Risk factors of breast cancer may be divided into preventable and non preventable. Their study belongs in the field of epidemiology.
Breast cancer, like other forms of cancer, can result from multiple environmental and hereditary risk factors. The term environmental, as used by cancer researchers, means any risk factor that is not genetically inherited.
For breast cancer, the list of environmental risk factors includes the individual person's development, exposure to microbes, "medical interventions, dietary exposures to nutrients, energy and toxicants, ionizing radiation, and chemicals from industrial and agricultural processes and from consumer products...reproductive choices, energy balance, adult weight gain, body fatness, voluntary and involuntary physical activity, medical care, exposure to tobacco smoke and alcohol, and occupational exposures, including shift work" as well as "metabolic and physiologic processes that modify the body's internal environment."
Some of these environmental factors are part of the physical
environment, while others (such as diet and number of pregnancies) are
primarily part of the social, cultural, or economic environment.
Although many epidemiological risk factors have been identified, the cause of any individual breast cancer is most often unknowable.
Epidemiological research informs the patterns of breast cancer incidence across certain populations, but not in a given individual. Approximately 5% of new breast cancers are attributable to hereditary syndromes, and well-established risk factors accounts for approximately 30% of cases.
The probability of breast cancer increases with age, but breast cancer tends to be more aggressive in younger people.
Men diagnosed with breast cancer tend to be older than women with breast cancer. They are more likely to be diagnosed with hormone-receptor positive tumors, with about six out of seven cases being estrogen-receptor positive. The overall prognosis is worse for men than for women
The more alcohol a woman drinks, the more likely she is to get breast cancer. The relationship is linear and dose-dependent. Even low levels of alcohol consumption carry some risk.
A study of more than one million middle-aged British women concluded that each daily alcoholic beverage increases the incidence of breast cancer by 11 cases per 1000 women.
This means that among a group of 1000 women who drink one alcoholic beverage per day, they will have 11 extra cases of breast cancer when compared to a group of women who drink less than one alcoholic beverage per week; a group of 1000 women who have four drinks per day will have an extra 44 cases of breast cancer compared to non-drinkers.
One or two drinks each day increases the relative risk to 150% of normal, and six drinks per day increases the risk to 330% of normal. Approximately 6% of breast cancers reported in the UK are due to women drinking alcohol.
The primary mechanism through which alcohol causes breast cancer is increased estrogen levels.
Another study showed no contribution of dietary fat intake on the incidence of breast cancer in over 300,000 women..
A randomized controlled study of the consequences of a low-fat diet, the Women's Health Initiative, failed to show a statistically significant reduction in breast cancer incidence in the group assigned to a low-fat diet, although the authors did find evidence of a benefit in the subgoup of women who followed the low-fat diet in a strict manner.
A prospective cohort study, the Nurses' Health Study II, found increased breast cancer incidence in premenopausal women only, with higher intake of animal fat, but not vegetable fat. Taken as a whole, these results point to a possible association between dietary fat intake and breast cancer incidence, though these interactions are hard to measure in large groups of women.
A study published in 2001 found higher levels of monounsaturated fatty acids MUFAs (especially oleic acid) in the erythrocyte membranes of postmenopausal women who developed breast cancer.
That same study discussed that a diet high in MUFAs is not the major determinant of erythrocyte membrane MUFAs, where most oleic acid in mammalian tissue is derived from the saturated stearic acid residue.
Where key conversion is controlled by the Delta9-desaturase, which also regulates the transformation of the other common saturated fatty acids (SFAs) (myristic and palmitic). The study discussed that fat content of the diet has an important effect on Delta9-d activity, while high levels of SFAs increase Delta9-d activity by twofold to threefold, whereas polyunsaturated fatty acids (PUFAs) decrease.
This conclusion was partially contradicted by a latter study, which showed a direct relation between very high consumption of omega-6 fatty acids (PUFAs) and breast cancer in postmenopausal women.
The literature support the following conclusions:
The study associated sub-optimal vitamin D levels with poor scores on every major biological marker that helps physicians predict a patient's breast cancer outcome.
The lead researcher stated, "Based on these results, doctors should strongly consider monitoring vitamin D levels among breast cancer patients and correcting them as needed."
The relative risk among women in the highest decile of Brassica vegetable consumption (median, 1.5 servings per day) compared to the lowest decile (virtually no consumption) was 0.58.
That is, women who consumed around 1.5 servings of Brassica vegetables per day had 42% less risk of developing breast cancer than those who consumed virtually none.
Researchers have long measured that breast cancer rates in an immigrant population soon come to resemble the rates of the host country after a few generations.
The reason for this is speculated to be immigrant uptake of the host country diet. The prototypical example of this phenomenon is the changing rate of breast cancer after the arrival of Japanese immigrants to America.
