endocrine disruptor

Could Altered Vitamin A Metabolism Be Responsible for Endometriosis and Fibroid Growth?

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vitamin A

Yes, and increased use of environmental toxicants may be partially to blame. Over the last decade researchers have uncovered connections between tissue level vitamin A activity – the retinoic acid pathway – hormone metabolism, and the cell cycle overgrowth noted in fibroid tumor development, breast and ovarian cancer, and endometriotic tissue growth. Moreover, researchers from the environmental side have found that the popular glyphosate-based herbicides alter vitamin A or retinoic acid metabolism which in turn alters androgen and estrogen metabolism. Connecting the dots, we may have a first step to reducing cell growth in these conditions; remove the toxicant exposure and increase nutritional resources. A second step may be to develop locally absorbed vitamin A, applied directly to the aberrant tissues.

What is Vitamin A?

Vitamin A, (retinol, carotene) is a fat-soluble nutrient that we derive solely from dietary sources. It is responsible for a myriad of functions in a vast number of tissues from the eye, to the ovary, to the heart. Historically, nutrition from diet, coupled with the old wives’ tales of good health, carrots for eyesight, and cod liver oil for all that ails you, were all that were needed to maintain healthy levels of Vitamin A in most individuals. However, with the increase in processed foods, modern farming, intense use of herbicides and pesticides, and the general replacement of the old wives’ nutritional wisdom with pharmaceuticals, many men, women, and children are vitamin A deficient and likely do not even know it. The WHO estimates vitamin A deficiency in 19 million pregnant women and 150 million children worldwide. When Vitamin A deficiency reaches its nadir night blindness, maternal mortality, and difficulty fighting infections are common. In women, the first signs of vitamin A deficiency may be unrecognized and include fibroids or endometriosis. Earlier signs of vitamin A deficiency in women could also be menorrhagia (heavy menstrual bleeding) that often precedes fibroid or endometriosis diagnosis, but research is lacking here, or even genital warts of the common HPV strains.

Why Retinoic Acid, Hormones, and Cell Growth

Retinoic acid (RA), is the form of vitamin A stored in the body. RA is what is called a paracrine, perhaps even an intracrine hormone regulator. That means it turns hormone metabolism on or off in the cells within its immediate vicinity (paracrine) or within its own cell (intracrine). This is compared to endocrine control of hormone metabolism – where hormones and the factors that regulate hormone synthesis and metabolism travel vast distances through the blood to reach their targets tissues (the hypothalamus-pituitary – ovarian system is an example of endocrine regulation) or autocrine where the hormone leaves its own cell only to turn around and bind to a receptor on that cell. In contrast, retinoic acid stays close to home and regulates local cell behavior, both internally and proximally. The vitamin A deficiency leading to fibroids or endometriosis represents a cell and tissue level disruption of the retinoic acid pathway that in turn interrupts the normal cell cycle (differentiation, proliferation, and apoptosis -cell death) and elicits all sorts of problems from decreased estrogen metabolism (too much estradiol at the cells), to cell overgrowth, or more specifically, not enough cell death where needed. The results include aberrant cell growth as in fibroids, tumors, and endometriosis.

Retinoic Acid, Progesterone and Estrogen Metabolism

With many women’s health conditions too much estradiol at the tissue level is at the root. Estradiol is an excitatory hormone that tells our cells to go forth and prosper. Progesterone, depending upon the tissue and the relative values of each circulating hormone can work synergistically to enhance estradiol’s actions or it can shut it down entirely via the upregulation of a specific estradiol metabolizing enzyme called 17 beta-hydroxysteroid dehydrogenase type 2  (17B -HSD2).  When these enzyme levels are high, more estradiol is converted to estrone. Since estrone is a less potent estrogen than estradiol, metabolism of estradiol to estrone somewhat inactivates the estrogen and slows cell proliferation. When the enzyme levels are low, more estradiol remains, and cell growth is enhanced.  Vitamin A or retinoic acid mediates the progesterone-dependent activation of this enzyme, effectively regulating estradiol concentrations locally. Too little retinoic acid or a disrupted retinoic acid pathway and estradiol is not converted to estrone – e.g. it is not inactivated. Cell proliferation dominates, while normal cell death or apoptosis is reduced. Fibroids, tumors, or endometriosis ensue.

What Causes Low Retinoic Acid or Reduced Functioning?

Vitamin A is derived entirely from diet. Foods high in vitamin A include brightly colored vegetables, dark leafy greens, carrots, pumpkin, sweet potatoes, bell peppers, and fatty fish oils, like cod liver oil and organ tissues like the liver. Meat and dairy also have high concentrations of vitamin A. Diets high in processed food do not contain sufficient vitamin A to maintain the proper cell cycle balance and so we get too much proliferation and too little apoptosis. Tissues grow and grow and do not die.

Alcohol intake reduces the body’s ability to metabolize retinoic acid because alcohol and the retinoic acid pathway use the same enzymes – alcohol dehydrogenase (ADH1) and aldehyde dehydrogenase (ALDH1) for metabolism. Alcohol competes for the enzyme and so vitamin A from diet cannot be converted to the usable retinoic acid.

