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anincreased risk of overall cancer risk, especially increasing the endometrioid sub-
type. On the contrary, the use of continuous estradiol-progestin, estradiol+intra-
uterine levonorgestrel intrauterine system, or tibolone had no signicant effect on
overall ovarian cancer risk [49]. Therefore, only sequential use of estradiol + pro-
gestin increases the overall risk of ovarian cancer.
A subsequent study from the same research group reported the incidence of pri-
mary fallopian tube cancer and the use of hormone therapy in women aged 50 or
older, which was identied from the Finnish Cancer Registry, excluding cases with
a previous salpingectomy [50]. The use of 5years or more of estradiol combined
with the levonorgestrel-releasing intrauterine system and the use of sequential estra-
diol and progestin treatment were both associated withan increased risk of fallopian
tube cancer. On the contrary, the treatment with only estradiol or continuous estra-
diol and a progestin did not increase the risk of the cited cancer.
5.4.5 Assisted Reproductive Technology
There is controversy regarding any possible increase in ovarian cancer risk in
women subject to assisted reproductive technology. It is likely that medication used
for fertility treatments may increase the risk of borderline ovarian tumors [51, 52].
However, results seem to depend on the fact of achieving or not pregnancy. It seems
that women who are successfully treated for infertility and give birth do not display
an increased ovarian cancer risk, when compared to those that remain nulliparous.
The latter women have a higher risk of EOCs. Another explanation could be that
infertility, per se, and not the used treatment, be the cause of an increased ovarian
cancer risk [53].
5.4.6 Tubal Ligation, Salpingectomy, andHysterectomy
Fallopian tube ligation and hysterectomy (if performed before age 35) reduce the risk of
EOC, particularly non-serous cancers [54, 55]. An Australian Cancer Study, a Danish
register-based case-control study, the OC3, and the Million Women Study reported that
tubal ligation has different preventive effects according to histologic types, with protec-
tion being higher for high-risk serous, endometrioid, and clear- cell carcinomas, while
results are controversial regarding mucinous carcinomas [29, 30, 56–58].
The effect of salpingectomy on ovarian cancer risk has been compared to that
achieved with tubal ligation. Madsen etal. [57] and Falconer et al. [59], respec-
tively, reported that salpingectomy reduced EOC in the Danish register-based case-
control study and in a national US population-based study. Results suggest that
opportunistic bilateral salpingectomy, aimed at removing the site where ovarian
cancer might originate, should be recommended when women are hysterectomized
due to benign conditions and among those seeking tubal ligation [14, 60].
Opportunistic salpingectomy should be encouraged instead of tubal ligation or
performed at the time of hysterectomy in order to reduce the risk of future fallopian
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and ovarian cancers. However, data of large prospective studies are not available to
conrm the value of opportunistic salpingectomy in the prevention of ovarian can-
cer. On the other hand, there are ongoing trials comparing the effect of salpingec-
tomy (without oophorectomy) with delayed oophorectomy in BRCA mutation
carriers [61].
Reports indicate that hysterectomy in young women due to benign conditions,
with conservation of the fallopian tubes and the ovaries, may also reduce the risk of
ovarian cancer [29, 54, 55]. However, there is no sense of performing a hysterec-
tomy while preserving the fallopian tubes, if childbearing is over. Therefore, it is
recommendable that hysterectomy be carried out with concomitant opportunistic
salpingectomy. In addition, surgery for pelvic oor disorders treated by hysterec-
tomy can include vaginal opportunistic salpingectomy excision [62–64].
Opportunistic distal salpingectomy can also be performed during a cesarean section
in women who are sure they have completed their family [65].
The safety of opportunistic salpingectomy has been conrmed in large cohorts
[66]. However, the conrmation of the real value of opportunistic salpingectomy in
the prevention of ovarian cancer may require a 20–30-year follow-up. On the other
hand, salpingectomy has also been challenged as a risk-reducing intervention [67].
5.5 Anthropometric Variables
5.5.1 Body Weight
Birth weight has not been associated with ovarian cancer risk [68]. Prospective
studies assessing the effects of body fat at ages 5 and 10, body mass index (BMI) at
age 18, and other anthropometric measures have reported a small relationship
between height and EOC risk [69].
