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There are emerging facts that obesity negatively affects male reproductive potential by reducing sperm quality. Furthermore, in particular it alters the physical and molecular structure of germ cells in the testes and ultimately affects the maturity and function of sperm cells. Recent studies have shown that male obesity also impairs offspring metabolic and reproductive health. It suggests that the paternal health cues are transmitted to the next generation with the mediator mostly likely occurring via the sperm. Interestingly the molecular profile of germ cells in the testes and sperm from obese males is altered with changes to epigenetic modifiers. Obesity causes male infertility in a number of ways. Here, you will read the 11 most important reasons why obesity is blamed for male infertility.

The changes in sperm and semen parameters ultimately affects the fertilization and pregnancy, even IVF treatment also.

Now, you will read 11 reasons that will explain why obesity is so dangerous for male fertility.

1. Obesity = White Adipose Tissues => Male Infertility

Obesity is associated with an increase in the number and size of adipocytes (Adipose Cells). Many proposed mechanisms explain the effect of obesity on male fertility with the focus on the influence of abnormal levels of adipose-derived hormones and adipokines related to reproductive organs and hormones on fertility. Total body fat, intra-abdominal fat and subcutaneous fat have all been associated with low levels of free and total testosterone in men.

(i) Hormonal Abnormalities

Many proposed mechanisms explain the effect of obesity on male fertility with the focus on the influence of abnormal levels of adipose-derived hormones and adipokines related to reproductive organs and hormones on fertility. Most obese men seeking infertility treatment present with a decreased ratio of testosterone to estrogen. This decrease is explained by over activity of the Aromatase Enzyme, which is expressed at high levels in white adipose tissues and is responsible for a key step in the biosynthesis of estrogens.

(ii) White Adipose Tissue As An Endocrine Organ

LiveScience explains the Endocrine system as: The endocrine system is the collection of glands that produce hormones that regulate metabolism, growth and development, tissue function, sexual function, reproduction, sleep, and mood, among other things.

White Adipose tissues release some hormones that have very crucial impacts on reproduction system. That may cause male infertility.

Leptin is one of the number of proteins secreted from white Adipocytes. Adipocytes are the adipose tissues cells. Excessive fat accumulation characteristic of obesity can, therefore, result in the altered release of Adipose-derive.

(iii) Effects of Leptin on Male Fertility

Leptin is produced mainly by adipose tissue, but can also be made by the placenta, stomach and skeletal muscles. As well as a higher prevalence of male infertility, obese individuals are reported to have higher circulating levels of leptin than non-obese individuals.

Leptin levels have also been linked with normal functioning in the reproductive system.

Leptin receptors are present in testicular tissue and the discovery of leptin in semen has established a link between this protein hormone and male reproductive function. Jope et al. also demonstrated the presence of leptin receptors on the plasma membrane of sperm, suggesting that leptin might directly affect sperm via the endocrine system.

(iv) Decrease in Testosterone due to Increase in Leptin

Excess levels of leptin are known to have a harmful effect on sperm production.

Furthermore increased leptin levels might decrease the levels of testosterone in the serum. That is the very important reason for male infertility.

(v) Resistin Secretion and Insulin Resistance

Resistin is another adipose tissue specific factor, which is reported to induce insulin resistance. Almost 80% of men with type 2 diabetes are also obese, and an increase in resistin secretion owing to a higher number of adipo cytes links obesity to type 2 diabetes. High circulating levels of insulin are present in the bloodstream as a consequence of insulin resistance in patients with type 2 diabetes.

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2. Decreased Testosterone Levels

A decrease in the testosterone:estrogen ratio is consistently displayed in obese infertile men. In a study by aggerholm et al., obese men had 6% higher levels of estradiol and 25–32% lower levels of testosterone than normal men. The severity of obesity determines the degree to which levels of estradiol are increased and testosterone decreased. The increased conversion of androgens into estrogens, which is a characteristic of obesity, depresses the function of the pituitary gland by disturbing normal feedback in the testis.

Most obese males have altered reproductive hormonal profiles in comparison to the normal.

These men have elevated estrogen and low testosterone and FSH levels. It has been reported that morbidly obese individuals, have reduced spermatogenesis associated with severely low testosterone levels contributing to male infertility.

3. Obesity, Sleep Apnea and Male Infertility

One of the consequences of obesity is sleep apnea. Sleep changes are thought to affect neuroendocrine function related to testosterone secretion. Boyar et al. have reported that testosterone increases the LH production during sleep in early and mid-puberty. Sleep apnea appears to be an independent predictor for low testosterone levels in severely obese men. The findings of another study suggest that obese infertile subjects have a difference in stage 2 and stage 3–4 sleep when compared with controls which correlates with lower LH and testosterone levels. Therefore, low testosterone level can be attributed to central suppression and differences in sleep patterns and sleep fragmentation.