A case control study of 362 Korean women also reported an association between mushroom consumption and decreased risk of breast cancer.
Obesity has been linked to an increased risk of developing breast cancer by many scientific studies. There is evidence to suggest that excess body fat at the time of breast cancer diagnosis is associated with higher rates of cancer recurrence and death.
Furthermore, studies have shown that obese women are more likely to have large tumors, greater lymph node involvement, and poorer breast cancer prognosis with 30% higher risk of mortality.
Weight gain after diagnosis has also been linked to higher rates of breast cancer recurrence or mortality although this finding is not consistent.
Weight gain is often less severe with newer chemotherapy treatments but one study found a significant risk of breast cancer mortality in women who gained weight compared to those who maintained their weight.
However, other cohort studies and recent clinical trials have not shown a significant relationship between weight gain after diagnosis and breast cancer mortality.
Weight loss after diagnosis has not been shown to decrease the risk of breast cancer recurrence or mortality. However, physical activity after breast cancer diagnosis has shown some associations with reducing breast cancer recurrence and mortality independent of weight loss.
Data for both weight loss and physical activity and the effect on breast cancer prognosis is still lacking.
There is debate as to whether the higher rate of breast cancer associated with obesity is due to a biological difference in the cancer itself, or differences in other factors such as health screen practices.
It has been suggested that obesity may be a determinant for breast cancer screening by mammography.
Seventeen scientific studies in the United States have found that as obesity increases in women over 40 years of age the rate of mammography reported decreases significantly.
When stratified by race (white vs. black) there was a stronger relationship between obesity and lack of mammography screening among white women.
Another study also found lower rates of mammography among those who were overweight and obese compared to those women who were of normal body mass index—this effect was only seen in white women.
Obese women are more likely to list pain associated with mammograms as a reason for not getting screened; however, leaner women also list this as a reason for avoiding mammograms.
Other reasons obese women may avoid mammography are due to lack of insurance, low income, or embarrassment at the procedure, although when these factors are accounted for, the effect of lower rates of screening are still significant.
In contrast, other studies have shown that mammography patterns did not differ among women who were obese compared to those at a healthy weight indicating that there may be biological differences in cancer presentation between these groups.
Increased blood levels of progesterone are associated with a decreased risk of breast cancer in premenopausal women.
A number of circumstances which increase exposure to endogenous estrogens including not having children, delaying first childbirth, not breastfeeding, early menarche (the first menstrual period) and late menopause are suspected of increasing lifetime risk for developing breast cancer.
However, not only sex hormones, but also insulin levels are positively associated with the risk of breast cancer.
In contrast, for instance, having the first live birth after age 30 doubles the risk compared to having first live birth at age less than 25. Never having children triples the risk. However the risks involved in having a child are significant.
Further, the cancers diagnosed in women who had ever used hormonal contraceptives were less advanced than those in nonusers, raising the possibility that the small excess among users was due to increased detection.
The relative risk of breast cancer diagnosis associated with current and recent use of hormonal contraceptives did not appear to vary with family history of breast cancer.
Some studies have suggested that women who began using hormonal contraceptives before the age of 20 or before their first full-term pregnancy are at increased risk for breast cancer, but it is not clear how much of the risk stems from early age at first use, and how much stems from use before the first full-term pregnancy.
The largest meta-analysis (1997) of data from 51 observational studies, indicated a relative risk of breast cancer of 1.35 for women who had used HRT for 5 or more years after menopause.
The estrogen-plus-progestin arm of the Women's Health Initiative (WHI), a randomized controlled trial, which randomized more than 16,000 postmenopausal women to receive combined hormone therapy or placebo, was halted early (2002) because health risks exceeded benefits.
One of the adverse outcomes prompting closure was a significant increase in both total and invasive breast cancers (hazard ratio = 1.24) in women randomized to receive estrogen and progestin for an average of 5 years.
HRT-related breast cancers had adverse prognostic characteristics (more advanced stages and larger tumors) compared with cancers occurring in the placebo group, and HRT was also associated with a substantial increase in abnormal mammograms. Short-term use of hormones for treatment of menopausal symptoms appears to confer little or no breast cancer risk.
A correlation was found between the use of hormonal contraceptives and subsequent reliance on hormone replacement therapy.
Additional randomized controlled trials have been published since the guidelines. The IBIS trial found benefit from tamoxifen.
In 2006, the NSABP STAR trial demonstrated that raloxifene had equal efficacy in preventing breast cancer compared with tamoxifen, but that there were fewer side effects with raloxifene.
The RUTH Trial concluded that "benefits of raloxifene in reducing the risks of invasive breast cancer and vertebral fracture should be weighed against the increased risks of venous thromboembolism and fatal stroke".
On September 14, 2007, the US Food and Drug Administration approved raloxifene (Evista) to prevent invasive breast cancer in postmenopausal women.
