Male obesity and alteration in sperm parameters

Ahmad O. Hammoud, M.D.,a Nicole Wilde, M.P.H.,a Mark Gibson, M.D.,a Anna Parks,a
Douglas T. Carrell, Ph.D.,a,b and A. Wayne Meikle, M.D.c,d
Division of a Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology; b Department of Andrology,
and c Department of Medicine and Pathology, University of Utah, School of Medicine; and d ARUP Institute for Experimental
Pathology, Salt Lake City, Utah

Objective: To study the effect of male obesity on sperm parameters and erectile dysfunction.
Design: Retrospective analysis.
Setting: Referral fertility center.
Patient(s): Couples presenting for infertility treatment.
Intervention(s): On presentation, all men reported their weight and height and filled out an intake form that in-
cludes questions regarding factors that affect male infertility, including presence of erectile dysfunction. Body
mass index (BMI) was divided into three groups: normal (BMI <25 kg/m2), overweight (25 kg/m2 % BMI <
30 kg/m2), and obese (BMI R30 kg/m2). Sperm parameters reviewed included sperm concentration and progres-
sively motile sperm count.
Main Outcome Measure(s): Oligozoospermia, low progressively motile sperm count, and self-reported erectile
dysfunction.
Result(s): The mean age of the study population was 32.8  0.3 years. Among the 526 patients, 10.2% (54 of 526)
were excluded because of the presence of a male factor known to affect fertility. The incidence of oligozoospermia
increased with increasing BMI: normal weight 5.32%, overweight 9.52%, and obese 15.62%. The preva-
lence of a low progressively motile sperm count was also greater with increasing BMI: normal weight 4.52%,
overweight 8.93%, and obese 13.28%. The incidence of erectile dysfunction did not vary across BMI cate-
gories when corrected for potential contributing factors.
Conclusion(s): Male obesity is associated with increased incidence of low sperm concentration and low progres-
sively motile sperm count. (Fertil Steril 2008;90:22225. 2008 by American Society for Reproductive Medi-
cine.)
Key Words: Male obesity, low sperm count, erectile dysfunction, sperm motility, sperm morphology

Obesity is associated with significant disturbance in the hor- couples with obese male partners; causes for this relationship
monal milieu that can affect the reproductive system (1, 2). might include behavioral, sexual dysfunction, or semen
This effect is clear in women who present with several repro- quality factors.
ductive disorders when they are in the two extremes of
The purpose of this study was to investigate the relation-
obesity or weight loss (3). In men this relationship is poorly
ship between BMI, measures of semen quality, and male sex-
characterized. Several reports showed that the accumulation
ual dysfunction in couples presenting for evaluation of
of fatty tissue in men is associated with a decrease in serum
infertility.
levels of total and free T (1) and an increase in serum levels
of E2 (2). This hormonal alteration may lead to low sperm
count. Jensen et al. and others reported a negative correlation MATERIALS AND METHODS
between obesity and various sperm parameters in the general
After institutional review board approval, we reviewed
population (4, 5). Newer data, from population studies, have
records of all couples who presented to a tertiary care center
suggested a relationship between increasing body mass index
for infertility evaluation in the last 2 years and who had a se-
(BMI) and male infertility (6, 7). The interaction between
men analysis. Data collected included patient demographics,
obesity and fertility has received increased attention owing
past medical and surgical history, and self-reported male
to the recent and rapid increase in the prevalence of obesity
sexual dysfunction. On presentation, all men reported their
in the developed world (8, 9). It is unclear how the findings
weight and height and filled out an intake form with questions
of poorer measures of semen quality in cohort studies relate
regarding the existence of factors that affect male fertility,
to the increased interpregnancy intervals found among
including smoking, alcohol use, substance abuse, type of
medication, past medical and surgical history, and various
Received August 15, 2007; revised October 5, 2007; accepted October 8, health questions including the presence of erectile dysfunc-
2007. tion. These forms were complemented by physician intake
Reprint requests: Ahmad O. Hammoud, M.D., Division of Reproductive
Endocrinology and Infertility, Department of Obstetrics and Gynecol-
notes that recorded a comprehensive medical history, with in-
ogy, Suite 2 B200, University of Utah, Salt Lake City, UT 84132 (FAX: formation focused on infertility. Weight and height were used
801-587-3795; E-mail: ahmad.hammoud@hsc.utah.edu). to calculate the BMI according to the standard formula:

2222 Fertility and Sterility Vol. 90, No. 6, December 2008 0015-0282/08/$34.00
Copyright 2008 American Society for Reproductive Medicine, Published by Elsevier Inc. doi:10.1016/j.fertnstert.2007.10.011
BMI weight/height2 (kg/m2). The male subjects were di- TABLE 1
vided into three groups according to the Centers for Disease
Control and Prevention classification: normal weight (BMI Distribution of risk factors for male infertility.
