estrogen Archives - Page 2 of 3

BPA and Other Gender Bending Plastics

Published on February 2, 2015

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An oft repeated theme in this journal is that measurement matters. From the basic concept that one cannot manage what is not measured to the more specific notion that research protocols in the lab should attempt to mimic real life as much as reasonably possible, we believe measurement is critical. In matters of health and hormones where complex systems with a myriad of ever-changing variables are the norm, this is difficult at best. Sometimes, however, the simple act of measuring these variables opens a world of insight. This is the case with BPA and other estrogenic plastics.

BPA and Estrogens

Bisphenol-A (BPA), the estrogenic activator leaching sperm from our men and damaging the ovaries of women came to the world’s attention several years ago after a vocal and strident outcry from moms. The FDA subsequently remitted, prohibiting BPA from baby bottles and sippy cups and a slew of newer ‘safer’ BPA-Free plastic products emerged, but are they really safer? Maybe not.

Simulating Real Life Usage: Measurement Matters

Until recently, no one had measured the estrogenic activity of the other compounds used to plasticize our food containers. Nor had anyone measured these compounds under real-world stressors, such as UV-radiation (sunlight), microwave radiation or in the dishwasher or with different types of solvent (to represent the food/drinks contained by these plastics). Indeed, as is often the case, we were lulled into a false sense of safety. We believed that since BPA was removed from plastics, the endocrine disruptors were also removed, when in fact the other compounds had simply not been measured.

As one might expect, once those tests were conducted, researchers found that most plastic products on the market today release chemicals that are estrogenic – even those marketed as BPA-Free. Baby bottles, where much of the BPA outcry began, can leech as many as 100 different chemicals especially when exposed to real-life stressors, sunlight, microwaves and dishwashers, all estrogenic in nature.

Sunlight, in particular, was especially adept at maximizing the release of estrogenic chemicals into the solvent. Who hasn’t left their water bottle in the car? And when the plastics were tested in both polar and non-polar solvents (most foodstuffs/drinks are a combination of both), the majority showed reliably detectable estrogenic activity.

What to Do With All of These Estrogens

Not to worry, according to the authors of the study, there are ways to create plastics that don’t elicit estrogenic activity and they don’t cost any more or require different manufacturing than those that do. It’s simply matter of choosing to utilize those plasticizers and associated chemicals instead of what we currently use. The question is whether major plastics manufacturers will pay heed to these warnings and make the switch. Did I mention the man-boobs and infertility from the extra estrogens?

The study: Most Plastic Products Release Estrogenic Chemicals: A Potential Health Problem That Can Be Solved

Postscript

The article above was published originally in October 2012. Over two years later, I am sad to say that not much has changed. Industry has repeatedly denied the safety issues with BPA and the other, presumably safe, BPA-free plastics. The current campaigns, much like those of the tobacco industry, proffer industry financed research as proof of product safety while discrediting any scientist who brings evidence to the contrary. It’s a common script followed by all chemical manufacturers; one that has yet to be successfully curtailed.

Migraines and Hormones: Behind the Curtain

by Angela A Stanton, PhD

Published on December 15, 2014

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Before puberty, migraines are three times more frequent in males than in females but after puberty the tides turn and females are more likely to suffer from migraines than males. An Oxford study found that females are twice as likely to have migraines and that

“brains are deferentially affected by migraine in females compared with males. Furthermore, the results also support the notion that sex differences involve both brain structure as well as functional circuits, in that emotional circuitry compared with sensory processing appears involved to a greater degree in female than male migraineurs.”

The overwhelming belief is that the connection is clear: the hormones kick in for women at puberty and that must be the reason. This begs the questions: 1) Do males have the same hormonal problems before puberty as females do after puberty? If hormones are at root of the problems, then there must be some similarities, right? 2) If female hormones are responsible for migraines, do all females have migraines when they reach puberty? 3) Do migraines cease when hormones stop changing after menopause? 4) What about pregnancy or postpartum, how do hormones impact women then? And finally, 5) Do men stop having migraines after puberty?

