The Skinny on Roundup, Sex and Sperm Part 2: studies not held by the safety agencies.

shell in sandThere are only TWO studies investigating sperm that decide the toxicity of the chemicals sprayed on our food held with USA EPA, World Health Organisation or Europe’s EFSA.

There is no study held with these agencies that evaluate toxicity of chemicals looking at the effect of Roundup or glyphosate on sperm at current levels of human exposure to the chemical.

Somehow, they just manage to ignore this pretty important part of assessing toxicity for our reproductive systems.


THESE ARE NOT HELD BY THE USA EPA, the World Health Organisation, or Europe’s EFSA:

These studies look at the effects of glyphosate AND Roundup at different periods of human development.  They also look at low levels of glyphosate and Roundup which are similar to human exposure levels.

And here they are (If you have more suggestions please forward them to me):

Glyphosate Study on mature rabbits:  Yousef : Described the harmful effect of glyphosate on semen quality after 6 weeks of post-treatment period in rabbits (of sub-lethal quantities, Safe Says Who understands at levels 38 and 380 mg/kg bw/day). Pesticide treatment resulted in a decline in body weight, libido, ejaculate volume, sperm concentration, semen initial fructose and semen osmolality.  This was accompanied with increases in the abnormal and dead sperm and semen methylene blue reduction time. The hazardous effect of these pesticides on semen quality continued during the recovery period, and was dose‐dependent.  These effects on sperm quality may be due to the direct cytotoxic effects of these pesticides on spermatogenesis and/or indirectly via hypothalami‐pituitary ‐testis axis which control the reproductive efficiency [1].

Roundup dosed perinatally then through to prepuberty:  Dallegrave 2007 examined the reproductive effects of Roundup on male and female offspring of Wistar rats treated with 50, 150 or 450 mg/kg of Roundup during pregnancy and lactation.  The study found that these doses of Roundup did induce adverse reproductive effects on male offspring.  Findings include a decrease in sperm number and daily sperm production during adulthood, an increase in the percentage of abnormal sperms, a dose-related decrease in the serum testosterone level at puberty, and signs of sperm cell degeneration during both periods. The study showed that Roundup is a reproductive toxin at non-maternally toxic doses [2].   This study showed that glyphosate Roundup administration from the perinatal period to lactation did not induce maternal toxicity but caused reproductive problems in male offspring, including a decrease in the number of sperm in the cauda epididymis affecting the daily production of sperm in adult life.  [2].

Roundup Prepuberty study:  Romano et al. 2010 demonstrated a significant reduction in serum testosterone concentrations and changes in the testicular morphology of male Wistar rats treated with Roundup during the prepubertal period, and these effects were demonstrated with even the lowest dose used in the experiment (5 mg/kg).  It was shown that glyphosate during this period causes an anti-androgenic effect, causing a reduction of serum testosterone and in the height of the seminiferous epithelium [3].

Roundup studies on human cells at very low doses:  A reduction in aromatase activity was observed in placental and embryonic human cells treated with low concentrations of a commercial formulation of glyphosate, which disrupted the conversion of steroids to estradiol.  [4] [5]  It has been shown that women occupationally exposed to this herbicide have reproductive disorders [5].

Estradiol has a critical impact on reproductive and sexual functioning.

Low, sub-agricultural doses:  A study exposed human liver HepG2 cells, to four different formulations and to glyphosate. The study measured cytotoxicity, plus genotoxicity, anti-estrogenic, and anti-androgenic effects. Study authors checked androgen to estrogen conversion by aromatase activity and mRNA. All parameters were disrupted at sub-agricultural doses with all formulations within 24h. These effects were more dependent on the formulation (Roundup) than on the glyphosate concentration. The researchers observed a human cell endocrine disruption from 0.5 ppm on the androgen receptor, for the most active formulation (R400), then from 2 ppm the transcriptional activities on both estrogen receptors were also inhibited on HepG2. Aromatase transcription and activity were disrupted from 10 ppm. Cytotoxic effects started at 10 ppm with the most sensitive, and DNA damages at 5 ppm. A real cell impact of glyphosate-based herbicides residues in food, feed or in the environment has thus to be considered, and their classifications as carcinogens/mutagens/reprotoxics is discussed. [6]