<25 kg/m2), overweight (25 % BMI < 30 kg/m2), and obese No. of
(BMI R30 kg/m2) (10). Diagnosis patients (%)
All subjects underwent comprehensive semen analysis Antisperm antibodies 1 (1.9)
within 1 month. Sperm parameters analyzed included sperm Chronic prostatitis 1 (1.9)
concentration (106 sperm/mL), total progressively motile Empty sella syndrome 1 (1.9)
sperm per ejaculate, and sperm morphology according to Epididymitis 1 (1.9)
the World Health Organization criteria (11). The prevalence Increased prolactin 1 (1.9)
of oligozoospermia, low total progressively motile sperm Klinefelters syndrome 1 (1.9)
per ejaculate, and decreased percentage of normally formed Orchitis 1 (1.9)
sperm was calculated and compared among the three BMI Testicular failure 1 (1.9)
groups. Oligozoospermia was defined as a sperm concentra- Hypospadias 2 (3.7)
tion of <20  106/mL. Low progressively motile sperm Chemotherapy 2 (3.7)
count was defined at thresholds of 10  106 motile sperm Hydrocele 3 (5.6)
per ejaculate and 5  106 progressively motile sperm per Undescended testis 5 (9.3)
ejaculate in two separate analyses. The cutoffs for low pro- Testicular cancer surgery 6 (11.1)
gressively motile sperm count were based on insemination Vasectomy reversal 11 (20.4)
data reporting reduced pregnancy rates with inseminations Varicocele 17 (31.5)
with specimens containing less than 10  106 progressively Total 54 (100)
motile sperm per inseminate (12, 13) or with 5  106 progres-
sively motile sperm per inseminate (14). Decreased percent- Hammoud. Male obesity and sperm count. Fertil Steril 2008.
ages of normally formed sperm were defined as <30% of
sperm exhibiting normal head morphology.
patients compared with normal-weight patients was 3.4
Finally, the prevalence of erectile dysfunction in relation to
(95% CI 1.1210.60). When 5  106 progressively motile
patient age, smoking status, alcohol use, use of antidepres-
sperm was used as the threshold for defining low total progres-
sant, and BMI was also evaluated.
sively motile sperm count, we obtained similar results: the
Means were reported as mean  standard error. The chi- prevalence of such counts was 3.2% among men with normal
square test for trend was used to compare frequencies. weight, 6.5% for overweight men, and 10.9% for obese men.
Logistic regression analysis was used when appropriate. (P.028) When we compared obese patients with non-obese
The statistical package SPSS 13.0 was used for analysis patients (normal weight and overweight), the OR of having
(SPSS, Chicago, IL). a high percentage of abnormal morphology was 1.6 (95%
CI 1.052.59).
The incidence of erectile dysfunction in our patient
RESULTS population was 9.2% (36 of 390). The incidence of erectile
Over a period of 2 years, 526 couples were seen. The mean dysfunction showed a trend to increase with increasing
age of male partners was 32.8  0.30 years. Among the 526
men, 10.3% (54 of 526) had a male factor known to affect fer-
tility. The distribution of those conditions is given in Table 1. FIGURE 1
After exclusion of patients with known male factor, the BMI Incidence of oligozoospermia in the different BMI
data were available for 83% of male patients (390 of 472). The groups (P .011).
mean BMI of the population was 28.5  0.26 kg/m2. The
distribution of the BMI groups was as follows: normal weight
24.1% (94 of 390), overweight 43.1% (168 of 390), and obese
32.8% (128 of 390). The overall prevalence of oligozoosper-
mia (defined as sperm count <20  106/mL) was 10.5% (41
of 349). The prevalence of oligozoospermia increased with in-
creasing BMI (P.011) (Figure 1). The odds ratio (OR) of
oligozoospermia in obese patients compared with patients
with normal BMI was 3.3 (95% confidence interval [CI]
1.199.14). The prevalence of low progressively motile sperm
count (defined as <10  106 progressively motile sperm) also
increased with BMI (P.018) (Figure 2). The OR of having Hammoud. Male obesity and sperm count. Fertil Steril 2008.
a progressively motile sperm count <10  106 in obese

Fertility and Sterility 2223

 FIGURE 2
Incidence of low progressively motile sperm count in
the different BMI groups (P .018).
Hammoud. Male obesity and sperm count. Fertil Steril 2008.
BMI; however, this trend did not reach statistical significance
(normal weight 6.4% [6 of 94], overweight 7.7% [13 of 168],
and obese 9.4 % [12 of 128], P.71). A logistic regression
model that corrected for age, smoking, alcohol use, antide-
pressant use, and BMI showed that age (OR 1.06; 95% CI
1.01.12) and intake of antidepressant (OR 8.5; 95% CI
2.430.1) were the only significant determinants of the
presence of erectile dysfunction.
