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American Journal of  Medical 
Science and Innovation (AJMSI) 

Obesity and Male Fertility: An In-Depth Review of  the Impact of  Elevated BMI
Solmaz Gul Sajjad1, Aarush Mohammad Sajjad2, Michael Fakih MD3, Muhammad Ahsan Akhtar MD Frcog4

Yasmin Sajjad MD Frcog4*

Volume 3 Issue 2, Year 2024
ISSN: 2836-8509 (Online)

DOI: https://doi.org/10.54536/ajmsi.v3i2.2540
https://journals.e-palli.com/home/index.php/ajmsi

Article Information ABSTRACT

Received: June 07, 2024
Accepted: July 13, 2024
Published: July 17, 2024

This paper discusses the complex relationship between obesity and male infertility in a 
detailed manner. According to the introduction, obesity-related infertility is importantly 
discussed since it affects some 15% of  couples in which half  cases are attributed for obesity-
related infertility is important to discuss since it affects some 15% of  couples, and half  
of  cases are attributed to male factors. The body of  the analysis discusses various factors 
related to obesity-associated male reproduction implications, including endocrinopathies 
insulin sensitivity, sperm DNA fragmentation, erectile dysfunction OSAS asshened semen 
characteristics chronic epididymitis and epigenetic changes. The above discussion on 
endocrinopathies shows that excessive white adipose tissues derail the HPG axis, triggering 
hormonal imbalances which lead to infertility. This paper explains the interaction between 
insulin resistance and testosterone levels in type 2 diabetes affected men. The paper also 
focuses on sperm DNA fragmentation, showing the association between obesity and increased 
levels of  sperm DNA damage, mitochondrial dysfunction and abnormality in morphology. 
Erectile dysfunction is focused on obesity-induced oxidative stress, inflammation and 
hormonal abnormalities that impair male reproductive function. Additionally, the role of  
sleep apnea in testosterone secretion and possible association between its severity to lower 
level of  this hormone are presented. There is a further discussion of  altered sperm traits, 
chronic epididymitis and epigenetic changes with regard to the obesity which gives us a broad 
perspective on male fertility. The paper then concludes its discussion regarding weight loss 
interventions restoring fertility, focusing on diet and exercise as means for reducing certain 
parameters associated with modifiable inflammatory markers linked to infertility. In summary, 
the general assessment highlights that obesity management is crucial in male infertility.

Keywords
Obesity, Male Infertility, Epigenetic 
Changes,  DNA Fragmentation, 
Erectile Dysfunction, Chronic 
Epididymitis

1 Nevill Hall Hospital, Abergavenny hospital, South Wales, United Kingdom 
2 Whiston Hospital, Mersey & West Lancashire Trust, United Kingdom 
3 Gynecological Endocrinology & Reproductive Medicine and First IVF Fertility Centre and Fakih IVF Centre Abu Dhabi, United 
  Arab Emirates
4 Reproductive Medicine, RCOG accredited sub specialist in Reproductive Medicine, Fakih IVF Fertility Centre Abu Dhabi, United 
  Arab Emirates
* Corresponding author’s e-mail: y.sajjad@btinternet.com

INTRODUCTION
As defined by ASRM, infertility is any patient with 
regular, unprotected intercourse and no known aetiology 
for either partner that suggests impaired reproductive 
ability. Evaluation should begin at 12 months for female 
partners under 35 and at six months for female partners 
35 or older. This danger accounts for 15% of  couples’ 
infertility, 50% of  which is male (Leslie et al., 2023). In 
contemporary countries, obesity is a major health issue 
that causes infertility (Chaudhuri et al., 2022). Over the 
last few decades, dramatic changes in semen quality 
have been found to be a universal trend due to civilised 
communities’ lifestyle modifications around the world, 
which are mostly sedentary and high in fast food and 
calories, which are considered the main causes of  obesity. 
This is making obesity more common and rising. Being 
overweight harms health. Being overweight or obese may 
cause infertility in men and make it harder for couples to 
conceive.
Obesity is linked to male infertility in many studies (Amiri 
& Tehrani, 2020). Obesity may disrupt the hypothalamic-
pituitary-gonadal (HPG) axis’ synchronised correlation and 

complicated signal connections with other reproductive 
hormones (Chaudhuri et al., 2022). Physical factors like 
supra pubic heavy adipose tissue deposits increase scrotal 
temperature, oxidative stress (OS), and pro-inflammatory 
mediators, impairing semen parameters (Chaudhuri et al., 
2022). Obesity also substantially disrupts sperm genetic 
and epigentic conformation, altering DNA methylation 
patterns and impairing spermatogonia, causing infertility 
(Cescon et al., 2020).  Given new evidence-based ideas 
concerning obesity-related male infertility, its cause and 
mechanism must be investigated. This article reviews 
obesity’s relationships with infertility characteristics that 
may affect male infertility directly or indirectly.

