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MOU 270502

REVIEW

CURRENT
OPINION Obesity and male infertility
Barbara E. Kahn and Robert E. Brannigan

Purpose of review
The prevalence of obesity has risen steadily for the past 35 years and presently affects more than a third of
the US population. A concurrent decline in semen parameters has been described, and a growing body of
literature suggests that obesity contributes to the male infertility. The purpose of this review is to examine
the effects of obesity on male fertility, the mechanisms by which impaired reproductive health arise, and the
outcomes of treatment.
Recent findings
Obesity alters the hypothalamic–pituitary–gonadal axis both centrally and peripherally, resulting in
hypogonadotropic, hyperestrogenic hypogonadism. Adipose tissue-derived factors, like leptin and
adipokines, regulate testosterone production and inflammation, respectively. Increased systemic
inflammation results in increased reactive oxygen species and sperm DNA fragmentation. Increased
testicular temperature because of body habitus and inactivity impairs spermatogenesis. The degree to
which obesity affects hormone levels, semen parameters, sperm DNA integrity, and pregnancy rates is
variable, which may be the result of other comorbid conditions. Treatment in the form of weight loss has
also had inconsistent results.
Summary
Multiple interdependent mechanisms contribute to the detrimental effect of obesity on male fertility. Large,
randomized control trials are needed to better characterize the therapeutic benefits of weight loss to restore
male reproductive potential.
Keywords
BMI, infertility, obesity, sperm, testosterone

INTRODUCTION THE HYPOTHALAMIC–PITUITARY–

The National Health and Nutrition Examination
Survey has tracked the prevalence of obesity,
defined as a BMI of greater than or equal to 30,
since the early 1960s [1,2]. Between 1980 and 2002,
the prevalence of obesity in adults, ages 20 and
older, has doubled [3]. The prevalence of obesity
has continued to rise on subsequent surveys, with
the most recent estimate involving 35.2% of men
&&
and 40.4% of women [4 ]. Not only has obesity
been associated with diabetes, cardiovascular dis-
ease, cancer, and an increased risk of all-cause
mortality, but also infertility [5–7]. Coincident with
the obesity epidemic, there have been several
studies demonstrating a decrease in semen quality
overtime [8–10]. Obesity may be contributing to
this trend, as it negatively impacts reproductive
function through numerous mechanisms, including
hormonal perturbations, elevated levels of inflam-
matory mediators and reactive oxygen species
(ROS), and increased testicular heat, which cumu-
latively can have substantial, detrimental effects
on spermatogenesis.
GONADAL AXIS IN OBESE MEN
Under normal conditions, gonadotropin-releasing
hormone is produced and released from the hypo-
thalamus, which stimulates the production and
release of follicle-stimulating hormone (FSH) and
luteinizing hormone (LH) from the anterior pitu-
itary. FSH and LH act on the testicle to stimulate
spermatogenesis and steroidogenesis, respectively.
Studies in the 1970s and 1980s first described the
hormonal abnormalities seen in the hypothalamic–
pituitary–gonadal (HPG) axis in obese men relative
to nonobese men. In these studies, obese men had
Division of Male Reproductive Surgery and Men’s Health, Department of
Urology, Northwestern University Feinberg School of Medicine, Chicago,
Illinois, USA
Correspondence to Professor Robert E. Brannigan, MD, Department of
Urology, Galter Pavilion, 675 North Saint Clair Street, Chicago, IL 60611,
USA. Tel: +1 312 926 5564; fax: +1 312 695 7030;
e-mail: r-brannigan@northwestern.edu
Curr Opin Urol 2017, 27:000–000
DOI:10.1097/MOU.0000000000000417

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Obesity and its impact on urological disease
KEY POINTS
 Obesity is increasing in prevalence and is a substantial
public health concern.
 Obesity results in hypogonadotropic, hyperestrogenic,
hypogonadism via central and peripheral pathways.
 Obesity is characterized by systemic inflammation,
which commonly increases ROS levels and can result in
abnormally high levels of sperm DNA fragmentation.
 Body habitus and inactivity are associated with
increased testicular heat, which can impair
spermatogenesis.
 Obesity has been linked to altered semen parameters,
increased sperm DNA damage, and decreased
pregnancy rates.
