With the onset of sedentary lifestyles, high-fat diets, and a general decline in physical activity, much evidence suggests that obesity is becoming a global pandemic [1, 2]. Obesity is reaching unprecedented levels in the Western world. One study revealed a prevalence of obesity in the USA of 19.8% [3], while another indicated a staggering 30% [4] . Reports have already shown that the world's overweight population has grown greater than its underweight population [4]. The World Health Organization (WHO) predicts that by 2015 approximately 2.3 billion adults will be overweight and that an additional 700 million will suffer from obesity [5],

Simultaneous to this alarming trend, there has been an apparent progressive increase in infertility rates over the past few decades. It has been indicated that 15% of all couples of reproductive age are infertile [6, 7], and up to 50% of all cases are believed to be due to the male factor alone [8]. Although still highly debated, the increased prevalence of overweight and obesity may account for the declining sperm counts over recent decades. According to a study conducted in 2000 by Swan et al., male sperm counts have been dropping by as much as 1.5% annually in the USA, as well as in other Western countries [9, 10]. Since these declines were not present in regions where obesity was less prevalent [9], this may further suggest a potential link between altered lifestyles, obesity, adverse health outcomes and, now, semen quality and male infertility [11].

As obesity trends continue to increase and expectation levels show no signs of decline, the interaction between obesity and fertility has received astonishing attention [3,4]. Nevertheless, obesityand its effecton sperm counthasjustrecentlybeen documented [11, 12]. Studies have shown a negative correlation between obesity and various sperm parameters in the general population [11, 12]. Some have suggested a relationship between body mass index (BMI) and male infertility [13, 14]. Evidently, there has been a higher probability of abnormal spermatozoa and infertility found in obese men [1].

Furthermore, obesity has been shown to be associated with significant disturbances in the hormonal milieu, which can adversely affect the reproductive system [15, 16]. These reports have illustrated that fat tissue accumulation in men causes subsequent lowered serum levels of total and free testosterone while simultaneously elevating estrogen serum levels [15, 16]. A study demonstrated that such fat accumulation resulted in oxidative stress (OS) from a dysregulation of adipocy-tokine and reactive oxygen species (ROS) production [17]. Interestingly, data has been in agreement with recent studies suggesting that systemic OS correlates with BMI [18,19]. The relationship of increasing levels of obesity and male-factor infertility calls for greater clinical awareness, as much evidence suggests that obesity may play a significant role with the rising subfertility rates.

The aim of this review is to discuss the relationships between obesity and male infertility. Moreover, it specifically explores the role of ROS production in obesity and its subsequent generation of OS, thereby directly and indirectly linking the effects of obesity on male reproductive potential.

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