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Abstract
Rising obesity rates around the world have had a profound impact on female
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reproductive health. Childhood obesity is associated with early onset of puberty,
menstrual irregularities during adolescence and polycystic ovary syndrome. Women of
reproductive age with high BMIs have a higher risk of ovulatory problems and tend to
respond poorly to fertility treatment. Strategies for fertility control can also be complex
since the efficacy and safety of hormonal contraceptives can be compromised by
increased body weight. Obesity can aggravate symptoms of pelvic organ prolapse,
stress urinary incontinence and increase the risk of endometrial polyps and
symptomatic fibroids. Weight reduction enhances reproductive outcomes, diminishes
symptoms of urinary incontinence and reduces morbidity following gynecological
surgery. Sustained and substantial weight loss is difficult to achieve with the lifestyle
and dietary measures that are currently available. A number of pharmacological
treatment options are available, and there are emerging data on reproductive outcomes
following surgical treatment for obesity.
Keywords
In 2005, approximately 1.6 billion adults worldwide were classed as overweight (BMI
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obese More
(BMI Download
>30). By 2015, these figures are PDF
obese [1]. Obesity is recognized as a major risk factor for a number of medical
conditions, including cardiovascular disease, diabetes, osteoarthritis and malignancies
of the colon and endometrium [201]. The aim of this review is to explore the impact of
obesity on benign gynecological conditions.
A literature search was performed using MEDLINE and EMBASE from 1989 to July
2009. The search terms were: obesity, puberty, infertility, PCOS, fertility treatment,
miscarriage, contraception, fibroid, endometrial polyp, urinary incontinence, pelvic floor
dysfunction, menopausal transition, anesthesia, surgery and weight management.
Relevant articles were identified and cross-references were checked.
Puberty
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High BMI scores at 3 years of age has been identified as a risk factor for the early onset
of puberty [2]. The impact of childhood weight gain on the time of the onset of puberty
has been the focus of much research. Data from a large population-based study from
Sweden suggest that for each unit increase in BMI, peak height velocity is brought
forward by 0.11 years [3]. This phenomenon of accelerated pubertal development can
be explained by the ‘critical weight hypothesis’, which proposes that menstruation is
established once a threshold weight of 48 kg or 17% body fat composition is achieved
[4,5]. A number of endocrine pathways linking childhood obesity with insulin resistance
and early onset of puberty have been described [6]. Prenatal growth restriction can be
accompanied by ‘catch-up’ growth in early infancy, resulting in increased deposition of
visceral fat [7,8], insulin resistance and compensatory hyperinsulinemia [9]. Accelerated
aromatization of adrenal and ovarian androgens in adipose tissue increases the
bioavail-ability of sex steroids, which promotes earlier adrenarche, pubarche and
thelarche [10,11]. It has been found that girls with an early onset of puberty are at
increased risk of ovarian hyper-androgenism and polycystic ovary syndrome (PCOS)
[12], as well as cardiovascular events in later life [13].
[15] and 3.1 (95% CI: 2.2-4.4) in those with a BMI greater than 27 [16]. Obesity is
associated with an increase in leptin and a decrease in adiponectin levels in the
circulation [17]. Leptin has a stimulatory effect on the hypothalamo–pitutary axis but
inhibits ovarian folliculogenesis [18,19], as well as lutenizing hormone (LH)- and
insulinmediated steroid production by granulosa and theca cells. Obesity related
hyperinsulinemia causes hyperandrogenemia, which results in granulosa cell apoptosis,
while peripheral conversion of androgens to estrogen in adipose tissue inhibits
gonadotrophin secretion [17].
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metabolic parameters in those who are already symptomatic [21]. Serine
phosphorylation of the insulin receptor prevents signal transduction to its substrate,
causing insulin resistance [23,24] and compensatory hyperin-sulinemia – a situation
that is exacerbated by obesity, particularly central obesity [25,26]. Hyperinsulinemia
inhibits hepatic production of sex hormone-binding globulin, thus increasing serum free-
androgen levels. Ovarian androgen production is facilitated by insulin, which, acting via
IGF1, also enhances LH-mediated steroidogenesis in the theca-cell system of the ovary
[27,28]. Serine phosphorylation of P450c17 increases 17,20-lyase activity, resulting in a
further increase in ovarian and adrenal androgen production [23]. Increased androgen
levels cause hirsutism, while peripheral conversion of excess androgens to estrogens
by adipocytes leads to menstrual disorders and anovulatory infertility.