Diethylstilbestrol (DES) is a synthetic form of estrogen. It has been used between the early 1940s and 1971. Pregnant women took DES to prevent certain pregnancy complications.
However, it also increased their risk of breast cancer. It also increased the risk of breast cancer in the prenatally exposed daughters after they have reached an age 40 years.
Furthermore, there is exposure to endocrine disruptors from the environment, in addition to phytoestrogens mentioned above in the diet section. See xenoestrogens in environmental factors below
The evidence to date generally supports an association between breast cancer and polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). dioxins and organic solvents, on the other hand, have only shown an association in sparse and methodologically limited studies, but are suggestive of an association. Overall, however, evidence is still based on a relatively small number of studies.
Beginning in the mid-1990s, a number of studies suggested an increased risk of breast cancer in both active smokers and those exposed to secondhand smoke compared to women who reported no exposure to secondhand smoke.
By 2005 enough evidence had accumulated for the [California Environmental Protection Agency] to conclude that breathing secondhand smoke causes breast cancer in younger, primarily premenopausal women.
The Agency concluded that the risk was increased by 70%, based on epidemiological studies and the fact that there are many mammary carcinogens in secondhand smoke.
The following year (2006) the US Surgeon General identified the same risk increase and concluded that the evidence is "suggestive," one step below causal.
There is some evidence that exposure to tobacco smoke is most problematic between puberty and first childbirth.
The reason is that breast tissue appears most sensitive to chemical carcinogens breast cells not fully differentiated until lactation.
The likely reason that the older studies of active smoking did not detect risks associated with smoking was that they compared active smokers to all nonsmokers (which includes many passive smokers).
The newer studies, which exclude passive smokers from the control group, generally show elevated risks associated with active as well as passive smoking.
The California Environmental Protection Agency has concluded that passive smoking causes breast cancer and the US Surgeon General has concluded that the evidence is "suggestive," one step below causal.
There is some evidence that exposure to tobacco smoke is most problematic between puberty and first childbirth.
The reason that breast tissue appears most sensitive to chemical carcinogens in this phase is that breast cells are not fully differentiated until lactation.
The risk increases with increased dose. In addition, the risk is higher in women irradiated before age 30, when there is still breast development.
Researchers at the National Cancer Institute (NCI) and National Institute of Environmental Health Sciences conducted a study in 2005 that suggests that artificial light during the night can be a factor for breast cancer by disrupting melatonin levels.
In 2007, "shiftwork that involves circadian disruption" was listed as a probable carcinogen by the World Health Organization's International Agency for Research on Cancer. (IARC Press release No. 180).
Multiple studies have documented a link between night shift work and the increased incidence of breast cancer.
A review of current knowledge of the health consequences of exposure to artificial light at night including the increased incidence of breast cancer and an explanation of the causal mechanisms has been published in the Journal of Pineal Research in 2007.
In the US incidence is significantly lower and mortality higher among black women and this difference appears to persist even after adjustment for economic status.
It is currently unclear if significant racial differences in incidence and mortality persist after adjustment for economic status between women of white, Hispanic and Asian origin in the US.
Several studies have found that black women in the U.S. are more likely to die from breast cancer even though white women are more likely to be diagnosed with the disease.
Even after diagnosis, black women are less likely to get treatment compared to white women.
Scholars have advanced several theories for the disparities, including inadequate access to screening, reduced availability of the most advanced surgical and medical techniques, or some biological characteristic of the disease in the African American population.
Some studies suggest that the racial disparity in breast cancer outcomes may reflect cultural biases more than biological disease differences.
However, the lack of diversity in clinical trials for breast cancer treatment may contribute to these disparities, with recent research indicating that black women are more likely to have estrogen receptor negative breast cancers, which are not responsive to hormone treatments that are effective for most white women.
Research is currently ongoing to define the contribution of both biological and cultural factors.
Part of the differences in incidence that is attributable to race and economic status may be explained by past use of hormone replacement therapy
However that study has been criticized for inaccuracy and another study found no substantial association between breast cancer and tea consumption in the overall, but found a weak inverse association between caffeine-containing beverages and risk of postmenopausal breast cancer.
Specifically about green tea, one study has found significant inverse association between risk of breast cancer and green tea intake in Asian women who were low soy consumers.
Aluminum salts, such as those used in anti-perspirants, have recently been classified as metalloestrogens.
In research published in the Journal of Applied Toxicology, Dr. Philippa D. Darbre of the University of Reading has shown that aluminum salts increase estrogen-related gene expression in human breast cancer cells grown in the laboratory.
Fortunately, this in-vitro association between aluminum salts and estrogen activity does not translate into an increased risk of breast cancer in humans.
The lack of association between underarm deodorants and breast cancer has been the subject of a number of research articles.
