Human Reproduction, Vol.24, No.7 pp.

1561 1568, 2009

Advanced Access publication on April 7, 2009 doi:10.1093/humrep/dep075

ORIGINAL ARTICLE Andrology

Associations between andrological

measures, hormones and semen
quality in fertile Australian men:
inverse relationship between obesity
and sperm output
T.M. Stewart 1,4, D.Y. Liu 1, C. Garrett 1, N. Jrgensen 2, E.H. Brown 3,
and H.W.G. Baker1
1
Department of Obstetrics and Gynaecology, The University of Melbourne and Melbourne IVF Reproductive Services, The Royal Womens
Hospital, Melbourne, Australia 2Department of Growth and Reproduction, Rigshospitalet, Copenhagen, Denmark 3School of Human
Biosciences, La Trobe University, Melbourne, Australia
4
Correspondence address. Tel: 61-3-8345-3723; Fax: 61-3-8345-3702 E-mail: tstewart@unimelb.edu.au

background: The World Health Organization developed a time to pregnancy (TTP) study (number of menstrual cycles taken to con-
ceive) to determine whether the average TTP is increasing and semen quality decreasing with time. The present study describes clinical,
semen and hormone characteristics obtained from male partners of pregnant women in Melbourne, Australia, and examines the associations
between these characteristics.
methods: Male partners (n 225) of pregnant women (16 32 weeks) who conceived naturally had physical examination, health and
lifestyle questionnaires, semen and hormone (FSH, LH, sex hormone-binding globulin, testosterone and Inhibin B) analyses.
results: Previously known associations between semen, hormone and clinical variables were conrmed as signicant: sperm numbers
(concentration and total sperm count) correlated positively with Inhibin B and inversely with FSH and left varicocele, while total testicular
volume correlated positively with sperm numbers and Inhibin B and inversely with FSH. However, only abstinence, total testicular volume,
varicocele grade and obesity (BMI . 30 kg/m2) were independently signicantly related to total sperm count. Compared with those with
BMI , 30 (n 188), obese subjects (n 35) had signicantly lower total sperm count (mean 324 versus 231 million, P 0.013) and
Inhibin B (187 versus 140 pg/ml, P , 0.001) but not FSH (3.4 versus 4.0 IU/l, P 0.6).
conclusions: Obese fertile men appear to have reduced testicular function. Whether this is cause or effect, i.e. adiposity impairing
spermatogenesis or reduced testicular function promoting fat deposition, remains to be determined.

Key words: fertile men / semen quality / gonadal hormones / time to pregnancy / obesity

women in Europe, USA and Japan (Jorgensen et al., 2001; Swan

Introduction
Scientic controversy and public concern surrounds the claims that
human fertility is declining globally because of reduced sperm pro-
duction. Since the publication of the Carlsen et al.s (1992) paper,
which claimed that human sperm concentration had declined by as
much as 50% over the past 50 years, there has been a continued
effort worldwide to provide evidence to either support or refute
this assertion (Carlsen et al., 1992). Prospective studies of andrological
characteristics (clinical, semen and hormone) have been conducted in
well-dened populations, specically male partners of pregnant
et al., 2003; Iwamoto et al., 2006). The World Health Organization
(WHO) Special Program of Research, Development and Research
Training in Human Reproduction also responded to the controversy
and developed a study Sentinel Surveillance of Semen Quality and
Time to Pregnancy to test whether human fertility is changing in differ-
ent regions of the world. It was planned to be a multi-centre colla-
borative epidemiological study but funding was not obtained. The
aim of the WHO surveillance study was to perform cross-sectional
studies of currently pregnant women and their partners at 3-year
time intervals to determine whether fertility and semen quality are

