Breast Cancer
乳腺癌
by Raymond Peat
It’s important to know the realities of cancer in the population, the death rate from cancer, and the effects of its aggressive diagnosis and treatment. Appreciating those, I think the need for a new attitude toward cancer can be seen.
了解癌症在人群中的真实情况、癌症的死亡率以及积极诊断和治疗的效果是很重要的。感谢这些，我认为我们有必要对癌症采取新的态度。
Official US data for the years 1990 to 1993 showed 505,300 cancer deaths in 1990, and 529,900 cancer deaths in 1993. This was an increase of roughly 1.3% per year (which was faster than the population growth) during the time in which Rodu and Cole (1996) and agencies of the U.S. government claimed the death rate was decreasing one half percent (0.5%) per year.
美国1990年至1993年的官方数据显示，1990年有50.53万人死于癌症，1993年有529900人死于癌症。在Rodu和Cole(1996)以及美国政府机构声称死亡率每年下降0.5%的时候，这大约是每年1.3%的增长(比人口增长快)。
This increase happened despite the abnormal population bulge in the number of people between the ages of 35 and 50, resulting from the postwar baby boom. Cancer incidence is about ten times higher among the older population than in this younger age range, so in this abnormally structured population, the death rate from cancer is much lower than it would be if the population composition were the same as before the war, and it is lower than it will be in ten or twenty years, when the population bulge reaches the prime cancer years.
尽管由于战后婴儿潮，35岁至50岁之间的人口数量异常增加，但这一增长仍然发生了。癌症发病率之间大约有十倍的老年人比年轻的年龄,所以在这个人口结构异常,癌症的死亡率是远低于如果人口组成是一样的在战争之前,它低于它将在十年或二十年,当人口膨胀达到癌症的黄金时期。
In 1994, total cancer deaths increased to 536,900 (an increase of 1.32% over 1993). The crude death rate per 100,000 population was 203.2 in 1990, in 1993 it was 205.6, in 1994 it had increased to 206. This, despite the population distortion caused by the baby boom,causing a scarcity of people in the age groups with the highest rates of cancer mortality.
1994年，癌症死亡总数增加到536 900人(比1993年增加了1.32%)。1990年粗死亡率为每10万人203.2人，1993年为205.6人，1994年增加到206人。尽管婴儿潮造成了人口扭曲，导致癌症死亡率最高的年龄组的人口稀缺。
In the U.S. in 1994 there were altogether 2,286,000 deaths. In a population of about 260 million, this was a death rate of less than 1% per year (about 0.88%). The chance of dying that year for any person was less than one in a hundred. That doesn’t mean that life expectancy is over 100 years, but that would be implied if we ignored the population bulge of the baby boomers, as the cancer statisticians are doing.
1994年，美国共有2286000人死亡。在约2.6亿人口中，每年的死亡率不到1%(约0.88%)。在那一年，任何人的死亡几率都不到百分之一。这并不意味着预期寿命超过100岁，但如果我们像癌症统计学家正在做的那样，忽略婴儿潮一代的人口膨胀，这就意味着预期寿命超过100岁。
When the U.S. Department of Health and Human Services, and every major medical journal in the United States lies about the simple statistics of cancer death rates, it’s clear that very powerful and dangerous social forces are operating.
当美国卫生和公众服务部，以及美国的每一个主要医学杂志对癌症死亡率的简单统计数据撒谎时，很明显，非常强大和危险的社会力量正在发挥作用。
Anyone who knows about the baby boom that started right after the second world war must also realize that in 1940, at the end of the great depression, when infant and childhood mortality was very high and people postponed having children, the population had a disproportionate number of old people, and that it would be outrageous to use the rate of cancer in the pre-war population to evaluate the rate of cancer in the post-war population. But that is what is being done, and the mass media are helping to prevent the public from questioning the official story about cancer.
谁知道婴儿潮开始第二次世界大战之后还必须意识到,在1940年,大萧条结束时,当婴儿和儿童的死亡率非常高,人们推迟生育,人口数量不成比例的老人,用战前人口的癌症发病率来评估战后人口的癌症发病率是令人无法容忍的。但这就是正在做的事情，大众媒体正在帮助防止公众质疑关于癌症的官方报道。
If the health of the population in 1940 is to be compared to that of a very differently constituted later population, the appropriate method is to compare the rate of death among people of a certain age. The death rate from leukemia, especially among children, was greatly increased in the post-war years, when people were being exposed to radiation from atomic bomb tests. The death rates among adults of various ages, from breast cancer, prostate cancer, and melanoma have steadily increased. Rodu and Cole, who declared victory in the war against cancer, said the decline in total cancer mortality began in 1991. (Cole and Rodu, 1996) If lung cancer is excluded, they say mortality from other cancers has been declining since 1950! (“The fifty-year decline of cancer in America,” Rodu and Cole, 2001.) The first time I saw this bizarre use of “age restandardization” was when Professor Bruce Ames was on a lecture tour for the American Cancer Society, and was speaking to the biology department at the University of Oregon. He showed a graph indicating that the mortality curves for most types of cancer in the U.S. had begun their downward curve in the late 1940s just after the A.C.S. came onto the scene. Even though I think the A.C.S. probably initiated the practice of age-standardizing with reference to the 1940 population, they don’t always find that date suitable for their purposes. In fund-raising literature showing their past success in curing childhood leukemia, they restandardized mortality with reference to the postwar year when the leukemia death rate was at its highest, with the result that their cures appeared to be steadily lowering the death rate. But the incidence rate varied according to the intensity of the radioactive intensity that pregnant women were exposed to, and so both the incidence and the mortality fell after atmospheric testing was stopped.
