Sperm Counts Are Plummeting, and Researchers Think They Know Why - News and Education Blog
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Sperm Counts Are Plummeting, and Researchers Think They Know Why

              A new study suggests that sperm counts are falling rapidly in developed countries such as North America, Europe, Australia, and New Zealand, and that the steep decline shows no signs of slowing.1 The new research—a meta-analysis that crunched data from over 180 different studies on sperm counts in men from 1973 to 2011—points to a worrying decline in male fertility that may be a warning for all of us.

“Declines in sperm count have implications beyond fertility and reproduction,” the researchers conclude. “Recent studies have shown that poor sperm count is associated with overall morbidity and mortality.”2 This new data, they say, “might be considered as a ‘canary in the coal mine’ for male health across the lifespan” and may be due to influences such as endocrine disruption from chemical exposures. In fact, the study’s lead researcher, epidemiologist Hagai Levine of the Hebrew University of Jerusalem, told BBC News that: “If we will not change the ways that we are living and the environment and the chemicals that we are exposed to…eventually…it may..[lead to] the extinction of the human species.”3

             Though that may sound a bit alarmist, there’s no doubt we are exposed to an unprecedented onslaught of chemicals in modern life--more than 80,000 chemicals have been registered for use in the United States, and an estimated 2,000 new ones are introduced annually. These include chemicals in foods and food wrapping, personal care products, prescription drugs, household cleaners, furniture, bedding, clothing, lawn care products and more. Many of these chemicals haven’t been tested for safety by our government.4

An alarming number of these new chemicals can function as endocrine disrupters—disrupting the body’s hormonal balance and harming the developmental, reproductive, neurological, and immune systems in humans and wildlife.5

            Neurobiologist Frederick Vom Saal, of the University of Missouri-Columbia, has been studying the harmful effects of endocrine disrupters since the 1970s. He has discovered that the familiar standards of toxicology don’t necessarily apply to endocrine disrupters. In fact, as Vom Saal told one of the world’s premier scientific journals, Nature: “Low doses of endocrine disrupters act in ways that are totally unpredicted by the traditional approaches of toxicology.” First of all, endocrine disrupters may exert their effects at astonishingly low exposure levels. Secondly, as Vom Saal explains, whereas classical toxicology looks at a kind of ascending “ski slope” graph of dose and response, endocrine disrupters often form “U” shaped graphs, where low doses are as powerful as high doses. And sometimes, their graphs undulate like successive waves.6

           Secondly, says Vom Saal, our entire biology is responsive to “phenomenally small amounts of hormones in terms of our behavior, our core physiology, our neuroendocrine system, and our ability to metabolize drugs.”7 We are exquisitely sensitive to estrogens, and today our environment is full of chemicals that can stimulate our estrogen receptors. Vom Saal studied extraordinarily low doses of the notorious bisphenol A-- an industrial chemical that has been used to make certain plastics and resins since the 1960s. The doses he studied were 2,500 times lower than other doses previously studied--between 2 and 20 micrograms per kilogram of body weight. He found these low doses still scrambled the male reproductive system in mice.8 That’s concerning, because in 2004 the U.S. Centers for Disease Control (CDC) found traces of BPA in nearly all of the urine samples it collected.9 Similarly, a 2010 Canadian study found BPA in the urine of 91% of the population.10

           BPA and its new relative, BPS, along with other endocrine disrupters such as phthalates used to soften plastics, perfluorooctanoic acid (PFOA) used in Teflon and brominated flame retardants, leach into food and water from containers and cookware, or soak through our skin from store receipts and furniture or enter our lungs in household dust.11,12,13 Correlations exist between the concentrations of perfluorinated carbons in household dust and the percentage of carpeting in the house.14 And most Americans spend more than 90 percent of their time indoors—at home, school, work, and in cars, exposed to dust full of shed chemicals.15

These chemicals are not only widespread in the environment, they persist, and are not easily removed or decomposed, leading to the common references of persistent organic pollutants (POPs). PFOA, for instance, does not easily break down in the environment; the human half-life is estimated at about 3 years.16 PFOA has specifically been found to harm the testicles in animal studies.17

Heavy metals can also be endocrine disruptors. Twenty different metals in the environment, including lead, cadmium, mercury, and arsenic are thought to affect male reproductive health.18,19,20 Arsenic, which is found in everything from chickens to rice to drinking water,21 is a well-known endocrine disruptor.22 One animal study tested the effects on male rabbits of exposure to drinking water containing arsenic, chromium, lead, benzene, chloroform, phenol and trichloroethylene. Everything from mating desire and ability to sperm quality and testosterone secretion were affected.23