Some of the answers to these questions will surprise you and may make you wonder if hormones have anything to do with migraines at all. In this post, I show you that while there are some connections between hormones and migraine they might not be the primary drivers of migraine. The relationship between hormones and migraine is not in the presence of hormonal changes but what those changes require in terms of brain energy, the lack of which causes migraines.

First, I would like to respond in quick the five questions I asked earlier: 1) Do males have the same hormonal problems before puberty as females do after puberty that causes them migraines? The answer to this is no. 2) If female hormones are responsible for migraines, do all females have migraines when they reach puberty? The answer to this also is no. 3) Do migraines stop after menopause? Many women have more migraines and some even start migraines in their menopause, so the answer is no. 4) Do migraine increase or decrease during pregnancy or postpartum? The answer is no during pregnancy, but yes postpartum. 5) Do men stop having migraines after puberty? No they do not.

It is not obvious that the cause of migraines must have anything to do with female monthly cycles and their associated hormones. Given also that many women have migraines after puberty, we are safe to assume that some other factors may play a role. It would be hard to envision a world full of children in which our evolutionary road took women to necessarily experience migraines with their menstrual cycles. So what is the connection to hormones; how do women end up with migraines; and why?

Rather than listing all the hormones that activate throughout the monthly cycle of a woman, let’s take a look at what is happening in the body of that woman backstage, during the hormonal changes. First, in a small review I cover in a few sentences what a migraine is.

Migraine is a collection of symptoms that have an underlying physiological mechanism based on chemical (ionic) imbalance in the brain. Migraine is a neurovascular event that Dr. Charles at UCLA called “spectacular neuro-physiological event” that changes the neurophysiology or chemistry of the brain itself. This can be seen using fMRI technology where oxygenation of brain regions shows where activity occurs during migraine—albeit this does not show why it occurs. The same article also suggests that though medications are available to treat the pain associated with migraines, half the sufferers do not receive any pain relief benefit from the drugs. I find this statement alone interesting because if migraine was truly understood, the pain medication would work for all. This clearly is not the case. To understand what is happening, we must think out of the box and leave behind the hormonal theory of migraines.

Moving Beyond the Hormone Migraine Theory

We now visit the female body all through a month. Let’s start two days after her menstrual cycle has ended. As female, we feel great, no pain, no bleeding, life is awesome. But what we don’t see works hard in the background using up important energy: the brain. Our hormonal changes are happening every moment of the day only we don’t feel it—hormonal changes are directed by the brain. Because we don’t feel the changes, we are ill-prepared for the inevitable day when it reaches a threshold point of not enough brain energy and the migraine starts. This typically happens 2-4 days prior to menses. I do not think migraines are caused by hormones, but rather they are triggered by the lack of energy available to the brain as the hormones cycle. When the brain runs out of energy, a wave of cortical depression begins in some part of the brain. This is what we feel as a migraine.

What actually happens that uses all that energy? After the menstrual cycle is over, the female body immediately prepares for the next menstrual cycle. There is no downtime for rest. The brain turns off one group of hormones and turns on others thereby manipulating how women see the world prior to and during estrus (fertile time). After a menstrual cycle is over, the brain turns on the estrogen to do a few things:

Prepare the uterus with a new fertile lining to accept the fertilized egg should one arrive and start a new life.
In order to make such fertilized egg happen, the egg must be prepared in the ovaries so hormones initiate the ripening of a new egg.
The woman’s body goes through amazing visible changes at this time of the month. If she had pimples, they magically disappear. If she was bloated, her bloating goes away. Her face becomes the most symmetrical it possibly can; the more symmetrical the more sexually appealing she becomes to the opposite sex.
She becomes extremely attracted to high testosterone males requiring her pheromones to change and to be able to sense a high testosterone pheromone male’s presence. This high testosterone attraction changes after estrus to attraction to low testosterone males for the safety of the child, should mating end in a baby.