如果要将1940年人口的健康状况与一个构成非常不同的后来人口的健康状况进行比较，适当的方法是比较某一年龄人群的死亡率。战后人们受到原子弹试验的辐射，白血病死亡率，特别是儿童白血病死亡率大幅上升。不同年龄的成人乳腺癌、前列腺癌和黑色素瘤的死亡率稳步上升。宣布战胜癌症的Rodu和Cole说，癌症总死亡率的下降始于1991年。(科尔和罗杜，1996)如果排除肺癌，他们说其他癌症的死亡率自1950年以来一直在下降!(“美国癌症发病率50年的下降，”Rodu和Cole, 2001年。)我第一次看到“年龄再标准化”这个奇怪的用法是在布鲁斯·埃姆斯教授为美国癌症协会巡回演讲时，当时他在俄勒冈大学的生物系演讲。他展示了一张图表显示美国大多数癌症的死亡率曲线在20世纪40年代末开始下降就在acs问世之后。尽管我认为acs可能是参照1940年的人口开始实行年龄标准化的，但他们并不总是觉得那个年龄适合他们的目的。在显示他们过去在治疗儿童白血病方面取得成功的筹款文献中，他们参照战后那一年白血病死亡率最高的年份重新规范了死亡率，结果他们的治疗似乎在稳步降低死亡率。但发病率随孕妇所接触的放射性强度而变化，所以在停止大气测试后发病率和死亡率都下降了。
Government officials, editors of the big medical journals, professors and broadcasters, have been able to get away with this huge statistical fraud. I suspect that they will soon feel encouraged to simply make up the data that they want, because eventually “age standardization” isn’t going to work to hide the actual increases in mortality. Since people with cancer usually die of something else, such as a stroke or heart failure, it will be no trick at all to make cancer mortality decline to be replaced by other causes of death. The precedent for such fabulizing of data exists in the FDA’s approval of AZT, and other less notorious drugs.
政府官员、大型医学期刊的编辑、教授和广播公司都能够逃脱这种巨大的统计造假。我怀疑，他们很快就会感到被鼓励去编造他们想要的数据，因为最终“年龄标准化”将无法掩盖死亡率的实际增长。由于癌症患者通常死于其他原因，如中风或心力衰竭，使癌症死亡率下降被其他死因取代将不是什么难事。美国食品和药物管理局(FDA)批准AZT和其他不那么臭名昭著的药物时，就有过这样的数据令人难以置信的先例。
Radiation, estrogen, and a variety of chemical pollutants are known to be the major causes of breast cancer, but the efforts of the cancer establishment have been directed toward denying that these avoidable agents are the cause of the great increase in breast cancer during the last several decades. The cancer industry, including major producers of chemotherapy drugs, subsidizes the American Cancer Society and “Breast Cancer Awareness Week,” and it is in their interest to convince the public that early detection and conventional treatment with surgery, chemotherapy, and radiation are winning the war against cancer. There is always light at the end of the tunnel, in the war against cancer, just as there was in the Vietnam war. Their consistent effort to dissuade the government from acting to reduce the public’s exposure to the known causes of cancer should make it clear that they are in the business of treating cancer, not eliminating it.
众所周知，辐射、雌激素和各种化学污染物是导致乳腺癌的主要原因，但癌症研究机构一直在努力否认这些可避免的因素是过去几十年来乳腺癌发病率大幅上升的原因。癌症行业，包括化疗药物的主要生产商，资助美国癌症协会(American cancer Society)和“乳腺癌意识周”(Breast cancer Awareness Week)，让公众相信早期发现和常规治疗(包括手术、化疗和放疗)正在赢得与癌症的战争，这符合他们的利益。在与癌症的战争中，总有一线光明，就像在越南战争中一样。他们一直努力劝阻政府采取行动减少公众对已知癌症原因的接触，这应该清楚地表明，他们是在治疗癌症，而不是消除癌症。
In the 1960s I read some articles in a small town newspaper about Leonell Strong’s cancer research, and his treatment by the American Cancer Society and the Salk Institute. Leonell Strong had developed strains of mice for use in cancer research. In some of the strains, 100% of the females developed mammary cancer. Strong had demonstrated that these strains had very high levels of estrogen. He showed me mice that he had treated with simple extracts of liver, that were free of cancer, and whose descendants remained free of cancer for several generations.