MATERIALS AND METHODS
This paper is written with an overview of  related articles 
published in Pubmed. A systematic review of  the literature 
was performed to identify the complex relationship 
between obesity and male reproductive potential. Our 
review considered studies that investigated the following 
outcomes: likelihood of  obesity on male infertility, 
sperm concentration and DNA fragmentation, erectile 



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dysfunction, epigenetic changes and effecting other 
male reproductive functions including endocrinopathies 
& insulin sensitivity. The review was carried out to 
include all published literature. No date restrictions were 
applied, but language was restricted to English. Studies 
were retrieved up to December 2023, with an updated 
search performed in February 2024. Inclusion criteria 
followed were for studies carried out on male adults aged 
>18 years without history of  reproductive disorders. 
Data had to be reported with men categorized by body 
mass index (BMI), including a normal weight group 
(BMI ≤ 25) and an obese group (BMI ≥ 30). All types 
of  quantitative research were eligible for inclusion in the 
review including case series and reports. The exclusion 
criteria applied were non-peer-reviewed sources, studies 
with low methodological quality, or irrelevant topics. For 
relevance screen search results typically involved multiple 
stages including screening titles and abstracts followed 
by full-text assessment. Data extraction from the  
included studies involved  a systematic process to record 
information, such as study design, sample characteristics, 
key findings, and quality assessment criteria.
We employed bibliometric and gap analysis to 
systematically analyse and synthesize the literature to 
identify patterns, themes, and gaps  on the subject of  
effect of  male  obesity on male reproductive potential 
that  helped us in the development of  this  review article. 
The limitations of  this  review article methodology 
included publication & selection  biases and constraints 
due to resources available to us and time constraints.
The literature review discusses complete relationship 
between obesity and male infertility.  It shows that excessive 
white adipose tissues derail the HPG axis, triggering 
hormonal imbalances causing hypogonadotropic 
hypogonadism, causing spermatogenesis disorder 
that  leads to infertility.  Obesity can affect levels of  
testosterone, Inhibin B, SHBG, and increase oestrogen 
and leptin. Moreover it explains the interaction between 
insulin resistance and testosterone levels in men with type 
2 diabetes. The paper also focuses on the association 
between obesity and increased levels of  sperm DNA 
damage, mitochondrial dysfunction, and abnormality in 
morphology. 
A broad perspective on male fertility has been provided 
by reviewing   the association between obesity- induced 
oxidative stress, hormonal impairment leading to male 
reproductive dysfunction, chronic epididymitis, and 
epigenetic changes.  The paper concludes its discussion 
on weight loss interventions for restoring fertility 
focusing on diet and exercise and  highlighting  that 
obesity management is crucial in male infertility.

LITERATURE REVIEW
Adipose tissue can be classified as brown adipose tissue 
and white adipose tissue. Brown adipose tissue contains 
multilocular adipocytes vast amounts of  mitochondria 
that express high levels of  uncoupling protein 1 (UCP-
1), this is leads to the thermogenic activity of  the tissue 