With all this activity going on in the female body that she cannot feel, she is in danger of exceeding the threshold of brain energy-shortage without prior notice or preparation. The cost of all of these activities behind the curtains in the female body is very high in terms of brain energy and hydration. These are sex-hormonal functions that only exist for a certain period of time during the female life. Females are known to be born with all of their eggs they will ever ripen for possible babies. Only these eggs are not “ripe” at birth. Every month one egg ripens in one of two ovaries (sometimes in both and sometimes in none). This egg breaks out of the ovary and starts its journey down the ovarian tube where it either gets fertilized by a sperm or not. If the egg is fertilized, it attaches to the wall of the uterus lining—later to become the placenta of the baby—and a new life cycle begins in the mother-to-be. If however there is no sperm able to penetrate the egg, while it descends in the ovarian tube, the egg will have to be cleared from the uterus together with the nutritious blood vessel rich lining created. This happens with the menstrual bleeding. This we can see and feel.

My Theory: Why Hormone Changes are not the Cause of Migraines

As shown earlier, migraines are not equally present in everyone’s life. Other factors, such as genetic predisposition to sensory organ hyper sensitivities (SOHS) that require more energy, may be the cause. Recent research hints at ionic balance (meaning energy available for use) is crucial in maintaining optimal function and the slightest imbalance can cause major problems (Wei et al.).

When the body is tasked with demanding activities the cells responsible for completing those extra tasks are doing extra chores and need extra energy. The brain regulates the creation of extra hormones for the menstrual cycle. The brain manages the clearing of the uterus after the fertile layer was not used.

By the third day after the cycle, the brain is ordering an egg to ripen—this takes extra energy. This is a once a month event. The brain must have extra energy to complete this task. Ever tried to run a marathon on empty or run your car the extra mile without fuel in your tank? Not possible. Something must break. The brain is the logical one for those who are predisposed to SOHS. If their brain runs out of energy, the neurons cannot generate voltage and stop creating neurotransmitters that instruct the production of hormones in the body. This leads to cortical depression and migraine.

Migraine during Pregnancy

Hands up: how many of you had migraines during pregnancy? Up to 75% of migraineurs do not have migraines during pregnancy. Why you may ask? There is more than one reason for this. The first and most important reason is that while the mom-to-be is pregnant, she has no menstrual cycles so the brain has no monthly cyclical job and it need not use extra energy. Even if the pregnancy comes with a menstrual flow here and there—as it sometimes happens—there is no egg that ripens and there is no uterus layer to remove. It is only a bit of bleeding but no extra energy was needed by the brain for this menstrual flow.

The second important factor is that during pregnancy the mom-to-be seems is more cognizant of what her and her baby-to-be needs. She eat more, tends to eat what she craves and is less likely to be good-looking-body conscious during this time. Pickles with ice cream are famous cravings of women. All the nutrients the brain craves for re-creating energy and feed the brain to prevent migraines: salt, calcium, magnesium, and fat that converts to sugar in the brain.

Migraine during Postpartum

After giving birth nearly, nearly all women immediately revert to eating for a good looking body, lose all the baby fat, and get back into the size zero genes. They stop eating brain-healthy after pregnancy (they never realized they ate brain healthy the first place). Nearly all women return to their migraines postpartum as they return to their old dietary habits.

Post-Menopausal and Menopausal Migraines

We are often told that after we enter menopause or are post-menopausal, our migraines will disappear. Yet, I talk to many women, who have more migraines after their fertile period of life has passed. I am one of those women who experienced more migraines in menopause than in early life. Thus, being no longer fertile, no longer ‘hormonal’ does not mean that we become migraine free; further pointing to the lack of connection of migraines to hormonal fluctuations. In menopause, many women are still very body conscious and watch their dress size more than their health. Others, however, recognize the value of a body supporting diet that may not create a body to fit into such small jeans but may be healthier for an older woman. This second group probably stops experiencing migraines (like I did) whereas the first group remains dehydrated and lacks brain nutrition to work those SOHS brains. They end up continuing their migraines as they had them before.

Of course, we already know from my previous posts that migraines are genetic so not everyone abusing her body will end up as migraineur. To be migraine free, everyone, male or female, must follow the rules of brain fuel.