DISCUSSION
The incidence of obesity in the United States is reaching
epidemic proportions. It has increased from 12% to 17.9 %
in the period from 1991 to 1998 (8). In the same period,
male obesity has increased from 11.7% to 17.9% (8). A
more recent study estimated the incidence of obese
individuals to be 30.6% (9). These values were reflected in
our study population. Taking into consideration the effect
of obesity on both male and female fertility, it is predictable
that, as time passes, the fertility of the general population will
be reduced as well.
The relationship between obesity and male infertility has
been described recently (57). However, there is controversy
regarding the extent of this relationship and its mechanisms.
For example, Jensen et al. (4) reported a higher prevalence of
oligozoospermia in overweight and obese men compared
with normal-weight men (24.4% vs. 21.7%). However, they
did not find any relationship between increasing male BMI
and percentage of motile sperm. In a group of 274 men, obe-
sity was also associated with a lower sperm count compared
with non-obese patients. This relationship was only found in
normozoospermic men (15). Kort et al. (16) found that BMI
correlated negatively with the total number of normal sper-
matozoa. They did not report on sperm count or morphology
in this study.
In our study, we showed that obesity is associated with an
OR of oligozoospermia of 3.3, in a large patient population.
2224 Hammoud et al. Male obesity and sperm count
We also showed that obesity is associated with reduced mo-
tile sperm count and increased incidence of abnormal mor-
phology. These results are an important addition to the
emerging evidences of the relationship between obesity and
male infertility.
The relationship between obesity and male infertility is
multifactorial. Obesity can cause male infertility by altered
spermatogenesis due to the endocrinology of hypoandrogen-
ism and increased E2 levels. Estradiol may have deleterious
effects on spermatogenesis (17, 18). Low T levels in obese
men are due to lower sex hormone-binding globulin, the
enhancement of negative feedback on gonadotropins by the
increased E2 (1, 19, 20), insulin resistance (21), and sleep ap-
nea (22, 23). A decrease in sperm count is known to contrib-
ute to male infertility (24, 25). Finally, studies have shown
that obesity is associated with an increased incidence of erec-
tile dysfunction that can contribute to infertility (26, 27). In
our study, sexual dysfunction showed a trend to increase
with increasing weight. The lack of statistical significance
might be attributed to the self-reported sexual dysfunction
in this retrospective study.
Our study has potential sources of bias. The first is the
self-reported height and weight by the male partners during
the initial visit. However, several reports showed that self-
reported BMI has a reasonable accuracy in predicting the
incidence of obesity. In men, the sensitivity and specificity
for determining clinical obesity (BMI R30) by the self-
reported BMI were 83% and 96%, respectively (28, 29).
The selection of the patient population from couples who
presented for infertility treatment can also be an element
of concern. In this population, the incidence of abnormal
sperm parameters is expected to be higher than in the gen-
eral population. The use of absolute frequencies in this pop-
ulation no doubt overestimates the incidence of abnormal
sperm parameters in relation to overweight and obesity.
However, the use of the OR allows extrapolation of the
effect of obesity we observed to the population at large.
Last, the fact that this was a retrospective study implies
that it is impossible to ascertain whether all patients under-
went the same comprehensive workup to rule out other
causes of male infertility. However, these factors are not
known to be associated with obesity and thus are not likely
to be confounders in the relationship between obesity and
altered sperm parameters.
In summary, we showed that there is a strong relationship
between overweight and obesity and altered sperm parame-
ters. The available data need to be complemented by future
cohort studies that define prospectively the extent of this
relationship and examine the effect of weight loss.
REFERENCES
1. Giagulli VA, Kaufman JM, Vermeulen A. Pathogenesis of the decreased
androgen levels in obese men. J Clin Endocrinol Metab 1994;79:
9971000.
2. Schneider G, Kirschner MA, Berkowitz R, Ertel NH. Increased estrogen
production in obese men. J Clin Endocrinol Metab 1979;48:6338.
Vol. 90, No. 6, December 2008
 3. Pasquali R, Pelusi C, Genghini S, Cacciari M, Gambineri A. Obesity
and reproductive disorders in women. Hum Reprod Update 2003;9:
35972.
4. Jensen TK, Andersson AM, Jorgensen N, Andersen AG, Carlsen E,
Petersen JH, et al. Body mass index in relation to semen quality and re-
productive hormones among 1,558 Danish men. Fertil Steril 2004;82:
86370.
5. Magnusdottir EV, Thorsteinsson T, Thorsteinsdottir S, Heimisdottir M,
Olafsdottir K. Persistent organochlorines, sedentary occupation, obesity
and human male subfertility. Hum Reprod 2005;20:20815.
6. Nguyen R, Wilcox A, Skjaerven R, Baird DD. Mens body mass index
and infertility. Hum Reprod 2007;22:248893.