Can Toxins Disrupt the Vitamin A Pathway?

Yes, but here is where it gets complicated. Environmental toxins like glyphosate used in common weed killers such as Round-up have a complex relationship with the vitamin A pathway and hormone metabolism. These herbicides and many pesticides are endocrine disruptors, meaning they disrupt ‘normal’ hormone metabolism, often towards a hyper-estrogenic state. Similarly, plastics like BPA and a host of industrial chemicals are also endocrine disruptors that move us towards hyper-estrogenism – a key component of fibroid and endometriosis.

Glysophate activates an enzyme called retinaldehyde dehydrogenase which increases retinoic acid synthesis. This is argued to be the mechanism by which environmental exposures during pregnancy cause birth defects. However, glyphosate also inhibits vitamin A metabolism by a similar mechanism as alcohol, by competing for ADH1 availability, thereby having the ability to reduce vitamin A synthesis. Glyphosate also increases aromatase activity (the enzyme that converts testosterone to estradiol), creating a hyper-estrogenic state and depending upon the time course and the exposure concentration, completely wipes out aromatase activity. So like any true hormone system, that uses a complex chain of compensatory reactions to maintain homeostasis, the reactions to environmental toxins are complicated and non-linear. Nevertheless, they warrant attention, particularly when one is suffering from a condition affected by the environmental toxin in question.

Managing Vitamin A Levels

To determine if you are vitamin A deficient, seek out a lab that specializes in micronutrient testing. The recommended daily values of vitamin A can be found in the Dietary Supplement Fact Sheet.

Vitamin A is a fat-soluble vitamin, meaning that it will be stored in fat, and toxicity from too much vitamin A is possible. It is rare, but nevertheless, if supplementing, vitamin A levels should be monitored by micronutrient testing.

My Two Cents

Much of the research presented here linking local vitamin A deficiencies with endometriotic, fibroid, and cancer growth has not crossed over into clinical care. Moreover, it is complex and far from settled. Except for cancer trials, mostly in males and mostly with oral supplementation, the research regarding dietary vitamin A is limited and mixed. However, I think a local application of an absorbable form of vitamin A or retinoic acid should be investigated for the treatment of endometriotic and fibroid growth in women. Similarly, dietary supplementation within acceptable levels and changes combined with environmental ‘cleaning’ may be of use, if only to improve the overall health status of women currently suffering from fibroids or endometriosis.

Postscript: This article was published previously in August 2013. 

Photo by Tamanna Rumee on Unsplash.

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Hormone Treatment During Pregnancy and Gender Variance in Later Life

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gendered brain

For as long as I can remember, I’ve always had an unusual partially feminine gender identity, but until recently I never consciously acknowledged it. Then, a couple of years ago I realised that, although at a conscious level I identify as male, my body language, my pattern of arousal and orgasm, and my instinctive social behaviour are all very much more like what you’d typically see in a woman rather than a man. In addition, I appear to be suffering from secondary hypogonadism (i.e. my brain regions that control hormones aren’t working correctly), and I have a “eunuchoid” body structure, which indicates that my testosterone production has been below normal all my life.

Is Being Transgendered Just One of Those Things?

Although it never became my career, as a student I excelled at both chemistry and biology, and I’ve retained an amateur interest in the sciences ever since. Most people seem to assume that being transgendered is “just one of those things”, but I resolved to use that background in science to try and figure out whether there was an actual physical explanation for it. Accordingly, I tried to discover as much as I could about sexual development in the unborn child, and the kinds of things that can go wrong with that process.

Sexual Blueprints

Our sex-determining chromosome, the Y chromosome, is far smaller than any of our other chromosome and only has a few dozen functional genes on it. Basically all the Y chromosome does is to tell your undifferentiated gonads to turn into testicles (without it they’ll turn into ovaries instead). All of the genetic blueprints for actually building a male or female body are located elsewhere in your genome, so everyone has the full set of instructions for both sexes.

By default the “female” instructions are what get followed during fetal development, but if there’s testosterone present, the “male” instructions will be followed instead. Ordinarily this system works quite well, and you’ll develop as one sex throughout the pregnancy (which one depending on whether you have testicles churning out testosterone or not).

An Endocrine Disruptor

What appears to have happened in my case is that the pregnancy was no different from that of any other male baby, except that partway through the second trimester, something catastrophic happened that severely disrupted my endocrine system, so that for a few weeks I wasn’t producing any testosterone. Following that, my endocrine system recovered and everything went back to normal for the remainder of the pregnancy. The result is that I was built using the instructions for male development for most of the pregnancy, but during the time I wasn’t producing any testosterone, the instructions for female development were followed instead. That seems to have happened after all my physical development had completed, but very early in the process of wiring up my brain’s permanent structure (all the things that are affected seem to be associated with evolutionarily ancient parts of the brain, which points to the period of female development having happened early on in the process of wiring up my brain).