Fuel for Migraines (Hormonal or Not)

What exactly is the fuel for migraines of any kind? I am leading you back to the first post on migraine that tells you what nutrition the brain needs to return to energy and fuel-filled comfortable homeostasis. The brain works on electricity, which requires specific charge differences inside and outside the cell’s membrane. This voltage is created by salt (sodium and chloride) in ample supply. Sodium also retains water inside the cells for hydrations and opens the sodium-potassium gate to allow nutritional exchange. I am also linking you back to the second post on migraines that explains the anatomy of migraines and what actually happens when the brain in not in homeostasis. How a migraine starts is now visible in fMRI. If you follow the posts I linked to and read the book on how to prevent and fight migraines, chances are, you may never have to face another migraine in your life.

Sources:

Fighting the Migraine Epidemic; A complete Guide. An Insider’s View by Angela A. Stanton, Ph.D. Authorhouse, February 2014. https://www.amazon.com/Fighting-Migraine-Epidemic-Complete-Migraines/dp/154697637X/ref=tmm_pap_swatch_0?_encoding=UTF8&qid=1518636023&sr=8-1
Why Women Suffer More Migraines Than Men by Patty Neighmond, NOR April 16, 2012 3:17 AM ET http://www.npr.org/blogs/health/2012/04/16/150525391/why-women-suffer-more-migraines-than-men
Her versus his migraine: multiple sex differences in brain function and structure by Maleki et al. BRAIN. 2012: 135; 2546–2559, http://brain.oxfordjournals.org/content/brain/135/8/2546.full.pdf
Hormones & desire Hormones associated with the menstrual cycle appear to drive sexual attraction more than we know. American Psychological Association By Bridget Murray Law. March 2011, Vol 42, No. 3 Print version: page 44 http://www.apa.org/monitor/2011/03/hormones.aspx
Human Oestrus by Steven W Gangestad, Randy Thornhill. The Royal Society, Proceedings B May 2008 http://rspb.royalsocietypublishing.org/content/275/1638/991
Ovulating Women are STRIPPING Men of their Money. Cal Poly Bio 502 class lecture notes article. A blog about human evolution, economics, and sexual physiology. Why do strippers make more money at different times of the month? By Hayley Chilton http://physiologizing.blogspot.com/2013/01/ovulating-women-are-stripping-men-of.html
Migraine and Children. Migraine Research Foundation http://www.migraineresearchfoundation.org/Migraine%20in%20Children.html
Prevalence and Burden of Migraine in the United States: Data From the American Migraine Study II; Richard B. Lipton, MD; Walter F. Stewart, MPH, PhD; Seymour Diamond, MD; Merle L. Diamond, MD; Michael Reed, PhD. Journal Headache; 646:657
Population-based survey in 2,600 women. Karli et al., The Journal of Headache and Pain October 2012, Volume 13, Issue 7, pp 557-565 http://link.springer.com/article/10.1007%2Fs10194-012-0475-0
Multisensory Integration in Migraine Todd J. Schwedt, MD, MSCI. Curr Opin Neurol. Jun 2013; 26(3): 248–253
Unification of Neuronal Spikes, Seizures, and Spreading Depression. Wei et al., The Journal of Neuroscience, August 27, 2014 • 34(35):11733–11743 • 11733

Estrogens Doth Make the Heart Grow Sweeter

by Chandler Marrs, PhD

Published on September 30, 2014

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For years researchers have postulated the cardio–protective effects of the endogenous estrogens, namely estradiol. Research published in 2012 in the journal Hypertension identifies a mechanism by which the estrogens regulate heart function. It appears that systemic estrogen receptors (ER alpha to be specific) and by association estradiol, the hormone that binds to the estrogen receptors, are necessary to regulate cardiac glucose metabolism. Glucose is critical for maintaining heart contractility and mass.

Using both ovariectomized (ovaries removed) and knockout mice (genes that regulate the receptors are knocked out or removed, producing animals without estrogen receptors), researchers found that cardiac glucose metabolism was significantly impaired. When a drug that increases estradiol actions was given to the ovariectomized animals, cardiac glucose function was restored.

Estrogen Receptors and the Heart Muscle

In another study researchers found that the number of estrogen receptors located on the heart nearly doubles during end-stage cardiac disease. Moreover, the patterns and locations of these estrogen receptors differ significantly between males and females. Since males die from heart failure more frequently and more rapidly than females, researchers speculate that the increase in cardiac estrogen receptors is a protective, compensatory reaction that slows down and maybe even prevents heart failure.

