Science in Society Archive

Important Books & Reports

Banishing Glyphosate

Banishing Glyphosate - Dr. Eva Sirinathsinghji, Dr. Mae-Wan Ho and others

Glyphosate/Roundup, falsely claimed by Monsanto to be safe and harmless, has become the world’s most widely and pervasively used herbicide; it has brought rising tides of birth defects, cancers, fatal kidney disease, sterility, and dozens of other illnesses - more

Ban GMOs Now

Ban GMOs Now - Dr. Mae-Wan Ho and Dr. Eva Sirinathsinghji

Health & environmental hazards especially in the light of the new genetics - more

Living Rainbow H2O

Living Rainbow H2O - Dr. Mae-Wan Ho

A unique synthesis of the latest findings in the quantum physics and chemistry of water that tells you why water is the “means, medium, and message of life” - more

The Rainbow and the Worm - the Physics of Organisms

The Rainbow and the Worm - the Physics of Organisms - Dr. Mae-Wan Ho

“Probably the Most Important Book for the Coming Scientific Revolution” - more

Organic Food during Mother’s Pregnancy Reduces Risk of Male Birth Defects

Expecting mothers eating mostly organic produce reduce risk of urogenital anomalies in male offspring Dr Eva Sirinathsinghji

A large epidemiological study links consumption of organic food with decreased rates of hypospadias and cryptorchidism, both common types of male urogenital birth defects [1]. This is the first prospective study to find a significant link between consumption of organic foods and reduced risk of hypospadias.

The study analysed over 37 000 women and children pairs, finding that women who consume any organic food during pregnancy are 0.42 times as likely to give birth to a boy with hypospadias as those who report seldom or never eating organic food. This decrease is modest but significant, and builds on a growing list of studies linking pesticides and other endocrine disrupters to these types of defects. Of all the food groups analysed (vegetables, fruit, cereal, dairy, eggs and meat), consumption of organic vegetables as well as organic dairy were most strongly associated with the protective effect, with baby boys 0.30 times as likely to get hypospadias when mothers consumed either organic dairy or organic vegetables. For cryptorchidism, a borderline negative association was found solely with the consumption of organic milk/dairy products, with those consuming this organic food group being 0.65 times as likely to give birth to a boy with the condition. Results were adjusted for food intakes, sociodemographic variables and lifestyle factors, though these factors had marginal influence on the results.

Published in Environmental Health Perspectives and led by Dr Anne Lise Brantsæter at the Norwegian Institute of Public Health in Oslo, the research used data collected from the Norwegian Mother and Child Cohort Study. It is an ongoing long-term prospective cohort study of 110 000 pregnant women that aims to provide a resource for assessing the role of environmental and other exposures in the health of women and their children, conducted by the Norwegian Institute of Public Health. For this study in particular, the data were used to uncover the unknown aetiology of these urogenital anomalies.

Rates of urogenital defects rising in many global regions

Hypospadias is a male birth defect of the urethra where the urinary opening is not at the correct location at the head of the penis. It is the second most common birth defect in boys, affecting approximately 1 in 250 people in the US, and 3 in 1 ooo in Europe [2]. Its prevalence has been rising in many parts of the world including numerous countries in Europe, Americas and Asia. Increased rates in 7 European countries were reported by the International Clearinghouse for Birth Defects Monitoring Systems, a non-governmental organisation of the World Health Organisation in the 1960s, 1970s and 1980s [3]. Concurrently, a Danish study reported rising rates from 0.24 % of the population in 1977 to 0.52 % in 2005, corresponding to an annual increase of 2.4 % [4]. In the US, The Centre for Disease Control and Prevention reported a doubling of rates from 1968 to 1993 [5]. This analysis included data from the population-based registry that uses active case studies in 22 hospitals and clinics in the 2 different states, Atlanta and Georgia. The US Birth Defects Monitoring Program which gathers discharge diagnoses of newborns across the country reports an increase in hypospadias from 20.2 per 10 000 live births in 1970 to 39.7 per 10 000 in 1993, almost a doubling of rates in a 14-year period [6].  Data from the Japanese International Clearinghouse for Birth Defects Surveillance and Research show that the prevalence of hypospadias in Japan from 1997 to 2002 and 2003 to 2006 were 3.43 per 10 000 and 4.23 per 10 000 births, respectively [7]. In China, rising rates are found in rural populations and in children of mothers with higher maternal age, with a national annual increase in prevalence of 7.43 % reported in one study [8]. There appears to be geographical variation in disease rates however, and not all regions or countries are seeing rises in disease but either levelling off or even decreases in disease rates, including California, Mexico, Israel, Australia and some parts of Europe [3].