Obese women with ovulatory problems respond poorly to ovulation induction by means
of anti-estrogens such as clomifene citrate. A systematic review of 13 studies also
identified obesity and insulin resistance as predictors of treatment failure following
gonadotrophin treatment. Obesity is positively correlated with gonadotrophin dose
(weighted mean difference: 771 IU; 95% CI: 700-842) and cycle cancellation (OR: 1.86;
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Moreovulation (OR: 0.44; 95% CI: PDF
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producing fewer follicles, women with high BMIs achieved similar rates of ovulation and
clinical pregnancy compared with their low-BMI counterparts [30].
210.08 IU; 95% CI: 149.12-271.05) and have a higher risk of miscarriage (OR: 1.33;
95% CI: 1.06-1.68). There was insufficient evidence to inform any meaningful
conclusions about the effect of BMI on live birth, cycle cancellation, oocyte recovery
and ovarian hyperstimulation syndrome [31].
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Early pregnancy loss
The reasons behind the association between high BMI and miscarriage are open to
debate. It has been suggested that obesity impacts on the ovarian environment,
resulting in impaired folliculogenesis and oogenesis. This hypothesis is supported by
studies demonstrating comparable miscarriage rates in obese and nonobese women
after adjusting for embryo and oocyte quality [35,36]. An alternative view is that obesity
has a detrimental impact on the uterine environment. Some studies have reported lower
pregnancy rates in obese women, even in cases where donated oocytes have been
used or where adjustments have been made for embryo quality, suggesting a problem
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Contraception
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cause a substantial weight gain of 9 kg over 5.5 years - possibly owing to increased
appetite [46]. A number of studies have explored the efficacy of hormonal contraception
in women with a high BMI. Analysis of data from a cohort of 755 female participants
suggests that women with a body weight of 70.5 kg or more have a significantly
increased risk of oral contraceptive failure (RR: 1.6; 95% CI: 1.1-2.4) compared with
women who weigh less. The highest risk of contraception failure was observed among
low-dose oral contraceptive users (RR: 2.6; 95% CI: 1.2–5.9) and very low-dose oral
contraceptive users (RR: 4.5; 95% CI: 1.4–14.4) [47]. By comparison with women with
a BMI less than 27.3, the risk of pregnancy was higher in women with a BMI greater
than 27.3 (OR: 1.58; 95% CI: 1.11–2.24) and higher still in women with a BMI greater
than 32.2 (OR: 1.72; 95% CI: 1.04–02.82) [48]. These results were not supported by
the analysis of National Survey of Family Growth data [49] which suggested a complex
relationship between obesity, socioeconomic factors and contraceptive use. A
multicenter trial in China found a dose– response relationship between weight and
failure rates associated with Norplant [50]. Results of secondary analyses of efficacy
studies have suggested that contraceptive failure associated with the transdermal
contraceptive patch (Ortho-Evra®) was increased in women whose bodyweight was
greater than or equal to 90 kg (≥198 lb) [51]. Reduced efficacy of hormonal
contraception in obese women could be due to lower plasma concentrations of the
Menopausal transition
The mean weight gain during the period of menopausal transition is 2.1 kg [55]. This is
mainly due to deposition of visceral fat [56] and results in an increased risk for diabetes,
metabolic syndrome and cardiovascular disease. In a longitudinal study on menopausal
women with constant body weight and unchanging levels of physical activity,
subcutaneous and visceral abdominal fat deposits were noted to increase during the
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menopausal transition. The increase was approximately 32% for subcutaneous and
44% for visceral fat [57]. Increase in visceral adiposity is associated with insulin
resistance, hypertension and hyperlipidemia [58]. Obesity also increases peripheral
conversion of androgens to estrogens, while high serum levels of unopposed estrogens
can encourage endometrial hyperplasia and cancer. In a study of abnormal
perimenopausal bleeding, obesity was shown to be independently associated with
heavy menstrual bleeding [59].
Women with PCOS, many of them obese [22], experience varying degrees of menstrual
irregularity. Even in the absence of PCOS, obesity has been associated with long and
irregular cycles. Women with a BMI of 35 have a fivefold higher risk of long cycles
compared with those with a BMI between 22 and 23 (OR: 5.4; 95% CI: 2.1–13.7) [60].
Upper body obesity is associated with menstrual disorders in obese women, even in the
absence of PCOS [61].
A cross-sectional study on 726 Australian women aged 26 to 36 years reported that the
comparison with women with a waist circumference less than 80 cm [62]. This further
highlights the link between visceral adiposity and menstrual irregularities.
