Breast cancer and its association with alcohol
Worldwide, more than a million women are However, while the association is consistent and
diagnosed with breast cancer every year, considered confirmed for consumers of three
accounting for 10% of all new cancers and 23% or more drinks per day (Rosenberg et al. 1993,
of all female cancer cases. Breast cancer incidence Longnecker 1994, van den Brandt et al. 1995,
rates vary considerably, with the highest rates in Swanson et al. 1997, Suzuki et al. 2010, Zhang and
the developed countries and the lowest rates in Holman 2011), for consumers of one to two drinks
developing countries (Cancer Research UK 2008). per day, the data is less consistent or erratic (Flatt
Breast cancer is the most common cancer in et al. 2010). Indeed, it has been suggested that
women in Australia, UK and the USA, where one in the relationship between alcohol consumption
eight women will be diagnosed with breast cancer and breast cancer is linear (Bowlin et al. 1997,
in Australia before the age of 85 (AIHW 2008), one Smith-Warner et al. 1998, Hamajima et al. 2003,
in nine will be diagnosed at some stage in their life Thygesen et al. 2008, Chen et al. 2011) or increases
in the UK (UK Office for National Statistics 2007), monotonically (Ellison et al. 2001, Tjonneland et al.
and one in four will be diagnosed at some stage 2003, Thygesen et al. 2008) for the average daily
in their life in the USA (CDC 2007). Breast cancer amount of alcohol consumed. The highest risk
incidence rates continue to increase with age, with has been associated with consumption of six or
the greatest rate of increase immediately prior to more drinks per day (Chen et al. 2011). It has also
been suggested that consumption patterns may
modify risk (Morch et al. 2007, Chen et al. 2011),
An association between alcohol consumption of such that the consumption of four to five drinks breast cancer
consumed per session may increase/double risk
The first purported positive association between by 50% compared to only one drink consumed per
alcohol consumption and breast cancer was session. Paradoxically, alcohol dependence does
reported in 1977 (Williams and Horm 1977), and not increase the risk of breast cancer (Kuper 2000).
since then approximately 100 epidemiological
studies have been published, which consistently It has also been suggested, but not substantiated,
support such as association (Longnecker 1994, Key that there is a positive relationship between the
et al. 2006). This association has been observed for duration (and hence accumulated amount) of
both pre- and post-menopausal women of all ages, alcohol consumption over the lifespan of a woman
and is observed to be independent of the type of and her risk of breast cancer, although age at
alcoholic beverage consumed (Rosenberg et al. commencement of alcohol consumption appears
1993, Longnecker 1994, Bowlin et al. 1997, Hamajima to be irrelevant (Longnecker et al. 1995a, 1995b,
et al. 2003, Petri et al. 2004, Key et al. 2006). The Bowlin et al. 1997, Swanson et al. 1997, Terry et
association may also be more significant for certain al. 2006, Chen et al. 2011). For example, the risk of
subtypes of breast cancer for example, hormone- breast cancer appears similar for cumulative alcohol
sensitive rather than hormone-insensitive subtypes consumption prior to 40 years of age and after 40
(Millikan et al. 2008, Dolle et al. 2009, Kwan et al. years of age (Chen et al. 2011). Again it has been
2009, Li et al. 2010, Kabat et al. 2011).
suggested but not substantiated that there is long
latency between onset of alcohol consumption
and onset of breast cancer of approximately 20 has been proposed that alcohol may modify the
years (Willett and Stampfer 1997, Thygesen et al. significance of these risk factors, and in particular,
2008), although some studies conversely suggest act additively with those risk factors that influence
that recent consumption is a better predictor the concentration of hormones in plasma. It has
of risk compared to retrospective consumption also been proposed that the factors other than
due to confounders such as aging, hormonal/ family history, may act additively with the family
menopausal status and body mass index (Ellison history risk factor, and also, that some of these risk
et al. 2001, Horn-Ross et al. 2004, McDonald et al. factors may be limited to those women who have
2004, Tjonneland et al. 2004, 2007).
