Male Infertility: Nutritional and Environmental Considerations

Male Infertility:
Nutritional and Environmental Considerations

This section is compiled by Frank M. Painter, D.C.
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FROM:   Alternative Medicine Review 2000 (Feb); 5 (1): 2838 ~ FULL TEXT

Steven Sinclair, ND, LAc


An estimated six percent of adult males are thought to be infertile. [1] Infertility is defined by most authorities as the inability to achieve a pregnancy after one year of unprotected intercourse. Conception is normally achieved within 12 months in 80-85 percent of couples using no contraceptive measures; thus an estimated 15 percent of couples attempting their first pregnancy will have difficulty conceiving. While certain cases of male infertility are due to anatomical abnormalities such as varicoceles, ductal obstructions, or ejaculatory disorders, an estimated 40-90 percent of cases are due to deficient sperm production of unidentifiable origin. [2]

      Diagnosis and Evaluation

While the focus of this article is on specific nutritional and environmental factors, there are other important diagnostic considerations when evaluating male infertility. These include endocrine abnormalities, such as hyper- and hypothyroidism or hypogonadism. Prescription drugs, including phenytoin, glucocorticoids, sulfasalazine, and nitrofurantoin all may have detrimental effects on sperm production and motility. [2] A detailed history of exposure to occupational and environmental toxins, recreational drugs and alcohol, excessive heat or radiation, and previous genitourinary infections should be elicited. Concurrent pathologies may also affect sperm production. Hepatic cirrhosis is associated with increased endogenous estrogens, which can suppress pituitary gonadotropin secretion and affect spermatogenesis. In addition, an estimated 80 percent of men with hemochromatosis have some degree of testicular dysfunction. Scrotal temperature is highly regulated by the body, and sperm production is greatly reduced at temperatures above 96º F. Men attempting to improve their fertility should not wear tight fitting pants or underwear (boxer shorts instead of briefs), an should avoid strenuous exercise, hot tubs, and baths.

      Semen Analysis

A normal semen sample should have a volume of 1.5-5.0 ml, with greater than 20 million sperm/ml. The number of abnormal sperm should be less than 40 percent, with greater than 30 percent of the sperm sample demonstrating proper motility. Unfortunately, conventional semen analysis is not a highly accurate predictor of fertility. Purvis et al reported, after surveying infertility clinics, that 52 percent of men with a sperm count below 20 million/ml were able to impregnate their partners and 40 percent of men with a sperm count below 10 million/ml were also able to conceive. [1] Conventional semen analysis often fails to identify infertile males with "normal" samples and conversely fails to identify fertile males with subnormal semen parameters. [3] Another confounding factor is variations in sperm density, motility, and morphology among multiple samples from the same subject.

More sensitive tests are available, including the post-coital test, which measures the ability of sperm to penetrate cervical mucus, and the hamster-egg penetration test, which measures the in vitro ability of sperm to penetrate hamster eggs. This test predicts fertility in an estimated 66 percent of cases, in comparison to 30 percent with conventional sperm analysis. [1]


The role of infection in idiopathic male infertility has been underestimated, in particular chronic asymptomatic chlamydial infections. [1 ] Chlamydia can reside in the epididymis and vas deferens, affecting sperm development and fertility. One study suggests approximately 28-71 percent of infertile men have evidence of a chlamydial infection. [4] The presence of anti-sperm antibodies may indicate an undiagnosed infection, and is estimated to be a relative cause of infertility in 3-7 percent of cases. In a study designed to examine the effects of antioxidants on anti-sperm antibodies, there was a significant correlation between beta carotene levels and antibody titers, suggesting dietary antioxidants are involved in mediating immune function in the male reproductive system. [5]

      Declining Sperm Counts

There is a growing body of scientific evidence supporting the idea that sperm counts have declined considerably over the last 50 years. Carlsen et al analyzed a total of 61 studies including 14,947 men from the years 1938 to 1991, for mean sperm density and mean seminal volume. Their results show a significant decline in mean sperm density from 113 million/ml in 1940 to 66 million/ml in 1990 (p<0.0001). Seminal volume decreased from an average of 3.40 ml to 2.75 ml (p=0.027).6,7 This demonstrates a 20-percent drop in volume and a substantial 58-percent decline in sperm production in the last 50 years. Three other recent reports also found semen quality has declined among donors over the last 20 years. [8-10] Because the decline in sperm production is relatively recent, one must suspect a combination of environmental, lifestyle, and dietary factors might be interfering with spermatogenesis.