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 1562
decreasing with time. Specically, time to pregnancy (TTP) and factors
affecting it were to be assessed by a short questionnaire administered
to currently pregnant women, and in selected eligible male partners
more detailed information was to be obtained by a further question-
naire, clinical examination, semen and hormone analyses. We have
undertaken the baseline phase of the WHO study in Melbourne,
Australia, with local funding. We describe clinical, semen and
hormone characteristics obtained from 225 male partners of pregnant
women and the associations between these characteristics.
Materials and Methods
Study population
Women pregnant between 16 and 32 weeks gestation who attended
either the antenatal clinic at The Royal Womens Hospital (RWH) or
private obstetric practices for routine management of pregnancy and child-
birth in Melbourne, Australia, between January 2000 and December 2002
were approached in the waiting areas and asked to complete the WHO
TTP questionnaire. If the current pregnancy was a natural conception
and if their partner was eligible (18 50 years, and both he and his
mother were born in Australia), he was invited to participate in a more
detailed evaluation. This included a physical examination, two semen ana-
lyses, measurement of reproductive hormones in blood and the com-
pletion of additional questionnaires. All women and men gave written
informed consent. The RWH Research and Ethics Committee approved
the project.
Questionnaires
The development and validation of the TTP questionnaire has been
described in detail (Stewart et al. 2001). In brief, the questionnaire for
women elicited information on socio-demographic factors, contraceptive,
pregnancy and reproductive history, and lifestyle factors, such as smoking
and illicit drug use.
Physical examination
The same experienced clinical andrologist examined each man including
blood pressure by mercury sphygmomanometer, body proportions
(height, arm span and leg length measured from pubis to oor), breasts
for gynaecomastia (dened as any palpable breast tissue), genitalia (with
the man both lying and standing), virilization (Tanner stages of pubic
hair) and volume of testes using a Prader orchiometer. Stretched penile
length was measured with a ruler, the end of which was pressed against
the pubis and the length to the tip of the glans read off to the nearest
1 mm while traction was exerted on the distal third of the shaft to
achieve the maximum length of the penis.
Semen analysis
Two semen samples at least 2 weeks apart from each subject by mastur-
bation after a stipulated 2 5 days abstinence were requested and the sub-
jects recorded the number of days since last ejaculation. The majority of
men produced the specimen onsite at the hospital although 20 men
requested a home collection. Semen analyses were performed by two
experienced clinical scientists who had good external quality control
(EQC) results, and there was no signicant difference between their
results in this study. One scientist assessed all morphology slides. All
sperm tests were performed after liquefaction of the semen at room
temperature within 2 h of collection. Sperm concentration by improved
Neubauer, volume by weighing the tube, motility and morphology were
assessed according to the WHO (1999) manual. Sperm morphology
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Stewart et al.
was assessed on smears prepared from semen after washing with 10 ml
of 0.9% sodium chloride to remove seminal plasma. Morphology slides
were stained with the Shorr method after the smears were xed in 90%
ethanol for 30 min. Sperm morphology was assessed according to
WHO (1999) using the strict method. For each sample 200 sperm from
at least 10 individual elds were assessed under oil immersion with a mag-
nication of 1000 under bright-eld illumination.
Hormone analysis
A blood sample was drawn from an antecubital vein, usually in the
morning, and serum was separated by centrifugation after clotting and
stored at 2208C. The frozen serum was sent on dry-ice to the Depart-
ment of Growth and Reproduction, Rigshospitalet, in Copenhagen,
Denmark, for a centralized analysis of the reproductive hormones: FSH,
LH, Inhibin B, total testosterone and sex hormone-binding globulin
(SHBG). FSH, LH and SHBG were measured by time-resolved immuno-
uorometric assay (Dela, Wallac, Turku, Finland), Testosterone by a
time-resolved ouroimmunoassay (Dela, Wallac, Turku, Finland) and
Inhibin B by a specic two-sided enzyme immunometric assay (Serotec,
UK). Intra- and inter-assay coefcients of variation (CV) for measurements
of both FSH and LH were 3 and 4.5%, respectively. Both CVs for Testos-
terone and SHBG were ,8 and ,5%, respectively. The intra- and inter-
assay CV for Inhibin B was 15 and 18%, respectively.
Statistical analysis
In general non-parametric tests were used because most of the data were
not normally distributed. The 2.5th and 97.5th percentiles or 5th percen-
tiles for total testicular volume (TTV), stretched penile length and semen
variables (because only low values are pathological) were calculated.
Distribution-free condence limits were calculated for the percentiles.
Correlations between and within clinical, semen and hormone character-
istics were examined by Spearmans rho (r) test. One-way analysis of var-
iance was used to assess the signicance of differences between
categories. Multiple linear regression analysis with various end-points,
such as sperm concentration, was used to determine which groups of
factors were independently signicantly associated, i.e. a parsimonious
model was chosen including only statistically signicant covariates. The
problem with multiple testing because of the large number of variables
and our interest in several end-points is recognized. A pragmatic approach
was used as follows. Factors known, expected or reported in the literature
to be related were included (e.g. age, duration of abstinence, season,
smoking, alcohol consumption, urogenital diseases). The remaining vari-
ables were included but were only considered further if they were
highly signicant (i.e. P , 0.001, with P , 0.05 being the signicance
level). Time of blood sampling was related to FSH (r 0.133, P 0.04)
and Inhibin B (r 20.280, P 0.001) levels and this was included as a
covariate in subsequent analyses. The FSH/Inhibin B ratio was calculated
as FSH multiplied by 100 divided by Inhibin B. Results of the rst semen
specimen were used for calculations of the relationships between
semen, clinical and hormone characteristics. Sperm concentration and
total sperm count (volume  concentration) were cube root transformed
and FSH, LH and Testosterone log-transformed for regression analysis.
The interval between specimen collection and start of semen analysis
was categorized as 30 min or .30 min; duration of abstinence as 1,
2, 3, 4 and 5 days; varicocele as absent (Grade 0), small cough
impulse only (Grade 1), moderate sized, palpable (Grade 2) and large,
visible enlargement (Grade 3); season as summer (December February),
autumn (March May), winter (June August) and spring (September
November); BMI as underweight ,20 kg/m2, normal ,25 kg/m2, over-
weight 25 30 kg/m2 and obese .30 kg/m2 (WHO 2000). TTV was
the sum of the left and right testis.
 Obesity and sperm count 1563