 The therapeutic benefits of weight loss on abnormal
hormone levels and semen parameters in obese men
need further study.
normal LH levels, decreased total testosterone
levels, and decreased sex hormone-binding globulin
(SHBG) levels [11–13]. Subsequent studies demon-
strated an inverse correlation between BMI and total
testosterone and SHBG [14,15]. The studies had
differing results regarding free testosterone levels
in obese men [11–16]. The discordant free testos-
terone results may be explained by variations in the
severity of the BMI. Giagulli et al. [17] demonstrated
that moderately obese men (BMI 30–35) had normal
LH pulsatility and free testosterone, whereas
severely obese men (BMI > 40) had decreased LH
levels, LH amplitudes, and free testosterone. The
decrease in LH pulse amplitude but not frequency
in obese men was further supported by Vermeulen
et al. [18]. Elevated estradiol levels because of aro-
matization of testosterone by peripheral adipose
tissue suppress the HPG axis via negative feedback
inhibition [16,19]. The perturbations in the HPG
axis in obese men described above have been sup-
ported in more recent studies as well. In a longitudi-
nal trial of 942 men ages 40–70 years enrolled in the
Massachusetts Male Aging Study, Derby et al. [20]
demonstrated that not only was BMI negatively
associated with total testosterone, free testosterone,
and SHBG, but also that these levels decline more
rapidly with age in obese men. The authors ponder
whether the hormonal abnormalities lead to
increased adiposity or increased adiposity leads to
hormonal abnormalities.
Adipose tissue, which was initially believed to
act solely as a reservoir for energy storage, also
produces hormonally active proteins involved in
satiety and metabolism as well as HPG axis
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&
regulation [21 ]. Leptin, one of the first adipose
tissue-derived factors discovered, is secreted by
&
white adipose tissue [21 ,22]. In rat models, leptin
stimulates gonadotropin-releasing hormone secre-
tion in the hypothalamus and FSH and LH secretion
in the anterior pituitary [23,24]. Leptin is also
believed to have a direct effect on regulation of
testosterone production in the testicle given the
presence of leptin receptors in Leydig cells [25].
Obesity generates a leptin resistant state, in which
high circulating leptin levels are correlated with
increased adiposity and lower testosterone levels
[26]. In another rodent model, Caprio et al. [27]
demonstrated that in cultured Leydig cells, elevated
leptin levels inhibit testosterone production despite
HCG stimulation, similar to mechanisms believed
to occur in obese men.
OBESITY AND THE TESTICLE
In addition to the effects of the hormonal abnor-
malities on spermatogenesis in obese men, sperm
quality is also affected by oxidative stress damage
and increased scrotal temperatures. Obesity is con-
sidered a proinflammatory state with production of
adipokines and cytokines by adiopocytes that result
&
in an increase in systemic inflammation [21 ].
During oxidative stress, ROS overwhelm the anti-
oxidant defenses of the cell leading to cellular dam-
age and death to which sperm are particularly
vulnerable [28]. Elevated seminal ROS are associated
with decreased sperm concentration, motility,
morphology, and increased frequency of DNA frag-
mentation [29,30].
Spermatogenesis is also adversely effected by
elevated testicular temperature [31]. Increased adi-
posity in the legs and pannus overlying the scrotum
may lead to increased testicular temperatures.
During cadaver dissection of a cohort of fertile
and infertile men, Shafik and Olfat [32] described
different scrotal fat patterns. They subsequently
performed lipectomy to remove the scrotal lipoma-
tosis from a series of infertile men with improve-
ments in semen parameters in 64.7% of study
participants and pregnancies in 19.6% [33]. In
addition to obesity, prolonged inactivity has
also been associated with increased scrotal tempera-
tures [34].
OBESITY AND OVERALL FERTILITY
STATUS
Obesity may affect all aspects of a male’s fertility,
including semen parameters, sperm DNA integrity,
and pregnancy outcomes. The effect of BMI on semen
parameters has been evaluated in numerous cohort
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MOU 270502
studies with conflicting results. In the first meta-
analysis performed, MacDonald et al. [35] found no
statistically significant association between BMI and
semen parameters. Given the heterogeneity of the
data in the 13 previously published, relevant studies,
only the data from five of the studies could be pooled
in the meta-analysis, which included 4853 men [35].