Estrogen Receptors, Glucose and the Healthy Heart

Under normal circumstances, healthy hearts derive most of their energy from free fatty acids with only a smaller percentage from glucose metabolism. During ischemic events or heart attacks, the metabolic balance switches and glucose metabolism increases significantly. Since estrogen receptors appear to mediate cardiac glucose metabolism, it is likely that circulating concentrations of estradiol, the hormone that binds to the estrogen receptor, also plays a role in heart health or, more specifically, in its ability to survive and recover post heart attack. The estrogen receptor-cardiac glucose connection may be the mechanism leading to the higher survival rates for women, especially women with higher circulating estradiol (pre-menopause).

Diabetes and Estradiol

Interestingly, in diabetic patients the metabolic pattern is reversed. Rather than an increase in glucose metabolism post heart attack, free fatty acid metabolism increases making it difficult for the heart to generate sufficient energy to recover. Researchers speculate that this may account for the increased rate of heart failure in individuals with diabetes. Indeed, in experimental (rodent) models of diabetes, research show that diabetics have lower estradiol levels. The research in humans is mixed.

Hormones Matter

These studies point to the importance of steroid hormones beyond their role in reproduction. The interplay between steroid hormones and cardiac function is but one example of many where the traditional view and nomenclature of reproductive, sex, or female hormones has become outdated and likely limits our understanding of health and disease.

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Adhesions – the Pain, Suffering and Frustration

by Roxie Fiste

Published on July 30, 2013

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My personal struggles with adhesions began shortly after a partial hysterectomy at age 33. Our daughter was just a toddler but there would be no more babies now that my uterus, riddled with growing tumors, had been removed. For over a year I had fought with my body, suffering with double menstrual cycles, pain, even having contractions as my body thought I was pregnant again! It took five pregnancy tests to prove to the doctors that I didn’t have a tube pregnancy going on. The first surgeon I had tried to save my uterus but the fibroids had grown inside as well as through its walls. He carefully cleaned off the endometriosis gathered around my ovaries believing they would function normally after surgery. It took about six weeks, but my energy levels eventually picked up to the point I actually felt good again.

My husband gave me a membership to a nearby health center as my healing process was ending. Being a full time mother and housewife did keep me very busy so working out gave me a couple of hours a week to clear my mind. Don’t get me wrong, I loved being a new mom, watching our daughter grow and change each day, but those few hours were greatly energizing. Eventually, I was even able to return to a little stargazing in late evenings after our daughter would go to bed. Life seemed to actually return to normal.

Six months later something began happening to the Me inside. Outwardly, I was unchanged, but emotionally and mentally I was becoming lost. The feelings were strange, frightening, as the real me seemed to drift off into the distance. It was after a rigorous workout that I felt something flopping around in my lower abdomen. It wasn’t painful until my GYN did a check which nearly caused me to pass out. Another surgery was scheduled which resulted in my left ovary, the size of a small orange, being removed. The surgeon reassured me that once I healed everything would be “normal” again. He had cleaned up my right ovary and removed some tiny adhesions. Life improved for about a month. For six months after that I began experiencing mood shifts, panic attacks, night sweats and two episodes of convulsions. My GP sent me to see a specialist to see if anything could be done for my mental state. This new doctor immediately set up an appointment with my GYN again. Something was physically wrong with me which was causing a disruption in my emotional and mental states. Surgery was once again scheduled. This time the doctor found endometriosis, adhesions and a dead ovary. After its removal I was placed on estrogen which completely righted the mental and emotional states. My family thought I was home free!