Table I Clinical, semen and hormone test results for 225 fertile Australian men

Variable Mean (SD) Median (range) Fifth percentile (CL)a or 2.5th and
97.5th percentiles (CL)b
.............................................................................................................................................................................................
Age (years) 35 (5) 34 (21 46) 27 (24 28), 45 (44 45)b
Height (cm) 180 (7) 180 (163198) 166 (163170), 193 (192195)b
Weight (kg) 87 (12) 85 (53 126) 64 (63 69), 117 (105 124)b
2
BMI (kg/m ) 27 (4) 26 (19 42) 20 (20 22), 34 (32 36)b
TTV (ml) 48 (10) 48 (20 90) 32 (30 34)a
Stretched penile length (cm) 15 (1.7) 14 (10 18) 12 (11 12)a
Semen volume (ml) 3.8 (1.6) 3.6 (0.7 10.0) 1.3 (1.0 1.7)a
6 a
Sperm concentration (10 /ml) 108 (80) 96 (4 532) 22 (18 25)
Total sperm count (106/ejaculate) 368 (298) 305 (17 3115) 65 (50 93)a
Total progressive motility (%) 53 (10) 54 (15 75) 34 (29 38)a
Normal sperm morphology (%) 16 (10) 14 (1 58) 3 (3 4)a
FSH (IU/l) 3.5 (1.9) 3.3 (0.8 13.8) 1.1 (0.9 1.3), 8.0 (6.7 9.9)b
LH (IU/l) 3.9 (1.5) 3.7 (0.7 8.9) 1.5 (1.1 1.8), 7.5 (6.7 8.3)b
Testosterone (nmol/l) 18 (6) 17 (7 40) 9 (8 11), 33 (28 35)b
SHBG (nmol/l) 31(13) 29 (8 90) 10 (9 14), 58 (50 70)b
Inhibin B (pg/ml) 179 (70) 172 (22 382) 63 (57 80), 328 (296 365)b
a
Fifth percentile is given for andrological and semen variables.
b
2.5 and 97.5th percentiles for other variables with distribution-free condence limits (CL).
TTV, total testicular volume; SHBG, sex hormone-binding globulin.