20世纪60年代，我在一个小镇的报纸上读到一些关于莱昂内尔·斯特朗(Leonell Strong)癌症研究的文章，以及美国癌症协会(American cancer Society)和索尔克研究所(Salk Institute)对他的治疗。莱昂内尔·斯特朗培育出用于癌症研究的小鼠品种。在一些菌株中，100%的女性患上了乳腺癌。斯特朗已经证明，这些菌株的雌激素水平非常高。他向我展示了用简单的肝脏提取物治疗过的老鼠，这些老鼠没有患癌症，它们的后代几代都没有患癌症。
Strong had received his PhD in genetics under T. H. Morgan. For a person trained in classical genetics, and who had spent his career developing the supposedly genetically determined cancer trait, the elimination of the trait by a few injections must have been hard to understand, but at least he tried to understand it.
斯特朗在t·h·摩根手下获得了遗传学博士学位。对于一个接受过古典遗传学训练的人来说，他的职业生涯中一直在研究被认为是由基因决定的癌症特征，通过注射几针来消除这种特征肯定很难理解，但至少他尝试去理解它。
When he had earlier demonstrated the presence of a virus in the milk of cancer-prone mice, and when he showed the role of heredity in cancer, he was popular with the cancer business, but when he showed that “genetic” cancer could be eradicated with a simple treatment, he became the object of official abuse. He said that the Salk institute had offered him a position to induce him to move with his large colony of mice from New York to San Diego, but when he arrived he found that he had no job, and his records of decades of research had been lost. He said that a memo which was discovered in a lawsuit revealed that the institute had just wanted his mice, and never intended to give him the promised job. For the cancer establishment, his discovery of a way to prevent cancer was not welcome.
早些时候他已经展示了一种病毒的存在在癌变老鼠的牛奶,当他显示,癌症遗传的作用,他与癌症流行业务,但当他表明,癌症可以根除“遗传”用一个简单的治疗,他成为官方虐待的对象。他说索尔克研究所给他提供了一个职位，诱使他带着他的一大群老鼠从纽约搬到圣地亚哥，但当他到达那里时，他发现自己没有工作，他几十年的研究记录也丢失了。他说，在一场诉讼中发现的一份备忘录显示，研究所只是想要他的老鼠，并没有打算给他承诺的工作。对于癌症研究机构来说，他发现的预防癌症的方法并不受欢迎。
In 1969, two years before the war against cancer had begun pouring public money into the pockets of the cancer establishment, Harry Rubin gave a lecture that criticized the cancer establishment’s claim that it was curing cancer. He cited a study by a pathologist who had looked for cancer in the tissues of people who had been killed in accidents. He found identifiable cancers in the tissues of everyone over the age of fifty that he examined. If everyone over 50 has histologically detectable cancer, then the use of biopsy specimens as the basis for determining whether a person needs treatment has no scientific basis.
1969年，在对抗癌症的战争开始将公共资金注入癌症机构的口袋的两年前，哈里·鲁宾做了一次演讲，批评了癌症机构声称他们正在治愈癌症的说法。他引用了一位病理学家的一项研究，该研究在事故中死亡的人的组织中寻找癌症。他在检查过的每个50岁以上的人的组织中发现了可识别的癌症。如果每个50岁以上的人都有组织学上可检测到的癌症，那么使用活检标本作为确定一个人是否需要治疗的基础是没有科学依据的。
The definition of a disease, and the recognition of its presence, has an important place in medicine, but understanding its cause or causes is essential for both treatment and prevention. The dominant belief in medicine is that diseases are significantly caused by “genes,” including diseases such as cancer, diabetes, psychoses, and neurological diseases. In Israel, ethnic groups that had never had much diabetes before immigrating, within a single generation had diabetes as often as other Israelis. Shortly after insulin became available for the treatment of diabetes, the incidence of the disease in the U.S. began to increase. The simple death rate from diabetes per 100,000 population is now higher than it was in 1920, before insulin treatment became available. Neurological diseases and autoimmune diseases, along with diabetes and cancer, have increased greatly in recent generations. These simply aren’t genetic diseases, and there should be a shift of resources away from useless or harmful treatments toward their prevention.
疾病的定义和对疾病存在的认识在医学中占有重要地位，但了解疾病的起因对于治疗和预防都是至关重要的。医学界的主流观点是，疾病很大程度上是由“基因”引起的，包括癌症、糖尿病、精神病和神经系统疾病。在以色列，移民之前从未患过糖尿病的少数民族，在一代人的时间内患糖尿病的频率与其他以色列人一样高。胰岛素可用来治疗糖尿病后不久，美国的糖尿病发病率开始上升。每10万人中糖尿病的简单死亡率现在比1920年胰岛素治疗尚未普及时要高。神经系统疾病和自身免疫性疾病，以及糖尿病和癌症，在最近几代人中大幅增加。这些根本不是遗传疾病，应该将资源从无用或有害的治疗转向预防。
Even when a disease’s cause isn’t clearly understood, it is essential to use logical thinking in diagnosing its presence. The presence of a certain gene or “genetic marker” is often thought to have great diagnostic significance, which it rarely has. But even gross “signs” of a disease can be used diagnostically only if we know that similar signs aren’t present in perfectly healthy people. When pains are thought to be the result of a herniated intervertebral disk, x-ray pictures may be produced as confirmation of the diagnosis. But when people without pains are just as likely to have herniated disks (about 2/3 of normal people have them), the diagnosis fails to be convincing. When x-rays or MRIs show “plaques” in the head, multiple sclerosis is often “confirmed,” but when normal medical students show just as many brain plaques, the diagnosis must be questioned. Similarly, when mature people who were perfectly healthy until they were killed by an accident are found to always have identifiable cancers, any diagnosis of cancer that is based on a similar histological specimen must be reconsidered.