Based on when genital development takes place and when the process of building the permanent structure of the brain begins, I was able to work out that whatever it was must have happened somewhere around 16 or 17 weeks after conception, at or very soon after the time my mother would have first felt me moving inside her. Knowing what she was like when I was younger, my immediate thought was that she must have had a depressive episode, decided that she couldn’t cope with another child so soon after the first, and taken an overdose of something in an attempt to bring on a miscarriage.

A DIY Abortion That Didn’t Take

A bit of snooping on maternity forums soon revealed that the first thing most unhappily pregnant women contemplating a DIY abortion seem to think of is an overdose of contraceptive pills. I was able to subsequently confirm that my parents were using birth control pills for contraception at the time – the high dosage first generation ones. There was also something otherwise completely inexplicable that happened later in my childhood, which makes me think she must have been hiding a guilty secret along those lines.

My mother passed away in 2010, and in a way I’m glad that happened before I discovered any of this, because I would have been angry with her and she didn’t deserve that. She did her best to be a good mother to me and to all her other children, and I don’t hold her responsible in any way for what happened. I can’t blame my father either. He lost 3 brothers during his childhood and then his first wife died on their honeymoon, so I can understand why he became so obsessed with the idea of having a large family.

Brain Sexual Identity and DES

One further thing that made me think an exposure to artificial female hormones is the cause of my conditions was reading in the book “Brain Sex” about a pattern of behaviour commonly shown by teenage boys whose mothers were given treatment with a drug called diethylstilbestrol or DES in an attempt to prevent miscarriage . The boys in the study were typically very shy, socially withdrawn, had low self esteem, were regarded as sissies, bullied, ostracised by their peers, with no ability to fight back when attacked and no interest in sport. The authors of the book described it as “feminized behaviour”, and my teenage years matched it so closely it could have come straight out of my school report!

The main hormonal component of the contraceptive pills my parents were using is norethisterone acetate, a progestin, whereas DES is an estrogen. What estrogens and progestins both have in common is that they are female hormone derivatives, and are basically completely incompatible with masculinity. Both types of hormone have the ability to disrupt testicular hormone production at quite modest doses, well below those commonly used for medical treatment for women.

DES was for many years used to chemically castrate men suffering from hormone-sensitive prostate cancer, while progestins are commonly used for chemical castration of sex offenders and transsexuals. If they also suppress testosterone in a male fetus, then any use of them during a pregnancy of a male child carries a risk of creating a baby who developed as the wrong sex for part of the pregnancy. This is what I think happened to me, and to the DES sons.

For nearly two years I’ve been trying to find out as much as I can about DES sons, reading their personal accounts of how they’ve been affected and chatting with them online. Among the ones I’ve had contact with or whose life stories I’ve read, there seems to be a very high incidence of both intersex-related genital abnormalities and gender dysphoria. As a group they seem to commonly experience many of the same problems I have (a genital abnormality, feminized behaviour as a teenager, low testosterone and problems with hormones, gender variance). The key difference is that on the whole they seem to be far more psychologically female than I am (which is exactly what you’d expect, considering that their exposure was for a much larger part of the pregnancy than mine). I think it’s quite likely that for most of them, their testosterone production was completely suppressed and they were developing as female throughout the time their mothers were on the drug!

DES and all other estrogens were withdrawn from use in pregnancy 30 years ago, however, treatments for prevention of miscarriage, based on progestins rather than estrogens, continue to be used to the present day. One of these involves a progestin called hydroxyprogesterone caproate, given as a weekly intramuscular injection of either 250mg or 500mg, starting 16 weeks into the pregnancy – just around the time I think my hormone exposure occurred. The difference is that this treatment continues to be administered for the remainder of the pregnancy. If this drug does suppress testosterone production in a male fetus, then it’s hard to imagine a treatment better suited to creating as baby with a male body but a female brain! I’m fairly sure that if you gave an adult man 250mg per week of this drug, his testosterone production would be seriously impaired. Why wouldn’t the same happen to a male fetus?

Females Affected Too

In this article, I’ve only been looking at the effects of artificial sex hormones on a male fetus, however it’s likely that, under the right circumstances, a female fetus could be affected too. This could happen if the external hormone mimics the action of testosterone (e.g.progestin induced virilization), or if it disrupts endogenous hormone production in a way that causes excessive androgens to be produced (hyperandrogenism).

Postscript: This article was published previously September 2013. 

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DES – The Drug to Prevent Miscarriage Ruins Lives of Millions

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DES ad

Let’s rewind time. We’re in 1970. My mum, like millions of other women, puts all her trust and last hopes of carrying a successful pregnancy in the hands of health professionals. She accepts to take a drug recommended and prescribed in good faith by her doctor without knowing that years later it would have devastating consequences not only on her health but the health of her daughter and possibly her grand-children. She takes Diethylstilbestrol (or DES in short), the first synthetic man made female sex hormone (oestrogen) widely prescribed for public use in the mistaken belief that it would prevent miscarriage and loss.