Results
Participation and characteristics of subjects
Of the 2100 pregnant women who were approached, 2061 com-
pleted the WHO TTP questionnaire (participation rate, 98%) and
928 had eligible male partners, of whom 225 participated in the
male study (participation rate, 24%). However, of the 225 men (all
were Caucasian), 2 did not provide semen but underwent physical
examination and hormone analysis, 2 did not have hormone analysis
but underwent physical examination and semen analysis and 1 did
not undergo physical examination or hormone analysis but had
semen analysis. Second semen analyses were obtained from 214
men, and analysis of these produced the same results for fth percen-
tiles and correlations as the rst sample, and are therefore not dis-
cussed further in this paper. Of the 223 couples that participated in
the semen study, 183 (82%) produced planned natural pregnancies
while 23 (10%) had contraceptive failures and 17 (8%) had other
unplanned pregnancies. None of the pregnancies were the result of
infertility treatment as this was a specic exclusion criterion for the
semen study. However, 13 had been investigated for infertility and 3
had been treated for male infertility in the past.
Clinical, semen and hormone results
The clinical, semen and hormone test results for 225 fertile men are
summarized in Table I. Of the 222 men who had clinical examination,
2 had absent right testes from testicular torsion in childhood. Eunu-
choidal proportions, dened as arm span exceeding height by 6 cm,
were evident in 30 men (14%). Mild gynaecomastia was present in
44 men (20%). The majority (95%, n 221) had Tanner stage six
pubic hair distribution. One man had slight Peyronie disease. Sixteen
men had moderate to large varicoceles. The mean (median) time
interval from specimen collection to start of semen analysis was
35.8 (30) min. Duration of abstinence ranged from 1 to 14 days
with a mean of 3.5 (3) days: only two men abstained for ,2 days
and 45 for .5 days. The percentages of semen samples delivered
during the different seasons were: 14.8% in summer, 29.6% in
autumn, 31.8% in winter and 23.8% in spring. Increasing time from
specimen collection to start of semen analysis has been shown to
be associated with reduced motility but this was not statistically signi-
cant in the present study. Signicant upward trends in semen volume
(P 0.024), concentration (P 0.001) and total sperm count (P ,
0.001) were observed with increasing abstinence up to 5 days
(linear effect) after which no further effect was observed for these
variables. Other semen variables were not signicantly affected by dur-
ation of abstinence. Season was not signicant for any semen variable.
Correlations among the clinical, semen
and hormone test results
There were strong correlations between BMI and mean arterial blood
pressure (r 0.332, P  0.001) and between TTV and stretched
penile length (r 0.266, P  0.001). Year of birth was not signicantly
correlated with any characteristic. Other signicant correlations were
between sperm concentration and percentage normal morphology
(r 0.357, P  0.001). Percentage normal morphology correlated
with total sperm count (r 0.273, P  0.001) and percentage