(Omran & Christian, 2020). White adipose tissue stores 
fat with fibroblasts, preadipocytes, mature adipocytes, 
and macrophages (Fernández-Sánchez et al., 2011). 
White fat deposits are greater in obese animals due to 
adipocyte hyperplasia and hypertrophy, and white adipose 
tissue may generate endocrine, paracrine, and autocrine 
chemicals (Fernández-Sánchez et al., 2011).  
Secondary hypogonadism in obese people may decrease 
spermatogenesis and cause erectile dysfunction (Cabler et 
al., 2010). Obese people have excess white adipose tissue, 
which increases testosterone to oestrogen conversion and 
reduces gonadotrophin release due to HPG axis negative 
feedback loop disruption. Spermatogenesis is disrupted 
by this. The increased oestrogen from this conversion 
reduces endogenous gonadotrophin release. Oestrogens 
inhibit GnRH pulsatility (Colaci et al., 2012). Fat men 
have increased amounts of  aromatization activity, 
adipose-derived hormones, and adipokines, which 
convert testosterone to oestrogen (Cabler et al., 2010). 
Endocrine and secretory white adipose tissue secretes 
several physiologically active peptides and proteins. These 
include adipokines, which include immunomodulators, or 
adipose-derived hormones including leptin, adiponectin, 
and resistin (Ren et al., 2022).
Adipose-derived hormones regulate food intake, insulin 
action, energy balance, lipid, and glucose metabolism. 
Increased white adipose tissue in obese males may 
enhance adipose-derived hormones (Gómez-Hernández 
et al., 2016). Additionally, adipose tissue and testicular 
Leydig cells contain aromatase cytochrome P450 enzyme, 
which is essential to oestrogen production. Thus, white 
adipose tissue is thought to cause enhanced oestrogen 
levels in obese men due to androgen conversion (Katib, 
2015; Palmer et al., 2012). White adipose tissue increases 
hypothalamic-mediated leptin production, which regulates 
energy intake and expenditure and decreases Leydig cell 
testosterone production. This may explain why obese 
men’s greater leptin levels may affect the HPG axis and 
lower testosterone synthesis (Khodamoradi et al., 2022). 
Sperm plasma membranes and testicular tissue have 
leptin receptors, indicating that leptin may operate on 
these receptors (Sengupta, Bhattacharya, and Dutta, 
2019). Leptin may directly affect sperm via the endocrine 
system independent of  HPD axis modifications (Isidori 
et al., 1999). FSH/LH ratios, inhibin B, and SHBG levels 
regulate sertoli cell activity and spermatogenesis. Males 
with high BMIs have lower hormone levels. Low LH 
and testosterone levels may cause hypogonadotropic 
hypodonadism and male infertility (Hohl and Ronsoni, 
2022). To conclude, obesity may diminish sperm counts 
due to impaired sertoli cell activity and HPG axis 
abnormalities caused by testosterone and oestrogen 
(Davidson et al., 2015).
Type 2 diabetic males should evaluate their testosterone 
levels. Secondary hypogonadism in males with type 2 
diabetes may result from peripheral and central insulin 
resistance, as well as the impact of  proinflammatory 
cytokines (TNFα and IL-6) on the HPG axis (Bhasin et 



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al., 2010). Increased insulin levels may lower SHBG levels 
in obese men’s livers, thereby increasing blood levels 
of  active unbound estogrens and testosterone. After 
SHBG correction, low testosterone levels were linked to 
insulin resistance and obesity. Insulin resistance affects 
testosterone and sperm production independently (Tsai 
et al., 2004; Palmer et al., 2012).
Sperm chromatin, a compact, organised structure, 
preserves genetic integrity. Obese males had more 
sperm with DNA fragmentation, poor mitochondrial 
membrane potential (MMP), and aberrant morphology 
and motility. These causes may cause male infertility 

(Durairajanayagam, 2018). Oxidative stress reduces 
sperm motility (Nowicka-Bauer and Nixon, 2020; Blumer 
et al., 2008). Continuous ATP generation by mitochondria 
in the midpiece controls sperm motility. Selective 
permeability of  the mitochondrial membrane maintains 
an electrolytical gradient between the inner and outside 
surroundings. This permits oxidative phosphorylation 
to produce enough ATP. However, excessive reactive 
oxygen species (ROS) damage phospholipid membranes, 
limiting oxidative phosphorylation and ATP generation 
(Fariello et al., 2012). Lower sperm mitochondrial activity 
was detected in obese males. 

Figure 1: Mechanisms involved and the effect on male infertility (Cabler et al., 2010)

Erectile dysfunction (ED) in males is the continuous 
inability to achieve or maintain an erection suitable to 
perform sexual activity (Geerkens et al., 2020). What 
we know so far shows that ED is more common in 
overweight men from childless couples than in other 
guys (Zhang et al., 2019). Sultan et al. (2023) say that men 
with a BMI of  28.7 or higher are 30% more likely to have 
ED than men with a normal BMI (<25). Overweight 
people and people with ED both have oxidative stress, 
inflammation, and insulin and leptin resistance, all of  
which can affect ovulation (Moon, Park, and Kim, 2019). 
A rise in fat levels in the blood, the release of  adipokin 
from adipocytes that have become too big, and the 
entry of  immune cells into the adipose tissues are some 
of  the most important signs of  obesity. These things 
cause insulin and leptin resistance (Shimobayashi et al., 
2018). Going against leptin also makes the brain release 
less gonadotropin-releasing hormone (GnRH). Because 
of  this, testosterone levels drop, which can lead to ED 
(Moon, Park, and Kim, 2019). Also, sexual dysfunction 
wasn’t linked to infertility caused by ED from a higher 
BMI. Instead, it was more likely due to other biological 
changes being harmed by being overweight (Nguyen et 
al., 2007).