Sleep apnea, independently and in the context of obesity, is emerging as a risk factor for hypogonadism, sexual dysfunction, and probably reduced fertility.

Men with hypogonadism, erectile dysfunction, and infertility should be screened for obesity and sleep apnea and correction of these modifiable risk factors can improve the overall reproductive potential.

Sleep apnea is characterized by a fragmented sleep course owing to repeated episodes of upper airway obstructions and hypoxia, and is often diagnosed in obese and diabetic males. Patients with sleep apnea have a disrupted nightly rise in testosterone levels and, therefore, lower mean levels of testosterone and lH compared with controls. In a study of sleep apnea in obese, control and lean patients, luboshitzky et al. concluded that the condition is associated with decreased pituitary–gonadal function and that the accompanying decline in testo sterone concentrations is the result of obesity, and to a lesser degree, sleep fragmentation and hypoxia. This disruption has been associated with abnormal spermatogenesis and male reproductive potential. That causes male infertility.

4. Obesity Causing Erectile Dysfunction

Low testosterone in young as well as old men may be associated with low grade systemic inflammation. It might be a part of the mechanism underlying adverse health outcomes of male hypogonadism as connection is not exclusively dependent on the amount of adipose tissue, but may also be an independent effect of androgens. Inflammation can promote erectile dysfunction. In particular, IL-6 and TNF-alpha disrupt the penile endothelium by creating high levels of ROS, which decrease Nitric Oxide Synthase (NOS) cofactor tetrahydrobiopterin and delay the hydrolysis of NOS inhibitor asymmetric dimethylarginine (ADMA).

Obesity adversely affects above stated molecules which as a result cause erectile dysfunction because nitric oxide facilitates normal erection.

Whereas the effects of sleep apnea on reproduction are confounding owing to obesity itself being a cause of male infertility, erectile dysfunction is significantly associated with obesity. Patients who are overweight or obese make up of 76% of men who report erectile dysfunction and a decrease in libido. Many studies have found an association between an increased incidence of erectile dysfunction and an increase in Bmi; hormonal dysfunction is central to the connection between obesity and erectile dysfunction. Erectile dysfunction is highly prevalent in men with both type 2 diabetes and obesity, and might act as a forerunner to cardiovascular disease in this highrisk population. Conversely, improved diabetes control and weight loss have been found to improve erectile function.

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5. Impaired Scrotal Temperature Causing Male Infertility

An elevated Bmi can impair or arrest spermatogenesis by causing an increase in scrotal temperature. Increased fat distribution in the upper thighs, supra-pubic area and scrotum in conjunction with the sedentary lifestyle often associated with obesity can result in increased testicular temperature.

It is therefore not surprising that increased testicular heat caused by increased adiposity in obesity has been proposed as a possible mechanism. It negatively impacts sperm parameters that becomes a big reason of male infertility.

Many studies have focused on genital heat stress as a potential cause of impaired semen quality in cases of sedentary occupations, the occurrence of frequent fever and varicocele. Hjollund et al. concluded that even a moderate physiological elevation in scrotal skin temperature is associated with substantially reduced sperm concentrations. Additionally, magnusdottir et al. found that the duration of sedentary posture correlated positively with increased scrotal temperatures, leading to a decrease in sperm density. In addition, exposure, occupationally, to hot environment, tight clothing also contribute to increased genital heat stress which can be a potential cause of impaired semen quality.

6. Male Obesity and Abnormal/Altered Semen Parameters

Abnormal semen parameters attributed to obesity include decreased sperm concentration, abnormal morphology, compromised chromatin reliability, and abnormal motility.

The relationship between obesity and male infertility can be attributed to more than just sexual dysfunction and other altered physical manifestations of obesity. Although spermatogenesis and fertility are not impaired in a majority of obese men, a disproportionate number of men seeking infertility treatment are obese. There have been several studies on the relationship between semen quality and obesity, with an inverse correlation between these parameters frequently being reported.

The body mass index (BMI) is associated with alterations in sperm parameters.

Obese men are three times more likely to exhibit a reduction in semen quality than men of a normal weight.

Hofny et al. studied that in obese fertile and infertile men BMI positively correlated with abnormal sperm parameters and negatively correlated with sperm concentration and motility. Some other studies reported that oligospermia and low progressively motile sperm concentration, increased with augment in BMI.