This next study by Romano et al. 2102 pulls a lot of the history of research into glyphosate and independent reproductive toxicology studies together and reveals how the glyphosate intake of the mother affects the developing child [8]:

What is shocking/surprising/confronting about this study is that the 50 mg/kg bw/day (so for example the MRL for flour and bread is 30mg/kg) was ONLY FED TO THE MOTHERS.  The offspring were never fed glyphosate.  I double checked with the study authors and they confirmed:  The product was administered only to the mothers during the late of the gestational period and first days of lactational phase’.

And this wasn’t even a test with Roundup – which is stronger and more effective.

Romano et al. 2012 summarised (remember, this is the offspring who were never directly fed the pesticide):

Females: increased estradiol serum concentrations and earlier puberty

Males:   increased estradiol serum concentrations, but sexual arousal, which estradiol is meant to stimulate, didn’t happen, the study authors believe this suggests that hormone signals may have been misinterpreted by the central nervous system somehow.

 Estrogens (such as estradiol) spermatogenesis can be disrupted to such an extent that the animals become infertile. (Wikepedia)

Increase in the latency to first mount, latency to first intromission, latency to mount after first ejaculation, suggesting an herbicide-mediated effect on the libido of the animals.

The actual Glyphosate Prepuberty study:  Romano et al. 2012 investigated the effect of gestational maternal glyphosate exposure (50 mg/kg, NOAEL for reproductive toxicity) on the reproductive development of male offspring.  The study authors assessed the sexual behavior of 60-day-old male rat offspring from females treated with glyphosate during the perinatal period.  Dams were exposed during the critical period of sexual hypothalamic differentiation – prepuberty.  This study suggests that maternal exposure to glyphosate disturbed the masculinization process.  Among other factors, sexual behavior is influenced by hormones, so the serum concentrations of testosterone, estradiol, FSH and LH were measured.

Study authors observed an increase in the latency to first mount, latency to first intromission, latency to mount after first ejaculation, suggesting an herbicide-mediated effect on the libido of the animals.  Increased estradiol serum concentrations were observed, likely due to the increase in testosterone, which leads to greater conversion of estradiol (Bardin and Catterall 1981; Knudsen and Max 1980). Estradiol is known to stimulate the sexual arousal in both females and males (Harding and Velotta 2011; Max and Knudsen 1980; Heindel and Kimberley 1989); however, it appears that this did not occur in these animals, suggesting that hormone signals may have been misinterpreted by the central nervous system. The early onset of puberty observed in this study suggests that the production of this hormone was initiated precociously in these animals. In addition, testosterone levels were also elevated, which may have contributed to change in the age at puberty onset. Because the rats reached puberty at an earlier age, the animals had lower body weights at puberty.

Besides the changes observed in the gonadal hormones, the evaluation at PND60 showed altered gonadotropins, with elevated LH mRNA expression, protein content in the pituitary gland and serum. The FSH mRNA expression was increased, while the protein and serum concentrations remained unaltered. The gonadotropins are produced and released by the stimulation of hypothalamic GnRH, and testosterone exerts negative feedback on LH production.

Thus, we may speculate that the glyphosate treatment may have caused (1) a permanent stimulus of LH production and (2) failure in the interpretation of the negative feedback mechanism. Because sex hormones may influence the spermatogenesis, we evaluated total sperm production, daily sperm production, sperm reserves and sperm transit at PND60. Perinatal glyphosate exposure increased the total and daily sperm production in the testes, which is associated with the increase in the height of the germinal epithelium of seminiferous tubules in histological sections. In addition, we assessed the sperm content in epididymis segments, noting that sperm reserves were increased in the caput, corpus and cauda segments. Sperm transit time, however, was reduced only in the cauda of the epididymis. These observations may be related to the increased testosterone, estradiol and LH serum concentrations. This study shows, for the first time, the effects on the reproductive development of male offspring from dams treated with glyphosate only in the perinatal period. We conclude that the exposure promotes behavioral changes and histological and endocrine problems in reproductive parameters and these changes are reflected by a hypersecretion of androgens and increased gonadal activity, sperm production and libido. It is not known whether the dose used in this study is in fact the levels of exposure of population to the glyphosate herbicide.