Now let’s fast forward. We’re in 2001 three decades after my mum took DES. I’m in a hospital ward anxiously waiting for the results of a scan. I’m pregnant. “We’re so sorry, but you know 1 out of 5 pregnancies end in miscarriage. You should try again” I’m told. My head is spinning. What did my Mum said again? DES, yes DES, I remember now. She mentioned when I was just a teenage girl that research had confirmed that the drug taken throughout her pregnancy to prevent miscarriage was responsible for all sorts of dreadful health issues including a rare form of vaginal cancer, infertility and high risks pregnancies. What if this was responsible for the loss of my baby, I ask. “DES? What is DES? Never heard of it!” replies the consultant on duty that day. ”If you keep miscarrying, we’ll investigate further” he adds.

I don’t listen and seek help and advice from an organization founded by a mother who had been prescribed this drug and advocates for the many families affected by DES. A Professor, expert in fertility treatment, confirms a congenital uterine malformation typical of DES exposure and confirms that I’m a DES daughter, one amongst millions of other women whose mothers took Diethylstilbestrol during pregnancy.

If you were born or pregnant in the US between 1938 and 1971, and until the mid-’80s in some European countries, you may have been exposed to DES too and you may suffer from the consequences of this drug without even knowing it. Diethylstilbestrol has put the mothers prescribed the drug, their daughters and sons exposed in utero, and potentially their grandchildren due to the trans-generational effects of this synthetic hormone, at risk for serious health problems including but not limited to: structural damages in reproductive organs, high risk pregnancies and miscarriage, cancer, infertility and possible immune system impairment. Many other suspected effects are still awaiting further research but funding is critically missing.

Often referred to as the “Silent Thalidomide” by the media, diethylstilbestrol is considered as the world’s first drug scandal. Despite evidence of its ineffectiveness and danger, it continued to be prescribed to pregnant women beyond 1971 when the first link between DES and a rare form of vaginal cancer (clear cell adenocarcinoma) was formally established in Boston, Massachusetts.

Even though this drug was given to pregnant women decades ago, it affects and continues to affect millions of families today and possibly for many years to come. Yet, diethylstilbestrol has been and still is a well-kept secret, a taboo subject not only in families but within the medical community too.

No drug manufacturers, health authorities, nor governments have ever taken responsibility for the long term health side effects of this drug.

Don’t Pharmaceutical companies have a responsibility to their consumers to provide a product that is safe?

Four sisters recently filed a lawsuit against drug manufacturer Eli Lilly. They feel that their breast cancer was a direct result of Eli Lilly’s negligence. Eli Lilly has never accepted responsibility nor apologized for the DES tragedy, even though the company has paid millions in out-of-court settlements and verdicts to DES Daughters and Sons who suffered injuries from their exposure. The Melnick sisters reached a settlement with the drug company a few weeks ago, but Eli Lilly has not accepted any responsibility. Outraged by Eli Lilly’s failure to fess up on DES, Patricia Royall, a plaintiff in one of the 72 pending DES breast cancer lawsuits in Boston federal court and the District of Columbia, is now calling on the general public to sign a petition urging the drug manufacturer to apologize for the DES tragedy. From all corners of the globe, Australia to France, the UK to the Netherlands, Ireland to the USA, DES victims are crying out for justice.

Diethylstilbestrol is a world drug disaster yet very few people know about its tragic health consequences or have even heard about it. Public health awareness campaigns are vital to reaching out to the millions of people who have been exposed to this harmful drug. People who are not aware of their exposure to DES are not receiving proper medical treatment, or making truly informed decisions about their healthcare, as a result. It is equally important to educate the next generations of health professionals who have never heard of DES so they can provide adequate care to DES victims for years to come.

DES DaughterDES is not something of the past. People who have been exposed to this drug years ago are battling with health issues and fighting for their lives as I’m writing this blog post. Who knows what health problems the grandchildren of the mothers who were prescribed this drug will have to deal with as they grow up. I want my daughters to receive adequate medical care and monitoring if they ever have to suffer the consequences of this drug. This is why together with my husband we support the great work done by the very few International DES Action Groups who are providing valuable information and are advocating for the DES victims.

If you’re concerned that you may have been exposed to DES, please don’t let doctors dismiss your concerns. Contact your local DES Action Group for professional advice and guidance.  Connect with me and other DES daughters via my blog: DES Daughter Network and my website: Journal of a DES Daughter. You have the right to know.

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This article was published previously on Hormones Matter in February 2013. 

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Awareness ribbons looped on lapels. Around trees. Through chain-link fences. Yellow for missing children and bone cancer. Red for heart

Update: Oral Contraceptive Use and Autism

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Kim Stifert

In a recently published article and subsequent post to Hormones Matters, I proposed that a link exists between oral contraceptive use and the prevalence of autism spectrum disorders in children. In that post, I point out that widespread oral contraceptive use is a risk factor that has been largely overlooked in the biomedical literature. Because oral contraceptives were specifically designed to mimic natural human hormones and disrupt normal endocrine function to prevent pregnancy, I think that there is good reason for concern that the synthetic hormones may be initiating the harmful neurodevelopmental effects that lead to autism spectrum disorders in children of women who have been exposed to oral contraceptives.