Obstructive sleep apnea (OSA) is a sleep-related 
breathing disorder and is characterised by a decrease 
or complete cessation in airflow in spite of  an ongoing 
effort to breathe. OSA occurs due to periodic narrowing 
and obstruction of  the pharyngeal airway during sleep., 
resulting in hypoxia and hypercapnia. (Osman et al., 
2018; Arnold et al, 2017). OSA can have an impact on 
daily life as it alters the suffers ability to have a calm 
and continuous nights’ sleep, and therefore can lead to 
increased daytime sleepiness, personality changes or 
cognitive difficulties related to fatigue (Arnold et al, 2017). 
OSA is more common amongst obese individuals and 
results in hypoxemia with each pause in breathing. The 
role of  OSA in male infertility is not well understood it is 
often associated with a decrease in morning testosterone 
concentration and a decline in pituitary gonadal function 
which are necessary for normal spermatogenesis. 
(Cojocaru et al., 2023; Cabler et al., 2010). It has been 
suggested that nocturnal testosterone rhythm is disrupted 
by sleep apnea due to sleep fragmentation (Katib, 
2015). Total and free testosterone levels were reduced 
in obese OSA men in comparison with age‐ and body 
weight‐matched control men. A negative correlation 
was established between severity of  sleep apnea and 



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testosterone levels, which was still true after adjusting 
for BMI and waist values. Therefore, it was suggested 
that the major factor responsible for the decrease in 
testosterone secretion in OSA is the severity of  sleep 
apnea (Katib, 2015).

RESULTS AND DISCUSSION
Sperm parameters such as concentration, sperm motility 
and morphology have shown to be affected by male 
obesity. There has also been some evidence suggesting 
that weight loss can efficiently lead to increased levels 
of  serum testosterone levels and hence increased 
sperm count. (Liu and Ding, 2017). A study reported 
that spontaneous and progesterone-induced acrosome 
reactions are potentially impaired in obese men (Liu 
and Ding, 2017). The correlation between male obesity 
and its impact on sperm acrosome reaction is sparingly 
documented in literature. However, it is reasonable to 
assume that spermatogenesis and sperm maturation is 
affected by obesity. This results in oxidative stress and 
membranous lipid alteration, which therefore cause 
defects in acrosome reaction (Aitken, 2020).
There have been several studies on both humans and 
animals, to show a correlation between obesity and a 
decreased in sperm DNA integrity. With obese males it has 
been shown that they often display an increase in sperm 
DNA damage, alterations to reproductive hormones and 
a decrease in sperm motility and sperm concentration 
(Leisegang et al., 2021). The main pathological mechanism 
described in literature to explain these changes has been 
an increase sperm oxidative stress with increases in 
BMI, mainly because of  a rise in seminal macrophage 
activation. Although the extent of  increase was small, 
this phenomenon led to a decrease in acrosome reaction, 
lower embryo implantation rates during IVF, decreased 
sperm motility and an increase in sperm DNA damage 
(Palmer et al., 2012). 
As for the alterations to reproductive hormones, an 
increased BMI led to a decrease in sperm concentration 
and serum testosterone but an increase in serum 
estradiol (Katib, 2015). It was also found that individuals 
with a higher BMI displayed an increase in chances of  
developing oligospermia. Obese men were 3.5 times 
more likely to have oligospermia than men who possess a 
normal BMI. However, this value was slightly higher than 
the chances of  developing oligospermia in overweight 
men (Hajshafiha et al., 2013). The chances of  developing 
oligospermia in overweight men was 3 times more likely 
than men with a normal BMI, therefore showing that a 
man doesn’t necessarily have to be classified as obese in 
order for his sperm count to be affected. 
One of  the disadvantages of  obesity is the increase in 
scrotal adiposity and subsequent increase in gonadal 
heat leading to an alteration in sperm production and 
parameters. The mechanism of  spermatogenesis is 
sensitive to heat and testicular function is dependent 
on body temperature and requires a temperature of  
2-4°C below body temperature in order to function 