Three years later, Sermondade et al. [36] published a
second meta-analysis, which aggregated original
data from 21 studies including 13 077 men. In this
meta-analysis, a significant J-shaped association was
revealed between BMI and abnormal sperm count,
defined as less than 40 million sperm per ejaculate.
The odds ratio with a 95% confidence interval for
oligozospermia or azoospermia in underweight
men (BMI < 18.5) was 1.15 (0.93–1.43), in over-
weight men (BMI 25–29.9) was 1.11 (1.01–1.21),
in obese men (BMI 30–39.9) was 1.28 (1.06–1.55),
and in morbidly obese men (BMI > 40) was 2.04
(1.59–2.62) [36]. The second meta-analysis differed
from the first, in that it dichotomized the semen
analyses results rather than analyzing them as con-
tinuous variables. It was also strengthened by its
ability to obtain original data, and therefore include
more studies.
Several studies have evaluated sperm DNA frag-
mentation as a surrogate marker for sperm function-
ality. DNA fragmentation index (DFI) greater than
30% by sperm chromatin structure assay has been
associated with decreased pregnancy rates via
natural conception, decreased pregnancy and deliv-
ery rates via intrauterine insemination, and
decreased pregnancy and delivery rates via IVF com-
pared with intracytoplasmic sperm injection
[37,38]. The presence of an elevated DFI can be
discordant with semen parameters, having been
identified in 20% of infertile men with normal
standard semen parameters [39]. Kort et al. [40] were
the first to demonstrate a significant correlation
between BMI and DFI on sperm chromatin structure
assay testing among a population of 520 healthy
men ages 26–45 years who presented for semen
analysis testing. The DFI of normal BMI men,
19.9  1.96%, was significantly lower than the DFI
in the overweight, 25.8  2.23%, and obese groups,
27.0  3.16% [40]. Another cross-sectional study by
&
Bandel et al. [41 ] demonstrated no association
between obesity and elevated DFI in a population
of 1503 men, of which 75% had proven fertility. The
lack of consensus in the studies suggests there are
other factors contributing to the abnormal semen
parameters and DFI in some obese men not present
in others. These factors may be overrepresented in
studies of mostly infertile men and underrepre-
sented in studies of mostly fertile men, leading to
conflicting results.
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Obesity and male infertility Kahn and Brannigan
Although it has been shown that female BMI
may adversely affect the results of assisted reproduc-
tive techniques, the impact of male BMI is less well
&&
elucidated [42 ]. In a population-based cohort
study of 12 566 Danish women and their partners
who underwent 25 191 cycles of IVF, both male and
female obesity decreased the odds of live birth [43].
Conversely, in a prospective cohort study of 721
couples undergoing their first fresh IVF cycle, nei-
ther male BMI, female BMI, nor couple BMI was
associated with fertilization rate, embryo score,
&&
pregnancy rate, or live-birth rate [44 ]. A meta-
analysis aggregated the data from these two studies
and three others and observed a statistically signifi-
cant decrease in live-birth rate via IVF or intra-
cytoplasmic sperm injection among obese men
&
compared with normal weight men [45 ].
INTERVENTIONS
With growing evidence that obesity adversely
affects male fertility by way of hormonal derange-
ments, oxidative stress, and testicular overheating,
efforts have focused on possible interventions
including weight loss by lifestyle modifications
and bariatric surgery, antioxidants, and aromatase
inhibitors. Hakonsen et al. [46] studied the effects
14 weeks of diet and exercise on hormones, semen
parameters, and DFI in 43 obese men. The study
participants with the largest weight loss, 17.2–
25.4%, had statistically significant increases in
sperm concentration, morphology, serum testoster-
one, SHBG, and testosterone : estradiol ratio. In this
study, there was no association between BMI and
DFI and no change in DFI with weight loss [46]. Reis
et al. [47] compared the effects of lifestyle modifi-
cation and gastric bypass on hormones and semen
parameters in morbidly obese men. In total, ten
morbidly obese men were randomized to either
lifestyle modifications with diet and exercise or
gastric bypass. Baseline hormones and semen
parameters were evaluated at time 0, 2 months after
intervention, and 24 months after intervention.
