone, and thyroid hormone would seem appropriate. Aspirin is coming to be
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widely accepted as an anticancer agent, and at moderate doses can cause cancer cells to die. It, like
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progesterone and thyroid, has a wide variety of anti-estrogenic effects. Especially when a tumor is
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painfully inflamed, aspirin’s effects can be quick and dramatic. However, people aren’t likely to be
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pleased if their cancer doctor tells them to “take aspirin and call me in six months.” Aspirin’s
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reputation for causing stomach bleeding causes people to avoid it, even when the alternative is
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something that’s seriously toxic to other organs, and it might just seem too ordinary to be considered
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as a powerful anticancer drug.
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</p>
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<p>
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Because of the toxic (carcinogenic, and anti-respiratory) effects of the “essential fatty acids,” which
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are usually stored in the tissues in very large quantities, it’s important to avoid the stresses or
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hunger that would release the fats into the blood stream. Estrogens and adrenalin and serotonin and
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growth hormone, and prolonged darkness, increase the release of the free fatty acids. Frequent meals,
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including some saturated fats such as coconut oil, and a balance of protein, sugars, and salts, will
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minimize the release of stored fats.
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</p>
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<p>
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The population trends toward greater obesity and earlier puberty, both of which are associated with a
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higher risk of breast cancer, suggest that the war against cancer is far from over. In the 19th century
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when the incidence of breast cancer was much lower than it is now, puberty usually occurred around the
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age of 17. In countries with a low incidence of breast cancer, puberty still occurs in the middle to
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late teens. People who are now 100 generally had puberty years later than girls do now. The biological
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changes now seen in children in the U.S. suggest that the incidence of degenerative diseases of all
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sorts is likely to increase as these children grow up.
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</p>
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<p>
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A metabolic approach to the prevention and treatment of cancer would have many beneficial side effects,
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such as producing generally healthier, happier and brighter babies.
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</p>
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<hr />
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<p><strong><h3>REFERENCES</h3></strong></p>
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<p>
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Radiat Res 1998 Sep;150(3):330-48 <strong>Mortality in beagles irradiated during prenatal and postnatal
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development. II. Contribution of benign and malignant neoplasia.</strong> Benjamin SA, Lee AC,
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Angleton GM, Saunders WJ, Keefe TJ, Mallinckrodt CH. To evaluate the lifetime carcinogenic hazards of
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exposure to ionizing radiation during development, 1,680 beagles received whole-body exposures to 60Co
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gamma rays or sham exposures. Eight groups of 120 dogs each received mean doses of 15.6-17.5 or
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80.8-88.3 cGy in early, mid- or late gestation, at 8, 28 or 55 days postcoitus or at 2 days after birth.
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Another group of 120 dogs received a mean dose of 82.6 cGy as 70-day-old juveniles and one group of 240
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dogs received a mean dose of 81.2 cGy as 365-day-old young adults. Sham irradiations were given to 360
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controls. Sexes were equally represented. In 1,343 dogs allowed to live out their life span, neoplasia
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was a major disease, contributing to mortality in 40% of the dogs. There was a significant increase in
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benign and malignant neoplasms occurring in young dogs (<4 years old), including fatal malignancies,
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after irradiation in the perinatal (late fetal and neonatal) periods. The lifetime incidence of fatal
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neoplasms was also increased in dogs irradiated perinatally. Three malignancies-lymphomas,
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hemangiosarcomas and mammary carcinomas-accounted for 51% of all fatal tumors. There was an apparent
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lifetime increase and earlier onset of lymphomas in dogs exposed as fetuses. Fatal hemangiosarcomas were
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increased in dogs irradiated early and late in gestation. Fatal mammary carcinomas were not increased by
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irradiation, although non-fatal carcinomas were increased after perinatal exposure. Myeloproliferative
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disorders and central nervous system astrocytomas appeared to be increased in perinatally irradiated
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dogs. These data suggest that irradiation in both the fetal and neonatal periods is associated with
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increased early onset and lifetime cancer risk.
