The Effect of Body Mass Index on Semen Quality
1,6,7Department of Obstetrics and Gynaecology, Kasturba Medical College, MAHE University, Manipal, Karnataka, India
2-4Department of Reproductive Medicine & Surgery (RMS), Kasturba Medical College, MAHE University, Manipal, Karnataka, India
5Division of Clinical Embryology, Kasturba Medical College, MAHE University, Manipal, Karnataka, India
8Department of Biostatistics, Gajra Raja Medical College, Gwalior, Madhya Pradesh, India; Jiwaji University, Gwalior, Madhya Pradesh, India
Corresponding Author: Anjali Mundkur, Department of Reproductive Medicine & Surgery (RMS), Kasturba Medical College, MAHE University, Manipal, Karnataka, India, Phone: +91 9686448802, e-mail: firstname.lastname@example.org
Received on: 30 June 2022; Accepted on: 14 September 2022; Published on: 28 December 2022
Introduction: Obesity is a major public health problem. Its impact on male infertility is controversial. We aimed to explore the relationship between increasing male body mass index (BMI) and the change in semen parameters and recognize the ones most affected.
Objectives: Explore the relationship between the male BMI and their semen parameters & recognize the most affected parameter.
Materials and methods: It is a prospective study involving 221 men who were distributed into groups according to the BMI (kg/m2)—underweight (<18.5), normal (18.5–22.9), overweight (23.0–24.9), and obese I (25–29.9) obese II (>30). Their semen analysis was done as a part of the routine evaluation, and that was correlated with the BMI. The statistical significance was determined using the p-value, obtained by analysis of variance (ANOVA) testing. p-value <0.05 was considered statistically significant.
Results: The pairs: normal vs obese I, normal vs obese II, and overweight vs obese I have statistically significant mean differences for the volume. The pairs: normal vs obese I and normal vs obese II have statistically significant mean differences for progressive motility. The pairs: normal vs obese I have a statistically significant mean difference for total motility while using a family error rate of 0.05.
Conclusion: Obese men had significantly reduced semen volume, progressive, and total motility. The sperm concentration and morphology also showed abnormal values with increasing BMI, but the relationship was not statistically significant. Oligospermia in the underweight group was incidentally noted. We concurred that maintaining a normal BMI augments a man’s fertility potential.
How to cite this article: Bansal S, Mundkur A, Adiga P, et al. The Effect of Body Mass Index on Semen Quality. Int J Infertil Fetal Med 2022;13(3):121-124.
Source of support: Nil
Conflict of interest: Dr Pratap Kumar is associated as the National Advisory Board Member of this journal and this manuscript was subjected to this journal’s standard review procedures, with this peer review handled independently of the Editor-in-Chief and his/her research group.
Keywords: Obesity, Oligospermia, Prospective observational study, Sperm motility and physically fit.
STATEMENT OF CLINICAL SIGNIFICANCE
Obesity is a widespread, manmade pandemic. Increasing BMI grossly reduces sperm volume and motility. Underweight men also have deranged semen parameters. Staying in shape and having an adequate BMI may ensure and improved fertility status.
Obesity is a global pandemic that’s massively affecting all age-groups and all sections of society. It is characterized by an accumulation of excess body fat or white adipose tissue, associated with adverse health outcomes and reduced life expectancy. According to the regional fact sheet provided by the district, the recorded incidence of obesity in men in the age-group of 15–49 years was 22.2% in the year 2015; it is expected to reach 35% in India overall by 2040 if the present trend continues.
Our convenient and “canned” eating habits, the sedentary lifestyle that we assume at our workplace and home, and the baseline neglect towards our health all put together are making us, to put it plainly, fat.
So much so that becoming overweight and eventually obese is now accepted by many as something that just happens as age progresses. Obesity is at an all-time high in developing and developed nations alike.