Glyphosate was shown to alter aromatase activity and decrease serum testosterone concentrations.  Thus, the aim of this study was to investigate the effect of gestational maternal glyphosate exposure (50 mg/kg, NOAEL for reproductive toxicity) on the reproductive development of male offspring.   Results suggest that maternal exposure to glyphosate disturbed the masculinization process and promoted behavioral changes and histological and endocrine problems in reproductive parameters. (Romano 2012) 


To help understand all the above terms please consult Wikipedia :

Spermatozoa formed in the testis enter the caput epididymis, progress to the corpus, and finally reach the cauda region, where they are stored. Sperm entering the caput epididymis are incomplete – they lack the ability to swim forward (motility) and to fertilize an egg. It stores the sperm for 2–3 months. During their transit in the epididymis, sperm undergo maturation processes necessary for them to acquire these functions. Final maturation is completed in the female reproductive tract (capacitation).

Testes are components of both the reproductive system and the endocrine system. The primary functions of the testes are to produce sperm (spermatogenesis) and to produce androgens, primarily testosterone.  Both functions of the testicle are influenced by gonadotropic hormones produced by the anterior pituitaryLuteinizing hormone (LH) results in testosterone release. The presence of both testosterone and follicle-stimulating hormone (FSH) is needed to support spermatogenesis. It has also been shown in animal studies that if testes are exposed to either too high or too low levels of estrogens (such as estradiol; E2) spermatogenesis can be disrupted to such an extent that the animals become infertile.

Aromatase, also called estrogen synthetase or estrogen synthase, is an enzyme responsible for a key step in the biosynthesis ofestrogens. aromatase is  responsible for the  aromatization  of  androgens into estrogens.  Inhibition of the enzyme leads to low estrogen levels.

Estradiol is the predominant estrogen during reproductive years both in terms of absolute serum levels as well as in terms of estrogenic activity.  Estradiol has not only a critical impact on reproductive and sexual functioning, but also affects other organs, including the bones.  For females, in precocious puberty, estradiol levels are inappropriately increased.


[1] Yousef, M.; et al, Toxic effects of carbofuran and glyphosate on semen characteristics in rabbits”, Journal of Environmental Science Health, B30, 4, 1995, 513-534

[2] Dallegrave, E., Mantese, F. D. et al. 2007. Pre- and postnatal toxicity of the commercial glyphosate formulation in Wistar rats. Arch Toxicol 81: 665–673

[3] Romano, R. M., Romano, M. A. et al. 2010. Prepubertal exposure to commercial formulation of the herbicide Glyphosate alters testosterone levels and testicular morphology. Archives of Toxicology 84(4): 309–317.

[4]  Benachour, N., Sipahutar, H., Moslemi, S., Gasnier, C., Travert, C., Séralini, G-E. 2007.  Time- and dose-dependent effects of roundup on human embryonic and placental cells. Archives of Environmental  Contamination and Toxicology 53, 126–33.

[5] Richard, S., Moslemi, S., Sipahutar, H., Benachour, N., Séralini, G-E. 2005. Differential effects of glyphosate and Roundup on human placental cells and aromatase. Environmental Health Perspectives 113: 716–20.

[6] Gasnier C, Dumont C, Nora Benachour N, Clair E, Chagnon MC, Seralini GE (2009) Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines. Toxicology 262:184–191

[7]  Romano MA, et al.  Glyphosate impairs male offspring reproductive development by disrupting gonadotropin expression.   Arch Toxicol. 2012 Apr;86(4):663-73. doi: 10.1007/s00204-011-0788-9. Epub 2011 Nov 26.

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