I propose that ethinylestradiol (EE2) is the likely offender. EE2, one of the synthetic compounds found in oral contraceptives, is known to be an endocrine disrupting compound that is capable of impairing the endocrine system and offspring. Endocrine disrupting compounds have the ability to cause harm by negatively affecting sensitive hormonal pathways in both animals and in humans. And, recent studies have suggested that endocrine disruptors can impact human physiological processes within cells, tissues and organs by modifications in gene regulation. The environmental scientific community has repeatedly cautioned us about exposure to endocrine disruptors in the womb or early in life, strongly advising that exposure is likely to be linked with neurodevelopmental disorders that include reduced IQ, ADHD, and autism.

The World Health Organization issued the State of the Science of Endocrine Disrupting Chemicals 2012. In the report, they comment that we are just beginning to understand the mechanisms through which exposure to endocrine disruptors can modify the development of specific tissues that lead to increased vulnerability to diseases and disorders later in life. In addition, we are just now becoming aware of the critical roles that hormones play in neurodevelopment, including the neuroendocrine circuits that control physiology and sex-specific behavior that could result in behavioral and psychiatric conditions and disorders.

In the realm of environmental risk factors, the oral contraceptive hypothesis I first proposed is compelling. As a group of agents, there are explicit documented mechanisms through which oral contraceptives can impact the oocyte and/or the developing embryo. Additional reasons for considering the role of oral contraceptives and autism include:

  1. The exposure concentration is directly administered and pharmacologically effective.
  2. The exposure to the endocrine disruptor may be of larger magnitude than other environmental exposures that mostly occur through passive secondary means.
  3. A temporal correlation exists between the increased prevalence of oral contraceptive use and the increased prevalence of autism spectrum disorders over the last fifty years.
  4. The possibility exists that the effects of EE2 could intensify over generations due to transgenerational transmission of altered epigenetic programming.
  5. Continued exposure across generations could possibly impart sensitivity to developing autism spectrum disorders.

After making the oral contraceptive hypothesis, I called for epidemiological study as a first step toward proving the hypothesis. An epidemiological study investigates the patterns, causes and effects of health and disease conditions in defined populations. These studies can be expensive and labor intensive but are usually the first step toward proving medical hypotheses. Understanding the difficulty of performing these studies, I decided to review once more the only recent study of oral contraceptive use and the development of autism spectrum disorders in children. In this study, I found the epidemiological evidence I needed.

In 2011, Kristin Lyall published a study called, Maternal early life factors associated with hormone levels and the risk of having a child with an autism spectrum disorder in the nurses’ health study II. In this study that explored various early life factors, Lyall reported that,

“Overall, distributions of the factors under study were similar between the cases and non-cases. In crude comparisons in the full study (66,445 women), cases were more likely to have had an early age at menarche, a longer time until cycle regularity, a longer duration of pregravid OC use in years, and a higher BMI at age 18, though only the oral contraceptive duration association was significant (p < 0.05)”.

A significant finding of Lyall’s study is that oral contraceptive exposure presented a statistically significant risk factor for children subsequently developing autism spectrum disorders. This information provides epidemiologic evidence of the association between oral contraceptive use and autism. The fact that this is a large study and that oral contraceptive exposure is statistically significant leads me to believe that my hypothesis has merit. This finding must be replicated. In the meanwhile, I will continue to explore the association between oral contraceptive use and autism.

References

Kerdivel G, Habauzit D, Pakdel F (2013) Assessment and Molecular Actions of Endocrine-Disrupting Chemicals That Interfere with Estrogen Receptor Pathways. International Journal of Endocrinology 2013:501851. doi: 10.1155/2013/501851.

Latham KE, Sapienza C, Engel N (2012) The epigenetic lorax: Gene-environment interactions in human health. Epigenomics 2012;4:383–402. doi: 10.2217/epi.12.31.

Lyall K, Pauls DL, Santongelo L (2011) Maternal early life factors associated with hormone levels and the risk of having a child with an autism spectrum disorder in the nurse’s health study II. Journal of Autism and Developmental Disorders May;41(5): 618-27.

Martínez NA, Pereira SV, Bertolino FA, Schneider RJ, Messina GA, Raba J (2012) Electrochemical detection of a powerful estrogenic endocrine disruptor: ethinylestradiol in water samples through bioseparation procedure. Analytica Chimica Acta Apr 20;723:27-32. doi: 10.1016/j.aca.2012.02.033.

Strifert, K (2014) The link between oral contraceptive use and prevalence in autism spectrum disorder. Medical Hypotheses, Volume 83, Issue 6, December 2014, Pages 718–725.

