estrogen

Discovering DES: Opening Pandora’s Box

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Diethylstilbestrol (DES) is a synthetic estrogen. Known as DES in the United States, it is more commonly known as stilboestrol in the UK and Australia. It was the first synthetic estrogen produced, developed by Sir E. Charles Dodds and colleagues in the UK in 1938.

Constructed from a chemical base, it produced the same feminizing effect as estrogens derived from animals (e.g. Premarin) but was more powerful and cheaper to produce. DES cost about two dollars per gram to produce compared to the three hundred dollars to produce natural estrogen.

Never patented, the DES formula was published in the magazine Nature on 15 February 1938, giving the world the first cheap and powerful estrogen. As it was never patented, within months drug companies around the world were working with this formula, vying to market this lucrative new product straight out of the lab.

This has been likened to opening Pandora’s Box, an action that turns out to have detrimental, unintended and far-reaching negative consequences.

Dodds was aware of what a powerful and potentially carcinogenic drug he had synthesised. In the months following the discovery, Dodds became increasingly concerned about the carcinogenicity of the newly synthesized drug. In his laboratory he noticed that men on his staff who handled and inhaled the stilboestrol powder were growing breasts, suggesting to him stilboestrol might cause breast cancer in men. He suggested that animal studies be carried out looking at the carcinogenicity of stilboestrol in male rodents. In 1940 a paper was published showing that stilboestrol caused mammary cancers in both male and female mice.

Many studies of a variety of experimental, agricultural and domestic animals were conducted in the 1940s and showed serious adverse effects of the drug including cancer, fetal death, and sterility of offspring.

Dodds never envisaged that stilboestrol would be given to healthy women and was against the automatic and “promiscuous” prescribing of estrogen: He was aghast when told it was being used to “prevent miscarriage”; particularly as he had conducted research showing the drug could prevent or end pregnancies in rabbits and rats. This made it a potential birth control or emergency contraceptive pill. However, Dodds said that the human female reproductive cycle was too delicate to introduce foreign substances into it, and he denounced the use of DES to prevent or end pregnancies.

The risk of cancer with these drugs was well known and documented. In fact Dodds himself spent many years thereafter warning that these drugs put women at serious risk of endometrial and breast cancer.

However it was all too late – Pandora’s Box was well and truly open.

Despite the controversy and warnings, the Age of estrogen had well and truly begun. Over the following decades, DES and other exogenous estrogens were marketed and prescribed for a bewildering, often contradictory, range of conditions: to slow and prevent aging; to stop hot flushes and as treatment for other menopausal symptoms; to prevent miscarriage, for pregnancy maintenance, as a pregnancy “tonic”; as the oral contraceptive pill; as the ‘morning after’ contraceptive pill; to stunt the growth of tall girls; to suppress lactation; as a hormonal pregnancy test; to treat acne…

What these uses have in common is that they were experimental; they often didn’t work; and they were never proven safe, frequently having serious, often unexpected, long-term health outcomes for those exposed to the drugs.

And, despite Dodds’ concern, it was healthy women who were “automatically and promiscuously” prescribed the drugs.

To quote Barbara Seaman from The Greatest Experiment Ever Performed on Women: Exploding the Estrogen Myth (2003),

I call the marketing, prescribing, and sale of these drugs an experiment because, for all these years, they have been used, in the main, for what doctors and scientists hope or believe they can do, not for what they know the products can do. Medical policy on estrogens has been to ‘shoot first and apologise later’ – to prescribe the drugs for a certain health problem and then see if there is a positive result.

It wasn’t until 1971 that the magnitude of the adverse effects of stilboestrol use started to emerge. DES emerged as a public health crisis in 1971 with the discovery of the ‘DES Cancer’, an aggressive, clear cell adenocarcinoma of the cervix/vagina, in DES daughters.

The discovery of this “biological time bomb” sent shock waves through the medical science community. Up until that time, based on the Thalidomide experience, it was thought any adverse effects of a drug given during pregnancy would show up immediately as “birth defects”. It was obvious that DES was a whole new ball game.