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Table II Non-parametric (Spearman) correlation coefcients for relationships between clinical, semen, hormone test
results and obese men with BMI > 30 kg/m2, compared with lower BMI
Variable TTV Left varicocele
.............................................................................................................................................................................................
Left varicocele 20.085
Obesity 0.070 20.048
Total sperm count 0.341 b 20.228 b
Inhibin B 0.379 b 20.109
b
FSH 20.244 0.033
a
Testosterone 0.147 0.046
a a
LH 20.171 20.004
a
P , 0.05; bP  0.001.
Bold values are statistically signicant.
progressive motility (r 0.359, P  0.001). Testosterone correlated
positively with SHBG (r 0.594, P  0.001).
Correlations between clinical, hormone
and semen characteristics
Interesting correlations found in the present study are summarized in
Table II. Other correlations were as follows: TTV correlated positively
with sperm concentration (r 0.359, P  0.001), increasing varicocele
grade was associated with a signicant (P  0.001) progressive
reduction in these variables, especially for total sperm count. For
example, the mean cube root total sperm count was 6.96 for men
without a left varicocele, 6.46 for Grade 1 varicocele, 5.51 for Grade
2 and 4.84 for Grade 3 (P  0.001). Inhibin B and FSH correlated signi-
cantly with sperm concentration: Inhibin B correlated positively with
concentration (r 0.276, P  0.001) while FSH was inversely corre-
lated (r 20.221, P  0.001). Interestingly, stretched penile length
was correlated positively with sperm concentration (r 0.228, P 
0.001), total sperm count (r 0.227, P  0.001), percentage pro-
gressive motility (r 0.218, P  0.001) and Inhibin B (r 0.223,
P  0.001) and correlated inversely with FSH (r 20.226, P 
0.001). Weight and BMI were inversely correlated with SHBG (respect-
ively, r 20.268, P  0.001 and r 20.349, P  0.001), Inhibin B
(r 20.278, P  0.001 and r 20.284, P  0.001) and testoster-
one (r 20.165, P , 0.05 and r 20.187, P , 0.05). Weight cor-
related negatively with sperm concentration (r 20.138, P , 0.05).
On the basis of BMI, males were grouped as underweight (,20 kg/
m2), normal (2025 kg/m2), overweight (25 30 kg/m2) and obese
(30 kg/m2); there was a nonlinear relationship with total sperm
count (Fig. 1). Fitting different curves to the total sperm count/BMI
relationship revealed statistical signicance (P between 0.02 0.05,
r 2 3%) with lower total sperm counts with both low and high BMI
and a peak about BMI 25. The ve men with BMI ,20 had low total
sperm counts but because of the small numbers we have not analysed
this further. The total sperm count was signicantly (P , 0.05) lower in
the obese men than in those with BMI ,30. The obese group (Table III)
had signicantly lower total sperm count, Inhibin B, SHBG and testoster-
one but not FSH. The FSH/Inhibin B ratio is signicantly (P 0.016)
higher in the obese group (3.4 (SD 3.0), n 36) than in the normal
and overweight range combined (2.4 (2.1), n 184).
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Stewart et al.
Obesity Total sperm count Inhibin B FSH Testosterone
20.163 a
20.247 b 0.384 b
0.028 20.207 a 20.325 b
20.103 20.016 0.128 a 0.116
0.062 20.171 20.201 a 0.434 b 0.27 b
Multiple linear regression
Modelling of factors associated with cube root total sperm count
showed only TTV, left varicocele, abstinence and the obese group
were independently signicant (Table IV). Omitting TTV did not
alter the signicance or the coefcients of the other factors greatly.
Results were similar for cube root sperm concentration (not shown).
Discussion
Previously established andrological associations of sperm output were
conrmed. As 90% of testicular volume is comprised of seminiferous
tubules, it is expected that testicular size would be closely related to
sperm output (Kothari and Gupta, 1974; Kaler and Neaves, 1978; van
Dop et al., 1980). Similarly, the relationships between TTV,
sperm number, FSH and Inhibin B are consistent with the literature
(Handelsman et al., 1984; Wang et al., 1985; Plymate et al., 1992;
Arai et al., 1998; Pierik et al., 1998). The presence and size of a var-
icocele was associated with lower sperm output also as described pre-
viously (MacLeodm, 1965; Rodriguez-Rigau et al., 1981; Chehval and
Purcell, 1992; WHO, 1992).
This study has also provided information on other less well-known
relationships, for example, the association between stretched penile
length and semen and hormone variables, and between obesity and
reduced sperm count. Interestingly, stretched penile length was corre-
lated positively with sperm concentration, total sperm count, percen-
tage progressive motility, TTV and Inhibin B and negatively correlated
with FSH. In a study such as this it is possible to nd unexpected
relationships between two variables that are correlated with other
factors. We suspect that the penile length sperm concentration
relationship is explained by the correlations with obesity: both
penile length and sperm count were lower with obesity. The smaller
penile length is probably attributable to underestimation of penile
length in obese subjects using a ruler to measure the distance from
the pubis to the tip of the glans of the stretched penis.
When compared with the fertile Danish men from the European
study (Jorgensen et al., 2001), the testosterone levels are lower in
the Australian men: median (2.5 97.5 percentiles) for Australian
men 17 (933) and 22 (11 36) for the Danish men. LH levels
were slightly higher in the Australian men 3.7 (1.5 7.5) than in the
 Obesity and sperm count 1565

Figure 1 Plot of individual results (n 225) and box plot of total sperm count from men with BMI , 20 kg/m2 (underweight), 20 25 (normal),
25 30 (overweight) and 30 (obese) (the arrow indicates outlier (3115  106) and the box represents the interquartile range with the bar represent-
ing the median value. Whiskers extend beyond the ends of the box as far as the minimum and maximum values).