The human papilloma virus is well known for its capability to immortalize breast cancer cells which is used in research, however the role of this viruses in human breast cancer remains controversial.
Humans are not the only mammals susceptible to breast cancer. Some strains of mice, namely the house mouse (Mus domesticus) are prone to breast cancer which is caused by infection with the mouse mammary tumour virus (MMTV or "Bittner virus" for its discoverer Hans Bittner), by random insertional mutagenesis.
This finding is taken to mean that a viral origin of human breast cancer is at least possible, though there is no definitive evidence to support the claim that MMTV causes human breast cancer.
For example, there may be critical differences between cancer pathogenesis in mice and people. A human homologue of the mammary virus has been described in 1971 and linked to human breast cancer in several small epidemiologic studies.
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Breast cancer, like other forms of cancer, can result from multiple environmental and hereditary risk factors. The term environmental, as used by cancer researchers, means any risk factor that is not genetically inherited.
For breast cancer, the list of environmental risk factors includes the individual person's development, exposure to microbes, "medical interventions, dietary exposures to nutrients, energy and toxicants, ionizing radiation, and chemicals from industrial and agricultural processes and from consumer products...reproductive choices, energy balance, adult weight gain, body fatness, voluntary and involuntary physical activity, medical care, exposure to tobacco smoke and alcohol, and occupational exposures, including shift work" as well as "metabolic and physiologic processes that modify the body's internal environment."
Although many epidemiological risk factors have been identified, the cause of any individual breast cancer is most often unknowable.
Epidemiological research informs the patterns of breast cancer incidence across certain populations, but not in a given individual. Approximately 5% of new breast cancers are attributable to hereditary syndromes, and well-established risk factors accounts for approximately 30% of cases.
Age
The risk of getting breast cancer increases with age. A woman is more than 100 times more likely to develop breast cancer in her 60s than in her 20s. If all women lived to age 95, about one in eight would be diagnosed with breast cancer at some point during their lives. However, the actual lifetime risk is lower than that, because 90% of women die before age 95, most commonly from heart attacks, strokes, or other forms of cancer.The probability of breast cancer increases with age, but breast cancer tends to be more aggressive in younger people.
Sex
Men have a much lower risk of developing breast cancer than women. In developed countries, about 99% of breast cancer cases are diagnosed in women; in a few African countries, which represent the highest incidence of male breast cancer, men account for 5–15% of breast cancer cases. The rate of breast cancer in men appears to be rising somewhat.Men diagnosed with breast cancer tend to be older than women with breast cancer. They are more likely to be diagnosed with hormone-receptor positive tumors, with about six out of seven cases being estrogen-receptor positive. The overall prognosis is worse for men than for women
Dietary factors
Alcohol
According to the International Agency for Research on Cancer, there is sufficient scientific evidence to classify alcoholic beverages as a Group 1 carcinogen that causes breast cancer in women. Group 1 carcinogens are the substances with the clearest scientific evidence that they cause cancer, such as smoking tobacco.The more alcohol a woman drinks, the more likely she is to get breast cancer. The relationship is linear and dose-dependent. Even low levels of alcohol consumption carry some risk.
A study of more than one million middle-aged British women concluded that each daily alcoholic beverage increases the incidence of breast cancer by 11 cases per 1000 women.
This means that among a group of 1000 women who drink one alcoholic beverage per day, they will have 11 extra cases of breast cancer when compared to a group of women who drink less than one alcoholic beverage per week; a group of 1000 women who have four drinks per day will have an extra 44 cases of breast cancer compared to non-drinkers.
One or two drinks each day increases the relative risk to 150% of normal, and six drinks per day increases the risk to 330% of normal. Approximately 6% of breast cancers reported in the UK are due to women drinking alcohol.
The primary mechanism through which alcohol causes breast cancer is increased estrogen levels.
Fat intake
Dietary influences have been examined since decades with conflicting results and so far failed to confirm any significant dependency. One recent study suggests that low-fat diets may significantly decrease the risk of breast cancer as well as the recurrence of breast cancer.Another study showed no contribution of dietary fat intake on the incidence of breast cancer in over 300,000 women..
A randomized controlled study of the consequences of a low-fat diet, the Women's Health Initiative, failed to show a statistically significant reduction in breast cancer incidence in the group assigned to a low-fat diet, although the authors did find evidence of a benefit in the subgoup of women who followed the low-fat diet in a strict manner.
A prospective cohort study, the Nurses' Health Study II, found increased breast cancer incidence in premenopausal women only, with higher intake of animal fat, but not vegetable fat. Taken as a whole, these results point to a possible association between dietary fat intake and breast cancer incidence, though these interactions are hard to measure in large groups of women.