While working out about seven months after my previous surgery, I felt a burning sensation deep in my lower back. I tried various exercises, massage, whatever would help my back improve. Nothing worked. It became a rather tedious nightmare just trying to do laundry, chase a toddler, cook a meal, etc.! How frustrating to have the deep, fiery pain continue to spread from my back to all the way around my lower abdomen! Someone we visited suggested it might be adhesions. She suggested that I go back to my GYN. By the time this fourth surgery came I could barely stand up straight. It had gotten hard to breathe and I could no longer sing in the choir. My surgeon found so many adhesions a laser could not be used. It took him 45 minutes to remove the enormous number of adhesions using a scalpel. He was worn out and frustrated by the way my body was producing them so before closing me up he placed special mesh along my abdominal wall, while trying to protect my intestines. To complete his attempt he added small implants of cortisone pellets into the areas covered by the mesh. Upon waking after this particular surgery I was quite nauseous. Multiple muscle spasms hit within hours of coming out of the anesthesia as well. The nurses were quite good at keeping me set up with Phenergan and piroxicam! One stopped the nausea and the other stopped the muscle spasms. It was not my normal way of dealing with pain – I preferred to take a couple of Tylenol 3’s, not injections of strong meds. Thankfully, after a couple of days in the hospital I went back to taking tablets instead of shots. My breathing returned to normal as well as the ability to take deep breaths to sing within a few days of surgery. This time my husband and I fully believed my life would get back on track.

For about a year I remained free of adhesions, going about normal activities, mommyhood, spontaneous adventures with my family. Within weeks of the anniversary of that last surgery the ring of fire returned. This is what my GYN called the ring of adhesions rapidly growing in my body. Over the next ten years I would have six more surgeries for adhesions. There were years I barely weighed 84 lbs before surgery. Other times I weighed as much as 105 lbs – my body just couldn’t adjust to the physical intrusions of the scar tissue.

In 2002 I had what would be my very last surgery for adhesions. There were a couple of complications which made healing more challenging – a hematoma in my abdomen caused searing pain and a near double surgery, (thankfully a specialist released me saying the hematoma would resolve on its own), and a serious bout with Epstein-Barr virus slowed healing to a snail’s pace. It took over a year to recover from the EBV. Looking back it is quite clear that my immune system was worn down, plus my vitamin D3 levels were very low, most likely from all of the surgeries I had starting, with my first surgery mid-pregnancy through 2002. Twelve altogether – not a world record, but definitely ENOUGH!

Menopause and the Body Fat Blues

by Chandler Marrs, PhD

Published on June 26, 2013

4552 views

Postmenopausal weight gain is a common problem for many women. Most suspect it has something to do with declining or changing hormones, but the mechanisms have remained unclear. Fat, researchers are learning, is not merely the inert blob we thought it was, but a complex endocrine organ capable of initiating and maintaining its own growth. Not good news for those of us who carry an over abundance of this cushy substance.

In a recent study measuring the mechanisms of subcutaneous thigh fat storage it was learned that the enzymes that direct whether we store or burn fat are re-regulated post menopause, presumably by hormone changes. Called adipocyte fatty acid storage factors, these proteins determine whether and how much fat is burned or stored. For post menopausal women, not only are there more post meal fatty acids but more fat is stored. What was interesting was the mechanism. There were no differences between the pre- and post- menopausal enzymes that broke down the fats (lipoprotein lipase), meaning the capacity to burn it remained unchanged. What changed was the capacity to store it.

The researchers found the two enzymes that determine fat storage rates (adipocyte acyl-CoA synthase and dicylglycerol acyltransferase) were significantly upregulated in postmenopausal women. Why they were upregulated was not clear. The standard presumption was made that declining ‘estrogen’ concentrations must somehow regulate the fat storage enzymes, but none of the estrogens were measured.

In a similar study looking at the role androgens and fat storage in men (diagnosed hypogonadal – low testosterone and eugonadal – ‘normal’ testosterone men), researchers found the hypogonadal men exhibited upregulated fat storage factors in the femoral area (butt and thigh). The pattern was consistent to that observed in postmenopausal women. Since neither testosterone, the other androgens or estradiol and other estrogens or even progesterone hormones were measured in either study, it is unclear which hormones or hormone patterns impact these fatty acid storage factors. What is clear, however, is that aging, whether chronological or endocrine, seems to increase fat storage.