即使一种疾病的病因尚不清楚，用逻辑思维来诊断它的存在也是至关重要的。某一特定基因或“遗传标记”的存在通常被认为具有重大的诊断意义，但这种情况很少发生。但是，只有当我们知道完全健康的人没有类似的症状时，即使是疾病的严重“症状”也可以用于诊断。当疼痛被认为是椎间盘突出的结果时，x线照片可以作为诊断的确认。但是，当没有疼痛感的人同样可能有椎间盘突出(大约2/3的正常人有椎间盘突出)时，诊断就不能令人信服了。当x光片或核磁共振成像显示大脑中有“斑块”时，多发性硬化症通常被“证实”，但当正常医学院学生显示同样多的大脑斑块时，诊断就必须受到质疑。同样地，当那些在意外事故中死亡之前完全健康的成年人被发现总是患有可识别的癌症时，任何基于类似组织学标本的癌症诊断都必须重新考虑。
By diagnosing something that is as common and trivial as dandruff as “cancer,” physicians can get a very high rate of cures, whether they use surgery, radiation, or chemotherapy. Abnormal cellular proliferation is usually harmless, but it has become an important part of a business that makes several billion dollars per year, with no definite benefits except the financial benefits for those in the business.
通过诊断一些像头皮屑这样普通而琐碎的东西，如“癌症”，医生可以得到非常高的治疗法，无论他们使用的是手术、放疗还是化疗。异常的细胞增殖通常是无害的，但它已经成为一个重要的业务的一部分，每年数十亿美元，没有明确的利益，除了经济利益的业务。
Before cancer treatment became culturally practically obligatory, and when fewer people died of cancer, some people lived into old age with clearly “malignant” cancers, and died of some other cause. The policy of leaving a cancer alone is now established for prostate cancer in old men. Until there is clear evidence to the contrary, a similar policy might be appropriate for many kinds of cancer.
在癌症治疗成为强制性的文化实践之前，当死于癌症的人越来越少的时候，一些人活到老年，明显患有“恶性”癌症，并死于其他原因。对于老年前列腺癌患者，不去管癌症的政策现已确立。除非有明确的相反证据，否则类似的政策可能适用于多种癌症。
If every year more people are treated for cancer, and every year more people die of cancer, one simply wonders whether fewer people would die if few were treated.
如果每年都有更多的人接受癌症治疗，每年都有更多的人死于癌症，人们不禁会想，如果很少人接受治疗，死亡人数是否会减少。
If the first rule of medicine is to do no harm, then the second rule, growing out of the first, would have to be to give no treatment without knowing what is being treated, and to have a valid basis for believing that the damage done by the treatment is not worse than the damage that the disease would cause. If cancer specialists haven’t demonstrated that their treatments improve their patients’ situation, then their professional activities aren’t justified; the statistics suggest that they aren’t.
如果医学的第一条规则是不伤害,然后第二个规则,第一,增长会给没有接受治疗,治疗不知道和相信有一个有效的基础治疗并不比造成的损害,这种疾病会导致的损害。如果癌症专家没有证明他们的治疗能改善病人的状况，那么他们的专业活动就不合理;统计数据表明，事实并非如此。
There simply isn’t a valid base of knowledge about the natural history of cancer development in humans to permit a valid judgment to be made about the meaning of particular signs or indicators or histological structures. The extensive use of mammograms has increased the diagnosis of “ductal carcinoma in situ” by more than 1000% (a 16- or 18-fold increase in some hospitals, and expected to double in the next decade), increasing the number of mastectomies and other treatments, but the increased treatments and early diagnosis haven’t produced any visible change in the death rate.
对于人类癌症发展的自然历史，根本没有一个有效的知识基础来允许对特定的迹象、指标或组织结构的含义作出有效的判断。乳房x线照片的广泛应用使“导管原位癌”的诊断率提高了1000%以上(在一些医院，这一数字增加了16或18倍，预计在未来10年将翻一番)，增加了乳房切除术和其他治疗的数量，但是增加的治疗和早期诊断并没有在死亡率上产生任何明显的变化。
The pathologists talk knowingly of “pre-neoplastic” conditions that indicate an increased risk of malignancy, but instead of data, what they have is an ideology about the nature of cancer. When they say that a growth pattern is premalignant or that a cell has a malignant structure, they might as well be talking about goblins, because the scientific basis for what they are saying is nothing but a belief in the ideology that cancer is “clonal,” that a particular cancer derives from a single defective cell. They are so self-assured, and have so many sources to cite about the “clonal nature of cancer,” that it seems impolite to suggest that they might simply be misusing language and logic.