Specific dietary fatty acids
Although many claims have been made in popular literature there is no solid evidence linking specific fats to breast cancer.A study published in 2001 found higher levels of monounsaturated fatty acids MUFAs (especially oleic acid) in the erythrocyte membranes of postmenopausal women who developed breast cancer.
That same study discussed that a diet high in MUFAs is not the major determinant of erythrocyte membrane MUFAs, where most oleic acid in mammalian tissue is derived from the saturated stearic acid residue.
Where key conversion is controlled by the Delta9-desaturase, which also regulates the transformation of the other common saturated fatty acids (SFAs) (myristic and palmitic). The study discussed that fat content of the diet has an important effect on Delta9-d activity, while high levels of SFAs increase Delta9-d activity by twofold to threefold, whereas polyunsaturated fatty acids (PUFAs) decrease.
This conclusion was partially contradicted by a latter study, which showed a direct relation between very high consumption of omega-6 fatty acids (PUFAs) and breast cancer in postmenopausal women.
Phytoestrogens
Phytoestrogens have been extensively studied in animal and human in-vitro and epidemiological studies. Research failed to establish any noticeable benefit and some phytoestrogens may present a breast cancer risk.The literature support the following conclusions:
- Plant estrogen intake in early adolescence may protect against breast cancer later in life.[21]
- The potential risks of isoflavones on breast tissue in women at high risk for breast cancer is still unclear.[22]
Calcium
Some studies have found a relationship between calcium intake and lowered breast cancer risk.- In the Nurse's Health Study, a high dietary intake of calcium showed 33% lower risk of breast cancer.
- Cancer Prevention Study II Nutrition Cohort Concluded 20% lower risk of breast cancer with 1250 mg of calcium intake.
- Women's Health Study shows an inverse association between total calcium intake and premenopausal breast cancer risk.
- Another two studies, one in France and another in Finland, showed significant inverse relation between calcium intake and breast cancer.
- Hypotheses
- Calcium reduces cell proliferation and induces differentiation in mammary glands.
- High calcium intake decreases fat-induced epithelial hypoproliferation of mammary gland and chemically induced carcinogenesis.
- Breast density is positively associated with breast cancer. Dietary calcium intake reduces the breast density.
- High calcium intake is associated with a reduced risk of benign proliferative epithelial disorders which are thought to be precursors of breast cancer.
Vitamin D
Vitamin D is related to reduced risk of breast cancer and disease prognosis. A 2011 study done at the University of Rochester Medical Center found that low vitamin D levels among women with breast cancer correlate with more aggressive tumors and poorer prognosis.The study associated sub-optimal vitamin D levels with poor scores on every major biological marker that helps physicians predict a patient's breast cancer outcome.
The lead researcher stated, "Based on these results, doctors should strongly consider monitoring vitamin D levels among breast cancer patients and correcting them as needed."
- Hypotheses
- Vitamin D metabolites (25 (OH) D, 1, 25 (OH) 2 D) promote cellular differentiation and it is important for chemoprevention.
- Low circulating levels of 25 (OH) D in adolescence may be an important predisposing factor for breast cancer risk in later life.
Brassica vegetables
In a study published in the Journal of the American Medical Association, biomedical investigators found that Brassicas vegetable intake (broccoli, cauliflower, cabbage, kale and Brussels sprouts) was inversely related to breast cancer development.The relative risk among women in the highest decile of Brassica vegetable consumption (median, 1.5 servings per day) compared to the lowest decile (virtually no consumption) was 0.58.
That is, women who consumed around 1.5 servings of Brassica vegetables per day had 42% less risk of developing breast cancer than those who consumed virtually none.
Country diet
A significant environmental effect is likely responsible for the different rates of breast cancer incidence between countries with different dietary customs.Researchers have long measured that breast cancer rates in an immigrant population soon come to resemble the rates of the host country after a few generations.
The reason for this is speculated to be immigrant uptake of the host country diet. The prototypical example of this phenomenon is the changing rate of breast cancer after the arrival of Japanese immigrants to America.
Mushrooms
In 2009, a case-control study of the eating habits of 2,018 women suggested that women who consumed mushrooms had an approximately 50% lower incidence of breast cancer. Women who consumed mushrooms and green tea had a 90% lower incidence of breast cancer.A case control study of 362 Korean women also reported an association between mushroom consumption and decreased risk of breast cancer.
Iodine deficiency
The protective effects of iodine on breast cancer have been postulated from epidemiologic evidence and described in animal models.Obesity and Lack of Exercise
Gaining weight after menopause can increase a woman's risk. A 2006 study found that putting on 9.9 kg (22 lbs) after menopause increased the risk of developing breast cancer by 18%. Lack of exercise has been linked to breast cancer by the American Institute for Cancer Research.Obesity has been linked to an increased risk of developing breast cancer by many scientific studies. There is evidence to suggest that excess body fat at the time of breast cancer diagnosis is associated with higher rates of cancer recurrence and death.