There are several studies stressing the importance of an appropriate weight and healthy lifestyle in women and how it positively influences their fertility potential.1
However, the published data suggesting the same for men is scarce. Obesity is the root cause leading us to a plethora of metabolic and physiological abnormalities, causing severe side effects related to health, fertility as well as life expectancy.
Infertility, per se, in the general population, mostly even in today’s time and age, is something that’s associated with women. But in reality, nearly 40% of the couples tagged as infertile are dealing with the “male” causes of infertility singularly. Male factor infertility is multifactorial, and obesity may potentially be the lone cause and an augmentative factor in many individuals.2
Obesity is said to affect spermatogenesis as well as the quality of the semen. Also, there is upcoming evidence suggesting that weight loss helps with improvement in semen quality.3
The data suggesting that male obesity is directly causative of male infertility is not yet definitive.4
The obesity noted in the men of reproductive age-group is a fast-rising trend, more like a way of life.
There is emerging data about obesity throwing light on how it works, incorporating different mechanisms in order to hamper sperm quality. It causes metabolic insults that can also reflect onto the upcoming generations of the affected males. The molecular makeup of the impaired sperm affects the subsequent embryo development.5
It causes an imbalance in the hypothalamic-pituitary-gonadal axis and a decrease in sex hormone binding globulin levels. That, by default, causes an increase in free testosterone, which is subjected to more peripheral conversion to estrogen. There is an associated rise in serum leptin levels, which lowers serum testosterone.6
Increased adiposity in the scrotal tissue raises its temperature and decreases spermatogenesis directly. It also leads to increased oxidative stress that inhibits the normal functioning of sperms and also makes them more prone to destruction. Sertoli cells are associated with germ cells, providing both nutritional and metabolic support, and this adhesion between the two is testosterone-dependent. But in the setting of obesity, testosterone is reduced, and this adhesion is weakened. The spermatids get phagocytosed.7
The rising prevalence of obesity and subfertility, accompanied by solid theories hinting towards an accountable link, is prodding us to formulate a potential intervention. It is our duty to conduct large-scale studies and clinical trials to constitute conclusive evidence. The main reason is that the solution to obesity is broadly achievable—a healthy lifestyle, revolutionary modifications in eating habits, and regular exercise. These are some “easy to inculcate” changes that can pay off with disproportionately rewarding long-term dividends.
MATERIALS AND METHODS
We conducted a prospective, observational study over 4 months. It included the consenting male partners of the couples that had come for subfertility evaluation at the Department of Reproductive Medicine and Surgery in a tertiary care hospital. A detailed history was taken, and an examination was performed for men attending the infertility clinic. Their semen sample was collected for analysis as a part of their routine evaluation.
All male partners of the infertile couples that attended the clinic during the study duration consented to be a part of the same.
Men with conditions like hypertension, diabetes mellitus, chronic kidney disease, occupation-related reasons such as—working in a furnace, chefs, etc., history of varicocele, known cryptorchidism or any other testicular anomaly, having undergone any scrotal/testicular surgery, which are the already known causes for deranged semen parameters, were excluded. Institutional Ethics Committee approval was sought before starting the study. A time-bound sample side was decided upon, and 221 participants were recruited.
For the consenting male partners, height and weight were measured, and the BMI was calculated according to the standard formula—weight (kg)/height (m2).
The participants were divided into groups as per their BMI. The BMI was arranged such that a set range was given for each of these groups—underweight, normal weight, and overweight, obese grades—I and II, as approved by the World Health Organization (WHO) for the Asian population.8
Semen collection and analysis were conducted as per the hospital protocol (Table 1).
|BMI category and range||Number of cases (%)|
|Underweight (<18.5)||5 (2.3)|
|Normal range (18.5–22.9)||49 (22.2)|
|Overweight (23–24.9)||49 (22.2)|
|Obese I (25–30)||85 (38.5)|
|Obese II (>30)||33 (14.9)|
The sample was collected via masturbation after a minimum of 3 days of abstinence. After collection, the semen sample was liquefied and analyzed as per the standard hospital protocol. The analysis was done for each semen sample, and the semen parameters were interpreted according to the criteria circulated by the WHO.