病理学家清楚地谈论“肿瘤前期”状况，这表明恶性肿瘤风险增加，但他们拥有的不是数据，而是关于癌症本质的意识形态。当他们说,经济增长模式是一个细胞癌变前的或恶性结构,他们谈论的也可能是妖精,因为他们说的科学依据不过是对癌症的意识形态是“克隆”,一个特定的癌症源于一个有缺陷的细胞。他们是如此自信，并有如此多的来源引用“癌症的克隆性质”，以至于认为他们可能只是在滥用语言和逻辑似乎是不礼貌的。
Isn’t a person derived from a single cell, and so, in that sense, “clonal”? As organs differentiate in the development of the organism, can’t organs be traced back to the cells from which they developed? Isn’t every tissue “a clone” in that sense? What is it that makes the “clonal” nature of cancer tissue so special? Isn’t it just that a nasty, mean, malignant tissue is, mentally, traced back to a “malignant” cell, by analogy with the way good tissues are traced back to good cells? If the tumor is odious, it must derive from an odious cell, and what could make that cell so hateful if it is genetically identical to the good cells? Therefore, the goblin reasoning goes, a genetic mutation must have produced the evil cell.
人不是由单细胞衍生出来的吗，所以，从这个意义上说，“克隆”?器官在有机体的发育过程中会发生分化，难道器官不能追溯到它们生长的细胞吗?从这个意义上说，不是每个组织都是“克隆”吗?是什么让癌症组织的“克隆”性质如此特殊?这难道不是说，一个令人讨厌的、卑鄙的恶性组织，在精神上可以追溯到一个“恶性”细胞，就像好的组织可以追溯到好的细胞一样吗?如果肿瘤是令人讨厌的，那么它一定来自于令人讨厌的细胞，如果这个细胞在基因上与好的细胞完全相同，又是什么让这个细胞如此令人讨厌呢?因此，按照妖精的推理，一定是基因突变产生了邪恶的细胞。
The actual evidence is that there are broad changes in tissues preceding the appearance of cancer. The goblin theory explains this by saying that a multitude of “precancerous”mutations occurred before the mutant cancer cell appeared. Harry Rubin has carefully shown experimentally and logically that cancer precedes the genetic changes that occur in tumors. But the ideology that cancer is the result of a genetic mutation forces its devotees to say that the genetic changes that can be found in a mature tumor must have occurred in one cell that was previously not malignant. An effect is identified as a cause.
实际的证据是，在癌症出现之前，组织有广泛的变化。“地精理论”解释说，在突变的癌细胞出现之前，就已经发生了大量的“癌前”突变。Harry Rubin在实验和逻辑上仔细地证明了癌症先于发生在肿瘤中的基因变化。但是，癌症是基因突变的结果的意识形态迫使它的追随者说，可以在成熟肿瘤中发现的基因变化，一定是发生在一个以前不是恶性的细胞中。结果被确定为原因。
The clonal-goblin theory of cancer leads logically to the conclusion that the cancer clone must be exorcised by surgery, chemotherapy, and/or radiation.
癌症的克隆地精理论从逻辑上得出结论，癌症克隆必须通过手术、化疗和/或放疗来驱除。
The biological theory of cancer, on the other hand, is inclined to view the normal and abnormal development of cells in terms of the cells’ responses to conditions.
另一方面，癌症的生物学理论倾向于根据细胞对环境的反应来看待细胞的正常和异常发育。
Estrogen and ionizing radiation are the most clearly documented causes of breast cancer. Their excitatory effects lead to inflammation, edema, fibrosis, and interruption of intercellular regulatory processes. Radiation is estrogenic, and increased estrogenic stimulation produces growth and temporary loss of differentiated functions. Estrogen and radiation aren’t the only things that can cause these systematic changes in the structure of tissues–for example, vitamin A deficiencies, hypothyroidism, chlorinated hydrocarbons, irritation, and lack of oxygen can cause similar changes–but estrogen and irradiation have been studied enough to give us a fairly distinct picture of the real processes involved in the development of cancer.
雌激素和电离辐射是乳腺癌最明确的病因。它们的兴奋作用导致炎症、水肿、纤维化和细胞间调节过程的中断。辐射是雌激素的，增加的雌激素刺激产生生长和暂时的分化功能丧失。雌激素和辐射并不是导致组织结构发生系统性变化的唯一因素，比如维生素A缺乏、甲状腺功能减退、氯代烃、刺激、缺氧也会导致类似的变化，但雌激素和辐射已经被充分研究，给我们提供了癌症发展过程中相当清晰的图像。
Polyunsaturated fats are another clearly identified cause of cancer, especially breast cancer. These fats synergize with estrogen, and sensitize to radiation. Their effects on the mother can be seen in the offspring, as an increased tendency to develop breast or prostate cancer.
多不饱和脂肪是另一个明确的致癌原因，尤其是乳腺癌。这些脂肪与雌激素协同作用，并对辐射敏感。它们对母亲的影响可以在后代身上看到，比如增加患乳腺癌或前列腺癌的可能性。
An individual’s hormone balance can be disrupted by exposure to radiation, estrogens, or unsaturated fats. The hormonal balance of the parent is imprinted upon the offspring, acting on the chromosomes, the liver, brain, genitals, pituitary, bones–in fact, the prenatal imprint can probably be found everywhere in the offspring.