Lead is a reproductive toxicant, and exposure to inorganic lead is detrimental to human semen quality.24 Male lead concentration significantly reduces the odds of conception in couples.25 Lead moves throughout ecosystems, with atmospheric lead being deposited in vegetation, and in the ground and water.26 According to the CDC, lead exposure can affect nearly every system in the body, and yet it often occurs with no obvious symptoms and goes unrecognized.27 Lead present in household dust can come from old paint or surrounding soil.28 Mercury, too, is a widespread contaminant in the environment. Atmospheric deposition is the primary source of mercury globally, and once in the atmosphere, mercury can circulate for years.29 Seafood and dental amalgams are other primary sources of mercury that many are exposed to.

           In general, levels of contaminants and potential toxins allowed in the USA are higher than in Europe, Australia and Canada. Fracking is increasingly common in the USA, and chemicals found in water near fracked gas sites may affect reproductive health. More than 15 million Americans live within one mile of hydraulic fracturing sites, and a review of over a hundred studies concluded these activities have potential for environmental release of a complex mixture of endocrine disrupting chemicals.30

Many of the endocrine disruptors that affect male fertility are actual estrogen mimics. There is a saying in estrogen biology, according to Dr. Vom Saal, which is this: “The estrogen receptor never met a phenol that it did not like.”7 Phenols are aromatic organic compounds that are joined in chains to synthesize polycarbonates, nylon, detergents, herbicides and numerous pharmaceutical medicines. The estrogen receptor has an affinity for a component of phenols. According to University of Missouri cell biologist and endocrinologist Wade Welshons, “99.9 percent of what turn out to be chemical estrogens have a phenolic hydroxyl group on the molecule, and any of those can bind to the estrogen receptor.”31 Welshons adds that: “Almost everything that binds to the estrogen receptor turns it on in some way.”

With all this potential for toxic exposure around us, what are we to do? One of the things we are beginning to recognize, at least where conception is concerned, is that having a healthy lifestyle, minimizing toxin exposures, and supporting the body to detoxify from these exposures is necessary far prior to the actual fusing of a sperm and an egg. Many people may not realize that it takes sperm about 2-3 months to develop and mature – if the toxicities are not removed or minimized prior to this, each of these sperm will be nesting and developing in a toxic bath with high levels of oxidative stress leading to DNA damage and impaired spermatogenesis.32 Although antioxidants are one means to improve male fertility,33,34 they are not adequate to overcome the potential damage that chemicals and heavy metals can wreak on the whole body including the reproductive system, and a comprehensive detoxification system is necessary.


1 Levine H, Jørgensen N, Martin0-Andrade A, et al. Temporal trends in sperm count: a systematic review and meta-regression analysis. Human Reproduction Update, 2017 July; 1-14. View Full Paper

2 Jensen TK, Jacobsen R, Christensen K, et al. Good semen quality and life expectancy: a cohort study of 43,277 men. Am J Epidemiol 2009;170: 559–565. See Abstract

3 Ghosh P, Spermcount drop ‘could make humans extinct’. BBC News Health. July 25 2017 [cited July 29, 2017] Available at: http://www.bbc.com/news/health-40719743

4 National Toxicology Program, US Department of Health & Human Services. February 1 2017 [cited July 29, 2017] Available at: https://ntp.niehs.nih.gov/about/index.html

5 National Institute of Environmental Health Sciences, Endocrine Disruptors. [Cited July 29, 2017] Available at: https://www.niehs.nih.gov/health/topics/agents/endocrine/index.cfm

6 Fagin, D. Toxicology: the learning curve. Nature (2012) Oct 25;490(7421):462-5 See Full Paper

7 Personal communication, November 2, 2007.

8 Angle BM, Do RP, Ponzi D et al. Metabolic disruption in male mice due to fetal exposure to low but not high doses of bisphenol A (BPA): evidence for effects on body weight, food intake, adipocytes, leptin, adiponectin, insulin and glucose regulation. Reprod Toxicol. 2013 Dec;42:256-68 View Full Paper

9 Centers for Disease Control and Information. Fact Sheet. Dec 23 2016 [cited July 29 2017] Available at: https://www.cdc.gov/biomonitoring/bisphenola_factsheet.html

10 Bushnik T, Haines D, Lavallois P et al. Lead and bisphenol A concentrations in the Canadian population. Health Rep 2010 Sep;21(3): 7-18 View Full Paper