This lead to a paradigm shift and DES was recognized as an endocrine disruptor. Prenatal exposure to an endocrine disruptor such as DES results in multiple, diverse serious effects that are latent and delayed, being manifest years after the original exposure.

However, it was the Australian study of Tall Girls that moved our understanding of endocrine disruption to a new level. The small study was truly groundbreaking and far-reaching in the implications of its findings. No one had ever researched the long-term effects of exposure to an endocrine disruptor at this critical time of development, i.e. puberty. Another important feature of this study is that while DES was initially used, it was replaced in the mid-1970s (probably as a result of the ‘DES cancer’ being discovered) by ethinyl estradiol. So a very important ‘incidental’ finding of this study is that ethinyl estradiol, the estrogen found in the oral contraceptive pill, is an endocrine disruptor.

An important paper published from this study showed that tall girls treated with estrogen in early adolescence were nearly twice as likely to experience unexplained infertility as adults when compared to the matched control group of untreated tall girls.

This finding was replicated and extended in a 2011 Dutch study that evaluated fertility and ovarian function. Interestingly the European treatment for tall girls was high doses of synthetic estrogen (ethinyl estradiol) in combination with cyclic progestin.  The impact of treatment on impaired fertility was even more pronounced than that observed in the Australian study. In terms of ovarian function, treated women were more likely of being diagnosed with premature ovarian failure.

A 2014 Swedish study found that the tall girl treatment regime was associated with an increased risk of melanoma.

Allied to this was the realization that DES causes epigenetic changes, resulting in the next and subsequent generations potentially being affected. Epigenetics refers to heritable traits in cells and organisms that do not involve changes to the underlying DNA sequence. Scientists believe that DES, as an endocrine disruptor, impairs and changes the normal pattern of gene expression i.e. when genes are turned on and off. It is thought that exposure to DES dysregulates the epigenome, with potential consequences for subsequent developmental disorders and disease manifesting in childhood, over the life course, or transgenerationally.

So DES is not only the first exogenous estrogen to be synthesized; it is the first compound to be recognized as an endocrine disruptor; and it is the primary model for environmental endocrine disrupting chemicals. In addition, it can be seen that DES is the primary model for pharmaceutical endocrine disrupting drugs.

Thus, the DES exposed are the ‘canaries in the coalmine’, the harbingers of the future.

Nearly 80 years ago Sir Charles Dodds inadvertently opened Pandora’s Box and we are still experiencing the unintended effects all these years later.

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This article was published originally on July 24, 2017.

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

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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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More Side Effects from Birth Control- The Liver and the Gallbladder

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This time of year, the holiday season, can be a time of overindulgence for many of us. And how can we talk about overindulgence without taking a look at the liver? To say the liver is important is an understatement. It is the body’s largest gland and while estimates of the number of functions of the liver vary, many textbooks generally cite around 500. Nearly everything we ingest, from drugs and alcohol to vitamins and nutrients, is metabolized by the liver. The vital role it plays in the functioning of our bodies makes the testimony from the 1970 Nelson Pill Hearings about the effects of oral contraceptives on the liver that much scarier.

Research Presented at the Nelson Pill Hearings

Dr. Victor Wynn was one of the first physicians to testify about the effects of hormonal birth control on the liver.

On page 6341 he states, “if you will take cells out of the liver and examine them under the electromicroscope of women taking oral contraceptive medication, you will find some extraordinary changes.” Of these and other changes caused by the pill, he says: “When I say these changes occur, I mean they occur in everybody, more in some than in others, but no person entirely escapes from the metabolic influence of these compounds. It is merely that some manifest the changes more obviously than others.”

Later to testify was Dr. William Spellacy who was specifically called upon to speak about the metabolic effects on the liver. His testimony about the liver begins, “The biochemical effects of the sex hormones on the liver are legion.” Below is a list of liver functions that, based on the research presented in Dr. Spellacy’s testimony, are altered or impaired (NPH 6427):

  • Lowering of total plasma protein level
  • Decrease in the albumin and gamma globulin and increases in other fractions
  • Tests may be abnormal in women on oral contraceptives without disease being present
  • Estrogen (including that in oral contraceptives) interferes with liver function and varies with dosage
  • Some women taking oral contraceptives have abnormally high blood bilirubin levels
  • 1/3 of women who have jaundice on oral contraceptives will get it when pregnant
  • Discontinuation of oral contraceptives “cures” jaundice

He summed up his thoughts on the liver damage caused by hormonal birth control:

“The immediate effects include the alteration of several of the laboratory tests used in medical diagnoses. Aggravation of existing liver disease, if present, to the point where jaundice may be seen has also been shown. There is no answer to the query of will permanent liver damage result from the use of the oral contraceptives.”