暴露在辐射、雌激素或不饱和脂肪中，个人的激素平衡会被破坏。父母的荷尔蒙平衡会影响后代，影响染色体、肝脏、大脑、生殖器、脑垂体、骨骼——事实上，胎儿时期的荷尔蒙平衡可能在后代身上无处不在。
It’s easy to reduce our exposure to radiation, by avoiding mammograms, bone density scans, and other x-rays of all sorts. Ultrasound and MRI can produce good images of any tissue without the deadly effects of ionizing radiation.
通过避免乳房x光片、骨密度扫描和其他各种x光片，我们很容易减少暴露在辐射下。超声波和核磁共振成像可以为任何组织提供良好的图像，而不会产生电离辐射的致命影响。
Polyunsaturated fats can be reduced by careful selection of foods, but the food industry is finding ways to contaminate traditionally safe foods, such as beef and milk, by using new kinds of animal feed. Still, milk, cheese, beef, and lamb are safe, considering their high nutritional content, and the remarkable purification that occurs in the rumen of cows, sheep, and goats. Some studies suggest a protective effect from saturated fat (Chajes, et al., 1999.)
多不饱和脂肪可以通过谨慎选择食品来减少，但食品工业正在寻找污染传统安全食品的方法，如使用新型动物饲料的牛肉和牛奶。尽管如此，牛奶、奶酪、牛肉和羊肉是安全的，考虑到它们的高营养含量，以及牛、绵羊和山羊瘤胃中显著的净化作用。一些研究表明饱和脂肪具有保护作用(Chajes等，1999年)。
Estrogenic influences can be significantly reduced by avoiding foods such as soy products and unsaturated fats, by eating enough protein to optimize the liver’s elimination of estrogen, and by using things such as bulk-forming foods (raw carrots, potatoes, and milk, for example) that stimulate bowel action and prevent reabsorption of estrogens from the intestine. Avoiding hypothyroidism is essential for preventing chronic retention or formation of too much estrogen.
避免食用豆制品和不饱和脂肪等食物，食用足够的蛋白质以优化肝脏对雌激素的消除，以及食用大块食物(生胡萝卜、土豆和牛奶，例如)刺激肠道活动并阻止肠内雌激素的再吸收。避免甲状腺功能减退对于防止雌激素的长期滞留或形成是至关重要的。
Some studies show that dietary starch, rather than fat, is associated with breast cancer. Starch strongly stimulates insulin secretion, and insulin stimulates the formation of estrogen.
一些研究表明，与乳腺癌有关的是膳食淀粉，而不是脂肪。淀粉强烈刺激胰岛素分泌，胰岛素刺激雌激素的形成。
Estrogen is formed in fat cells under the influence of cortisol, and this formation is suppressed by progesterone and thyroid. Postmenopausal obesity is associated with increased estrogen and breast cancer. The prevention of weight gain, and supplementation with thyroid and progesterone if necessary, should be protective against many types of cancer, especially breast, kidney, and uterine cancer.
雌激素是在皮质醇的影响下在脂肪细胞中形成的，而这种形成受到孕酮和甲状腺的抑制。绝经后的肥胖与雌激素增加和乳腺癌有关。预防体重增加，必要时补充甲状腺和孕酮，可以预防多种癌症，特别是乳腺癌、肾癌和子宫癌。
Prenatal or early life exposure to estrogens, including phytoestrogens, or to irradiation, or to polyunsaturated oils, increases the incidence of mammary cancers in adulthood.
产前或早期暴露于雌激素，包括植物雌激素，或辐射，或多不饱和油，会增加成年期乳腺癌的发病率。
Protein deficiency prenatally or early in life causes a life-long excess of serotonin. Feeding an excess of tryptophan, the precursor of serotonin, during pregnancy produces pituitary and mammary tumors in the offspring. Serotonin, besides being closely associated with the effects of estrogen (e.g., mediating its stimulation of prolactin secretion) and polyunsaturated fats, can be metabolized into carcinogens.
产前或生命早期的蛋白质缺乏会导致血清素长期过量。在怀孕期间，喂养过量的色氨酸(血清素的前体)会在后代中产生垂体和乳腺肿瘤。5 -羟色胺除了与雌激素(如调节其刺激催乳素分泌)和多不饱和脂肪的作用密切相关外，还可代谢为致癌物。
Prenatal protein deficiency and excess unsaturated oils predispose to a developmental pattern involving hypothyroidism and hyperestrogenism; puberty occurs at an earlier age, along with a tendency to gain weight. Inflammatory processes (e.g., “autoimmune diseases”) are usually intensified under those conditions. Inflammation itself increases the effects of estrogen and serotonin.