optimally (Gao et al., 2022) An increase in temperature 
of  1°C can result in a 14% reduction in spermatogenesis, 
and therefore a decrease in efficient sperm production 
(Durairajanayagam, Agarwal, and Ong, 2015). An increase 
in temperature is related to reduced sperm motility, 
increased sperm oxidation stress, increased sperm DNA 
damage, testicular germinal atrophy, spermatogenic 
arrest and a reduced level of  inhibin B, with is a marker 
for spermatogenesis (Durairajanayagam, Agarwal, and 
Ong, 2015).
These all lead to lower sperm counts, therefore, it is 
crucial to maintain testicular temperatures slightly lower 
than that of  the body to avoid abnormal spermatogenesis 
associated with male infertility (Durairajanayagam et al., 
2014). The temperature within the testis is maintained 
by characteristics of  the scrotal sac including minimal 
subcutaneous fat, thin skin, scant hair distribution and 
dense sweat glands (Ilacqua, Francomano, and Aversa, 
2018). In order to maximize heat loss, the cremaster 
muscle surrounding the testes and spermatic cords, and 
the dartos muscle from beneath the scrotal skin all relax. 
The relaxation of  these muscles causes the testes to 
descend away from the abdomen and the scrotal skin to 
loosen (Fahmy, 2022). These characteristics increase the 
total surface area to allow for easy heat dissipation. 
Another mechanism by which lower temperatures 
are maintained within the testis is a counter-current 
mechanism involving the testicular arteries and veins 
(Aldahhan and Stanton, 2021). There is a heat exchange 
of  warmer inflowing arterial blood versus the colour 
outgoing venous blood. This system allows the cooler 
arterial blood to travel to the testis, and removes warmer 
venous blood (Rizzoto and Kastelic, 2020).
There are several factors other than increased scrotal 
tissue that can raise scrotal temperature, either by 
whole body increase or a local increase. Local elevation 
of  scrotal temperature is often a result of  direct heat 
exposure or effect of  body temperature and diminished 
physiological testicular cooling mechanisms (Sheynkin 
et al., 2005). Such exposures include the use of  laptop 
computers, plastic lined diapers in children, prolonged 
car driving, sedentary lifestyles, the use of  tight jockey 
shorts. Testicular heat stress caused by this increase in 
scrotal adiposity can subsequently causes oxidative stress. 
The increase in oxidative stress can therefore impair sperm 
motility, sperm-oocyte interaction and DNA integrity. The 
combination of  increase in temperature and lack of  activity 
also impairs spermatogenesis (Durairajanayagam, 2018). 
The membrane of  sperm consists of  saturated fatty 
acids, such as myristic acid, palmitic acid and stearic 
acid, as well as unsaturated fatty acids such as oleic acid, 
arachidonic acid, palmitoleic acid and docosahexaenoic 
acid. The composition of  such fatty acids within 
spermatozoa are vital for sperm functions such as 
motility, viability and fertility (Martínez‐Soto, Landeras, 
and Gadea, 2013). Whereas polyunsaturated fatty acids, 
such as docoseahecaenoic acid (DHA), related to sperm 
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Ravina et al., 2018). These unsaturated fatty acids are also 
susceptible to reactive oxygen species (ROS) and cause lipid 
peroxidation. Therefore, excess ROS found in obese males 
has the potential to result in lipid peroxidation causing poor 
membranal lipid fluidity, alterations to acrosome reaction 
and sperm motility (Sinha and Gupta, 2018). 
It was found that the regulation of  fatty acid metabolism 
in the testis may be altered by BMI, hence resulting in 
changes to fatty acid composition of  spermatozoa. This 
suggests that sperm quality in men with high BMI may 
be vastly affected by changes to fatty acid compositon 
of  spermatozoa (Andersen et al., 2016). Membrane 
cholesterol is another key constituent of  spermatozoa, 
and this varies during sperm maturation and capacitation. 
The main role of  mammalian spermatozoa is to fertilize 
their female contrary, the oocyte, and the capacity to 
achieve this phenomenon is gained during a multi-step 
process known as “posttesticular maturation” (Ramal 
Sanchez et al., 2018).
Cholesterol plays a vital role in the modifcations of  the 
composition of  sperm plasma membrane which are 
crucial for fertility (Rajoriya et al., 2020). These epididymal 
maturation steps prepares sperm cells for capacitation, 
which is the next maturation step, and also relies on 
the plasma membrane cholesterol (Visconti et al., 2011). 
To summarise, levels of  cholesterol in sperm is highly 
variable, but it has been suggested the higher sperm 
cholesterol levels in obese males have a contribution to 
infertility. The mechanism of  this is due to that fact that 
development of  acrosomal responsiveness and ability 
to fertilise in vitro is affected by cholesterol content of  
sperm. These changes are thought to lead to alteration 
to sperm morphology, decreased motility and premature 
acrosome reaction (Liu and Ding, 2017).
Although the current mechanism is unknown, it is 
evident that obese men have redundant areas of  fat found 
at the suprapubic and inner thigh regions which can cause 
mechanical inflammation to the scrotal contents. This 
include epididymitis, in which during physical activities 
the friction from rubbing and sheering forces can result 
in inflammation (Katib, 2015). Any changes to the 
epididymis, regardless of  the cause, alters the environment 
within the epidydmis. Such changes can have a knock-on 
effect on sperm maturation and inflammation can thus 
lead to scarring and cyst formation which subsequently 
results in blockage of  epididymal ducts (Schagdarsurengin 
et al., 2016). Although either one or both of  the ducts can 
be blocked, cases that involve bilateral epididmytis have 
more impact on male fertility.  
DNA methylation and acetylation of  histones is dyanmic 
and are vital processes for the function of  normal 
spermatogenesis, and therefore a successful pregnancy. 
DNA methylation involves the reversible attachment of  
a methyl group to a nucleotide in a heritable manner (Ge 
et al., 2017). Epigenetic changes regulate gene expression 
and transcription intensity without changing the 
genetic information within DNA. These include DNA 
methylation, hydroxymethylation, histone modifcations 