The honorary Chairman of the Population Crisis Committee, a “pro-pill” organization focused on population control added his two cents about the effects of oral contraceptives on the women using them. “While metabolic alterations affecting the liver and other organs do result from use of the pill, there is no evidence at this time that they pose serious hazards to health;” General William Draper, Page 6705.

Of course, we shouldn’t assume that just because a medication causes a “legion” of biochemical effects on the livers of otherwise healthy women that there will be any lasting problems, right?

Research Since the Hearings

“Women more commonly present with acute liver failure, autoimmune hepatitis, benign liver lesions, primary biliary cirrhosis, and toxin-mediated hepatotoxicity,” according to a 2013 article in Gastroenterology and Hepatology.

Like I mentioned in my piece about rheumatoid arthritis, whenever a health issue affects women disproportionately, there is often a connection with hormonal birth control. While this study doesn’t specifically mention that, it does call for further studies assess the role of sex hormones and other behaviors on liver problems in women.

These connections were well-documented at the 1970 Nelson Pill Hearings but the subsequent research gets more confusing.

Timeline of Liver Research

1980: Lancet published an article showing the connection between malignant liver tumors and women using oral contraceptives.

1989: The British Journal of Cancer found “confirmation in this population of the association between oral contraceptives and hepatocellular carcinoma” and “the relative risk was significantly elevated in long-term users [of oral contraceptives].”

1992:This study, the largest to date, adds to the number of investigations demonstrating an increased risk of primary liver cancer with use, particularly long-term use, of oral contraceptives.”

2006:Long-term use of oral contraceptives (OCs) and anabolic androgenic steroids (AASs) can induce both benign (hemangioma, adenoma, and focal nodular hyperplasia [FNH]) and malignant (hepatocellular carcinoma [HCC]) hepatocellular tumors.”

Yet a 2015 meta-analysis concluded that “oral contraceptive use was not positively associated with the risk of liver cancer.” However, the analysis also conceded that “a linear relationship between oral contraceptives use and liver cancer risk was found.” And the authors noted the need for further research into specific formulations of oral contraceptives and the duration of usage.

It makes you wonder how we went from pretty convincing and highly damning connections between oral contraceptives and liver cancer to no positive association at all. Did all the scientists from the 1960s to 2006 get it wrong? Or is something else going on here?

What About the Gallbladder?

Perhaps we can look at the liver’s little buddy, the gallbladder, for some more information. The two are intimately connected in that the liver is constantly making bile and sending it to the gallbladder for storage and dispensation. Like problems with the liver, women are more likely to develop gallstones than men. According to the National Institute of Diabetes and Digestive and Kidney Diseases, “Extra estrogen can increase cholesterol levels in bile and decrease gallbladder contractions, which may cause gallstones to form. Women may have extra estrogen due to pregnancy, hormone replacement therapy, or birth control pills.”

This was proven shortly after the Nelson Pill Hearings. According to the revised edition of The Doctors’ Case Against The Pill by Barbara Seaman:

“The Pill also has serious adverse effects on the gallbladder, and women who take the Pill face an increased risk of someday facing surgery for gallstones. Pill use causes higher levels of cholesterol saturation in the bile, according to a study reported in the New England Journal of Medicine in 1976. This high level of fate in the bile is considered ‘an early chemical stage of gallstone disease,” according to Dr. Donald Small of the Boston University School of Medicine… The risk of gallbladder disease rises with the length of time a woman has been on the Pill… In some studies, Pill users are two and a half times as likely to suffer from gallstones as comparable women.”