Table III Mean (SD, n) cube root total sperm count and serum hormone concentrations in three BMI groups

BMI (kg/m2) Cube root total sperm FSH (IU/l) Inhibin B Testosterone SHBG
p
countb (3 3 106) (pg/ml)a (nmol/l)b (nmol/l)a
.............................................................................................................................................................................................
,25 6.8 (2, 75) 3.6 (2, 75) 192.7 (65.7, 75) 19.1 (6.4, 75) 36.7 (14.7, 75)
2530 6.9 (2, 110) 3.3 (2, 109) 182.5 (73, 109) 17.5 (5.3, 109) 29.3 (10.3, 109)
.30 6.1 (1, 35) 4.0 (2, 36) 139.8 (47.9, 36) 16.7 (5.8, 36) 25.9 (10.8, 36)
a b
One-way analysis of variance, P  0.001, P , 0.05.

Danish men 3.5 (1.6 6.6) while SHBG levels were similar; 29 (10 58)
and 30 (11 63), respectively (Andersson et al., 2004). All serum ana-
lyses (ours and the Europeans) were assessed centrally at the same
laboratory in Copenhagen. The likely explanation for the difference
in the testosterone levels is different timing of the blood sampling in
the two studies with respect to the diurnal variation in testosterone
with its peak in the early morning (Diver, 2006). The time of sampling
in the current study was 0800 to 1900, median 1133 h, and in the
Danish study 0615 1245, median 0750 h.
Inverse relationship between BMI
and testicular function
We conrmed that BMI and obesity had signicant inverse correlations
with SHBG, Inhibin B and testosterone (Seidell et al., 1990; Pasquali
et al., 1991; Svartberg et al., 2003; Jensen et al., 2004; Winters
et al. 2006). The lower sperm concentration in the obese men was
not accompanied by signicant correlations between BMI and any
semen variable or TTV. Other studies have also shown an inverse
relationship between obesity and semen quality (Jensen et al., 2004;
Kort et al., 2006; Aggerholm et al., 2008; Hammoud et al., 2008).
Hammoud et al. (2008) retrospectively examined 526 infertile patients
and found that oligozoospermia and a low progressively motile sperm
count (dened as ,10  106 progressively motile sperm) were more
frequent with increasing BMI. However, the study was limited by the
use of self-reported height and weight measurements (Hammoud
et al., 2008). In another study, Aggerholm et al. (2008) used data
derived from ve separate occupational and environmental
population-based semen studies to create one data base (n
2139). Men who were overweight were found to have a slightly
lower adjusted sperm concentration and total sperm count than
men with a normal BMI (Aggerholm et al., 2008). Young Danish mili-
tary conscripts (n 1558) with either low or high BMI (,20 kg/m2
or .25 kg/m2) had lower sperm numbers and percentage normal
morphology than those with BMI in the normal range (Jensen et al.,
2004). This study had 14% of subjects with BMI ,20 whereas our

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 1566 Stewart et al.