Data from the large prospective EPIC cohort indicate that obesity (BMI≥30.0kg/
m
2
vs. <25kg/m
2
) is associated with an increased EOC risk, although the associa-
tion was weaker in pre- versus postmenopausal women. Height, weight gain, and fat
distribution were not associated with an increased risk, although waist-hip ratio was
associated with a higher risk of mucinous tumors [70]. Results from the Nurse’s
Health and Women’s Health Initiative (WHI) cohorts failed to demonstrate any
inuence of obesity overovarian cancer risk [71, 72]. A recent study among African
American women pointed out that ovarian cancer risk was signicantly elevated in
women with a BMI≥40kg/m
2
as compared with those with a BMI<25, and there
was an association between this cancer risk and weight gain after age 18 comparing
the highest versus the lowest quartile. In postmenopausal women (MHT users and
nonusers), ovarian cancer risk increased by 15% per 5kg/m
2
increase of BMI or 6%
per 5kg of weight gain [73].
Despite this, a later meta-analysis of 47 studies reported a 12% increase in EOC
risk for obese women (>30kg/m
2
), after adjusting for different confounding factors
such as MHT use [74]. Furthermore, a morerecent meta-analysis of prospective
studies found a non-linear increase in ovarian cancer for each 5 units of BMI
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increase. This rise started with a BMI of 28kg/m
2
andhigher.In addition, there was
no association between ovarian cancer and weight gain, hip circumference, or waist-
hip ratio [75]. It is important to note that obesity does not seem to increase the risk
of the most aggressive (or lethal) cancers and that associations are similar
amongMHT users and nonusers [76].
Adult weight gain has been related to female endocrine-related cancers, particu-
larly among non-MHT users. Thus, a meta-analysis found that for each 5kg increase
in adult weight, ovarian cancer risk increased in postmenopausal women, both in
low MHT and non-MHT users [77]. These results suggest the importance of pre-
venting weight and obesity in young women.
The links between obesity and higher ovarian cancer risk are probably mediated
by alterations in sex steroid hormones, insulin- related alterations and inammation.
Excessive weight has been related to invasive endometrioid, low-grade invasive
serous, and invasive mucinous ovarian carcinomas as well as borderline serous
tumors. In addition, the risk is similar in postmenopausal MHT users and nonusers.
These studies provide evidence that excessive body weight is a modiable risk
factor for ovarian cancer, especially among postmenopausal women.
5.5.2 Height
It has been suggested that altered insulin growth factor (IGF) 1 levels may inuence
early-life body size and adulthood cancer risk. In the two cohorts of the Nurses’
Health Study, height was associated with anincreased relative risk of EOC [69]. A
pooled analysis of 12 prospective cohorts that collectively included more than a half
million women from North America and Europe reported that taller women (>1.69m
vs. <1.60m) have an increased EOC risk (both pre- and postmenopausal), while
there was no statistical difference observed between those with increased BMI com-
paredtothose with a normal BMI (BMI>29.9kg/m
2
vs. 18.5–23kg/m
2
) [78].
A meta-analysis of case-control studies found that IGF-1 and IGF binding pro-
tein- 3 levels were lower in patients with ovarian cancer [79]. Another meta-analysis
(of prospective studies) reported that there was no signicant inuence of IGF-1/
IGF binding protein-3 on the ovarian cancer risk [80].
5.6 Diet, Physical Activity, andOther Modifiable
Lifestyle Factors
5.6.1 Diet
Some diets have been postulated to protect against cancer. For example, the
Mediterranean diet might decrease the incidence of various cancers by genomic
actions and by increasing levels of the sex hormone-binding globulin [81, 82].
However, there is no signicant evidence demonstrating that the adherence to the
Mediterranean diet reduces ovarian cancer risk [83].
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A potential link between thedietary inammatory index and the risk of EOC was
analyzed among African American women. A 10% increase in EOC risk was
observed for each unit change in the energy-adjusted dietary inammatory index,
and this association was higher in women aged over 60 [84].
In a randomized controlled trial of postmenopausal women, the adherence to a
low-fat diet for 4years decreased ovarian cancer risk [85]. One meta-analysis found
that egg consumption wasrelated to ovary cancer, although the dose-response was
unclear. A signicant effect of egg intake on ovarian cancer has been reported in
case-control studies, but not in cohort studies [86].
Studies related to the vitamin D endocrine system and carcinogenesis have pro-
duced controversial results. In vitro studies suggest that vitamin D may have a role
in cancer prevention. Results from observational clinical studies are masked by con-
founding factors. However, Ong etal. [87] reported a signicant association between
decreased vitamin D levels in Europeans and ovarian cancer risk. They used a
Mendelian randomization assessment to overcome the usual statistical errors
observed in conventional studies. However, further studies are needed before rec-
ommendations can be proposed regarding vitamin D supplementation and ovarian
cancer risk.