Endometrial polyps
Hormonal factors related to estrogen excess, such as obesity, have been implicated in
the patho-genesis of endometrial polyps [63]. Onalan et al. demonstrated that women
with a BMI greater than 30 were more likely to have endometrial polyps than women
with a BMI less than 30 (52 vs 15%). Obesity was an independent predictor for the
development of endometrial polyps [63] and positively correlated with their size and
multiplicity. Most endometrial polyps are benign, with malignancy reported in only 1.5%
of cases [64]. Postmenopausal status, hypertension and obesity are risk factors for
malignant transformation within endometrial polyps in women without a history of
tamoxifen treatment [65].
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Fibroids
Obesity has been linked with uterine fibroids. In a retrospective study, those presenting
with uterine fibroids were more likely to be obese (50 vs 25%) or severely obese (16 vs
7.2%) than a general population of women [66]. In a prospective cohort study in the
USA, BMI and weight gain exhibited a complex relationship with the risk of developing
fibroids [67]. In a separate study, fibroids were associated with a BMI greater than 25,
concurrent hypertension [68], occult obesity and upper body fat distribution [69]. The
risk of developing fibroids is tripled in women with a bodyweight of 70 kg or more in
comparison with those who weigh less than 50 kg [70]. It is possible that obesity causes
a relative hyperestro-genic state, which encourages fibroid growth [70], although not all
studies are in accordance with this hypothesis [71].
Urinary incontinence
A large cohort study demonstrated a link between BMI and urinary incontinence.
Increased waist circumference, in particular, was associated with stress urinary
incontinence, possibly as a result of raised intra-abdominal pressure caused by central
obesity [72]. The severity of incontinence appears to be influenced by the duration of
obesity. Women who had been overweight or obese since the age of 20 years were
more likely to report severe incontinence than those who gained weight later in life [73].
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intervention targeting weight loss among overweight and obese women led to a
reduction in the frequency of self-reported episodes of urinary incontinence [74].
A systematic review of 29 studies concluded that overweight and obesity increased the
risk of urinary incontinence - especially stress urinary incontinence [75]. A second
systematic review suggested that surgery for stress urinary incontinence in obese
women was as safe, but less effective, than similar surgery performed in nonobese
women [76].
Female pelvic organ prolapse is a common condition with a multifactorial etiology [77].
The prevalence of pelvic floor dysfunction is highest (57%) in morbidly obese women
(BMI >40), and considerably higher (53%) in severely obese women (BMI >35)
compared with that (44%) in obese women (BMI >30) [78]. Data from the Women's
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Health Initiative (WHI) study demonstrate that 55.7% women gained weight over a
period of 5 years (mean: 4.43 kg ± 5.95), during which time the proportion of those with
prolapse increased from 40.9-43.8% [79]. In this study, exacerbation of cystocele,
rectocele and uterine prolapse was noted among women who were overweight (BMI
between 25 and 29.9) or obese (BMI ≥30) at baseline. In overweight and obese
women, worsening of symptoms of cystocele occurred in 32 and 48%; rectocele in 37
and 58%; and uterine prolapse in 43 and 69%, respectively [79]. Furthermore, a small
degree of weight loss (10%) was associated with borderline worsening of uterine
prolapse (OR: 0.93; 95% CI: 0.88-0.97), minimal regression of cystocele (OR: 1.03;
95% CI: 1.00–1.05) and rectocele (OR: 1.04; 95% CI: 1.01–1.07) [79]. This suggests
that the damage to the pelvic floor caused by obesity is probably irreversible. Other
studies have shown that surgically induced weight loss has a beneficial effect on
symptoms of pelvic floor disorders in morbidly obese women [80]. The impact of obesity
on different aspects of gynecology has been summarized in Table 1.
Anesthesia
Abdominal surgery in obese women takes lon-ger, is associated with greater blood loss,
post-operative pyrexia, increased wound infection and increased hospital stay [85].
Since operative exposure is limited, panniculectomy could be considered in some
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situations [86] during a gyne-cological procedure. In these cases difficulty with
operative exposure is reduced, and these patients are better served intraoperatively
[87]. Mass closure [88], subcutaneous drains and prophylactic antibiotics [89] are
recommended in order to minimize wound disruption. The vaginal route can be
employed for hysterectomy, if appropriate. Compared with nonobese women, operating
time and blood loss are higher during vaginal hysterectomy in obese women [90]; the
risk of wound infection can be minimized.