The Outcome Measures
Explore the relationship between the male BMI and their semen parameters.
Recognize the most affected parameters.
Approval to conduct the study, which explained its nature in complete detail, was sought from the Institutional Ethics Committee. A written informed consent was obtained from the men who agreed to participate in the study (their participation being completely voluntary).
We analyzed the data using the Statistical Package for the Social Sciences software; the results have been represented in percentages and frequencies. The statistical significance was determined using the p-value obtained by ANOVA testing.
From the patient profile, statistically significant results (i.e., p < 0.05) indicate that the group means are not equal for volume, progressive motility, and total motility. However, ANOVA does not identify the particular pairs with significantly different groups’ means. In order to explore the differences between multiple groups’ means, post hoc tests were applied. Going by our ANOVA results, we have five groups that require 10 relative equations to cover all the combinations. We’ll use a post hoc test and specify that the family of 10 comparisons should collectively produce a familywise error rate of 0.05. The post hoc test used here is Tukey’s method, that is, the most commonly used method for comparing all possible pairs (Table 2).
|BMI category (N)||Volume (mL)||Concentration (million/mL)||Progressive motility (%)||Total motility (%)||Morphology (%)|
|Underweight (5)||3.2 ± 1.48||26.6 ± 8.56||38 ± 9.27||54 ± 10.54||6.2 ± 0.83|
|Normal (49)||3.6 ± 1.20||37.1 ± 20.93||43.57 ± 3.88||60.14 ± 15.4||6.4 ± 4.39|
|Overweight (49)||3.37 ± 1.11||34.59 ± 19.17||39.77 ± 10.77||58.1 ± 16.58||9.06 ± 13.73|
|Obese I (85)||2.69 ± 1.24||29.59 ± 21.63||35.21 ± 11.61||52.11 ± 15.20||5.6 ± 4.11|
|Obese II (33)||2.71 ± 1.72||26.64 ± 13.15||33.72 ± 14.24||51.15 ± 17.58||5.09 ± 3.41|
*<0.05- statistically significant difference
From the post hoc analysis, we inferred:
The pairs: Normal vs obese I, normal vs obese II, and overweight vs obese I have statistically significant mean differences for the volume.
The pairs: Normal vs obese I and normal vs obese II have statistically significant mean differences for progressive motility.
The pairs: Normal vs obese I have a statistically significant mean difference for total motility while using a family error rate of 0.05.
Age and BMI: A body mass index of >25 is common in the age group of 30–40. This is the primary age bracket to attain reproductive potential (Figs 1 and 2) (Table 3).
|Pairs for comparison||Volume||Progressive motility||Total motility|
|Mean difference||p-value||Mean difference||p-value||Mean difference||p-value|
|Underweight vs normal||−0.4673||0.921||−5.571||0.872||−5.943||0.931|
|Underweight vs overweight||−0.1776||0.998||−1.776||0.998||−3.902||0.985|
|Underweight vs obese I||0.5047||0.891||2.788||0.988||2.082||0.999|
|Underweight vs obese II||0.4970||0.910||4.273||0.952||3.048||0.995|
|Normal vs overweight||0.2898||0.754||3.796||0.550||2.041||0.969|
|Normal vs obese I||0.9721||0.0001||8.360||0.002||8.025||0.041|
|Normal vs obese II||0.9643||0.004||9.844||0.004||8.991||0.091|
|Overweight vs obese I||0.6823||0.015||4.564||0.242||5.984||0.222|
|Overweight vs obese II||0.6745||0.095||6.048||0.194||6.951||0.296|
|Obese I vs obese II||−0.0077||1.00||1.484||0.977||0.966||0.998|
Overweight and obese men had reduced concentration of sperm as compared to men with normal BMI but with no statistical significance. Total motility reduced significantly with an increasing BMI. Progressive motility was, however, the most affected parameter, and it showed a gross reduction with an elevation in the BMI.