Studies analyzing the association between dietary intake of acrylamide and EOC
risk have not been able to demonstrate any effect [88]. In a large prospective
Japanese cohort, no association was observed between acrylamide and ovarian can-
cer [89]. Other dietary components have not been associated with ovarian cancer
risk, including the intake of ber or of curcumin or a high-starch diet, although there
might be several confounding factors that have not been taken into account.
5.6.2 Physical Activity
The effect of recreational physical activity on ovarian cancer risk is inconclusive or
controversial [90]. The protective effect of recreational physical activity is more consis-
tent among case-control studies, while benets have been reported in some cohort stud-
ies [91]. Nevertheless, recent evidence shows that physical inactivity is independently
associated with an increased risk of someparticular histologic subtypes of EOC [92].
A prospective study assessing the effect of physical activity on ovarian cancer risk
found that in premenopausal women risk increased with low to high levels of cumula-
tive physical activity, while physical activity was not associated with ovarian cancer in
postmenopausal women [93]. These investigations, not completely comparable, pro-
vide controversial results that do not currently allow providing recommendations
regarding the preventive effect of physical activity on ovarian cancer risk.
5.6.3 Perineum Exposure toBody Powder andVaginal Douching
There is some evidence from case-control studies that the use of powder on the
perineum (genital powder) is associated with an increased EOC risk, but the data are
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conicting. The modest increased risk seems to be for invasive serous, endometri-
oid, and clear-cell carcinomas and borderline tumors in genital but not in non-
genital powder users [94]. The same study found no signicant trend in the risk with
increasing number of lifetime applications of genital powder. Despite this, a case-
control study of Afro-American women showed a dose-response effect for duration
and the lifetime number of applications of genital powder and EOC risk. In addi-
tion, non-genital powder use was linked to non-serous EOC [95]. A recent meta-
analysis of case-control and cohort studies reported that perineal talc use increases
ovarian cancer risk. In addition, this increased risk was signicant for serous and
endometrioid subtypes, although not for mucinous or clear-cell subtypes [96].
The prospective cohort Sister Study (involving 50,884 women with a sister with
breast cancer) found little association between baseline perineal talc use and subse-
quent ovarian cancer. Douching was more common among talc users, and douching
at baseline was associated with an increased subsequent risk of ovarian cancer. The
authors of the Sister Study concluded that douching, but not talc use, was associated
with an increased ovarian cancer risk [97].
5.6.4 Alcohol, Coffee, andTea Consumption
Alcohol consumption does not seem to inuence ovarian cancer risk [98, 99].
However, low alcohol consumption may reduce the risk of ovarian cancer, but this
may depend on the type of alcohol and the age at which it was consumed [100]. Red
wine consumption protects against ovarian cancer risk as compared with noncon-
sumption, but the consumption of white wine, beer, or spirits does do not confer
protection. The protection conferred by red wine is greatest when consumption is
initiated before the age of 50 [101].
It seems that coffee or tea consumption may not reduce EOC risk [102]. However,
higher black tea intake may have a protective effect against several cancer variants
[103]. A Danish case-control study reported that coffee consumption and total caf-
feine consumption (combination of tea and coffee) were associated with a small
reduction in ovarian cancer risk [104]. However, a Canadian study did not nd any
effect of coffee, tea, and caffeine intake on the ovarian cancer risk [105].
5.6.5 Cigarette Smoking
Cigarette smoking has been associated with certain histologic subtypes of ovarian
cancer [106]. The large Norwegian-Swedish Women’s Lifestyle and Health cohort
analyzed national registries according to different measures of smoking exposures
and adjusted for confounding factors. This study found that women who smoked for
more than 20years had three times the risk of developing borderline EOCs as com-
pared to never smokers, and there was an almost signicant relation for mucinous
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tumors. In addition, there was also a signicant dose-response effect with smoking
intensity and duration for both borderline and serous tumors [107].
The same authors reported new information from the Norwegian cohort regard-
ing smoking and primary invasive and borderline tumors by histologic types [108].
Current smokers who had smoked for more than 10years had a very much higher
risk of developing mucinous ovarian cancers than never smokers, but smoking was
not associated with serous or endometrioid ovarian cancers. The OC3 reported that
smoking 20 packs/year was associated with an increased risk of mucinous cancers
and a decreased risk for clear-cell cancers [30].