a positive family history of breast cancer (Gapstur
et al. 1992, Horn-Ross et al. 2004). Consequently, it
In addition, light to moderate alcohol consumption has been proposed but not proven that the positive
after diagnosis of breast cancer generally does association between alcohol and breast cancer
not appear to be associated with a recurrence of may be restricted primarily to women who have a
breast cancer (Reding et al. 2008, Flatt et al. 2010), positive family history of breast cancer (Vachon et
although increased body mass index may influence al. 2001).
any association (Homes et al. 1999, Kwan et al. 2010).
Further, light to moderate alcohol consumption Potential interaction between steroid hormones
after diagnosis of breast cancer also appears also and alcohol
not be associated with overall mortality (Holmes et Concerning the plasma concentration of the sex
al. 1999, Dal Maso et al. 2008, Franceschi et al. 2009, or steroid hormones as a risk factor for breast
Kwan et al. 2010), or it may actually reduce the risk cancer, there is a positive association between
of overall mortality (Reding et al. 2008, Barnett et al. the risk of development of breast cancer and the
2008). There may, however, be an association with concentration of these hormones for both pre- and
heavier consumption in developing, for example, post-menopausal women; the steroid hormones
estrogen receptor positive breast cancer in the include androgens, such as testosterone, and
contralateral breast (Li et al. 2009).
estrogens, such as estradiol, estrone and estriol
Risk factors for breast cancer and alcohol
(Brinton et al. 1986, Bergkvist et al. 1989, Colditz et
al. 1990, Steinberg et al. 1991, Colditz et al. 1995,
The errancy of the data suggests that causation of Dorgan et al. 2001, The Endogenous Hormones
breast cancer may be multi-factorial. The primary and Breast Cancer Collaborative Group 2002, Kaaks
risk factors for breast cancer are purported to be: et al. 2005a,b, Eliassen et al. 2006). One source of
lifestyle; inherited gene mutations and hence family endogenous estrogens is the aromatization of
history; medical history; reproductive history (such androgens to estrogens, and alcohol has been
as early menarche, nulliparity and late menopause); observed to increase this aromatization; the
endogenous/exogenous hormones (such as conversion occurs primarily in the ovary for pre-
hormone replacement therapy); body mass index; menopausal women and peripherally for post-
and environmental exposure to carcinogens. It menopausal women (Figure 1).
Figure 1. Primary mechanisms for the production of estrogens
In pre-menopausal women: dehydroepiandrosterone (DHEA) ——> androgens (testosterone) ———> estrogens (estradiol) In post-menopausal women: androgens (androdstenedione) ———> estrogens (estrone)
Breast cancer and its association with alcohol - 2
An elevated concentration of testosterone or in plasma which is positively associated with a
estradiol may increase the risk of breast cancer decreased risk of mortality from cardiovascular
approximately six- and five-fold, respectively disease. For example, from a meta-analysis of 38
(Dorgan 1994, 1996), where the risk may be epidemiological studies by Longnecker in 1994,
proportional to concentration (The Endogenous daily consumption of one alcoholic drink was
Hormones and Breast Cancer Collaborative Group associated with an 11% (7 to 16%) increased risk
2002). Indeed, Reichman et al. (1993) observed in of breast cancer compared with abstainers while
pre-menopausal women that the concentration from a subsequent meta-analysis of 53 studies by
of DHEA sulfate, testosterone and estradiol Clavel-Chapelom in 2002, daily consumption of one
increased across the menstrual cycle following the alcoholic drink was associated with only a 7.1% (5.5
consumption of alcohol as did Muti et al. (1997) to 8.7%) increased risk. Furthermore, the pattern of
and Rinaldi et al. (2006). The increase in sulfated alcohol consumption influences the concentration
DHEA implies that alcohol may also increase the of the steroid hormones circulating in plasma, such
production of DHEA sulfate in the adrenal cortex that chronic and heavy intake of alcohol is observed
through its effect on the hypothalamic-pituitary- to lead to early menopause, a lower concentration
adrenal axis (Rivier 1996, Dorgan 2001). Gavaler of gonadotrophins post-menopausally and an
and van Thiel (1992) and Rinaldi et al. 2006 reported increased concentration of the steroid hormones
similar observations in post-menopausal women post-menopausally (Gavaler and van Thiel 1987).
