Breast cancer and the environment

Breast cancer

Breast cancer is a disease of great importance to public health. According to the International Agency for Research on Cancer of the World Health Organization, breast cancer is the most frequently occurring among women in the world.

Rates of new cases are higher in industrialized countries, but rising rapidly in some developing countries. In the few developed countries where screening programs on a large scale have become routine recently, part of the increase can be attributed to improved screening mammography, which allows you to locate small tumors years before what could have been detecting by other means. Although the increased use of mammography may explain part of the increase in the number of cases detected in the United States and some other developed country, it cannot explain the recent increases and quite substantial that have occurred in parts of Central Europe and Asia were not carried out screening campaigns.

For more than three decades ago, scientists have systematically identified a number of risk factors that most believed to be responsible for up to 40 percent of all cases of breast cancer. Among the risk factors that have been established for breast cancer, include having menstrual periods that begin before age 12 and end after 55. Not having children or having them later in life, not to breastfeed their children, exposure repeated at relatively high doses of radiation from an early age, obesity after menopause and a family history of breast cancer in a close relative who has had before the age of 40 years. It is suspected, that other factors may increase the risk, but the data are less clear. Among these are: drinking alcohol daily, lack of vigorous exercise, low intake of vitamin D and fiber, smoking or passive and active living near chemical plants.

Despite the persistent public attention is given to predisposing to breast cancer genes inherited, less than one in ten cases occur in women born with defects in genes most important breast cancer have been identified to date: BRCA1, BRCA2, and ATM. It is believed that breast cancer, like everyone else, arises from a process in several steps involving sequential or simultaneous damage to several genes that control the growth and maturation of cells. Genetic damage can also occur when a cell bad copy their own DNA during cell division and fails to repair that error. Metabolic differences in how the body processes the compounds are affected by genetic factors may also influence the risk of developing cancer.

Breast cancer

So although certain risk factors for breast cancer, such as age at menarche, diet, and genetic predisposition are well known for several years, many breast cancers occur in women who do not attend any of these factors. Scientists do not know explain why today more cases of breast cancer occur. However, a growing body of evidence suggests that complex external environment including the general behavior, diet and exposure to chemicals-physical elements and plays a major role in increasing breast cancer. The general environment can induce breast cancer by two different mechanisms: environmental exposure can damage the genes directly, or can affect overall production of regulatory growth hormones such as are estrogen, progesterone and other similar substances produced naturally.

The time when exposure occurs may be just as important as the degree of exposure to one or more of these risk factors so as regards the development of the disease, and prenatal exposure is especially important.

They have obtained more evidence that environmental factors influence the development of breast cancer by observing that there is considerable geographic variation in breast cancer cases between both ethnic groups and within those groups. There have been studies that have shown that Asian women living in the United States have higher rates of breast cancer than those living in their countries of origin.

There are many data showing that the cumulative exposure of women to estrogen increases the risk of developing breast cancer. The longer a woman is exposed to estrogen throughout their lives, the more likely of developing this cancer. Women who begin menstruating at an early age and enter menopause at an older age, for example, are more vulnerable to breast cancer than women who menstruate for less time in their lives. The reduction of estrogen by surgical removal of the ovaries may reduce cancer risk significantly; breastfeeding, which lowers the cumulative exposure to estrogen by altering the regular menses, also reduces some risk. In addition, women with toxemia during pregnancy have lower hormone levels. A recent study suggests that the daughters of these women have a lower risk of breast cancer, possibly because their breast cells, when they were developing, were subject to lower levels of circulating hormones prenatally.

How do can influence estrogen and other hormones that increase the risk of breast cancer?

It is believed that hormones, especially those that are not linked to proteins and are rapidly excreted through normal metabolism, promote growth genetically damaged breast cells, causing them to become clinically relevant cancers. The times when cells are dividing rapidly, as in the prenatal period and puberty are also times when there is greater vulnerability to genetic damage likely to cause disease because repair mechanisms cannot operate at a comparable to the speed of cell growth. Studies suggest that prenatal exposure to high levels of estrogen increases the risk of breast cancer in offspring, perhaps because permanently affects the sensitivity of breast cells to estrogen. These tests on the role of natural hormones in the risk of cancer have led to the hypothesis that perhaps the synthetic hormones also can influence. Over the last three decades, there has been a convergence of several lines of studies indicating that a number of synthetic compounds that are used can usually modify or mimic the action of natural estrogen in the body. Some of these compounds that mimic hormones can be beneficial, such as those typically found in plants or fish. By contrast, other compounds that mimic hormones seem to be generally harmful, such as those often found in pesticides, plastics, and fuels. In human experimental studies conducted in animals and have detected higher levels of some of these compounds in organisms, they showed alterations in hormone function or had other health problems, including developmental defects and behavior.