World Health Organization (2012) State of the Science of Endocrine Disrupting Chemicals 2012 Summary for Decision-Makers. Available at: www.who.int/ceh/publications/endocrine/en/

 

 

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The Dangers of Glyphosate Herbicides

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Do we know what we’re eating? That’s the question that I constantly ask myself, because I know that at this point in time, my own regulations are the only thing protecting my health. It seems that the moment I become lax with my rules, I am quickly reminded why I must enforce them.

Monsanto is a corporation that manufactures herbicide and genetically engineered plants. Today, I learned that Roundup and other herbicides from the Monsanto corporation are made with a chemical ingredient called glyphosate. Glyphosate has been linked to a number of health-related issues ranging from birth defects to endocrine disruption (the endocrine system regulates the hormones in our body). Unfortunately, Monsanto’s products are used around the world. Products like Roundup are not just used to kill weeds in homes and the agricultural industry, but also to deter plant growth on railroad tracks, sidewalks and roads. This means that farmers, government workers and consumers are constantly spraying glyphosate on the ground, which is why it should come as no surprise that scientists are finding increasing levels of glyphosate in our groundwater. Even if we choose organic food (which is still recommended, since glyphosate is absorbed by plants treated with Roundup), our water cycle, including our drinking water, is being contaminated. In fact, glyphosate was detected in 60% to 100% of rain samples in Mississippi and Iowa.

Monsato, Malformations, Miscarriages and More

Consumers, workers and bystanders alike are affected by the use of glyphosate. Uninformed consumers purchase glyphosate-sprayed products and are exposed to the toxin. Agricultural workers handle the chemical directly. And then there are those that do not use the herbicide or consume the treated products, but are exposed to glyphosate nonetheless. This is particularly the case for those that live in close proximity to agricultural businesses that use Monsanto’s herbicides, such as Roundup.

Residents and doctors of Argentina and Paraguay began reporting a host of serious health effects, including birth defects, miscarriages, infertility and cancer. Those affected lived in regions where glyphosate was regularly used, linking abnormal health conditions to the pervasive chemical.

Argentinian scientists took this cue and began to study glyphosate, finding that exposure to glyphosate did cause birth defects in the embyros of chickens and frogs. Glyphosate has even been tied to an increase in spontaneous abortion and infertility among the cattle that are fed Roundup treated alfalfa.

Scientists from the University of Caen, in France, conducted an experiment using glyphosate doses that were less than the maximum residue limit (legal limit) and discovered that the chemical caused endocrine disruption. More specifically, the scientists found estrogen receptors were inhibited (blocking estrogen hormones from activating cells) with just 2 ppm (2mg/kg). The legal limit in the US is 5 ppm.

Dr. Don M. Huber, a plant pathologist who is part of the USDA National Plant Disease Recovery system, stated that there are, “more than 40 diseases reported with the use of glyphosate, and that number keeps growing as people recognize [glyphosate’s] association [with disease].”

Clearly, we should be concerned.

What about Government Health Regulations?

While only 2.03 mg/kg of glyphosate is needed to cause birth defects in chicken and frog embryos, government regulations, referred to as the maximum residue limit, allow 5 mg/kg of glyphosate residue in the US and a whopping 20 mg/kg in the European Union. The question isn’t how does this protect, but rather, who does this protect?

Unfortunately, government regulations are often set in place to protect corporations from liabilities. When citizens attempt to sue, corporations can state that they have complied with the law and that toxins are within the legal limit. Concerned parties may seek retribution from the government, but at this point, our tax dollars are being used for litigation.

What’s a Girl to Do? Take Action!

We start by sharing information with others to make a change. Litigation may be costly, but changing government regulations is not. (Corporations take the financial hit). Tell your friends, tell your co-workers, tell your neighbors.

This isn’t just a female-specific matter (though miscarriages and infertility concern us), since glyphosate is associated with a myriad of health issues and wreaks havoc on our crops by promoting plant diseases. Contact your senators and house representatives and let them know that you want regulations that protect your crops, your water resources, and your well-being. CLICK HERE to sign the petition to ban glyphosate-based herbicides.

Of course, if you’re worried your voice won’t be heard, the best way to make a statement is with your consumption habits. Every time you make a purchase, you cast a vote. Pay extra special attention to labels, buy organic and avoid products sprayed with glyphosate-based herbicide. Remember that corn chips may be processed from corn that has been treated with glyphosate. Let your money show that you don’t support the use of glyphosate, because money speaks.

Glyphosate Petition Review

The current petition against glyphosates was created on SignOn.org. I have recently been informed that emails associated with SignOn.org may start to pile up in your inbox. If this is the case, feel free to unsubscribe at any time to eliminate the onslaught of emails. Any recommendations for sites that create petitions without the spam would be greatly appreciated. Thanks for your support!

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BPA Exposure Linked to Egg Maturation Errors and Infertility

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Bisphenol A (BPA), the polycarbonate, endocrine disrupting plastic is pervasive in the environment.  A recent National Health and Nutrition Examination Survey detected BPA in the urine of 95% of the participants. Along with other toxins, BPA has been found in the placenta and follicular fluid of pregnant women.  Given its estrogenic actions and its ability to disrupt the normal equilibrium of maternal and placental hormones, scientists have begun to investigate what role BPA might have on infertility, pregnancy complications and fetal development. What they are finding is not good.