Furthermore, studies have shown that obese women are more likely to have large tumors, greater lymph node involvement, and poorer breast cancer prognosis with 30% higher risk of mortality.
Weight gain after diagnosis has also been linked to higher rates of breast cancer recurrence or mortality although this finding is not consistent.
Weight gain is often less severe with newer chemotherapy treatments but one study found a significant risk of breast cancer mortality in women who gained weight compared to those who maintained their weight.
However, other cohort studies and recent clinical trials have not shown a significant relationship between weight gain after diagnosis and breast cancer mortality.
Weight loss after diagnosis has not been shown to decrease the risk of breast cancer recurrence or mortality. However, physical activity after breast cancer diagnosis has shown some associations with reducing breast cancer recurrence and mortality independent of weight loss.
Data for both weight loss and physical activity and the effect on breast cancer prognosis is still lacking.
There is debate as to whether the higher rate of breast cancer associated with obesity is due to a biological difference in the cancer itself, or differences in other factors such as health screen practices.
It has been suggested that obesity may be a determinant for breast cancer screening by mammography.
Seventeen scientific studies in the United States have found that as obesity increases in women over 40 years of age the rate of mammography reported decreases significantly.
When stratified by race (white vs. black) there was a stronger relationship between obesity and lack of mammography screening among white women.
Another study also found lower rates of mammography among those who were overweight and obese compared to those women who were of normal body mass index—this effect was only seen in white women.
Obese women are more likely to list pain associated with mammograms as a reason for not getting screened; however, leaner women also list this as a reason for avoiding mammograms.
Other reasons obese women may avoid mammography are due to lack of insurance, low income, or embarrassment at the procedure, although when these factors are accounted for, the effect of lower rates of screening are still significant.
In contrast, other studies have shown that mammography patterns did not differ among women who were obese compared to those at a healthy weight indicating that there may be biological differences in cancer presentation between these groups.
Hormones
Persistently increased blood levels of estrogen are associated with an increased risk of breast cancer, as are increased levels of the androgens androstenedione and testosterone (which can be directly converted by aromatase to the estrogens estrone and estradiol, respectively).Increased blood levels of progesterone are associated with a decreased risk of breast cancer in premenopausal women.
A number of circumstances which increase exposure to endogenous estrogens including not having children, delaying first childbirth, not breastfeeding, early menarche (the first menstrual period) and late menopause are suspected of increasing lifetime risk for developing breast cancer.
However, not only sex hormones, but also insulin levels are positively associated with the risk of breast cancer.
Pregnancy, childbearing and breastfeeding
Lower age of first childbirth, compared to the average age of 24, having more children (about 7% lowered risk per child), and breastfeeding (4.3% per breastfeeding year, with an average relative risk around 0.7) have all been correlated to lowered breast cancer risk in large studies. Women who give birth and breast-feed by the age of 20 may have even greater protection.In contrast, for instance, having the first live birth after age 30 doubles the risk compared to having first live birth at age less than 25. Never having children triples the risk. However the risks involved in having a child are significant.
Hormonal contraception
Hormonal contraceptives may produce a slight increase in the risk of breast cancer diagnosis among current and recent users, but this appears to be a short-term effect. In 1996 the largest collaborative reanalysis of individual data on over 150,000 women in 54 studies of breast cancer found a relative risk (RR) of 1.24 of breast cancer diagnosis among current combined oral contraceptive pill users; 10 or more years after stopping, no difference was seen.Further, the cancers diagnosed in women who had ever used hormonal contraceptives were less advanced than those in nonusers, raising the possibility that the small excess among users was due to increased detection.
The relative risk of breast cancer diagnosis associated with current and recent use of hormonal contraceptives did not appear to vary with family history of breast cancer.
Some studies have suggested that women who began using hormonal contraceptives before the age of 20 or before their first full-term pregnancy are at increased risk for breast cancer, but it is not clear how much of the risk stems from early age at first use, and how much stems from use before the first full-term pregnancy.
Hormone replacement therapy
Data exist from both observational and randomized clinical trials regarding the association between menopausal hormone replacement therapy (menopausal HRT) and breast cancer.The largest meta-analysis (1997) of data from 51 observational studies, indicated a relative risk of breast cancer of 1.35 for women who had used HRT for 5 or more years after menopause.
The estrogen-plus-progestin arm of the Women's Health Initiative (WHI), a randomized controlled trial, which randomized more than 16,000 postmenopausal women to receive combined hormone therapy or placebo, was halted early (2002) because health risks exceeded benefits.
One of the adverse outcomes prompting closure was a significant increase in both total and invasive breast cancers (hazard ratio = 1.24) in women randomized to receive estrogen and progestin for an average of 5 years.