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</p>
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<p>
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Int J Cancer 1999 Nov 26;83(5):585-90. <strong>Fatty-acid composition in serum phospholipids and risk of
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breast cancer: an incident case-control study in Sweden.</strong> Chajes V, Hulten K, Van Kappel AL,
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Winkvist A, Kaaks R, Hallmans G, Lenner P, Riboli E. “. . . women in the<strong><hr /></strong>”
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</p>
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<p>
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Tumori 2000 Jan-Feb;86(1):12-6 <strong>Factors of risk for breast cancer influencing post-menopausal
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long-term hormone replacement therapy.</strong> Chiechi LM, Secreto G. <strong>“. . . growing
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evidence points to increased breast cancer risk in HRT long-term users, and the adverse effect
|
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would, obviously, overwhelm any other benefit. At present, the risk/benefit ratio of HRT is an
|
||
object of hot debate . . . .”
|
||
</strong>“We conclude that some biologic and clinical markers, namely android obesity, bone density,
|
||
mammographic density, androgen and estrogen circulating levels, alcohol consumption, benign breast
|
||
disease, and familiarity, should be carefully considered before prescribing long-term HRT. <strong>Our
|
||
analysis suggests that HRT could increase the risk of breast cancer and useless in preventing
|
||
coronary heart disease and osteoporotic fractures</strong> when administered in women with
|
||
positivity for one or more of these markers.”
|
||
</p>
|
||
<p>
|
||
Cancer 1996 Nov 15;78(10):2045-8. <strong>Declining cancer mortality in the United States.</strong> Cole
|
||
P, Rodu B.
|
||
</p>
|
||
<p>
|
||
<strong><em>Preventing Breast Cancer:</em></strong>
|
||
<strong><em>The story of a Major, Proven, Preventable Cause of This Disease.</em></strong> John W.
|
||
Gofman, M.D., Ph.D. 1996. “This book uncovers the major cause of the recent breast-cancer incidence in
|
||
the USA. The author shows that past exposure to ionizing radiation --- primarily medical x-rays --- is
|
||
responsible for about 75 percent of the breast-cancer problem in the United States. The good news: Since
|
||
the radiation dosage given today by medical procedures can be significantly reduced without interfering
|
||
with a single useful procedure, numerous future cases of breast-cancer can be prevented. The author
|
||
recommends specific actions to start breast-cancer prevention now, not ten years from now.”
|
||
</p>
|
||
<p>
|
||
Am J Public Health 1998 Mar;88(3):458-60. <strong>Geographic variations in breast cancer mortality: do
|
||
higher rates imply elevated incidence or poorer survival?</strong> Goodwin JS, Freeman JL, Freeman
|
||
D, Nattinger AB. <strong>“Mortality rates from breast cancer are approximately 25% higher for women in
|
||
the northeastern United States than for women in the South or West.</strong> This study examined the
|
||
hypothesis that the elevation is due to decreased survival rather than increased incidence.” “The
|
||
elevated mortality in the Northeast is apparent only in older women. For women aged 65<strong><hr
|
||
/></strong>CONCLUSIONS: Those seeking to explain the excess breast cancer mortality in the Northeast
|
||
should assess survival and should examine differences in cancer control practices that affect survival.”
|
||
</p>
|
||
<p>
|
||
Nutrition 1999 May;15(5):392-401 <strong>The influence of maternal diet on breast cancer risk among
|
||
female offspring.</strong> Hilakivi-Clarke L, Clarke R, Lippman M. The induction of breast cancer is
|
||
a long process, containing a series of biological events that drive a normal mammary cell towards
|
||
malignant growth. However, it is not known when the initiation of breast cancer occurs. One hypothesis
|
||
is that a high estrogenic environment during the perinatal period increases subsequent breast cancer
|
||
risk. There are many sources of extragonadal estrogens, particularly in the diet. The purpose of this
|
||
paper is to review the evidence that a high maternal intake of dietary fats increases serum estrogens
|
||
during pregnancy and increases breast cancer risk in daughters. Our animal<strong>
|
||
studies show that a high maternal consumption of corn oil consisting mainly of linoleic acid
|
||
(omega-6 polyunsaturated fatty acid, PUFA), increases both circulating estradiol (E2) levels during
|
||
pregnancy and the risk of developing</strong> carcinogen-induced mammary tumors among the female rat
|
||
offspring. A similar increase in breast cancer risk occurs in female offspring exposed to injections of
|
||
E2 through their pregnant mother. Our data suggest that the mechanisms by which an early exposure to
|
||
dietary fat and/or estrogens increases breast cancer risk is related to reduced differentiation of the
|
||
mammary epithelial tree and increased number of mammary epithelial cell structures that are known to the
|
||
sites of neoplastic transformation. These findings may reflect our data of the reduced estrogen receptor
|
||
protein levels and protein kinase C activity in the developing mammary glands of female rats exposed to
|
||
a high-fat diet in utero. In summary, a high dietary linoleic acid intake can elevate pregnancy estrogen
|
||
levels and this, possibly by altering mammary gland morphology and expression of fat- and/or
|
||
estrogen-regulated genes, can increase breast cancer risk in the offspring. If true for women, breast
|
||
cancer prevention in daughters may include modulating the mother's pregnancy intake of some dietary
|
||
fats.