Cryptorchidism is diagnosed when one or both testicles have not descended into the scrotum. Prevalence varies depending on geographical location, with rates between 2-8 % of all male births [9]. Prospective cohort studies have indicated an increased prevalence of the defect in England (1950s-1980s) and Denmark (1960s-2000) [10].

Hypsospadias, hormones and endocrine disrupting chemicals

The development of the external male genitalia is a complex process that involves both androgen hormone-dependent and independent pathways that are also susceptible to other endocrine and environmental influences. Non-hormonal influences that have been identified include foetal growth restriction and preeclampsia (a condition of pregnant women characterised by high blood pressure and protein in the urine), which have been consistently associated with hypospadias, suggesting that placental insufficiency may be a factor [11]. It is known that maternal diet influences placental function, level of inflammation and foetal nutrient supply [12], indicating that diet may be related to hypospadias via this mechanism.

Hormonal influences tie into their complex involvement in the development of the reproductive system early in foetal life. Initially, male and female reproductive systems follow a similar pattern of development and at 6 weeks of age, the differentiation of external genitalia is yet to take place. At 9-10 weeks the sex determining region of the Y chromosome (SRY) is required to initiate male gonadal differentiation including the differentiation of testicular Sertoli cells, as well as Leydig cells which produce testosterone. Testosterone induces the development of the epididymis (a highly convoluted duct behind the testis, along which sperm passes to the vas deferens), vas deferens and seminal vesicles. By the 10-12th week, the genitalia are distinguishable externally. Testosterone is also a substrate for the enzyme, 5α-reductase, which converts testosterone to dihydrotestosterone. This even more potent androgen drives growth of the external genitalia and prostate [13].

Studies of the genetics of hypospadias point towards hormonal abnormalities as a key cause. Though it is considered a complex disease with both genetic and environmental causes, some single gene traits can lead to hypospadias, including partial androgen insensitivity syndrome, testosterone 5α-reductase deficiency and Drash syndrome [14]. Clinical studies also indicate that defects in testosterone metabolism or testosterone receptors are a potential cause of hypospadias. Exposure to synthetic oestrogens and progestins used for contraceptives or assisted reproduction have been linked to the defect.

Animal studies show the importance of hormone-dependent pathways in reproductive development. Blocking dihydrotestosterone in rabbits results in feminisation of male reproductive organs in rabbits. Rats exposed to antiandrogens leads feminisation as well as cryptorchidism. Pesticides such as linuron and vinclozolin cause feminisation of external genitalia and abnormal urethral opening in rats and mice.  Phthalates, chemicals added to a large variety of products from pharmaceutical pills to gelling & emulsifying agents, agricultural adjuvants, building materials, personal care products as well as paints, textiles and plastic products such as children’s toys and food packaging, also act as antiandrogens and have been shown to cause feminisation and hypospadias in male rats (see [14] for summary of animal studies of hormonal roles in reproductive development.) Human studies have also found a link of hypospadias to phthalate exposure. It is thought that human exposure to phthalates happens most commonly through ingestion, either by the contamination of food via its use as an adjuvant for pesticides or food packaging, as well as sucking of children’s toys. It has been detected in most food groups from meats to vegetables and grains [15].