7. Sallmen M, Sandler DP, Hoppin JA, Blair A, Baird DD. Reduced fertility
among overweight and obese men. Epidemiology 2006;17:5203.
8. Mokdad AH, Serdula MK, Dietz WH, Bowman BA, Marks JS,
Koplan JP. The spread of the obesity epidemic in the United States,
1991-1998. JAMA 1999;282:151922.
9. Hedley AA, Ogden CL, Johnson CL, Carroll MD, Curtin LR, Flegal KM.
Prevalence of overweight and obesity among US children, adolescents,
and adults, 1999-2002. JAMA 2004;291:284750.
10. Overweight, obesity, and health risk. National Task Force on the
Prevention and Treatment of Obesity. Arch Intern Med 2000;160:
898904.
11. World Health Organization. Manual for the examination of human semen
and sperm-cervical mucus interaction. 4th ed. Cambridge: Cambridge
University Press, 1999.
12. Ombelet W, Vandeput H, Van de Putte G, Cox A, Janssen M, Jacobs P,
et al. Intrauterine insemination after ovarian stimulation with clomi-
phene citrate: predictive potential of inseminating motile count and
sperm morphology. Hum Reprod 1997;12:145863.
13. Miller DC, Hollenbeck BK, Smith GD, Randolph JF, Christman GM,
Smith YR, et al. Processed total motile sperm count correlates with
pregnancy outcome after intrauterine insemination. Urology 2002;60:
497501.
14. Khalil MR, Rasmussen PE, Erb K, Laursen SB, Rex S, Westergaard LG.
Homologous intrauterine insemination. An evaluation of prognostic fac-
tors based on a review of 2473 cycles. Acta Obstet Gynecol Scand
2001;80:7481.
15. Koloszar S, Fejes I, Zavaczki Z, Daru J, Szollosi J, Pal A. Effect of body
weight on sperm concentration in normozoospermic males. Arch Androl
2005;51:299304.
Fertility and Sterility
16. Kort HI, Massey JB, Elsner CW, Mitchell-Leef D, Shapiro DB, Witt MA,
et al. Impact of body mass index values on sperm quantity and quality.
J Androl 2006;27:4502.
17. Akingbemi BT. Estrogen regulation of testicular function. Reprod Biol
Endocrinol 2005;3:51.
18. Oliva A, Spira A, Multigner L. Contribution of environmental factors to
the risk of male infertility. Hum Reprod 2001;16:176876.
19. Strain GW, Zumoff B, Kream J, Strain JJ, Deucher R, Rosenfeld RS,
et al. Mild hypogonadotropic hypogonadism in obese men. Metabolism
1982;31:8715.
20. Haffner SM, Valdez RA, Stern MP, Katz MS. Obesity, body fat distribu-
tion and sex hormones in men. Int J Obes Relat Metab Disord 1993;17:
6439.
21. Tsai EC, Matsumoto AM, Fujimoto WY, Boyko EJ. Association of bio-
available, free, and total testosterone with insulin resistance: influence of
sex hormone-binding globulin and body fat. Diabetes Care 2004;27:
8618.
22. Luboshitzky R, Zabari Z, Shen-Orr Z, Herer P, Lavie P. Disruption of the
nocturnal testosterone rhythm by sleep fragmentation in normal men.
J Clin Endocrinol Metab 2001;86:11349.
23. Luboshitzky R, Lavie L, Shen-Orr Z, Herer P. Altered luteinizing hor-
mone and testosterone secretion in middle-aged obese men with obstruc-
tive sleep apnea. Obes Res 2005;13:7806.
24. Slama R, Eustache F, Ducot B, Jensen TK, Jorgensen N, Horte A, et al.
Time to pregnancy and semen parameters: a cross-sectional study among
fertile couples from four European cities. Hum Reprod 2002;17:50315.
25. Bonde JP, Ernst E, Jensen TK, Hjollund NH, Kolstad H, Henriksen TB,
et al. Relation between semen quality and fertility: a population-based
study of 430 first-pregnancy planners. Lancet 1998;352:11727.
26. Seftel A. Male hypogonadism. Part II: etiology, pathophysiology, and
diagnosis. Int J Impot Res 2006;18:2238.
27. Chung WS, Sohn JH, Park YY. Is obesity an underlying factor in erectile
dysfunction? Eur Urol 1999;36:6870.
28. Bolton-Smith C, Woodward M, Tunstall-Pedoe H, Morrison C. Accuracy
of the estimated prevalence of obesity from self reported height and
weight in an adult Scottish population. J Epidemiol Community Health
2000;54:1438.
29. Gillum RF, Sempos CT. Ethnic variation in validity of classification of
overweight and obesity using self-reported weight and height in
American women and men: the Third National Health and Nutrition
Examination Survey. Nutr J 2005;4:27.
2225