My Journey from DES Advocate to Author

by Judith Barrow

Published on June 20, 2013

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My name is Judith Barrow and I am an author. I have been connected with DES Action UK and USA since I heard a programme about Stilboestrol (Diethylstilbestrol in the USA) (DES) on the radio many years ago. I learned several years ago that a relative was affected by this drug.

The damage DES causes is very personal and as private person, she didn’t want anyone to know that she had been exposed to DES. So I became her front person. I did the research for her. I contacted the DES organizations on her behalf. What I found changed my life and led me to write a book. Here is my story.

DES and Endometriosis

I’d known for many years that my relative suffered with chronic endometriosis, and that she had anatomical deformities. Ultimately, it was discovered that she had a narrowing of the cervical canal which resulted in increasingly painful menstruation. Then I heard a Radio Four programme called ‘You and Yours’ which included an article on DES. I realized that a lot of the content applied to my relative.

I made the inquires for her. First to DES Action UK, which was still extant then (they folded last year due to lack of funds and support). I sent for their newsletter and went online. The more we read, the more we were convinced that she had been exposed in utero to Stilboestrol. Like many private families, her mother initially denied it. This caused family problems, so she didn’t pursue the issue any further.

The information she gained from the DES groups made her aware that she needed to have the annual cervical smear (the only specialists for this test for DES Daughters is in Ireland). The more research I carried out, the more aware I became of the damages DES had caused.

After a year of communicating with DES Action UK, I was asked to write an article appealing for DES Daughters and Mothers to come forward and tell their stories. It was hoped that the group would get more members and that, if more voices were heard, then perhaps the British Government would listen.

The stance of the Government is twofold; that those pregnant women who were prescribed the drug were given it so far in the past that to raise it as an issue now would only cause ”unnecessary concern.” They believed it was a problem to be discussed privately between the mothers and the drug companies. I disagreed.

Following the article, many women contacted me to tell their stories. Some were heartbreaking; one daughter had six miscarriages before giving up the struggle to conceive (she then, happily, adopted a lovely little girl). Another Daughter had too many health problems to list but amongst them she suffered from endometriosis, uterine fibroids, paraovarian cysts. It was no wonder she was depressed. Her mother wrote many letters to the Government. Ultimately the reply came back – “Thank you for your letter, future correspondence will be noted and filed but not responded to…” The mother cried when she told me. I was so angry for her.

But the DES Daughter story; the one I first came across when I knew of Stilboestrol and DES Action UK, that really affected me was from one of the initial members. I enclose part of the interview, and further comment, from the article in The Sunday Independent: Sunday 22 January 2012 (this decided me to self-publish the book; it gave credence and veracity to the story. It reads as follows:

Thousands of women could be at risk from ‘silent Thalidomide’

A drug intended to prevent miscarriage is blamed for causing cancer in the daughters – and possibly even granddaughters – of women who took it decades ago. By Sarah Morrison and Jaymi McCann

The first recorded “DES daughter” in Britain, Heather Justice, 59, from Jarrow, was 25 when she found out she had vaginal cancer and would have to undergo a hysterectomy and partial vaginectomy. Although she found records showing her mother had been given DES in the 1950’s, she was unable to bring a case to court – (in the UK, because she could not identify which manufacturer had produced the drug. However, a US lawyer did help her get some compensation there.
Also, she says –“it is impossible for anyone to find the manufacturer of the drug in this country, not just me, as it was never patented. It was the surgeon who performed my hysterectomy who asked my mother if she knew what she had taken. He knew it must have been DES because of the rare type of cancer I had. He was also the one who found her medical records with the generic name of the drug”:- added after this interview)
After years of fighting the legal system, she says she feels disillusioned. “One of the problems is that unlike Thalidomide, where you see the problem the minute the baby was born, women who took DES had healthy babies,” she says. “Problems were hidden until the teens and twenties, by which point we were forgotten about. When I asked my mum what she had taken, she didn’t even remember the name of the stuff. It is a complete and utter minefield.”…

It took almost nine years to research, to contact women from different countries and piece together a story. Although I am not a DES Daughter – and like many others in the UK still are – I was totally unaware of this drug, until that one radio show on DES. The more I discovered the angrier I became. That these women are still fighting for recognition, acknowledgement from the pharmaceutical companies after so long is a disgrace.