In the most recent set of experiments, researchers from Brigham and Women’s in Boston, found that in vitro BPA exposure to human eggs – oocytes, prevented the egg’s ability to mature and disrupted chromosome alignment and organization at the lowest dose possible; a dose lower than levels normally found in women’s ovaries.

The experiment used eggs discarded from patients undergoing IVF/ICSI cycles. The eggs were divided into two groups, those to be exposed to varying doses of BPA and a control group. Sibling pairs, eggs from the same mom, were placed into both the BPA and the control groups equally to reduce the possibility that any maturation errors in egg development might be linked other factors related to maternal infertility, such as age, weight or general health.

The eggs exposed to even the lowest doses of BPA failed to mature appropriately and higher doses were linked to an increased rate of error and maturation failure. Researchers note that this was preliminary study, but that their findings indicate BPA exposure might be linked into infertility at the most basic level – egg health and maturation.

From our perspective, this study suggests that couples contemplating pregnancy should eliminate BPA and other environmental toxicant exposure well before attempting to conceive. For couples having difficulties conceiving, it might be worth testing urinary BPA and other endocrine disruptors such as phthalates and reducing exposure to these chemicals prior to undergoing costly fertility treatments. Here are the four most effective ways you can minimize your exposure to BPA:

  1. Drink filtered tap water. This helps avoid water that has leached BPA from plastic containers.
  2. Use stainless steel water bottles or certified “BPA-free” containers.
  3. Avoid all canned foods, which are often lined with BPA containing resins. Eat fresh, non-processed, organic foods and avoid storing in plastic bags.
  4. Avoid the use of plastic utensils and dishes.

BPA is likely not the only source of endocrine disruptors. All plastics under normal conditions release estrogenic compounds. It may be wise to avoid plastics in general. Additional research on removing BPA and other chemicals from your diet can be found here.

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Of BPA and Endocrine Disruptors: New Research, Same Flaws

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BPA, MBP, estradiol

Bisphenol A or BPA is the ubiquitous estrogenic compound used to create plastics. It leaches into our food stuffs and because of its hormone-like qualities elicits a myriad of health issues in adults but especially in children and most especially when exposed in utero or during key developmental phases.

As we cover the expanding research base on BPA, it becomes increasingly clear that traditional methods of toxicology do not work for understanding endocrine disruptors – the man-made chemicals that alter our hormone pathways . A case in point, the latest research on BPA.

Exposure in Adults

A report published online in June of 2011 and presented at a prominent toxicology conference in February 2013, measured BPA exposure levels over a 24-hour period in adults fed a high BPA diet (lots of canned food and water from plastic bottles). The report showed that the concentration of BPA measured from blood was below the level of detection in most of the study participants, even though urine concentrations were extremely high and indicated exposure levels above the 95th percentile of the US population.

From urine tests, researchers were able to detect an average 84% – 97% of the dosed BPA and its metabolite, BPA glucuronide – indicating a high rate of clearance from the body. The ranges varied widely by time of day (morning tests showed significantly less clearance) and gender of participant (women did not process the hormone as well as men).

The researchers argue that their failure to detect BPA in blood, combined with the high concentration in the urine meant that risk was minimal. Their reasoning, even though BPA exposure was high, most of the BPA was cleared from the body rapidly and efficiently; no harm, no foul.

Medical and science marketers latched on to this and soon every major and minor media outlet was reporting that risks were minimal. Here are just a few headlines.

No Ill Effects Found in Human BPA Exposure, says the Wall Street Journal

Majestically Scientific Federal Study on BPA has Stunning Findings: So Why is the Media Ignoring it? – says Forbes

No toxic effects from controversial food packet, says expert – the Guardian

Ahh, where to begin?

Flaws in the Research

Conflicts of interest. Always look for industry sponsorship of for research, see my previous post on evaluating endocrine research for details. The relationship between the investigators in the present study and industry are muddled, but they do exist. For more information, click here.

Below the level of detection. When researchers report that their tests are unable to detect a visible pathology or measure a particular compound that any reasonable person would expect to be present, the test is likely at fault. Below the level of detection, means just that. It does not mean the compound was not present or that it was not exerting effects, only that the tests were not sensitive enough to measure the compound. This was case here and I suspect as testing methods improve, we’ll see higher detection levels in blood.

High clearance is not the same as never exposed.  In this study, not all of the hormone was recovered in the urine, only an average of 84% – 97%. That sounds like a lot. With hormones, however, small amounts do great damage. Why?  Because steroid hormones are stored in fat (and other tissues). They accumulate over time and metabolize into a myriad of different hormones (metabolites), some more potent than the parent compound. After the initial exposure and certainly after repeated exposures, our bodies become little (or big) hormone factories, storing and creating more and more hormones and hormone metabolites.