HRT-related breast cancers had adverse prognostic characteristics (more advanced stages and larger tumors) compared with cancers occurring in the placebo group, and HRT was also associated with a substantial increase in abnormal mammograms. Short-term use of hormones for treatment of menopausal symptoms appears to confer little or no breast cancer risk.
A correlation was found between the use of hormonal contraceptives and subsequent reliance on hormone replacement therapy.
Hormonal therapy
Hormonal therapy has been used for chemoprevention in individuals at high risk for breast cancer. Overall it is recommended only in very special circumstances. In 2002, a clinical practice guideline by the US Preventive Services Task Force (USPSTF) recommended that "clinicians discuss chemoprevention with women at high risk for breast cancer and at low risk for adverse effects of chemoprevention" with a grade B recommendation.Selective estrogen receptor modulators (SERMs)
The guidelines were based on studies of SERMs from the MORE, BCPT P-1, and Italian trials. In the MORE trial, the relative risk reduction for raloxifene was 76%.[65] The P-1 preventative study demonstrated that tamoxifen can prevent breast cancer in high-risk individuals. The relative risk reduction was up to 50% of new breast cancers, though the cancers prevented were more likely estrogen-receptor positive (this is analogous to the effect of finasteride on the prevention of prostate cancer, in which only low-grade prostate cancers were prevented). The Italian trial showed benefit from tamoxifen.Additional randomized controlled trials have been published since the guidelines. The IBIS trial found benefit from tamoxifen.
In 2006, the NSABP STAR trial demonstrated that raloxifene had equal efficacy in preventing breast cancer compared with tamoxifen, but that there were fewer side effects with raloxifene.
The RUTH Trial concluded that "benefits of raloxifene in reducing the risks of invasive breast cancer and vertebral fracture should be weighed against the increased risks of venous thromboembolism and fatal stroke".
On September 14, 2007, the US Food and Drug Administration approved raloxifene (Evista) to prevent invasive breast cancer in postmenopausal women.
Endocrine disruptors
Many xenoestrogens (industrially made estrogenic compounds) and other endocrine disruptors are potential risk factors of breast cancer.Diethylstilbestrol (DES) is a synthetic form of estrogen. It has been used between the early 1940s and 1971. Pregnant women took DES to prevent certain pregnancy complications.
However, it also increased their risk of breast cancer. It also increased the risk of breast cancer in the prenatally exposed daughters after they have reached an age 40 years.
Furthermore, there is exposure to endocrine disruptors from the environment, in addition to phytoestrogens mentioned above in the diet section. See xenoestrogens in environmental factors below
Factors in the physical environment
According to a review, the main mechanisms by which environmental compounds increase breast cancer risk are acting like hormones, especially estrogen, or affecting susceptibility to carcinogenesis.The evidence to date generally supports an association between breast cancer and polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). dioxins and organic solvents, on the other hand, have only shown an association in sparse and methodologically limited studies, but are suggestive of an association. Overall, however, evidence is still based on a relatively small number of studies.
Tobacco
Until recently, most studies had not found an increased risk of breast cancer from active tobacco smoking.Beginning in the mid-1990s, a number of studies suggested an increased risk of breast cancer in both active smokers and those exposed to secondhand smoke compared to women who reported no exposure to secondhand smoke.
By 2005 enough evidence had accumulated for the [California Environmental Protection Agency] to conclude that breathing secondhand smoke causes breast cancer in younger, primarily premenopausal women.
The Agency concluded that the risk was increased by 70%, based on epidemiological studies and the fact that there are many mammary carcinogens in secondhand smoke.
The following year (2006) the US Surgeon General identified the same risk increase and concluded that the evidence is "suggestive," one step below causal.
There is some evidence that exposure to tobacco smoke is most problematic between puberty and first childbirth.
The reason is that breast tissue appears most sensitive to chemical carcinogens breast cells not fully differentiated until lactation.
The likely reason that the older studies of active smoking did not detect risks associated with smoking was that they compared active smokers to all nonsmokers (which includes many passive smokers).
The newer studies, which exclude passive smokers from the control group, generally show elevated risks associated with active as well as passive smoking.
Passive smoking
Breathing secondhand smoke increases breast cancer risk by 70% in younger, primarily pre-menopausal women.The California Environmental Protection Agency has concluded that passive smoking causes breast cancer and the US Surgeon General has concluded that the evidence is "suggestive," one step below causal.
There is some evidence that exposure to tobacco smoke is most problematic between puberty and first childbirth.
The reason that breast tissue appears most sensitive to chemical carcinogens in this phase is that breast cells are not fully differentiated until lactation.
Radiation
Women who have received high-dose ionizing radiation to the chest (for example, as treatments for other cancers) have a relative risk of breast cancer between 2.1 to 4.0.The risk increases with increased dose. In addition, the risk is higher in women irradiated before age 30, when there is still breast development.