(i) Sperm Count & Concentration – Negatively Affected

Chavarro et al. found that men with a BMI greater than 25 kg/m2 had a lower total sperm count than men of normal weight, and the measured volume of ejaculate decreased steadily with an increasing BMI.

Obese men are three times more likely than healthy men of normal weight to have a sperm count of fewer than 20 million/ml, also known as oligospermia.

Among 1,558 Danish military recruits, there was a negative association between total sperm count and increasing BMI; there was also a consider able decrease in total sperm count and concentration. These findings have been corroborated by other studies.

(ii) Sperm Motility – Badly Affected

Some consensus on the effects of obesity on sperm motility has been established. Hofny et al. found that the BMI correlated negatively with sperm motility.

Hammoud et al. concluded that the incidence of low progressively motile sperm count increased with increasing BMI.

Fejes et al. concluded that the waist and hip circumference of men correlated negatively with the total motile sperm count as well as the rapid progressively Motile Sperm Count.

7. Male Obesity and DNA Fragmentation

Kort et al. found that an increase in the DNA Fragmentation index (DFI) accompanied an increasing BMI, demonstrating that obesity might compromise the integrity of sperm chromatin. DFI is the percent of sperm in a semen sample that have increased levels of single or double strand breaks in nuclear DNA. A young and healthy man has about 3–5% of sperm with fragmented DNA while a level of 25–30% DFI places a man attempting natural conception at a statistical risk for infertility.

Typically, males presenting with a high DFI will have reduced fertility. As a result, their partners may display an increased incidence of miscarriage.

An increase in the BMI above 25 kg/m2 causes an increase in sperm DFI and a decrease in the number of normal chromatinintact sperm cells per ejaculate, relative to the degree of obesity. Men with type 2 diabetes also present with a significantly higher number of severe structural defects in sperm compared with sperm from controls (P <0.05).

8. Male Obesity Affecting Pregnancy and IVF Results

Ramlau-Hansen et al. reported that normal BMI females with overweight or obese male partners have increased odds ratio for increased time to conceive compared with couples with normal weight male partners.

An increase of pregnancy loss in couples undergoing assisted reproduction therapy (ART) partly appears to be because of reduced blastocyst development, sperm binding, and fertilization rates during in vitro fertilization (IVF), when the male partner is overweight or obese.

9. Male Obesity Disturbing Fertilization and Pregnancy

In the last 5–10 years it has been demonstrated that maternal obesity is associated with changes to the oocyte that negatively impact embryo development, which reduces subsequent pregnancy establishment after in vitro fertilization.

Only recently in the last 2–3 years, the impact of an obese male partner on embryo development and pregnancy has been assessed.

Currently, there is mounting evidence that male obesity may be equally implicated in reducing fertility and embryo health. Couples with an overweight or obese male partner, with a female of normal body mass index (BMI), have increased odds ratio for increased time to conceive compared with couples with normal weight male partners. In part, this effect appears to be due to reduced blastocyst development, sperm binding and fertilization rates during in vitro fertilization (IVF), when the male partner is overweight or obese. These embryology based findings which have established that male obesity at the time of conception impairs embryo health, therefore reducing implantation and live birth rates are paralleled by animal models of male obesity. This highly suggests a functional change to the molecular makeup of sperm that impacts directly on both sperm function but also on subsequent embryo development.

10. Male Infertility and Health of Next Generation

Data from a rat model of diet induced obesity and reduced glucose tolerance demonstrated that paternal obesity compromised pancreatic function through altered gene transcription and islet cell dysfunction in female offspring.

Epidemiology studies have concluded that obese fathers are more likely to father an obese child.

Taken together these data suggest that paternal obesity at the time of conception has a marked effect on offspring health therefore, directly implicating the sperm as the mediator for these changes, likely through a molecular mechanism that is transmitted to the resultant embryo and offspring.

11. Abdominal Fat and Pycological Distress: Inter-linked

The abdominal adiposity has been linked with psychological distress and it has been argued that stress exposures promote abdominal fat deposition and infertility is also bound to increase psychological stress.

Males who experienced more than two stressful life events before undergoing infertility treatment were more likely to be classified below WHO standards for sperm concentration, motility, and morphology.


Altered hormonal profile is the suggested underlying cause and adipocytokines seem to have some role in obese infertile males. It is important that the treatment for infertility in obese men differs from that of normal weight infertile men and that focus is placed on reproductive abnormalities that are associated with obesity.

Weight loss is the cornerstone treatment in obese infertile men.

In some studies improvement toward healthy BMI by weight loss in men was associated with an increase in total sperm count and semen volume. The men who lost weight through natural (diet and/or exercise) methods experienced a high increase in androgen and inhibin B levels and an improvement in semen parameters.


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