|
||
</p>
|
||
<p>
|
||
Mol Cell Biochem 1998 Nov;188(1-2):5-12 <strong>Timing of dietary fat exposure and mammary
|
||
tumorigenesis: role of estrogen receptor and protein kinase C activity.</strong> Hilakivi-Clarke L,
|
||
Clarke R. The possible association between a high fat diet and increased breast cancer risk has remained
|
||
controversial. This largely reflects the conflicting data obtained from migrant, case control and animal
|
||
studies, which generally support this association, and cohort studies which often fail to show a link
|
||
between fat and breast cancer. The mammary gland is particularly sensitive to estrogens during fetal
|
||
development, leading us to hypothesize that dietary fat levels during this period may significantly
|
||
influence breast cancer risk. Using chemically-induced mammary tumors in rats as our experimental model,
|
||
<strong>we have demonstrated the ability of a maternal diet, high in the polyunsaturated fatty acid
|
||
(PUFA) linoleic acid, to alter mammary gland differentiation, accelerate the onset of sexual
|
||
maturation, and increase breast cancer risk.</strong> The mammary glands of female rats exposed to a
|
||
high-fat diet in utero have more of the undifferentiated structures (terminal end buds) and fewer of the
|
||
differentiated structures (alveolar buds) than the glands of rats exposed to a low-fat diet in utero.
|
||
Furthermore, these mammary glands contain lower levels of total estrogen receptors and have reduced
|
||
total protein kinase C activity. <strong>These effects appear to be mediated by an increase in the serum
|
||
estradiol levels of pregnancy, which are elevated at least 30% in pregnant dams fed a high-fat
|
||
diet.</strong> Furthermore, the administration of estradiol to pregnant dams produces effects on
|
||
mammary gland development, onset of puberty and sensitivity to chemical carcinogenesis comparable to
|
||
those seen in the offspring of rats fed a high fat diet during pregnancy. Our results, thus, support the
|
||
hypothesis based on epidemiological<strong>
|
||
data that high maternal estrogen levels increase daughters' breast cancer risk. The results also
|
||
suggest that a high-fat diet may be an important factor in increasing pregnancy estrogenic activity.
|
||
</strong>
|
||
</p>
|
||
<p>
|
||
Proc Natl Acad Sci U S A 1997 Aug 19;94(17):9372-7. <strong>A maternal diet high in n - 6
|
||
polyunsaturated fats alters mammary gland development, puberty onset, and breast cancer risk among
|
||
female rat offspring.</strong> Hilakivi-Clarke L, Clarke R, Onojafe I, Raygada M, Cho E, Lippman M.
|
||
<strong>We hypothesized that feeding pregnant rats with a high-fat diet would increase both circulating
|
||
17beta-estradiol (E2) levels in the dams and the risk of developing carcinogen-induced mammary
|
||
tumors among their female offspring. Pregnant rats were fed isocaloric diets containing 12% or 16%
|
||
(low fat) or 43%</strong> or 46% (high fat) of calories from corn oil, which primarily contains the
|
||
n - 6 polyunsaturated fatty acid (PUFA) linoleic acid, throughout pregnancy. The<strong>
|
||
plasma concentrations of E2 were significantly higher in pregnant females fed a high n - 6 PUFA
|
||
diet. The female offspring of these rats were fed with a laboratory chow from birth onward, and when
|
||
exposed to</strong>7,12-dimethylbenz(a)anthracene had a significantly higher mammary tumor incidence
|
||
(60% vs. 30%) and shorter latency for tumor appearance (11.4 +/- 0.5 weeks vs. 14.2 +/- 0.6 weeks) than
|
||
the offspring of the low-fat mothers. The high-fat offspring also had puberty onset at a younger age,
|
||
and their mammary glands contained significantly higher numbers of the epithelial structures that are
|
||
the targets for malignant transformation. Comparable changes in puberty onset, mammary gland morphology,
|
||
and tumor incidence were observed in the offspring of rats treated daily with 20 ng of E2 during
|
||
pregnancy. These data,<strong>
|
||
if extrapolated to humans, may explain the link among diet, early puberty onset, mammary parenchymal
|
||
patterns, and breast cancer risk, and indicate that an in utero exposure to a diet high in n - 6
|
||
PUFA and/or estrogenic stimuli may be critical for affecting breast cancer risk.
|
||
</strong>
|
||
</p>
|
||
<p>
|
||
Oncol Rep 1998 May-Jun;5(3):609-16 <strong>Maternal genistein exposure mimics the effects of estrogen on
|
||
mammary gland development in female mouse offspring.</strong> Hilakivi-Clarke L, Cho E, Clarke R.