Pesticides are the other obvious candidate for the observed disparity in disease rates between those eating organic versus conventional foods. Several classes of pesticide have been shown to have endocrine disrupting effects including glyphosate, 2,4-D, atrazine, endosulfan, linurin, vinclozolin and dichlorodiphenyldichloroethylene (DDE) [16]. A metal-analysis of 9 studies found a marginal but significant risk of hypospadias associated with both maternal and paternal exposures to pesticides, reporting a 1.4 times increased chance of getting hypospadias following maternal pesticide exposure [17]. Individual studies have found increased rates of hypospadias children of people living or working in agricultural environments in North Indian boys [18] and increased cryptorchidism in gardeners in Denmark [19]. Greek boys with hypospadias as well as their parents show the presence of organophosphate and organochlorine pesticides in hair samples, with mother’s showing significantly higher levels than the fathers, though was limited by a lack of control [20].       

Glyphosate herbicides have also been suggested to contribute to hypospadias in a recent review of the decline of health in both people and wild animals in the state of Montana, USA, in the last 20 years, that correlates with the increased use of glyphosate [21]. Glyphosate has been widely reported to cause birth defects and has been shown to disrupt endocrine pathways such as the retinoic acid signalling pathway and aromatase enzyme activity, which converts testosterone precursors to oestrogens (see [22] Banishing Glyphosate, Special ISIS report). This latter mechanism may cause a disruption of testosterone signalling that could lead to the development of hypospadias, though this is yet to be mechanistically studied.

Hypospadias, cryptorchidism and “testicular dysgenesis syndrome”

Some researchers have further suggested that hypospadias and cryptorchidism are related and share a common cause along with other abnormalities in male reproductive health that have risen sharply in the last 50 years, terming the group of abnormalities as “testicular dysgenesis syndromes” (TDS). Other abnormalities grouped into this category include testicular cancer and reduced sperm quality. Testicular cell cancer is the commonest form of cancer in young men in many countries, and is associated with impaired semen quality and lower fertility rates (see [23] Glyphosate/Roundup & Human Male Infertility, SiS 62).

To conclude

Studies such as this one highlight our need to protect the integrity of our food supply and urges us to further investigate the potential harm we are causing to our children. Endocrine disruption not only leads to developmental problems but other illnesses such as cancers. Contamination of our food supply and environment with such chemicals should be avoided at all costs.