Improvements in BMI were seen in the gastric
bypass group at 2 months. Improvements in testos-
terone were seen in the gastric bypass group at 24
months. No significant changes were seen in the
lifestyle modification group at either interval. No
changes in semen parameters were seen [47]. Two
case reports describe significant worsening of semen
parameters following bariatric surgery, including
six patients who developed azoospermia within
15 months of a Roux-en-Y gastric bypass, one
patient who worsened from oligospermia to crypto-
spermia 6 months after Roux-en-Y gastric bypass,
one patient who developed worsening oligospermia
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Obesity and its impact on urological disease
3 and 6 months after Roux-en-Y sleeve gastrectomy,
and one patient who demonstrated reversible wor-
sening from normal to severe oligoastheno-
teratospermia at 10 and 13 months after sleeve
gastrectomy with return to baseline at 24 months
&&
[48,49]. Bardisi et al. [50 ] are the first investigators
to describe improved semen parameters following
bariatric surgery in the form of sleeve gastrectomy.
Overall semen parameters were unchanged
12 months after surgery, but on subgroup analysis
there was a statistically significant improvement in
sperm concentration among the azoospermic and
oligospermic patients which was unrelated to the
&&
degree of weight loss [50 ].
Antioxidants have been proposed to treat excess
free radicals responsible for DNA fragmentation. A
Cochrane review of 48 randomized control trials
determined there was low-quality evidence that
antioxidants may improve pregnancy rates and
live-birth rates, though these were not specific to
obese men [51]. Aromatase inhibitors to block the
conversion of testosterone to estradiol and correct a
low testosterone : estradiol ratio have been shown
to improve sperm concentration and motility in
oligozospermic patients [52]. Again, this has not
been studied specifically in an obese cohort, but
the Pavlovich et al. study did consist of 24%
obese men.
METABOLIC SYNDROME AND MALE
INFERTILITY
Metabolic syndrome is a highly prevalent condition
comprised of numerous physiological abnormal-
ities, of which obesity is just one component. Facets
of metabolic syndrome, according to the National
Cholesterol Education Program Adult Treatment
Program III criteria include three of the five follow-
ing parameters:
(1) Waist circumference more than 40 inches;
(2) Blood pressure more than 130/85 mmHg;
(3) Fasting triglyceride level more than 150 mg/dl;
(4) Fasting high-density lipoprotein less than
40 mg/dl;
(5) Fasting glucose more than 100 mg/dl.
Kasturi et al. [53] thoroughly summarized the
links between metabolic syndrome (MetS) and male
infertility, and these extend well beyond patho-
physiology specifically linked to obesity. They pro-
pose a MetS–male infertility paradigm, in which the
component abnormalities of metabolic syndrome
(diabetes mellitus type II, hypertension, dyslipide-
mia, and obesity) collectively impair the HPG axis,
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spermatogenesis, and sexual functioning with resul-
tant deleterious effects on overall reproductive
potential in affected men. Deeper discussion of
the MetS–male infertility paradigm is beyond the
scope of this article, but the manuscript by Kasturi
&&
et al. [53] and more recently by Morrison et al. [54 ]
thoroughly detail the complicated and highly dis-
ordered reproductive pathophysiology experienced
by affected men.
CONCLUSION
Obesity is a systemic disease with several interrelated
mechanisms contributing to a suboptimal environ-
ment for sperm production. Hormonal abnormalities
related to increased adiposity blunt the HPG axis
leading to decreased intratesticular testosterone
levels necessary for spermatogenesis. Elevated scrotal
temperatures because of body habitus and inactivity
can also impair semen parameters. Increased
systemic inflammation in obesity can lead to ROS
and sperm DNA fragmentation, which is associated
with reduced pregnancy rates.
Numerous therapeutic interventions for infer-
tility linked to obesity have been studied, with
varying degrees of promise. Intuitively, optimiz-
ation of waist circumference and BMI should result
in restored reproductive potential. However, weight
loss efforts by lifestyle modification or bariatric
surgery do not consistently result in optimized hor-
monal levels or semen parameters. Given the com-
plex interplay between the components of MetS–
male fertility, the inconsistent therapeutic benefit
seen with weight loss may point to as yet untreated
facets of metabolic syndrome that are exerting
ongoing deleterious effects on male reproductive
physiology.
Acknowledgements
None.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
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