      Environmental Risk Factors

Current evidence suggests there may be environmental reasons for deteriorating sperm quality, including occupational exposure to various chemicals, heat, radiation, and heavy metals. [11,12] In addition, exposure to environmental estrogens and pesticides has been linked to alterations in spermatogenesis. Lifestyle risk factors are also significant, including cigarette smoking, alcohol consumption, chronic stress, and nutritional deficiencies. [13]

      Xeno-Estrogens and Pesticides

Increased exposure to estrogens is thought to be responsible for not only prenatal testicular damage, but may also contribute to post-natal depression of testicular function and spermatogenesis. Exogenous estrogens impact fetal development by inhibiting the development of Sertoli cells, which determine the lifelong capacity for sperm production.

Circulating estrogens also inhibit enzymes involved in testosterone synthesis and may directly affect testosterone production.

The synthetic estrogen, diethylstilbestrol (DES), is a well-documented example of this problem. DES was prescribed from 1945 to 1971 to millions of women during pregnancy. Male offspring from those women had a higher incidence of developmental problems of the reproductive tract, as well as diminished sperm volume and sperm count. [5]

Synthetic estrogens are still widely used in the livestock, poultry, and dairy industries. Men wishing to improve their fertility and sperm quality probably should avoid hormone-containing dairy products and meats and opt instead for organic or hormone-free foods.

Many commonly-used pesticides, such as organochloride compounds, have estrogenic effects within the body. Chemicals such as dioxin, DDT, and PCBs are known to interfere with spermatogenesis. One study which examined the effect of DDT on male rat sexual development found low levels of DDT caused degeneration in sperm production, a decrease in the total number of sperm, and a reduced number of Leydig cells. The authors hypothesize that DDT acts as an hormonal disrupter, damaging the seminiferous epithelium and lowering local testosterone levels. [14]

      Dietary and Lifestyle Factors

In addition to avoiding exogenous estrogens and pesticides, there are other dietary factors to consider. Adequate intake of essential fatty acids is important to ensure proper membrane fluidity and energy production in sperm cells. High dietary intake of hydrogenated oils, particularly cottonseed oil, has been shown to have a negative impact on sperm cell function. Not only does cottonseed oil contain toxic pesticide residues, it also contains high levels of the chemical gossypol, which can interfere with spermatogenesis. [15] In Nigeria, a randomized, controlled trial was designed to evaluate the effect of dietary aflatoxin on infertile men. Forty percent of the 50 infertile men in the study had aflatoxin in their semen samples, compared to eight percent of the fertile control group. Infertile men exposed to dietary aflatoxin had a 50-percent higher number of abnormal sperm than controls. [16]

      Heavy Metals

Another environmental concern with infertility is the toxic effects of heavy metals on sperm quality and production. In Hong Kong, infertile males were found to have approximately 40-percent higher hair mercury levels than fertile males of similar age. [17] Occupational exposure to lead has been shown to cause a significant decrease in male fertility. [18] Considering the occupational and environmental prevalence of heavy metals and their potentially negative interactions with the neuroendocrine system, a hair analysis should be included in the diagnostic work-up of idiopathic male infertility.

      Cigarette Smoking

Cigarette smoking has been associated with decreased sperm count, alterations in motility, and an overall increase in the number of abnormal sperm. [19] A study designed to evaluate seminal zinc levels in smokers and non-smokers found that although smokers did not have significantly lower zinc levels than non-smokers, seminal cadmium levels were significantly increased, especially in those smoking more than one pack per day. [20] Experimental evidence also suggests nicotine can alter the function of the hypothalamic-pituitary axis, affecting growth hormone, cortisol, vasopressin, and oxytocin release, which then inhibits the release of luteinizing hormone (LH) and prolactin. [21] Cigarette smokers were also shown to have higher levels of circulating estradiol and decreased levels of LH, follicle-stimulating hormone (FSH), and prolactin than non-smokers, all of which potentially impact spermatogenesis. Smokers with low prolactin levels also demonstrated defects in sperm motility. [22]



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