|
||
Human and animal data indicate that a high maternal estrogen exposure during pregnancy increases breast
|
||
cancer risk among daughters. This may reflect an increase in the epithelial structures that are the
|
||
sites for malignant transformation, i.e., terminal end buds (TEBs), and a reduction in epithelial
|
||
differentiation in the mammary gland. Some phytoestrogens, such as genistein which is a major component
|
||
in soy-based foods, and zearalenone, a mycotoxin found in agricultural products, have estrogenic effects
|
||
on the reproductive system, breast and brain. The present study examined whether in utero exposure to
|
||
genistein or zearalenone influences mammary gland development. Pregnant mice were injected daily with i)
|
||
20 ng estradiol (E2); ii) 20 microg genistein; iii) 2 microg zearalenone; iv) 2 microg tamoxifen (TAM),
|
||
a partial estrogen receptor agonist; or v) oil-vehicle between days 15 and 20 of gestation. E2,
|
||
genistein, zearalenone, and tamoxifen all increased the density of TEBs in the mammary glands. Genistein
|
||
reduced, and zearalenone increased, epithelial differentiation. Zearalenone also increased epithelial
|
||
density, when compared with the vehicle-controls. None of the treatments had permanent effects on
|
||
circulating E2 levels. Maternal exposure to E2 accelerated body weight gain, physical maturation (eyelid
|
||
opening), and puberty onset (vaginal opening) in the female offspring. Genistein and tamoxifen had
|
||
similar effects on puberty onset than E2. Zearalenone caused persistent cornification of the estrus
|
||
smears. These findings indicate that maternal exposure to physiological doses of genistein mimics the
|
||
effects of E2 on the mammary gland and reproductive systems in the offspring. Thus, our results suggest
|
||
that genistein acts as an estrogen in utero, and may increase the incidence of mammary tumors if given
|
||
through a pregnant mother. The estrogenic effects of zearalenone on the mammary gland, in contrast, are
|
||
probably counteracted by the permanent changes in estrus cycling.
|
||
</p>
|
||
<p>
|
||
Am J Public Health 1991 Apr;81(4):462-5 <strong>Does increased detection account for the rising
|
||
incidence of breast cancer?</strong> Liff JM, Sung JF, Chow WH, Greenberg RS, Flanders WD. “The
|
||
incidence of breast cancer has been increasing over time in the United States.” “To determine the role
|
||
of screening in this increase, trends in the incidence of in situ and invasive carcinoma of the breast
|
||
were evaluated using records of the metropolitan Atlanta SEER program between 1979 and 1986.” “The
|
||
average annual age-adjusted incidence of invasive disease rose 29 percent among Whites and 41 percent
|
||
among Blacks. Incidence increased in all age groups.” “Asymptomatic tumors accounted for only 40 percent
|
||
of the increased incidence among whites and 25 percent of the increased incidence among blacks, with
|
||
mammography as the principal contributing procedure.” “These data suggest that increased detection
|
||
accounts for some but not all of the rising incidence of breast cancer in the United States.”
|
||
</p>
|
||
<p>
|
||
J Clin Oncol 2001 Jan 1;19(1):239-41. <strong>The fifty-year decline of cancer in america.</strong> Rodu
|
||
B, Cole P. Department of Pathology, School of Medicine, and the Department of Epidemiology, School of
|
||
Public Health, University of Alabama at Birmingham, Birmingham, AL. PURPOSE: From 1950 to 1990, the
|
||
overall cancer mortality rate increased steadily in the United States, a trend which ran counter to
|
||
declining mortality from other major diseases. The purpose of this study was to assess the impact of
|
||
lung cancer on all-cancer mortality over the past 50 years. METHODS: Data from the National Centers for
|
||
Health Statistics were used to develop mortality rates for all forms of cancer combined, lung cancer,
|
||
and other-cancer (all-cancer minus lung cancer) from 1950 to 1998. RESULTS: <strong>When lung cancer is
|
||
excluded, mortality from all other forms of cancer combined declined continuously from 1950 to 1998,
|
||
dropping 25% during this period. The decline in other-cancer mortality was approximately 0.4%
|
||
annually from 1950 to 1990 but accelerated to 0.9% per year from 1990 to 1996 and to 2.2% per year
|
||
from 1996 to 1998.</strong>
|
||
<strong><em>CONCLUSION: The long-term decline is likely due primarily to improvements in medical care,
|
||
including screening, diagnosis, and treatment.</em></strong>
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
J Mammary Gland Biol Neoplasia 1998 Jan;3(1):49-61 <strong>Role of hormones in mammary cancer initiation
|
||
and progression.</strong> Russo IH, Russo J. “Administration of carcinogen to pregnant, parous or
|
||
hormonally treated virgin rats, on the other hand, fails to elicit a tumorigenic response, a phenomenon
|
||
attributed to the higher degree of differentiation of the mammary gland induced by the hormonal
|
||
stimulation of pregnancy. In women a majority of breast cancers that are initially hormone dependent are
|
||
manifested during the postmenopausal period. Estradiol plays a crucial role in their development and
|
||
evolution.”
