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One in five healthy men between the ages of 18 and 25 produce abnormal sperm counts. In men without fertility problems, the average sperm count has halved, 20 percent of young European men have sperm counts at a level likely to result in infertility, and a further 40 percent have sperm counts likely to result in delayed pregnancy (Word Health Organisation). Demands for assisted reproductive technology (ART) are growing; in Denmark, for example, more than seven percent of all children born in 2007 were conceived using ART.
In parallel with the decline in semen quality, there has been a rise in testicular germ cell cancer. This type of cancer is initiated during foetal development, and, in many countries, is the commonest cancer in young men (15 to 35 years of age). Testicular germ cell cancer is associated with impaired fertility even prior to cancer development.
Congenital malformations, such as, undescended testis appear also to have been increasing in the Western World. These are also risk factors for fertility problems.
Testosterone, the male hormone, is the major driver of male reproductive development and function. Suppression of its levels within the adult testis shuts down sperm formation and induces infertility. In America, there has been a substantial decline in testosterone levels that does not appear to be connected to health status, lifestyle or age. A sharp reduction started just after the introduction of GM crops and concomitant increase in the use of glyphosate-based herbicides (specifically 'Roundup'*).
“The mammalian (including human) testis is a sensitive ... biomonitor of potential toxic effects” (Brake and Evenson).
In the same way that such sensitivity makes it useful for testing the toxicity of a substance, the testis can be the first tissue to be damaged by exposure to toxins from the environment.
Several avenues of scientific investigation are suggesting that glyphosate or Roundup may be a key fertility-damaging environmental toxin.
Back in pre-GM days, one life-long glyphosate rat feeding study indicated an increased incidence of Leydig cell tumours (Cox). Leydig cells produce testosterone in the testis.
Glyphosate has since been described as an endocrine disruptor by one team of scientists. They found that pre-pubertal feeding of Roundup to rats led to decreased testosterone levels, and that maternal feeding of Roundup to rats led to a disturbed masculinisation process in male offspring. (Romano)
In another study, feeding Roundup to pregnant rats led to male offspring with low testosterone, decreased sperm counts and increased abnormal sperm cells. (Dellagrave)
Exposure to very low levels of Roundup has been found to cause Leydig cell damage. At non-toxic levels, Roundup and glyphosate led to a 35 percent drop in testosterone in rats. At higher concentrations of the herbicide other testicular cells were damaged. Glyphosate on its own was toxic to Sertoli cells which support and nourish the developing sperm cells. (Clair)
Concern about adverse reproductive effects observed in male agricultural workers exposed to Roundup at pre-pubertal age led Brazilian scientists to examine the herbicide's effects within rat testis cells. They found Roundup-induced activation of multiple stress-response pathways and membrane alterations leading to harmful calcium overload. (Cavalli)
The underlying problem in all these studies seems to be that glyphosate and Roundup cause accumulation of oxidants or 'reactive oxygen species' (ROS) inside cells. ROS are normal intermediates in the processes of energy generation. However, any toxin which interferes with any stage in these processes will create a 'dam', inducing a harmful accumulation of the intermediate ROS. Oxidants cause damage to the cell and seem to be associated with all chronic diseases. They can damage DNA and cell membranes, and can cause cancer.
One researcher demonstrated that Roundup can compromise the membranes of the cell mitochondrial bodies. The mitochondria are the site of energy-generation, and are where ROS arise. Functioning mitochondria are vital for sperm development and motility. Mitochondria also have their own DNA which can be damaged by any accumulated ROS.
High levels of ROS have been identified as a marker for human male infertility irrespective of sperm normality or abnormality.
Readers may remember a mouse feeding experiment in which sperm development was used as a biomarker to search for evidence of toxins in GM soya (Brake and Evenson). This study found identical sperm maturation profiles in animals fed GM and non-GM chow over four generations. In 2008, it was used to refute Russian scientist Irina Ermakova's multi-generational feeding study on rats which reported stunted growth and infertility.
Unfortunately, neither set of experiments included any measurement of the glyphosate or Roundup content of the feed used: this could be an important factor in the divergence between the results.
Also unfortunately, Brake and Evenson didn't record sperm number, only the ratios between sperm-cells at different stages of development. In humans, it seems sperm cell counts can be reduced by as much as 60-80 percent before fertility is impaired. If mice exhibit a similar such relationship, it's possible that a significant decline in testicular function was missed.
The mice were never allowed to survive much beyond puberty. This could mean that any cumulative effects from exposure to glyphosate or Roundup, from reduced testosterone, or from DNA damage had minimal opportunity to reveal themselves.
The jury is still out, but there's plenty of evidence there for YOU to insist that the precautionary principle be applied before the human race sprays itself to extinction.
We need focused, independent science to confirm or refute any role played, not only by glyphosate, but by the many varieties of Roundup formula, and by the many GM crops which accumulate them, in the on-going decline in male fertility.
- Glyphosate/Roundup & Human Male Infertility, Institute of Science in Society Report, 19.03.14
- Denise G. Brake and Donald P. Evenson, 2004, A generational study of glyphosate-tolerant soybeans on mouse fetal, postnatal, pubertal and adult testicular development, Food and Chemical Toxicology 42
- Caroline Cox, Northwest Coalition for Alternatives to Pesticides, Fall 1995, Glyphosate, Part 1: Toxicology, Journal of Pesticide Reform 15:3
- R. M. Romano, et al., 2010, Prepubertal exposure to commercial formulation of the herbicide glyphosate alters testosterone levels and testicular morphology, Archives of Toxicology 84
- R. M. Romano, et al., 2011, Glyphosate impairs male offspring reproductive development by disrupting gonadotropin expression, Archives of Toxicology November
- Émilie Clair, et al., 2012, A glyphosate-based herbicide induces necrosis and apoptosis in mature rat testicular cells in vitro, and testosterone decrease at lower levels, Toxicology in Vitro 26
- V. LdeL. O.Cavalli, et al., 2013, Roundup disrupts male reproductive functions by triggering calcium-mediated cell death in rat testis and Sertoli cells, Free Radical Biology and Medicine 65