Treatment of Male Infertility Secondary to Morbid Obesity

Mara Y. Roth; John K. Amory; Stephanie T. Page


Nat Clin Pract Endocrinol Metab. 2008;4(7):415-419. 

In This Article

Discussion of Diagnosis

There are numerous causes of male infertility, which accounts for roughly one-third of all infertility among couples (see "Differential Diagnosis of Infertility After Normal Puberty"). In patients who have undergone normal puberty, the differential diagnosis of infertility is extremely broad. Some cases are thought to be due to inherited genetic defects.[3] Only recently has obesity been recognized as a significant contributor to male infertility.[4] Current estimates suggest that over 30% of the male population in the US are considered to be obese (defined as a BMI >30 kg/m2) -- a number that continues to rise. Obesity could thus contribute substantially to the rates of hypogonadism and, potentially, to the rates of infertility.[5] Several studies show a direct correlation between a rise in BMI and a decline in both free and total blood testosterone levels.[1,4,6] Further studies have correlated this decline in testosterone levels with a rise in infertility rates,[7] and others have found a relationship between increased BMI and decreased sperm concentrations, sperm motility, and fertility rates.[8,9]

In general, secondary hypogonadism is an uncommon, but usually treatable, cause of male infertility.[3] In these patients, low serum testosterone levels result from loss of gonadotropin stimulation to Leydig and Sertoli cells within the testes, which leads to low testosterone production and decreased spermatogenesis, respectively (Figure 1). Aromatase is expressed in the intercellular septa of fat tissue and converts testosterone to 17ß-estradiol.[10]

Obesity is one of the causes of secondary hypogonadism (see "Differential Diagnosis of Infertility After Normal Puberty"). In obese men, increased adipose tissue results in increased aromatase activity and a relative elevation in estradiol levels, which inhibits gonadotropin secretion from the pituitary.[10] Several studies have shown that men with an increased BMI have a linear rise in serum 17ß-estradiol.[4,10] Interestingly, estradiol levels in obese men do not frequently surpass the normal range, so some investigators have suggested that the ratio of testosterone to estradiol is more clinically useful in diagnosing estrogen excess in men than the absolute estradiol level alone.[10,11] In addition, assessment of estradiol levels in men can be particularly challenging since most clinical assays are optimized to measure levels in the normal female range and are not well validated for measurement of male estradiol levels.[12] Clearly, clinical symptoms such as gynecomastia as well as laboratory data should be considered in the evaluation of hypogonadotropic hypogonadism.


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