and Hankinson et al. (1995, 1998) also reported an
increase in the plasma concentration of estrone, Potential interaction
which is purported to be a primary source of replacement therapy and alcohol
estradiol in breast cancer cells, following the Post-menopausal women on estrogen replacement
consumption of alcohol. Furthermore, the effect therapy (ERT) who consume alcohol are generally
of alcohol on the sex hormones is both acute and observed to have a significantly elevated plasma
concentration of estradiol as compared with women
not using ERT (Ginsberg et al. 1996 and Gavalar
The data shows also that there is a dose dependent 1998). Ginsberg et al. (1996) observed an increase
response to alcohol on the aromatization of of approximately 300%, which corresponds to the
testosterone and on the subsequent concentration preovulatory peak in the menstrual cycle, where the
of estradiol in plasma, which then peaked and changes in the circulating concentration of estradiol
plateaued (Longnecker et al. 1995); this was significantly correlated with changes in the blood
consistent with the risk of breast cancer in concentration of alcohol on both the ascending
consumers of alcohol compared to abstainers and descending limbs of the blood alcohol curve.
(Longnecker et al. 1988). Purported mechanisms The plasma concentration of this steroid hormone,
by which alcohol may increase the concentration which correlated with the plasma concentration
of steroid hormones include: stimulation of of follicle stimulating hormone (FSH), is correlated
ovarian theca cells to produce androgens through with total amount of alcohol consumed per week
increased pituitary luteinizing hormone secretion; (Gavalar 1998); interesting Gavalar also observed an
induction of androgen catabolism in the liver; and/ increase in the concentration of estrone. However,
or increased liver aromatase activity leading to an the interaction of alcohol and ERT is not simple as the
increased conversion of androgens to estrogens.
dose-response relationship of ERT is inverse when a
The question remaining is at what level of moderate amount of alcohol is consumed (Gavaler
moderate consumption the elevation of risk 1998).
occurs, and then relative risk (risk benefit ratio) Consequently, accumulating data suggests that
when compared with other causes of death, such alcohol consumption is most strongly associated
as cardiovascular disease, which increases in post- with the risk of breast cancers that are hormonally
menopausal women as a consequence of a reduced responsive, such as lobular (5-10% of all cancers)
concentration of estradiol in plasma; estrogens and hormone receptor positive tumors (estrogen
significantly lower the concentration of cholesterol receptor positive (ER+), such as ER+PR+ and ER+PR-
Breast cancer and its association with alcohol - 3
subtypes) (66%) (Enger et al. 1999, Li et al. 2003,
cancer, the gene has been observed to be mutated
Terry et al. 2006, Suzuki et al. 2008, Li et al. 2010,
in 15 to 50% of tumors (Olivier and Hainaut 2001).
Kabat et al. 2011) as well as with the risk of tubular
(2%) (Rosenberg et al. 2006); this is consistent with
The concurrent consumption of alcohol and folate
data suggesting that ERT is most strongly associated
(at least 300 mg/day) has been observed to reduce
with lobular cancers (Li et al. 2000, 2008, 2010,
the relative risk of alcohol-induced breast cancer
Zanetti-Dallenbach et al. 2008). Data also suggests
to 1.05 for women consuming greater than 15
that no or a negative association observed for triple
g alcohol/day or one and a half standard drinks,
negative breast cancer (ER-/PR- or ER-/PR) or basal-
but was only 0.55 for women consuming greater
like breast cancer (Millikan et al. 2008, Dolle et al.