Based on these observations, my colleagues in the Laboratory for Cancer Research Strang-Cornell New York City and I have hypothesized that the same environmental exposures that disrupt hormones may play a role in the development of breast cancer, they alter the effects of natural estrogen. Our theory is that some of these xenoestrogens may increase the risk of cancer to adversely affect the metabolism of estrogen while others xenoestrogens from plants like soy can protect against the disease. Natural estrogens and xenoestrogens can lead to breast cancer through the same mechanism. Both natural estrogens own body as xenoestrogens can bind to estrogen receptors and alter the quantity and quality of estrogen produced in the body. Estradiol, which is the main class of estrogen women generating metabolized in the body in different ways, which produce very different effects on the body. It is believed that there are “good” forms and “bad” of these metabolites of estrogen. The good estrogen appears to promote cellular repair and prevent the onset of cancer by enhancing protective factors in the cell cycle that are not conducive to cancer. On the contrary, the bad estrogen seems to stimulate damage to the protective genes that cause cancer, and increase the total quantities of free hormones; either of these two factors can trigger the accelerated growth of breast cells. This stimulated growth increases the chances of occurrence and genetic damage is maintained. Studies in animals and humans suggest that there is a relationship between elevated levels of bad estrogen and an increased risk of breast cancer.

Although there is still no conclusive evidence for this hypothesis, recent experimental analyzes have come to provide further support for this theory. Strang my colleagues and I discovered that cells from human breast cancer had bad estrogen levels more than four times higher than in normal breast cells. When organochlorines were added to breast cancer cells pesticides, the proportion of the amount of good and bad estrogen varied significantly. These pesticides, which tend to accumulate in fat cells, may somehow have influenced the formation of different metabolites of estrogen. These and other findings led us to hypothesize that exposure to certain types of xenoestrogens present in the environment may explain part of the increase in the incidence of breast cancer by altering the ratio of good estrogen and bad in breast tissue. A limited number of studies that were conducted in the 1970s and 1980s found that women who had higher levels of DDT metabolites in blood were at greater risk of developing breast cancer.

In contrast, to these experimental studies on the ability to alter the hormones found in chemicals, studies in humans have not been systematically finding an association between some residues of lipophilic pesticides and breast cancer.

In three recent studies has not been able to find any connection between the risk of breast cancer and the presence of the body of metabolites of DDT, suspected estrogen is a simulator. However, in these studies, both women suffering from breast cancer as those with which they compared them, showed levels of metabolites pesticide DDT that was almost only a sixth of those detected in the United States later 1960. Furthermore, not in all these experiments could obtain information about possible prenatal exposure to xenoestrogens harmful, nor on the history of prolonged use of, or exposure to, potential bad or good xenoestrogens, such as those found in plants, fish, and fiber. In short, research is inconclusive.

Achieve document the role of potentially harmful xenoestrogens, as are some organochlorine pesticides long life, it presents a formidable challenge to epidemiological research. In part, this is because other adjuvants, both positive and negative, cannot be easily measured factors and may have a relatively greater importance. For example, among some of the relevant sources of bad estrogens that may be causing breast cancer could be exhibitions, occurred two or three decades before materials are in widespread use, such as plastics, fuels, and drugs, none of which I could detect years later since they do not accumulate in fat. This idea is consistent with a recent study that found that postmenopausal women who had never breastfed had a much higher risk of developing breast cancer when compared them with those that did have breastfed their children. Breastfeeding can make them happen materials, such as organochlorines, infants breast. While this may reduce the risk of a woman developing breast cancer, the consequences that may suffer long-term children who have been exposed to higher levels of such contaminants in breast milk are a cause of concern.

How could they penetrate the body harmful xenoestrogens and act on breast cells and brain development? A way that seems very likely through animal fats in the diet. Synthetic harmful xenoestrogens tend to accumulate in fatty tissue and up the food chain. Some synthetic xenoestrogen ends up in food because once you have entered the environment may persist and accumulate for more than 50 years. People living in areas where pollution could be exposed to harmful xenoestrogen by just breathing the air or drinking contaminated water. You can also provide occupational exposures to xenoestrogens, for example in chemical laboratories and industrial plants.

Some researchers such as Stephen Safe at the University Of Texas A & M, they doubt that xenoestrogens play a role in the onset of breast cancer. They note that people are exposed to tiny amounts of potent chemicals found in the environment and are much less potent than natural estrogens, such as those produced in the body or are derived from plants. In addition, estrogens found in plant foods such as soy seems that decrease harmful estrogenic effects, canceling the influences of bad estrogen. These observations are correct, but they are incomplete. While any synthetic xenoestrogen can penetrate the blood in very small amounts compared to the body’s own natural hormones. However, once inside the body, many lipophilic synthetic xenoestrogens tend to remain for decades in tissues and not easily excreted. By contrast, estrogen derived from plants typically degrades quickly in the body. Thus, it seems unlikely that natural estrogens that people normally consume in your diet can completely cancel the activity of persistent and cumulative synthetic compounds.

We are aware that xenoestrogens cannot be the cause of all cases of breast cancer occurring. The fact that recently have found low levels of organochlorines in the blood and fat encouragingly tells us who have succeeded some efforts in the past to reduce or prohibit the use of such compounds. However, the variety of substances that can alter hormone metabolism seems to be very extensive and is not yet well characterized. The combined effect on human and ecological health remains a matter of serious concern. Unlike what happens with other established factors that affect the risk of breast cancer, such as early menstruation and late menopause, exposure to synthetic xenoestrogens may be reduced or controlled through public policies? In addition, the beneficial xenoestrogens, such as those found in broccoli, soy and fish might be useful to prevent the disease from occurring or recurring. If reduce avoidable exposures to harmful xenoestrogens and encourage the use of beneficial substances that make it possible only a fifth of breast cancers that occur each year, millions of women would be avoided this difficult disease, and increased spending taxpayers would save on treatment and care. These perspectives are too promising to dismiss them.

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