Metabolites matter. Hormones are shape shifters. Every time they meet an enzyme, the interaction between the enzyme and the hormone creates a new, similar, but differently shaped hormone. Hormones are never ‘one and done’ metabolizers. Even though a large percentage of the original hormone and its primary clearance metabolite were measured from urine in the present study, one cannot assume that there were not still other metabolites circulating within the body and wreaking havoc.

BPA has metabolites. This is critical and often ignored in toxicology research. BPA is a hormone like substance and as such, it metabolizes into many different forms. BPA has metabolites that are more potent than BPA itself. New research shows that BPA metabolizes into a compound called 4-methyl-2,4-bis(4-hydroxyphenl)pent-1-ene or MBP for short. MBP is 1000-fold stronger than BPA in its estrogenic effects. MBP binds strongly to both types of estrogen receptors (ERa and ERb) and may change the activity of the cell, displacing native or endogenous estradiol. So within that 3%-16% range of BPA not cleared, comes a compound 1000 times stronger than the BPA itself. As the research progresses, who knows how many other active and potent metabolites from BPA or MBP we’ll see. With hormones, nothing is simple or straightforward.

What this Means

Avoid medical marketing, it’s usually incorrect. Learn how to evaluate endocrine disruptor research. Once you get the hang of it, you’ll be able to dismiss faulty research at a glance. More importantly, learn about hormone systems and environmental hormone disrupting chemicals. Otherwise, our children will bear the brunt of our ignorance.

A good review article: Bisphenol A and the Great Divide: A Review of Controversies in the Field of Endocrine Disruption.

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BPA in Plastic Bottles: What’s the Big Deal About ‘Little Beards’?

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“The only thing that I heard is if you take plastic and put it in the microwave and heat it up, it gives off a chemical similar to estrogen. And so, I mean, in the worst case, some women might have little beards”   

~Paul LePage, Governor of Maine

Long ago, I cut a deal with my best friend: if one of us is on our death bed unable to care for ourselves, the other will tweeze her friend’s “man hairs.”  It may sound vain to some, but there is dignity even in death. When my mom lay dying in her hospice bed, I plucked the dark hair from her chin and upper lip, trimmed her nails, and brushed her hair, because I knew she wouldn’t want to “be seen like that”.  It was the least I could do after all those years she spent caring for and grooming me.

So I took great offense when Maine Governor Paul LePage–exhibiting astounding ignorance (even for a politician) of the delicate balance of human chemistry–made his remark about “women might have little beards.”  As if a woman having a little beard was no big deal, right?

Now before you go accusing me of over-reacting to media and environmentalist hype about the side effects of BPA–or bisphenol A- a compound added to plastic bottles and other packaging materials to increase flexibility, transparency, durability–first consider what a “big deal” it is in the scientific community.Two recent studies in Italy and Germany show that suboptimal storage conditions—such as prolonged exposure to sunlight and high temperatures—can cause leaching of BPA in plastic bottles into fluid contents resulting in high levels of estrogenic activity in plastic-bottled water. In other words, plastic bottles can leach chemicals that disrupt the endocrine system.

The endocrine system is responsible for making our hormones. Hormones are substances that help to control activities in your body. Different types of hormones control reproduction, metabolism (food burning and waste elimination), growth and development, and yes, even facial hair. Hormones also control the way you respond to your surroundings, and they help to provide the proper amount of energy and nutrition your body needs to function.While too few studies have been conducted to know with certitude about potential human health effects of drinking plastic−bottled beverages, as Lisbeth Prifogle of Hormones Matter reported previously, investigators have found that BPAs combined with the xenoestrogens in our environment cause male fish to grow eggs in their testes, female deer mice to pick males who weren’t exposed to BPA in a controlled environment, hyperactive rats (some scientist speculate that endocrine disruptors could be linked to the rise in ADHD amongst school children) and many other strange behaviors in the animal kingdom.

The National Toxicology Program’s Center for the Evaluation of Risks to Human Reproduction, suggests, in response to the European studies, that people move away from polycarbon−ate plastics [due BPA concerns].

In women with PCOS or other hormone problems, BPA can be especially problematic. Researchers from Athens report:

“Blood levels of BPA were nearly 60 percent higher in lean women with PCOS and more than 30 percent higher in obese women with the syndrome when compared to controls. Additionally, as BPA levels increased, so did concentrations of the male sex hormone testosterone and androstenedione, a steroid hormone that converts to testosterone.”

So Governor LePage, if you’re reading this, let me see if I can help you understand what the “big deal” is. Suppose you were exposed to an everyday chemical that made your breasts “a little” larger or your testes produce eggs. Or what if BPA led to sexual dysfunction in men? No big deal, Right? What’s a little Viagra between friends.Sources:

International Journal of Hygiene and Environmental Health, March 2009
Environmental Science and Pollution Research, March 2009

Environmental Health Perspectives, “Estrogens in a Bottle?”, June 2009

This image (or other media file) is in the public domain, per US public domain laws, because its copyright has expired. For more information see the file at wikimedia commons.

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