Light at night and disturbance of circadian rhythm
In 1978 Cohen et al. proposed that reduced production of the hormone melatonin might increase the risk of breast cancer and citing "environmental lighting" as a possible causal factor.Researchers at the National Cancer Institute (NCI) and National Institute of Environmental Health Sciences conducted a study in 2005 that suggests that artificial light during the night can be a factor for breast cancer by disrupting melatonin levels.
In 2007, "shiftwork that involves circadian disruption" was listed as a probable carcinogen by the World Health Organization's International Agency for Research on Cancer. (IARC Press release No. 180).
Multiple studies have documented a link between night shift work and the increased incidence of breast cancer.
A review of current knowledge of the health consequences of exposure to artificial light at night including the increased incidence of breast cancer and an explanation of the causal mechanisms has been published in the Journal of Pineal Research in 2007.
Racial and Socio-Economic Factors
Incidence and mortality vary with race and social status. Incidence rises with improving economic situation, while mortality is tied to low economic status.In the US incidence is significantly lower and mortality higher among black women and this difference appears to persist even after adjustment for economic status.
It is currently unclear if significant racial differences in incidence and mortality persist after adjustment for economic status between women of white, Hispanic and Asian origin in the US.
Several studies have found that black women in the U.S. are more likely to die from breast cancer even though white women are more likely to be diagnosed with the disease.
Even after diagnosis, black women are less likely to get treatment compared to white women.
Scholars have advanced several theories for the disparities, including inadequate access to screening, reduced availability of the most advanced surgical and medical techniques, or some biological characteristic of the disease in the African American population.
Some studies suggest that the racial disparity in breast cancer outcomes may reflect cultural biases more than biological disease differences.
However, the lack of diversity in clinical trials for breast cancer treatment may contribute to these disparities, with recent research indicating that black women are more likely to have estrogen receptor negative breast cancers, which are not responsive to hormone treatments that are effective for most white women.
Research is currently ongoing to define the contribution of both biological and cultural factors.
Part of the differences in incidence that is attributable to race and economic status may be explained by past use of hormone replacement therapy
Factors with inconclusive research
Tea
One research published in 2009 has show that moderate green or black tea consumption (three or more cups per day) can reduce breast cancer risk by 37% in women younger than 50 years old, comparing with women who drank no tea at all. But no association was found for overall women.However that study has been criticized for inaccuracy and another study found no substantial association between breast cancer and tea consumption in the overall, but found a weak inverse association between caffeine-containing beverages and risk of postmenopausal breast cancer.
Specifically about green tea, one study has found significant inverse association between risk of breast cancer and green tea intake in Asian women who were low soy consumers.
Factors with minimal or no impact
Abortion
The abortion-breast cancer (ABC) hypothesis (supporters call it the abortion-breast cancer link) posits induced abortion increases the risk of developing breast cancer; it is a controversial subject and the current scientific consensus has concluded there is no significant association between first-trimester abortion and breast cancer risk.Bras
There is no scientific evidence to prove that any kind of Brassiere can cause cancer.Deodorants
Much has been made of the possible contribution of aluminum-containing underarm antiperspirants to the incidence of breast cancer, since the most common location of a breast cancer is the upper outer quadrant of the breast.Aluminum salts, such as those used in anti-perspirants, have recently been classified as metalloestrogens.
In research published in the Journal of Applied Toxicology, Dr. Philippa D. Darbre of the University of Reading has shown that aluminum salts increase estrogen-related gene expression in human breast cancer cells grown in the laboratory.
Fortunately, this in-vitro association between aluminum salts and estrogen activity does not translate into an increased risk of breast cancer in humans.
The lack of association between underarm deodorants and breast cancer has been the subject of a number of research articles.
Fertility treatments
There is no persuasive connection between fertility medications and breast cancer.Folic acid (folate)
The results of the studies about the influence of dietary folic acid on breast cancer have been contradictory.Viruses
Several kind of viruses are suspected to play a role or cause breast cancer, among them human papilloma virus, human cytomegalovirus and the Epstein-Barr virus.The human papilloma virus is well known for its capability to immortalize breast cancer cells which is used in research, however the role of this viruses in human breast cancer remains controversial.
Humans are not the only mammals susceptible to breast cancer. Some strains of mice, namely the house mouse (Mus domesticus) are prone to breast cancer which is caused by infection with the mouse mammary tumour virus (MMTV or "Bittner virus" for its discoverer Hans Bittner), by random insertional mutagenesis.
This finding is taken to mean that a viral origin of human breast cancer is at least possible, though there is no definitive evidence to support the claim that MMTV causes human breast cancer.
For example, there may be critical differences between cancer pathogenesis in mice and people. A human homologue of the mammary virus has been described in 1971 and linked to human breast cancer in several small epidemiologic studies.
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