产前蛋白质缺乏和过多的不饱和油易导致甲状腺功能减退和雌激素过多的发育模式;青春期发生在更早的年龄，伴随着体重增加的趋势。炎症过程(如“自身免疫性疾病”)通常在这些情况下加剧。炎症本身会增加雌激素和血清素的作用。
Both preventively and therapeutically, the use of the antiinflammatory and antioxidative substances such as aspirin, caffeine, progesterone, and thyroid hormone would seem appropriate. Aspirin is coming to be widely accepted as an anticancer agent, and at moderate doses can cause cancer cells to die. It, like progesterone and thyroid, has a wide variety of anti-estrogenic effects. Especially when a tumor is painfully inflamed, aspirin’s effects can be quick and dramatic. However, people aren’t likely to be pleased if their cancer doctor tells them to “take aspirin and call me in six months.” Aspirin’s reputation for causing stomach bleeding causes people to avoid it, even when the alternative is something that’s seriously toxic to other organs, and it might just seem too ordinary to be considered as a powerful anticancer drug.
无论是预防还是治疗，使用抗炎和抗氧化物质如阿司匹林、咖啡因、孕酮和甲状腺激素似乎是合适的。阿司匹林作为一种抗癌药物正逐渐被广泛接受，适度的剂量会导致癌细胞死亡。就像孕酮和甲状腺一样，它有各种各样的抗雌激素作用。尤其是当肿瘤发炎时，阿司匹林的效果会迅速而显著。然而，如果癌症医生告诉他们“服用阿司匹林，6个月后打电话给我”，人们可能不会高兴。阿司匹林引起胃出血的名声使人们避免使用它，即使它的替代品对其他器官有严重的毒性，它可能看起来太普通了，不能被认为是一种有效的抗癌药物。
Because of the toxic (carcinogenic, and anti-respiratory) effects of the “essential fatty acids,”which are usually stored in the tissues in very large quantities, it’s important to avoid the stresses or hunger that would release the fats into the blood stream. Estrogens and adrenalin and serotonin and growth hormone, and prolonged darkness, increase the release of the free fatty acids. Frequent meals, including some saturated fats such as coconut oil, and a balance of protein, sugars, and salts, will minimize the release of stored fats.
由于“必需脂肪酸”的毒性(致癌和抗呼吸)作用，这些脂肪酸通常大量储存在组织中，因此避免压力或饥饿是很重要的，因为这些压力或饥饿会将脂肪释放到血液中。雌激素、肾上腺素、血清素和生长激素，以及长时间的黑暗，增加了游离脂肪酸的释放。经常吃饭，包括一些饱和脂肪，如椰子油，以及蛋白质、糖和盐的平衡，将最小化储存脂肪的释放。
The population trends toward greater obesity and earlier puberty, both of which are associated with a higher risk of breast cancer, suggest that the war against cancer is far from over. In the 19th century when the incidence of breast cancer was much lower than it is now, puberty usually occurred around the age of 17. In countries with a low incidence of breast cancer, puberty still occurs in the middle to late teens. People who are now 100 generally had puberty years later than girls do now. The biological changes now seen in children in the U.S. suggest that the incidence of degenerative diseases of all sorts is likely to increase as these children grow up.
人口趋向于肥胖和早熟，这两者都与乳腺癌的高风险有关，这表明对抗癌症的战争远未结束。在19世纪，乳腺癌的发病率比现在低得多，青春期通常发生在17岁左右。在乳腺癌发病率低的国家，青春期仍然发生在青少年的中晚期。现在100岁的人青春期通常比现在的女孩晚几年。目前在美国儿童身上看到的生物变化表明，随着这些儿童的成长，各种退化性疾病的发病率可能会增加。
A metabolic approach to the prevention and treatment of cancer would have many beneficial side effects, such as producing generally healthier, happier and brighter babies.
用新陈代谢的方法来预防和治疗癌症会有很多有益的副作用，比如产生更健康、更快乐和更聪明的婴儿。
REFERENCES
Radiat Res 1998 Sep;150(3):330-48 Mortality in beagles irradiated during prenatal and postnatal development. II. Contribution of benign and malignant neoplasia. Benjamin SA, Lee AC, Angleton GM, Saunders WJ, Keefe TJ, Mallinckrodt CH. To evaluate the lifetime carcinogenic hazards of exposure to ionizing radiation during development, 1,680 beagles received whole-body exposures to 60Co gamma rays or sham exposures. Eight groups of 120 dogs each received mean doses of 15.6-17.5 or 80.8-88.3 cGy in early, mid- or late gestation, at 8, 28 or 55 days postcoitus or at 2 days after birth. Another group of 120 dogs received a mean dose of 82.6 cGy as 70-day-old juveniles and one group of 240 dogs received a mean dose of 81.2 cGy as 365-day-old young adults. Sham irradiations were given to 360 controls. Sexes were equally represented. In 1,343 dogs allowed to live out their life span, neoplasia was a major disease, contributing to mortality in 40% of the dogs. There was a significant increase in benign and malignant neoplasms occurring in young dogs (<4 years old), including fatal malignancies, after irradiation in the perinatal (late fetal and neonatal) periods. The lifetime incidence of fatal neoplasms was also increased in dogs irradiated perinatally. Three malignancies-lymphomas, hemangiosarcomas and mammary carcinomas-accounted for 51% of all fatal tumors. There was an apparent lifetime increase and earlier onset of lymphomas in dogs exposed as fetuses. Fatal hemangiosarcomas were increased in dogs irradiated early and late in gestation. Fatal mammary carcinomas were not increased by irradiation, although non-fatal carcinomas were increased after perinatal exposure. Myeloproliferative disorders and central nervous system astrocytomas appeared to be increased in perinatally irradiated dogs. These data suggest that irradiation in both the fetal and neonatal periods is associated with increased early onset and lifetime cancer risk.