Table IV Linear regression of cube root total sperm

Study strengths and weaknesses
count in 223 fertile men with and without TTV included A possible weakness is the inclusion of only fertile couples in the
as a factor study as this may reduce or obscure a more signicant relationship
between obesity and other semen analyses results had infertile sub-
Model Factor Coefcient (SE) P-value r2 jects been included. The strengths of this study were the prospec-
........................................................................................
tive design and the blind ascertainment of results of clinical, semen
With TTV Constant 2.34 (0.51) ,0.001 37.0
Abstinence 0.40 (0.06) ,0.001 and hormone data by the same clinician and scientists. Also all
(days) hormone analyses were performed centrally in a facility in Copenha-
TTV (ml) 0.069 (0.009) ,0.001 gen which also participated in the European and US studies of part-
Left varicocele 20.39 (0.14) 0.006 ners of pregnant women (Jorgensen et al., 2001; Swan et al., 2003).
.30 BMI, 20.77 (0.25) 0.002
Our laboratory participated in two EQC programs, the Australian
Obese
External Quality Assurance Schemes for Reproductive Medicine
Without Constant 5.77 (0.25) ,0.001 21.5
TTV Abstinence 0.37 (0.06) ,0.001 and an International EQC program conducted by Dr Niels Jrgen-
(days) sen. Obtaining a representative sample of the general male popu-
Left varicocele 20.55 (0.12) ,0.001 lation is a near impossibility since few men volunteer, and
.30 BMI, 20.69 (0.28) 0.013 previous experience indicates that volunteers disproportionately
obese
represent those who are concerned about their fertility, either
because of previous testicular disorders or suspected infertility
(Bonde, 1990; Handelsman, 1997; Larsen et al., 1998; Cohn
et al., 2002). The design of this study allowed assessment of this
type of selection bias and this will be reported separately. The
study had only 2% with low BMI and although they had lower total
semen analysis results provide useful normative data for our geo-
sperm counts than those in the BMI 20 30 groups no strong claims
graphic region. They have been included in a WHO-sponsored
can be made because of the small numbers. A BMI value of
report (Cooper et al., in preparation) and the reference values
.25 kg/m2 was associated with lower numbers of normal
for the 5th Edition of the WHO Semen Analysis Manual (date of
chromatin-intact-motile sperm cells per ejaculate in a study of 520
publication is unknown at this stage).
men from infertile couples (Kort et al., 2006). Other smaller studies
have also shown a negative relationship between obesity and semen
quality (Fejes et al., 2005; Koloszar et al., 2005; Magnusdottir et al., Conclusion
2005). One study failed to nd an inverse association between In conclusion, this study has provided useful normative data for
obesity and semen quality (Pauli et al., 2008). A few studies have fertile Australian men. As well as conrming many well-established
also shown that male obesity is associated with an increased risk of andrological associations, there was a lower sperm concentration in
infertility (Sallmen et al., 2006; Nguyen et al., 2007; Ramlau-Hansen obese men with BMI .30. Whether this is cause or effect, in terms
et al., 2007). The risk of infertility may be particularly high if the of adiposity reducing spermatogenesis or reduced testicular function
female partner is also overweight or obese (Ramlau-Hansen et al., promoting fat deposition, remains to be determined.
2007).
Concerning the cause and effect relationship of the association
between obesity and reduced sperm concentrations, most authors Acknowledgements
assume that the obesity must be impairing testicular function and do
not consider the alternative possibility, that defective spermatogenesis We would like to thank the Department of Growth and Reproduc-
predisposes to obesity. There are many reports of hypogonadotrophic tion, Rigshospitalet, Copenhagen, Denmark, for analysing our serum
hypogonadism associated with gross obesity and indications that it can samples. We would also like to thank the obstetricians in private prac-
be treated with aromatase inhibitors (Cohen, 2008; Loves et al., 2008; tice who allowed us to approach their patients and Ms Ming Li Liu for
Roth et al., 2008). However, none of the subjects in this study showed technical assistance.
features of gonadotrophin deciency, and FSH levels are not low in the
obese group. The FSH/Inhibin B ratio was signicantly higher in the
obese group which, together with the inverse relationship between
Funding
FSH and total sperm count, is consistent with a primary testicular The Royal Womens Hospital Research Advisory Committee and Mel-
defect. Thus we suggest reduced testicular function may predispose bourne IVF provided funding of this project.
to, or aggravate, obesity. It has been known from traditional animal
husbandry that castration increases body fat (Hausberger and
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Submitted on September 25, 2008; resubmitted on February 27, 2009; accepted on
March 3, 2009