What is DES?

DES, a synthetic oestrogen, was created by Charles Dodds in the UK in 1938. It was expected to help prevent miscarriages. Years later, he raised concerns about DES but by then very few in the medical field were listening. Doctors prescribed Stilboestrol to pregnant women between the nineteen forties and seventies, believing it was safe. The women had no reason to doubt but, too late, they learned the horrible truth. Not only was DES ultimately proved to be ineffectual, it caused drastic damage to their children: An increased risk for infertility, vaginal/cervical cancer in young women and breast cancer in later life are but the start. Scientific studies continue add to the growing list of serious medical problems caused by exposure before birth. Hormones Matter has covered DES here, here and here.

Now researchers are investigating whether DES health issues are extending into the next generation, the so-called DES Grandchildren. Millions around the world were exposed to DES, but this tragedy flies under the radar of general consciousness. I set out to change that. These women and men should not suffer in silence.

From that initial contact with DES UK, my life changed drastically. I have become an advocate for DES education, research and services. I wrote a book to publicize the depth of suffering women, their children and grandchildren exposed to DES experience, often silently. Ten percent of proceeds from the book sales go directly to DES research. I hope that my work will in some small way help change that.

To learn more about my book click: Silent Trauma.

To learn more about DES action groups: DES Action Groups Worldwide

Hormones, Hysterectomy and the Hippocampus

by Chandler Marrs, PhD

Published on April 5, 2013

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hormones, hysterectomy and the hippocampus

New research, conducted on rodents, suggests that pre-menopausal hysterectomy with ovariectomy induces changes in the hippocampus (memory center of brain) making it hypersensitive to ischemic stressors (reduced blood flow). In contrast, ischemic stressors did not cause hippocampal damage in non-ovariectomized female rats or even gonadectomized male rats

The hippocampus, located in the temporal lobe of the brain, is responsible for working memory formation, storage and retrieval. Researchers have long known that damage to cells in the hippocampus cause significant problems in short-term, long-term and working memory, ranging from mild cognitive decline to complete impairment. Certain cells in the hippocampus are particularly sensitive to the amyloid protein buildup associated with Alzheimer’s disease.

In the current study, removal of the ovaries and the associated long-term estradiol deprivation made the hippocampus hypersensitive to ischemic stressors and induced a myriad of events leading to significant hippocampal CA3 cell damage and cell death. The long term estradiol deprivation also led to increased amyloid production and associated neurodegeneration. As one might expect, damage and disruption to the hippocampus, the brain’s memory center, was associated with the animal’s ability to learn, remember and function.

What was particularly interesting, female animals who retained their ovaries and were exposed to the same ischemic stressor demonstrated neither the brain damage nor the decline in cognitive function. Similarly, male animals whose gonads were removed, suffered no notable brain damage or cognitive decline either. It was only the female animals whose ovaries were removed and whose systems were deprived of estradiol for a long period of time.

When estradiol was added back to the ovariectomized female animals shortly after the surgery, the female animals were able to weather the ischemic stressor and hippocampal damage was reduced significantly. However, when the estradiol was added back after an extended period of deprivation, it had no effect on the hippocampal damage or subsequent decline in memory.

Estradiol is important for cognitive function.

It is important to note, that animal researchers use 17B-estradiol, the same form of estradiol produced in the ovaries. In contrast, researchers who study human memory, often supplement with synthetic estrogens (Premarin, Prempro etc.), which is molecularly different than what is produced in our bodies. Indeed, the synthetic estrogen is actually about 20 different estrogenic compounds synthesized from pregnant horse urine. With synthetic hormone replacement therapy (HRT), recently renamed menopausal hormone therapy (MHT), the difference in molecular structure, as well as the long chain of metabolites that MHT produces, lead to an increase in the number of illnesses and may or may not be protective against the diminished estradiol induced hippocampal damage or the associated cognitive decline.

Of BPA and Endocrine Disruptors: New Research, Same Flaws

by Chandler Marrs, PhD

Published on April 3, 2013

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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.

Hormones Matter

Where health, hormones, and a whole bunch of other stuff, make sense.

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