than 600 mg/day of folate. Indeed, the concurrent
2009, Kwan et al. 2009, Trivers et al. 2009, Kabat et
supplements reduces the relative risk to 0.74 for
women consuming greater than 15 g alcohol/day
The suggestion of a further increased risk of breast
compared to those not using vitamins (Zhang et al.
cancer by post-menopausal woman who use ERT
1999). The interaction between alcohol and folate
and who are also light to moderate consumers
has been observed to be primarily limited to estrogen
of alcohol remains controversial (Suzuki et al.
receptor negative (ER-) breast cancer tumors (Zhu
2005, Nielsen and Gronbaek 2008), in particular
and Williams 1998, Sellers et al. 2002, Zhang et al
as ERT decreases the risk of other diseases such
2005), which is consistent with an interaction of
as cardiovascular disease (Ross et al. 1981, Szklo
alcohol and folate on breast tissue tumors being
et al. 1984, Stampfer et al. 1985), osteoporosis
mainly through the primary metabolite of alcohol,
(Hutchinson et al 1979, Weiss et al. 1980, Paganini-
acetaldehyde, which is directly carcinogenic as
Hill et al. 1981), and dementias such as Alzheimer’s
well as indirectly carcinogenic via folate depletion,
disease (Tang et al. 1996, Zuccala et al. 2001, Ganguli,
independent of circulating estrogens and estrogen
et al. 2005, Stampfer et al. 2005, McDougall et al.
2006, Reid et al. 2006, Wright et al. 2006) and hence
decreases the risk of death from all causes (Bush et
Potential interaction between inherited gene
al. 1983, Criqui et al. 1988, Thun et al. 1997). mutations and alcohol Inherited mutations in the BRCA-1 and BRC-2 Potential interaction between folate and alcohol
genes confer significantly increased lifetime risks
An adequate consumption of folate, however, may
of breast cancer, in particular for BRCA-1 mutation
reduce the increased risk of breast cancer associated
carriers less than 50 years of age (Wooster et al.
with alcohol consumption (Zhang et al. 1999, 2005,
1995; Tavtigian et al. 1996, Antoniou et al. 2003).
Rohan et al. 2000, Sellers et al. 2001, Baglietto et al
In contrast to the general population, light to
2005, Stolzenberg-Solomon et al. 2006, Tjonneland
moderate alcohol consumption does not appear
et al. 2005, 2006). For example, while alcohol
to increase the risk of breast cancer in women
interferes with DNA synthesis and repair, folate is
carrying a BRCA-1 gene mutation although higher
involved in DNA synthesis, repair and methylation.
amounts may be multiplicative (McGuire et al. 2006,
In animal models, folate supplementation reduces
Dennis et al. 2010, Dennis et al. 2011), which may
DNA strand breaks in the p53 gene (Kim et al. 2000);
reflect hormone receptor status; estrogen receptor
the P53 protein regulates the cell cycle to prevent
negative tumors account of 80% of tumors in BRCA-
genome mutation, and hence functions to suppress
1 mutation carriers (Foulkes et al. 2004, McDonald et
tumors. It can activate DNA repair proteins when it
al. 2004, Zhang et al l 2007). Risk appears increased in
recognizes damaged DNA, hold the cell cycle at the
women carrying a BRC-2 gene mutation and appears
G1/S regulation point on DNA damage recognition
additive with increased body mass index (Dennis
to prevent uncontrolled cell division and can
et al, 2011). Light to moderate wine consumption,
initiate apoptosis, the programmed cell death, if
however, actually may be protective for BRCA-1 but
the DNA damage proves to be irreparable. Cancer
not BRCA-2 mutation carriers (Dennis et al. 2010,
occurs when the rate of proliferation of mutated
cells greatly exceeds the rate of apotosis. In breast
Breast cancer and its association with alcohol - 4
Other potential mechanisms of action for alcohol activation of these enyzmes (Anderson et al. 1995). in breast cancer
While these observations are yet to be confirmed in
Concerning biological or environmental exposure, human breast tissue, the induction of cytochrome
alcohol is purported to influence the local and P4502E1 is associated with an increased production
systemic metabolism of mammary carcinogens. Risk of reactive oxygen species that are associated with
is the sum of numerous factors, each with a small DNA damage including single and double strand
risk, such that the summed risk is high from the breakage (Wright et al. 1999, Koch et al. 2004),
enhancing or synergistic effects or influences of the where breast tissue tumors contain an approximate
risk factors. It is suggested that approximately 50% nine-fold higher concentration of these DNA
of breast cancer is not related to genetic/hormonal modifications (Li et al. 1999).