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
Hum Reprod 1999 Aug;14(8):2155-61<strong>
|
||
Tryptophan ingestion by pregnant rats induces pituitary and mammary tumours in the adult female
|
||
offspring.
|
||
</strong>Santana C, Martin L, Valladares F, Diaz-Flores L, Santana-Herrera C, Milena A, Rodriguez Diaz M
|
||
“. . . maternal ingestion of tryptophan induced a marked rise in 665-day-old offspring in the incidence
|
||
of both pituitary prolactinomas (62%) and mammary adenomas (49%). Present data suggest that tryptophan
|
||
regulates serotonergic differentiation during early development. A transitory modification of the
|
||
tryptophan concentration in the fetal brain induces a permanent increase in hypothalamic serotonin level
|
||
and, in addition to modifying the release of prolactin, increases the incidence of tumours in the
|
||
hypophysis and mammary gland.”
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
JAMA 1977 Feb 21;237(8):789-90. <strong>Breast cancer induced by radiation. Relation to mammography and
|
||
treatment of acne.</strong> Simon N.<strong></strong>This communication reports cases of 16 women in
|
||
whom cancer of the breast developed after radiation therapy for acne or hirsutism, suggesting another
|
||
group at higher risk than is generally expected for cancer of the breast.<strong>
|
||
It is prudent to regard the carcinogenic effect of radiation on the breast as proportional to dose
|
||
without a threshold. Mammography in young women should be ordered only selectively, not for
|
||
screening.</strong>
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
Rev Interam Radiol 1977 Oct;2(4):199-203. <strong>Cancer of the breast--induction by radiation and role
|
||
of mammography.</strong> Simon N.
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
Eur J Clin Nutr 1999 Feb;53(2):83-7. <strong>Western nutrition and the insulin resistance syndrome: a
|
||
link to breast cancer.</strong> Stoll BA. “The incidence of breast cancer in the Western world runs
|
||
parallel to that of the major components of the insulin resistance syndrome--hyperinsulinaemia,
|
||
dyslipidaemia, hypertension and atherosclerosis. Evidence is reviewed that the growth of breast cancer
|
||
is favoured by specific dietary fatty acids, visceral fat accumulation and inadequate physical exercise,
|
||
all of which are thought to interact in favouring the development of the insulin resistance syndrome.”
|
||
“Experimental evidence suggests that hyperinsulinaemia and its concomitants can increase the promotion
|
||
of mammary carcinogenesis and the mechanism is likely to involve increased bioactivity of insulin-like
|
||
growth factor 1 (IGF-1). Case-control and cohort studies have shown that higher serum levels of IGF-1
|
||
are associated with increased breast cancer risk.” “Nutritional and lifestyle modifications that improve
|
||
insulin sensitivity may not only decrease a tendency to atherosclerosis but also reduce breast cancer
|
||
risk in women.”
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
Strong, Leonell C, <strong><em>Biological Aspects of Cancer and Aging,</em></strong> Oxford, Pergamon
|
||
Press, 1968.
|
||
</p>
|
||
<p> </p>
|
||
<p>
|
||
Ethn Dis 1999 Spring-Summer;9(2):181-9. <strong>Secular trend of earlier onset of menarche with
|
||
increasing obesity in black and white girls: the Bogalusa Heart Study.</strong>
|
||
<hr />
|
||
<strong>in black girls (11.4+/-1.3 vs 12.3+/-1.4 years) and white girls (11.5+/-1.3 vs 12.3+/-1.3
|
||
years). Furthermore, twice as many girls in the second cohort had reached menarche by ages younger
|
||
than 12 years</strong> (P<0.001).” <strong>“Since increases in body fatness and related early
|
||
onset of menarche are risk factors for disorders in adult life including cardiovascular disease and
|
||
breast cancer, the secular trend in the increasing incidence of obesity throughout the United States
|
||
is becoming a major public health problem.”</strong>
|
||
</p>
|
||
<p> </p>
|
||
</article>
|
||
</body>
|
||
</html>
|