Obesity has implications for laparoscopic entry [91], and open laparoscopy is a
preferred option. Placement of additional ports may be technically challenging since
obesity can make it difficult to visualize abdominal wall vessels. A high BMI increases
the likelihood of conversion to open surgery during laparoscopy [92]. The benefits are
reduced postoperative pain and morbidity, and quicker recovery [93].
Comorbidities
Weight management
Moderate weight reduction of 5–10% has been shown to reduce the risk of
comorbidities [95] and encourage resumption of ovulation in anovulatory women
[96,97]. Lifestyle modification, diet and exercise are still considered to be central to any
obesity management strategy [98,99]. Pharmacological agents are useful adjuncts to
exercise and dietary therapy [100] and bariatric surgery is increasingly being used as a
final option by some women.
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Lifestyle changes, such as a healthy diet and regular exercise help in weight reduction.
The loss of 5–10% of body weight results in an improvement in ovarian morphology in
women with PCO [101]. Weight loss can encourage resumption of spon-taneous
ovulation and conception [96,101]. In a recent review of the literature, an expert panel
appointed by the Androgen Excess and PCOS Society (AEPCOS) concluded that
lifestyle modification was of paramount importance for treating metabolic complications
and improving ovulatory function in overweight and obese women with PCOS [102]. In
a meta-analysis of 18 RCTs, Wu et al. found that a combined diet-plus-exercise
program provided greater long-term weight loss than a diet-only program. However,
sustained weight loss is difficult to achieve and both diet-only and diet-plus-exercise
programs are associated with partial weight gain over time [103].
Pharmacological interventions
This degree of weight loss has not been a requirement for approval of the currently
marketed drugs, and none of the marketed antiobesity drugs produce weight losses of
10% or more [106].
Orlistat, which inhibits pancreatic and other lipases, thus inhibiting fat absorption and
thereby decreasing the progression of diabetes. It has gastrointestinal side-effects
[107];
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by modifying CNS neurotransmission. It is associated with increases in blood
pressure and pulse rate [107] and is not recommended for use by women who are
trying to conceive;
Metformin
The role of metformin in weight loss has been widely debated, and several authors
have questioned its effectiveness [109,110]. A recent meta-analysis of 14 RCTs
Contents in resulted
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longer duration of therapy (>8 weeks) [111]. A recent Cochrane review concluded that
metformin alone (OR: 2.12; 95% CI: 1.50-3.0) or in combination with clomifene (OR:
3.46; 95% CI: 1.97-6.07), increases ovulation rates in women with PCOS [112].
Metformin also increases the clinical pregnancy rate, but has no influence on the live
birth rate [112]. A recent RCT concluded that menstrual patterns improved with
metformin therapy in women with insulin resistance [113].
Surgical treatment may be the last resort for some women who are unresponsive to
other interventions for weight loss. A Swedish study demonstrated an estimated 24%
reduction in the adjusted overall mortality rate in those treated surgically compared with
conventionally treated controls [114]. Weight loss surgery reduces caloric intake by
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modifying the anatomy of the gastrointestinal tract via restriction, malabsorption or a
combination of the two techniques. The ensuing changes alter peptides that may
regulate appetite and satiety [115]. Bariatric surgical techniques include gastric bypass
(open and laparoscopic), laparoscopic adjustable gastric banding and bili-opancreatic
diversion (with or without duodenal switch) [116].
A systematic review of 136 studies involving 22,094 patients, 72.6% being women, with
a mean age of 39 years (range: 16–64 years) showed that effective weight loss was
achievable in morbidly obese patients following bariatric surgery. A substantial majority
of patients with diabetes, hyperlipidemia, hypertension and obstructive sleep apnea
experienced complete resolution or improvement [117]. In women of reproductive age,
menstrual irregularities [118] and PCOS may be completely resolved after bariatric
surgery [119]. Following bariatric surgery, morbidly obese women have improved fertility
and a reduced risk of obstetric complications, such as gestational diabetes,
macrosomia and hypertensive disorders of pregnancy [120]. However, pregnancy
should be avoided during rapid weight loss [121]. Intrauterine growth retardation and
nutritional deficiencies during pregnancy are the likely risks after bariatric surgery [120].
The impact of weight loss has been summarized in Table 3.
Executive summary
Magnitude of obesity
1.6 billion adults are currently overweight and 400 million are obese.
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Obesity & puberty
BMI at 3 years of age and childhood obesity are associated with early onset
puberty.
Obesity management
Lifestyle modification, diet and exercise are the cornerstones of any weight
loss program.
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Pharmacotherapy may aid weight loss.
Future perspective
The authors have no relevant affiliations or financial involvement with any organization
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pending, or royalties.
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