risk factors, but is related to the environment as Alcohol may additionally influence alterations in cell
observed from cultural/geographic correlations cycle behaviour such as cell cycle duration leading
for risk. With respect to environmental exposure to to the hyperproliferation of mutated cells, that is,
carcinogens, metabolism in the body may either uncontrolled cell division; nutritional deficiencies,
activate or detoxify the carcinogen. For example:
such as methyl-, vitamin E-, folate- pyridoxal
carcinogen —> toxic intermediates —> detoxified —>excreted phosphate-, zinc- and selenium-deficiencies;
and alterations of the immune system eventually
resulting in an increased susceptibility to certain
virus infections such as hepatitis B virus and hepatitis
whereby, a decrease in or inhibition of metabolism, There is also accumulating data that the primary
increases the exposure of the circulating carcinogen metabolite of alcohol, acetaldehyde, is partly
in the blood to organs/tissues, such as the breast.
responsible for alcohol-associated carcinogenesis.
Because alcohol is not itself genotoxic and nor Acetaldehyde is directly carcinogenic and
tumorigenic in animals, potential mechanisms mutagenic interfering with both DNA synthesis
for the positive association between alcohol and repair. It also binds to cellular proteins and DNA
and breast cancer include the facilitation of forming stable protein and DNA adducts, which
carcinogens into cells, the induction of carcinogen result in physical and functional impairment of the
activating enzymes, the inhibition of DNA repair cell and consequently in an immunological cascade
and the promotion of tumors. Potential ubiquitous reaction, and in the occurrence of replication
carcinogens include N-nitrosamines, to which errors and/or mutations in oncogenes or tumor
people are exposed from sources such as tobacco suppressor genes (Dellarco 1988, Fang and Vaca
and N-nitrosodimethylylamine (NDMA). The former 1995, Nakamura et al. 2003). Acetaldehyde also
carcinogen is metabolized by cytochrome P4502E1 degrades folate in the colon, where a folate dietary
enzymes in the liver, such that in the presence deficiency has been associated with an increased
of alcohol, this metabolism is inhibited and the risk of breast, pancreatic and colon cancer (Gloria et
unmetabolized carcinogen circulates in the blood al. 1997, Duthie et al. 2000, Hussien et al. 2005).