and non-coding RNA expression (Mendelson, 2017). 
Genetic modifications can be affected by genetic and 
environmental factors, one of  these being obesity. It has 
been found that increased BMI can lead to alterations 
in DNA methylation (Dick et al., 2014; Ozanne, 2015). 
Furthermore, it has been suggested that children born 
to obese fathers are more likely to suffer from metabolic 
disease and develop childhood obesity. Therefore, 
suggesting that paternal obesity can contribute to the 
health of  offspring (Soubry et al., 2016). Consequently, 
it has been shown that paternal obesity can influence 
epigenetic modifications in sperm.
It has been suggested that weight loss can lead to an altered 
androgen profile and therefore improve semen quality. It 
is evident that obesity in males has a negative effect on 
fertility, hence sperm function and subsequent impact on 
offspring. Therefore, interventions such as alterations to 
diet and exercise are able to reverse the obesity state and 
hence the alter the impact on sperm and offspring. By 
altering BMI, this has a cumulative effect at changes at the 
molecular level, thereby decreasing oxidative stress and 
any DNA damage (Savini et al., 2013).
It has been shown in the literature that numerous studies 
suggested that weight loss naturally by dieting and/or 
exercise led to an increase in androgen, inhibin B and sex 
hormone-binding globulin levels and decreased serum 
concentrations of  insulin and leptin (Kasturi, Tannir, 
and Brannigan, 2008). These changes result in improved 
semen parameters in obese men (Chavarro et al., 2010). 
Moreover, weight loss by the reduction of  adipose tissue 
coupled with exercise or a low-fat and low energy diet 
has been seen to be linked to a decrease in TNFα, IL-6 
and other inflammatory cytokine levels related with 
infertility (Manna and Jain, 2015). Other than the fertility 
issue many other health issues are also related to obesity 
including  Non-alcoholic fatty liver disease which is  the 
most common liver disease and is closely linked with 
obesity and metabolic syndrome Onyango, (VC et al . 
2023). Therefore by adopting weight loosing strategy it 
will not only imorove the fertility but also will help with 
general well-being. 

CONCLUSION 
Obesity can have physical and psychological impacts 
along with other serious comorbidities. As discussed 
above, the literature has proven that obese men are at risk 
of  increased chances of  infertility due to mechanisms 
involving hormonal, physical, adipokine and cytokine 
changes. These changes can eventually lead to abnormal 
sperm parameters, changes to sperm function and sperm 
molecular composition. Offspring from obese fathers 
also have the potential to develop metabolic disorder, and 
childhood obesity. 

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