In Afro-American women, smoking was associated in a higher degree to serous
ovarian cancer than for all types of ovarian cancers. In addition, compared to never
smokers, serous ovarian cancer risk was increased in lifetime ever smokers, in for-
mer smokers who quit within 0–2years of diagnosis, and in relation to total pack-
years smoked among lifetime smokers. In addition, smoking was not associated
with mucinous ovarian cancer [109].
5.6.6 Nonsteroidal Anti-Inflammatory Drugs
andAnalgesic Treatment
Nonsteroidal anti-inammatory drugs (NSAIDs) and some analgesics may have
chemopreventive actions against cancer from different organs. Pooled data from
population-based and case-control studies of ovarian cancer reported that aspirin
use was associated with a lower ovarian cancer risk, while non-aspirin NSAIDs and
acetaminophen use was not. In addition, the reduction of cancer risk was strong
with daily aspirin use as compared with other dosages, while for non-aspirin
NSAIDs, the risk reduction was strong for high-dose use [110]. The same authors
also reported a prospective analysis of the OC3 regarding analgesic use and ovarian
cancer risk. They analyzed data from 13 studies, nding that women who use aspi-
rin daily have a slightly lower risk of developing ovarian cancer than infrequent/
nonusers [111]. This result was similar to the risk reduction observed in case- control
analyses.
Low-dose aspirin (150mg/day for ≥5years) may reduce the risk of EOCs in
terms of histological types, the strongest inverse associations observed for muci-
nous and endometrioid tumors [112].
The African American Cancer Epidemiology Study on the EOC risk analyzed
the effect of aspirin and non-aspirin NSAIDs and acetaminophen use on ovarian
cancer risk [113]. The study found that NSAIDs (aspirin and non-aspirin) signi-
cantly reduced this risk, while acetaminophen had no protective effect. It is likely
that ovarian follicle rupture during ovulation releases uid containing prostaglan-
dins and other compounds that induce inammation [114], which can potentially be
neutralized by NSAIDs. Therefore, small doses of NSAIDs may be a preventive
intervention for women at high risk of ovarian cancer. In addition, it seems that
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anti- inammatory drugs may improve ovarian cancer prognosis when used along
with chemotherapy [115].
5.6.7 Occupation Risk Factors forOvarian andPrimary
Fallopian Tube Cancer
The risk of EOC was examined according to occupation in a Canadian population-
based case-control study, adjusting for confounders (BMI, OC use, menopause hor-
mone therapy, previous genital surgery, among others). The authors reported an
increased risk of EOC for teaching and related occupations, bookkeepers and
accounting clerks, and educational service and noninstitutional health service
employees [116].
An Australian population-based case-control study assessed the association of
lifetime environment ultraviolet radiation exposure and both invasive and border-
line ovarian cancers in women aged 18–79years. Women in the highest tertile of
daily average of environment radiation exposure were at the lowest risk of EOCs
than those in the lowest tertile [117]. This study suggests that there is an inverse
association between ovarian cancer risk and ultraviolet exposure.
In a Scandinavian study, correlation between occupation and the risk of primary
fallopian tube cancer was reported among 2206 cases and more than 50 occupations
[118]. The authors found that the risk of primary cancer was signicant among
smelting workers, artistic workers, hairdressers, packers, nurses, shop workers, and
clerical workers. These ndings were sustained for the different included countries.
The risk was signicantly low for farm-working women, painters, and chemical
process workers.
5.7 Comorbidity andOvarian Cancer Risk
5.7.1 Endometriosis
Women who had endometriosis during their reproductive years are at a higher
risk of developing endometrioid and clear-cell tumors (type I EOC) [29]. The
older a woman is when ovarian endometriosis is diagnosed, the higher the risk
of ovarian cancer [119]. An international collaborative investigation comprising
13 case- control studies reported an association between a history of endome-
triosis and an increased risk of clear-cell, low-grade serous, and endometrioid
invasive cancers, while there was no association with the risk of mucinous or
high-grade serous invasive ovarian cancers or borderline serous and mucinous
tumors [120].
There is evidence for shared genetic risk between endometriosis and almost all
histologic types of ovarian cancer. The strongest correlation is between endometrio-
sis and clear-cell carcinoma and endometrioid and low-grade serous carcinomas,
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while high-grade serous carcinoma (which often arises from the fallopian tubes)
had a weaker genetic correlation with endometriosis [121]. These ndings suggest
shared genetic susceptibility factors.
A meta-analysis reported that endometriosis was associated with an increased
risk of EOC, and tubal ligation had a protective effect [80]. In that review, hysterec-
tomy did not have any signicant effect on ovarian cancer risk in women with endo-
metriosis. The relationship between endometriosis and malignant transformation to
ovarian cancer may be related to epigenetic factors exerting effects over the ectopic
endometrium [122].