Article first published 30/09/15



References

  1. Brantsæter AL, Torjusen H, Meltzer HM, Papadopoulou E, Hoppin JA, Alexander J, Lieblein G, Roos G, Holten JM, Swartz J, Haugen M. Organic Food Consumption during Pregnancy and Hypospadias and Cryptorchidism at Birth: The Norwegian Mother and Child Cohort Study (MoBa). Environmental Health Perspectives 2015 Jul 9. [Epub ahead of print]
  2. Hypospadias, Wikipedia, 22nd September 2015
  3. Paulozzi LJ. International Trends in rates of hypospadias and cryptorchidism. Environmental Health Perspectives 1999, 107, 297-302.
  4. Lund L, Engebjerg MC, Pedersen L, Ehrenstein V, Nørgaard M, Sørensen HT. Prevalence of hypospadias in Danish boys: a longitudinal study, 1977-2005. European Urology 2009, 55, 1022-6.
  5. Paulozzi LJ, Erickson JD, Jackson RJ. Hypospadias trends in two U.S. surveillance systems. Pediatrics 1997, 100, 831-834
  6. March of Dimes, Metropolitan Atlanta Congenital Defects Program, and California Birth Defects Monitoring Program, MoD/MACDP/CBDMP. Leading Categories of Birth Defects. March 2001.
  7. Kurahashi N, Murakumo M, Kakizaki H, Nonomura K, Koyanagi T, Kasai S, Sata F, Kishi R. The estimated prevalence of hypospadias in Hokkaido, Japan. Journal of Epidemiology2004, 14, 73-7.
  8. Li Y, Mao M, Dai L, Li K, Li X, Zhou G, Wang Y, Li Q, He C, Liang J, Zhu J. Time trends and geographic variations in the prevalence of hypospadias in China. Birth Defects Research A. Clinical & Molecular Teratology 2012, 94, 36-41
  9. Virtanen HE, Bjerknes R, Cortes D, Jørgensen N, Rajpert-De Meyts E, Thorsson AV, Thorup J, Main KM. Cryptorchidism: classification, prevalence and long-term consequences. Acta Paediatrica 2007, 96, 611-6.
  10. Virtanen HE, Toppari J. Epidemiology and pathogenesis of cryptorchidism. Human Reproduction Update 2008, 14, 49-58
  11. Thorup J, Nordenskjold A, Hutson JM. Genetic and environmental origins of hypospadias. Current Opinion in Endocrinology, Diabetes, and Obesity 2014, 21, 227-232.
  12. Thornburg KL, O'Tierney PF, Louey S. Review: The placenta is a programming agent for cardiovascular disease. Placenta 2010, 31, S54-59.
  13. Blaschko SD, Cunha GR, Baskin LS. Molecular mechanisms of external genitalia development. Differentiation 2012,84, 261-8
  14. Nordenskjöld A. Genetic and clinical studies on hypospadias. Advances in Experimental Medicine & Biology 2004, 545, 73-84.
  15. Rudel RA1, Perovich LJ. Endocrine disrupting chemicals in indoor and outdoor air. Atmospheric Environment (1994). 2009, 43, 170-181.
  16. Del Pup L, Mantovani A, Luce A, Cavaliere C, Facchini G, Di Francia R, Caraglia M, Berretta M. Oncology Reports 2015, 34, 3-11.
  17. Rocheleau CM, Romitti PA, Dennis LK. Pesticides and hypospadias: a meta-analysis. Journal of Paediatric Urology 2009, 5, 17-24.
  18. Samtani R, Bajpai M, Ghosh PK, Saraswathy KN. Hypospadias Risk among North-Indian Children. Annals of Health & Health Sciences 2014, 1, 61-64 DOI: 10.5958/j.2322-0422.1.1.012
  19. Weidner IS, Møller H, Jensen TK, Skakkebaek NE. Cryptorchidism and hypospadias in sons of gardeners and farmers. Environmental Health Perspectives 1996, 106, 793-6.
  20. Michalakis M, Tzatzarakis MN, Kovatsi L, Alegakis AK, Tsakalof AK, Heretis I, Tsatsakis A. Hypospadias in offspring is associated with chronic exposure of parents to organophosphate and organochlorine pesticides. Toxicology Letters 2014 Oct 15;230, 139-45
  21. Hoy J, Swanson N, Seneff S. The High Cost of Pesticides: Human and Animal Diseases. Poultry, Fish & Wildlife Sciences 2015, 3, 132. doi:10.4172/2375- 446X.1000132
  22. Banishing Glyphosate. Special ISIS report, 2015. http://www.i-sis.org.uk/Banishing_Glyphosate.php
  23. Ho MW. Glyphosate/Roundup & Male Infertility,Science in Society 62, 14-17.
  24. Paulozzi LJ. International trends in rates of hypospadias and cryptorchidism. Environ Health Perspect. 1999;107:297–302

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Todd Millions Comment left 4th October 2015 07:07:35
I have some intimate background with the crypto version of this-which wasn't genetic.Unless clumsiness in inherited. I apparently managed to pass the umbilicus through my legs as I wrapped it round my neck a couple of times.Then I hit the chute.Mom said 'I wasn't blue-I was purple,like a plum'.She also related that she saw this,then I was 'gone' and the door was slammed.This was when the oxygen tanks were kept outside the operating and delivery rooms too keep the ether fumes (and a spark)from turning the hospitals into blast furnaces.If O2 was needed-a hose was run in.I would assume that the veteran ww2 nurse in attendance noted my colour and that the had doctor froze up and did what such tended too do in such situations -So she may have pushed up the nut as she raced for the oxygen tank whilst pulling the cord off my neck.If so I owe her thanx. A week later the doctor used me as a lab rat for a procedure he would have read about(but turned out hadn't actually performed before)based on-If I screw up,he's retarded by oxygen deficiency and so it won't mater(too him) as the evidence will be cleared away with the mandatory sterilization when he is 14. This didn't happen but-the screw up is too be kept in mind when you use these studies.Much in this field was and is still -a balls up.

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