together with the alcohol. The coexposure of the Alcohol is metabolised to acetaldehyde by the
carcinogen and alcohol to tissues has been observed enzyme alcohol dehydrogenase (ADH), where
approximately 96-98% of ADH activity occurs in the
In addition, cytochrome P4502E1 enzymes have liver but it also expressed and regulated by other
been observed in animal breast tissue and there tissues including breast tissue (Seitz et al. 1998,
is greater expression of these enzymes in breast Wright et al. 1998, Triano et al. 2003). Individuals
tissue tumors compared to normal breast tissue, differ in their ability to metabolise alcohol because
such that high concentration of circulating of genetic differences in ADH; ADH is encoded by
carcinogen may be activated by the cytochrome at least five different genes that result in enzyme
P4502E1 enzymes and/or alcohol may induce the classes of different metabolic activity for alcohol and
Breast cancer and its association with alcohol - 5
hence concentration of circulating acetaldehyde Although animal studies show that alcohol does
(Bosron and Li 1986). For example, Class 1 ADH not initiate or promote tumorogenesis and may
polypeptide subunits are encoded by three specific actually decrease the incidence of tumors, some
gene loci, ADH1A (_ ), ADH1B (_ ) and ADH1C studies also show that alcohol may effect or enhance
( ) where, in vitro, the (_ )-a polypeptide subunit metastasising tumors (Weiss et al. 1995, Swanson et
encoded by the ADH1C*1 variant metabolises al. 1997), and that this effect is dependent on the
alcohol to acetaldehyde 2.5-times faster than stage of alcohol consumption, that is, pre- or post-
the ADH1C*2 variant (Lee et al. 2006), and the - treatment with a carcinogen, and on the amount of
1 polypeptide subunit encoded by the ADH1B*2 alcohol consumed. While it is unknown what stage
variant metabolises alcohol to acetaldehyde 100- of carcinogenesis is affected by alcohol, recent
times faster than the subunits encoded by the research implies that alcohol acts at a late stage of
ADH1B*1 variant, but has a lower affinity for alcohol carcinogenesis (Weiss et al. 1995, Swanson et al.
(Hurley et al, 1990). Several studies have examined 1997).
an association between the different polypeptide
subunits and risk of breast cancer with conflicting Conclusions
and hence inconclusive results (Freudenheim et al. While there is an indisputable association between
1999, Hines et al. 2000, Lilla et al. 2005, Sturmer et alcohol consumption and the risk of breast cancer,
al. 2005, Terry et al, 2006, Visvanathan et al. 2007, the mechanisms behind the association require
Kawase et al. 2009, Larsen et al. 2010). Results further elucidation. This risk of breast cancer
from one recent study supports an association should not, however, be considered in isolation
between ‘fast’ metabolisers of alcohol per se and from the risk of other factors for mortality, such as
hence the ‘fast’ appearance of acetaldehyde and an cardiovascular disease, whereby cardiovascular
increased risk of breast cancer (Terry et al. 2006), disease is the primary cause of mortality in the
where women with the fast metabolising ADH1C*1 industrialised or westernised world. Indeed, the light
variant and hence ADH1C*1,1 genotype have been to moderate consumption of alcohol is associated
observed to be 1.8-times more at risk for breast with a significantly reduced risk of mortality from
cancer than women with other genotypes (Coutelle cardiovascular disease and from all causes, for
et al. 2004). Intriguingly, the expression of ADH1 is both men and women, irrespective of age and
breast tissue is decreased in invasive breast cancers ethnicity (Boffetta and Garfinkel 1990, Marmot
(Triano et al. 2003). The results of another recent and Brunner 1991). Thus, it may be advisable for
study, however, also suggests that slow converters women to enumerate and evaluate their risk factors
of alcohol to acetaldehyde may also be at increased for cardiovascular disease and for breast cancer, in
risk of developing breast cancer, which implies that addition to the amount and pattern of their alcohol
both alcohol and its primary breakdown product consumption, before considering abstaining from
acetaldehyde could be contributing compounds alcohol. Creina Stockley MSc Clinical Pharmacology, MBA; is Health and Regulatory Information Manager, AWRI and a member of AIM’s Social Scientific and Medical Council.
Breast cancer and its association with alcohol - 6
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GUIDE TO EXTRAVASATION MANAGEMENT IN ADULT & PEDIATRIC PATIENTS Large, well-designed, controlled clinical trials RELATED POLICIES in humans are not available to support theNursing Standard of Practice & Procedures: 1) Extravasations, Patient Management of 2) Care of the Patient by a Non-Chemotherapy Certified RN guidelines. Available data generally consists ofcase reports, trial
(The Memoirs of an Interesting and Unusual Girl)We've all heard how men and women are created equal; their journeys, however, are not. Occasionally there comes a life that spans the human condition. A life comedic, tragic, and compelling. A life spent in migration, character forged in pain, innocence dashed on misplaced trust. Hers is a life which she now views with humor, poignancy and meaning