11 Begley TH, et al. Perfluorochemicals: potential sources of and migration from food packaging. Food Addit Contam. 2005 Oct;22(10):1023-31 View Abstract

12 Franko J, et al. Dermal penetration potential of perfluorooctanoic acid (PFOA) in human and mouse skin. J Toxicol Environ Health A. 2012;75(1):50-62. View Abstract

13 D'Hollander W, et al. Perfluorinated substances in human food and other sources of human exposure. Rev Environ Contam Toxicol. 2010;208:179-215 View Abstract

14 Kubwabo C, et al. Occurrence of perfluorosulfonates and other perfluorochemicals in dust from selected homes in the city of Ottawa, Canada. J Environ Monit. 2005 Nov;7(11):1074-8. View Abstract

15 Klepeis NE1, Nelson WC, Ott WR et al. The National Human Activity Pattern Survey (NHAPS): a resource for assessing exposure to environmental pollutants. J Expo Anal Environ Epidemiol. 2001 May-Jun;11(3):231-52. View Abstract

16 Zhang T, et al. Perfluorinated compounds in human blood, water, edible freshwater fish, and seafood in China: daily intake and regional differences in human exposures. J Agric Food Chem. 2011 Oct 26;59(20):11168-76 View Abstract

17 Liu W, et al. Involvement of NRF2 in Perfluorooctanoic Acid-Induced Testicular Damage in Male Mice. Biol Reprod. 2015 Aug;93(2):41 View Abstract

18 Sengupta P. Environmental and occupational exposure of metals and their role in male reproductive functions x Drug Chem Toxicol. 2013 Jul;36(3):353-68 View Abstract

19 Alcser KH, Brix KA, Fine LJ et al. Occupational mercury exposure and male reproductive health.Am J Ind Med. 1989;15(5):517-29. View Abstract

20 Hanf V, Forstmann A, Costea JE et al. Mercury in urine and ejaculate in husbands of barren couples.

Toxicol Lett. 1996 Nov;88(1-3):227-31. View Abstract

21 Chung JY, Yu SD, Hong YS. Environmental Source of Arsenic Exposure J Prev Med Public Health. 2014 Sep; 47(5): 253–257. View Full Paper

22 Davey JC, Nomikos AP, Wungjiranirun M et al. Arsenic as an endocrine disruptor: arsenic disrupts retinoic acid receptor-and thyroid hormone receptor-mediated gene regulation and thyroid hormone-mediated amphibian tail metamorphosis. Environ Health Perspect. 2008 Feb;116(2):165-72. View Abstract

23 Veeramachaneni DN, Palmer JS, Amann RP. Long-term effects on male reproduction of early exposure to common chemical contaminants in drinking water. Hum Reprod. 2001 May;16(5):979-87. View Abstract

24 Sallmén M. Exposure to lead and male fertility. Int J Occup Med Environ Health. 2001;14(3):219-22. View Abstract

25 Buck Louis GM, Sundaram R, Schisterman EF et al. Heavy metals and couple fecundity, the LIFE Study.Chemosphere. 2012 Jun;87(11):1201-7. View Full Paper

26 Greene D. Effects of Lead in the environment. LEAD Action News 1993 (1):2 View Full Paper

27 Centers for Disease Control. February 9, 2017 [Cited July 29, 2017] Available at: https://www.cdc.gov/nceh/lead/

28 Laidlaw MA, Zahran S, Pingitore N et al. Identification of lead sources in residential environments: Sydney Australia.Environ Pollut. 2014 Jan;184:238-46 View Abstract

29 Mercury in the Environment. Fact Sheet 146-00. October 2000. [Accessed July 29, 2017] Available at: http://www.usgs.gov/themes/factsheet/146-00/index.html

30 Kassotis CD, Tillitt DE, Lin CH et al. Endocrine-Disrupting Chemicals and Oil and Natural Gas Operations: Potential Environmental Contamination and Recommendations to Assess Complex Environmental Mixtures. Environmental Health Perspectives, 2015

31 Neimark J. The Dirty Truth About Plastic. Discover Magazine (2008) April 18. View Full Paper

32 Heller CG, Clermont Y. Spermatogenesis in man: an estimate of its duration. Science. 1963 Apr 12;140(3563):184-6. View Abstract

33 Yang HS, et al. Effects of alpha-tocopherol on cadmium-induced toxicity in rat testis and spermatogenesis. J Korean Med Sci. 2006 Jun;21(3):445-51. View Full Paper

34 Sheweita SA, et al. Mechanisms of male infertility: role of antioxidants. Curr Drug Metab. 2005 Oct;6(5):495-501. View Abstract

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