Int J Cancer 1999 Nov 26;83(5):585-90. Fatty-acid composition in serum phospholipids and risk of breast cancer: an incident case-control study in Sweden. Chajes V, Hulten K, Van Kappel AL, Winkvist A, Kaaks R, Hallmans G, Lenner P, Riboli E. “. . . women in thehighest quartile of stearic acid had a relative risk of 0.49 (95% confidence interval, 0.22-1.08) compared with women in the lowest quartile (trend p = 0.047), suggesting a protective role of stearic acid in breast-cancer risk.”
Tumori 2000 Jan-Feb;86(1):12-6 Factors of risk for breast cancer influencing post-menopausal long-term hormone replacement therapy. Chiechi LM, Secreto G. “. . . growing evidence points to increased breast cancer risk in HRT long-term users, and the adverse effect would, obviously, overwhelm any other benefit. At present, the risk/benefit ratio of HRT is an object of hot debate . . . .” “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. Our analysis suggests that HRT could increase the risk of breast cancer and useless in preventing coronary heart disease and osteoporotic fractures when administered in women with positivity for one or more of these markers.”
Cancer 1996 Nov 15;78(10):2045-8. Declining cancer mortality in the United States. Cole P, Rodu B.
Preventing Breast Cancer:The story of a Major, Proven, Preventable Cause of This Disease. 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.”
Am J Public Health 1998 Mar;88(3):458-60. Geographic variations in breast cancer mortality: do higher rates imply elevated incidence or poorer survival? Goodwin JS, Freeman JL, Freeman D, Nattinger AB. “Mortality rates from breast cancer are approximately 25% higher for women in the northeastern United States than for women in the South or West. 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 years and older, breast cancer mortality is 26% higher in New England than in the South, while incidence is only 3% higher. Breast cancer mortality for older women by state correlates poorly with incidence (r = 0.28). 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.”
Nutrition 1999 May;15(5):392-401 The influence of maternal diet on breast cancer risk among female offspring. 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 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 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.
Mol Cell Biochem 1998 Nov;188(1-2):5-12 Timing of dietary fat exposure and mammary tumorigenesis: role of estrogen receptor and protein kinase C activity. 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, 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. 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. 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. 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 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.
Proc Natl Acad Sci U S A 1997 Aug 19;94(17):9372-7. A maternal diet high in n - 6 polyunsaturated fats alters mammary gland development, puberty onset, and breast cancer risk among female rat offspring. Hilakivi-Clarke L, Clarke R, Onojafe I, Raygada M, Cho E, Lippman M. 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% or 46% (high fat) of calories from corn oil, which primarily contains the n - 6 polyunsaturated fatty acid (PUFA) linoleic acid, throughout pregnancy. The 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 to7,12-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, 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.
Oncol Rep 1998 May-Jun;5(3):609-16 Maternal genistein exposure mimics the effects of estrogen on mammary gland development in female mouse offspring. 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.
Am J Public Health 1991 Apr;81(4):462-5 Does increased detection account for the rising incidence of breast cancer? 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.”
J Clin Oncol 2001 Jan 1;19(1):239-41. The fifty-year decline of cancer in america. 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: 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.CONCLUSION: The long-term decline is likely due primarily to improvements in medical care, including screening, diagnosis, and treatment.
J Mammary Gland Biol Neoplasia 1998 Jan;3(1):49-61 Role of hormones in mammary cancer initiation and progression. 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.”
Hum Reprod 1999 Aug;14(8):2155-61 Tryptophan ingestion by pregnant rats induces pituitary and mammary tumours in the adult female offspring. 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.”
JAMA 1977 Feb 21;237(8):789-90. Breast cancer induced by radiation. Relation to mammography and treatment of acne. Simon N.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. 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.
Rev Interam Radiol 1977 Oct;2(4):199-203. Cancer of the breast–induction by radiation and role of mammography. Simon N.
Eur J Clin Nutr 1999 Feb;53(2):83-7. Western nutrition and the insulin resistance syndrome: a link to breast cancer. 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.”
Strong, Leonell C, Biological Aspects of Cancer and Aging, Oxford, Pergamon Press, 1968.
Ethn Dis 1999 Spring-Summer;9(2):181-9. Secular trend of earlier onset of menarche with increasing obesity in black and white girls: the Bogalusa Heart Study. Wattigney WA, Srinivasan SR, Chen W, Greenlund KJ, Berenson GS. “Secular trends in onset of menarche and obesity were examined 14 years apart in two biracial (black-white) cohorts of girls aged 8 to 17 under study for cardiovascular risk. The first cohort (N=1,190, 64% white) was examined in 1978-1979, the second (N=1,164, 57% white) in 1992-1994.” “The onset of menarche occurred at an earlier age in the second cohort compared with the first cohort (P<0.0001), both 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 (P<0.001).” “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.”