To date, the protective role of opportunistic bilateral salpingectomy among
women with previous endometriosis has not been specically addressed.
5.7.2 Pelvic Inflammatory Disease
Pelvic inammatory disease/salpingitis increases the risk of serous borderline and
invasive ovarian cancers [123–125]. An Australian population-based study reported
an increased risk of high-grade serous ovarian carcinoma associated with pelvic
inammatory disease, but not with infertility or the diagnosis of endometriosis [31].
This data support the participation of inammatory processes in the carcinogenesis
of some epithelial ovarian cancers.
Although there are no reports addressing the value of salpingectomy in women
with inammatory adnexal processes, salpingectomy might exert the same protec-
tive role as it does in women without an inammatory process.
5.7.3 Long Menstrual Cycles andPolycystic Ovary Syndrome
Long and irregular menstrual cycles and polycystic ovary syndrome (PCOS) were
not initially related to ovarian cancer risk; however, when histologic subtypes were
taken into account in the analysis, menstrual cycle irregularities among women who
had never used oral contraceptives and those who were overweight were associated
with a reduced risk of high-grade serous EOCs and an increased risk of serous bor-
derline tumors [126].
The association between lifetime number of ovulatory cycles and epithelial ovar-
ian cancer risk has been reported, supporting the hypothesis that incessant ovulation
contributes to the pathogenesis of ovarian cancer [84]. Women with menstrual cycle
intervals of more than 35days have a lower risk of invasive ovarian cancer in com-
parison with those reporting cycle lengths of ≤35days. Also women with irregular
menstrual cycles have a lower risk of invasive ovarian cancer as compared to those
women with regular cycles [127].
A meta-analysis of few observational studies in women <55years suggests that
PCOS did not increase ovarian cancer risk [128]. Ovarian cancer risk does not seem
to be increased in women with PCOS [127].
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5.7.4 Epithelial Ovarian Borderline Tumors
A signicant number of epithelial ovarian borderline tumors are diagnosed at early
stages, and fertility-sparing surgery can be used in women without children and
those with localized tumors [129, 130]. However, tumor recurrence may affect
10–18% of patients who retain ovarian tissue [131, 132], and it seems that mucinous
tumors have a higher recurrence risk than serous types [128]. Therefore, pregnancy
should be attempted as soon as possible, in women who wish to do so. However,
there is no clear evidence that radical treatment, hysterectomy, or bilateral salpin-
gectomy reduces the risk of recurrence or malignant progression.
5.7.5 Previous Malignant Diseases
Girls and women who had suffered a germ cell tumor are more prone to have a sec-
ond malignant ovarian cancer [133]. An Australian population study reported that
breast cancer increases the rate of high-grade serous ovarian cancer threefold [31].
5.8 Conclusions
To date, ovarian cancer screening and early diagnosis are not feasible. There are
some general recommendations (Table5.1) from the current knowledge based on
risk and protective factors. The use of combined oral contraceptives for more than
5years, salpingectomy, and hysterectomy may reduce the risk of ovarian cancer.
Prevention of obesity and weight gain may also contribute at reducing ovarian
cancer risk. Reproductive factors, such as parity and breastfeeding are individual
Table 5.1 Risk and protective factors for ovarian cancer
Risk factors Protective factors
Increased age Breastfeeding (>1year)
Family history (rst degree) of ovarian cancer: BRCA1-2
mutations; Cowden syndrome, Lynch syndrome
Multiparity (>3 births)
Height (taller women) Combined oral contraceptives
Obesity (>29.9kg/m
2
) but more important ≥40kg/m
2
Fallopian tube ligation or
salpingectomy
Increase in adult body mass index (>5kg/m
2
) Hysterectomy
Diet with a high inammatory index Low-fat diet for at least 4years
Physical inactivity Red wine
Exposure to talc powder Black tea
Smoking Nonsteroidal anti-inammatory
drugs (aspirin and non-aspirin)
Endometriosis
Pelvic inammatory disease
Previous history of epithelial ovarian borderline tumor
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elections. Factors related to healthy lifestyles such as physical activity, alcohol con-
sumption or smoking, body talc use, and moderate red wine and NSAIDs consump-
tion may be a part of general health recommendations. Patients with a history of
endometriosis, pelvic inammatory disease, and ovarian borderline tumors should
be appropriately treated and followed up.
Competing Interest None to declare.
Funding: None.
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