The combined sperm defects were more commonly noted as compared to lone defects with increasing weight.
It was an incidental observation in the present study that low BMI may also affect sperm concentration. We wish to emphasize that a deviation from the normal BMI leads to deranged semen parameters. The study demonstrated that the best quality of semen was noted in those who were in the adequate BMI range.
The presence of oligospermia in the study population was noted in 31 individuals (14.02%). [Amongst the ones with low BMI– one (20%), normal BMI– nine (18%), overweight men– 14 (28%), obese I– six (7%), and obese II– one (3.33%)]. It was observed that there was no clear-cut decline in terms of oligospermia as the BMI increased.
This study showed that with the increase in BMI, the quality of ejaculation deteriorates.
Semen volume reduced with the increasing weight, as per our observation. A reduced volume indicates either the semen production is compromised or there is a partial/complete obstruction at some level in the male genital tract.
This is in line with one of the largest studies equating BMI with semen parameters, which was conducted by Bieniek et al. They concurred that semen volume, concentration, and motility were hampered by increasing BMI. It was thus established that semen parameters demonstrated mild but significant relationships with BMI, possibly contributing to subfertility.9
In this study, we demonstrated that sperm motility also comes down with a hiking BMI. Both progressive and total motility was reduced.
Oligospermia was noted in those with abnormal BMI. The underweight population also had a group of men affected by it. It is important to determine the cause of the lower than normal BMI. Whether it was sudden, aggressive weight loss, or some chronic disease, all these conditions that induce stress to have the potential to fiddle with the hypothalamic-pituitary-gonadal axis. This results in troublesome hormonal imbalances.
Malnutrition may be a direct cause of lowered spermatogenesis.
However, reduced sperm concentration was demonstrated in those with a risen BMI as well, but more so in the overweight group compared to the obese group.
In a study by Kozopas et al., it was found that obese men were more likely to have oligozoospermia and azoospermia.10
A study by Ramaraju et al. showed that an increasing BMI hampers sperm concentration.
Therefore, it is difficult to frame a relationship. Probably, a larger sample size would have given more clarity.
The motility decreased with increasing weight as per the study by Ramaraju et al., wherein the progressive motility was more affected, very much in line with our study.11
Various other studies have also reported a negative correlation between obesity and sperm parameters, including volume, sperm count, and motility.
Natalia et al. inferred that no significant difference in the semen parameters was observed between the obese and control group, except for an increase in the number of abnormal spermatozoa.12
The purpose of this study was to find conclusive data stating that obesity is quite instrumental in causing a subfertile status in men. The idea behind proving the same is that a simple change, such as assuming a healthy lifestyle, may be a major therapeutic intervention.
At the outset, the study showed significant results and had the pros of being simple and noninvasive. The main disadvantage of the study is that no intervention was done, and we don’t have any data suggesting that losing the extra weight improved the semen parameters. Although our conclusion is encouraging, the sample size was time bound, and a higher number would have added more value to the study.
Obesity led to a reduction in semen volume and motility evidently. Oligospermia was noted in those with a lower than normal BMI. Physically fit men with an adequate BMI had the best quality semen. A larger study with hormonal evaluation, DNA fragmentation tests along with lipid profiling is needed for a more elaborate understanding.
An abnormal BMI, either high or low, is detrimental to semen quality. Men with a normal BMI are more likely to have sperm with the ideal parameters.
We would like to thank Dr. Ravishankar, Assistant Professor, Department of Biostatistics, Vallabh Bhai Patel Chest Institute, Delhi University, New Delhi, India.
Suvrati Bansal https://orcid.org/0000-0002-3129-3104
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