A meta-analysis conducted in 1993 found “Oral contraceptive use is associated with a slightly and transiently increased rate of gallbladder disease” and “Considering…the rapidly changing formulas of oral contraceptives, the authors suggest that the safety of new oral contraceptives be evaluated by studying bile saturation and biliary function rather than by waiting for gallbladder disease to develop.”

A much more recent study (2011) found that there was even more risk of gallbladder disease with the newer formulations:

  • Long-term use of an oral contraceptive is associated with an increased risk of gallbladder disease compared with no use
  • There was a small, statistically significant increase in the risk of gallbladder disease associated with the use of desogestrel, drospirenone and norethindrone compared with levonorgestrel
  • Both estrogen and progesterone have been shown to increase the risk of gallstones
  • Estrogen has been shown to increase cholesterol production in the liver, with excess amounts precipitating in bile and leading to the formation of gallstones
  • Progesterone has been shown to decrease gall-bladder motility, which impedes bile flow and leads to gallstone formation

The gallbladder shows us that these hormones are damaging the body.

What Now?

So what do you do when you have a gallbladder that’s not functioning properly? The current practice is to take it out! Of course, removing the gallbladder is not the quick fix many think it is and often leads to other health complications like irritable bowel syndrome, acid reflux, and Sphincter of Oddi Dysfunction.

What about when your liver isn’t functioning properly? That’s not as simple. You can’t just take a liver out. How can the gallbladder, an organ so fundamentally connected to the liver, experience drastic and dangerous changes from hormonal birth control but the liver is supposedly unaffected? Have we researched ourselves out of that problem by declaring that it isn’t a problem? Has there been some spin-doctoring going on when it comes to the liver?

As Dr. Wynn said at the hearings, “There are more than 50 ways in which the metabolic functions of the body are modified, and to say therefore that normal physiological function has been demonstrated in the years of oral contraception is to overlook a very large amount of information.”

I think a very large amount of information has indeed been overlooked.

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More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

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This article was first published December 15, 2016.

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Improving Male and Female Fertility with Vitamin D

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Vitamin D is essential to a healthy life, at any stage, yet its effectiveness is often overlooked by practitioners treating parents who are trying to conceive. The overwhelming majority of infertility cases are treated with drugs or surgical procedures, and are successful less than 50 percent.

Supplementation presents a simple, safe, inexpensive, and potentially effective approach to preparing for fruitful conception. In this article, I address vitamin D’s role in reproduction, evidence supporting the positive effect of this nutrient on fertility, and how to become vitamin D healthy parents.

Vitamin D’s Role in Reproduction

The human reproductive system comprises billions of cells. Every cell in the female and male reproductive systems contains genetic codes as well as a receptor to receive vitamin D.
Vitamin D is actually a steroid hormone produced by our body. We manufacture vitamin D when we take a quality vitamin D3 supplement, expose our skin to optimal sun light, or consume lots of fatty fish or vitamin D3-fortified foods.

Cells in the female reproductive system (including the ovaries, fallopian tubes, uterus, placenta, and decidua) are replete with vitamin D receptors. The male reproductive system cells (including the testes, prostate, and urethra) also are abundant with vitamin D receptors.

When we have ample amounts of activated vitamin D, it binds with its receptor to regulate genes in our reproductive system. For example, activated vitamin D in the female reproductive system controls the genes involved in estrogen production. Vitamin D also regulates several genes during the process of embryo implantation.

Conversely, when the reproductive system lacks activated vitamin D, genes essential to conception are not expressed. Hence, the chances of achieving successful conception are diminished.

Both Mom and Dad Need Vitamin D for Fertility

For many couples, getting pregnant and carrying a pregnancy to term present daunting challenges. But few understand how vitamin D plays a role in fertility of both biological parents. Scientific research indicates that the significant prevalence of vitamin D deficiency correlates to the incidences of infertility cases in women and men:

  • Researchers in Milan, Italy conducted a study of 335 women who were candidates for in vitro fertilization (IVF). Published in the August 14, 2014 issue of The Journal of Clinical Endocrinology & Metabolism, the study demonstrated that the women with vitamin D levels of more than 30 ng/mL (75 nmol/L) enjoyed the highest chance of pregnancy. The researchers concluded vitamin D is an emerging factor influencing female fertility and IVF outcome.
  • Greek researchers recently examined 30 years of scientific literature on the role of vitamin D in human reproduction. The accumulated evidence suggests that vitamin D is significantly involved in the reproductive system of both genders. Regarding fertility, the researchers noted that vitamin D status is associated with semen quality and sperm count, motility, and morphology. Moreover, they concluded that there also is a positive effect of vitamin D supplementation on testosterone concentrations and fertility outcomes. The review was published in a 2013 issue of the International Journal of Clinical Practice.
  • An Australian fertility specialist, Anne Clark, M.D., presented findings to the 2008 Fertility Society of Australia Conference that demonstrated the role of low vitamin D in men. More than one-third of the 794 men who underwent a vitamin D blood serum test were determined to be deficient in vitamin D (as well as folate). Among the couples where the male completed supplementation treatment for nutritional deficiencies, more than one-half conceived naturally or with minimal treatment.

How to Become Vitamin D Healthy Parents

In today’s modern indoor living, the most effective source of vitamin D3 (cholecalciferol) is an oil-based soft gel or liquid supplement. Vitamin D3 supplements are available over the counter in retail and online stores. Beware of vitamin D prescriptions as most contain vitamin D2 (ergocalciferol) that is much less effective than vitamin D3.

The amount of vitamin D3 depends upon your vitamin D level, derived from a simple blood test called 25(OH)D. Assume you are vitamin D deficient (most people are) and get your blood tested by your healthcare practitioner.

Based on the results of your test, supplement daily with vitamin D3 to safely increase your blood levels. A number of vitamin D experts believe a healthy vitamin D range is at least 50 to 80 ng/mL (125 to 200 nmol/L).

Repeat the test in three to six months. Increase or maintain your daily D3 dose in response to your current level. Getting within range will take time (at least months) but rest assured that you will be gaining vitamin D wellness that should increase your chances of getting pregnant.

Vitamin D’s benefits do not end with fertility! Stay tuned for my next Hormones Matter article “Maternal Vitamin D: Pregnancy and Beyond.”

Editor’s Note: Susan Rex Ryan is an award-winning author who is dedicated to vitamin D awareness. Her extensive collection of health articles can be found on Hormones Matter as well as on her vitamin D blog at smilinsuepubs.com. Follow Sue on FB “Susan Rex Ryan” and Twitter @vitD3sue.

Hormones Matter does not provide medical advice, diagnosis or treatment.

Copyright © 2014 by Smilin Sue Publishing, LLC
All rights reserved.

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Uterus and Ovaries: Fountain of Youth

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Numerous studies have shown a strong correlation between removal of both ovaries / bilateral oophorectomy (castration) and accelerated aging as measured by an increased risk of chronic health conditions. Hysterectomy / uterus removal with preservation of both ovaries is also associated with some of these chronic conditions. These include heart disease, stroke, metabolic syndrome, osteoporosis, hip fracture, lung cancer, colorectal cancer, dementia, Parkinsonism, impaired cognition and memory, mood disorders, sleep disorders, adverse skin and body composition changes, adverse ocular changes including glaucoma, impaired sexual function, more severe hot flushes and urogenital atrophy. Wow, that’s quite a list!

Ovaries: Health Powerhouses

This 2016 article titled “Study: Remove ovaries, age faster” sums up the findings of Mayo Clinic researchers proving yet again the harmful and unethical practice of ovary removal. The study found that ovary removal (oophorectomy) is associated with a higher incidence of 18 chronic conditions and should be discontinued in women who are not at high risk for ovarian cancer. Although this study cites the increase in chronic conditions in women who undergo oophorectomy before age 46, other studies have shown that oophorectomy even after menopause does more harm than good. Here is one that showed that to be true up to age 75.

The ovaries have both reproductive and endocrine functions as detailed in this International Menopause Society article. After menopause, the ovaries produce mostly androgens, some of which are converted into estrogen. Testosterone levels are more than 40% lower in women without ovaries compared to intact women. Women without their uterus likewise have lower levels but not as low as women without ovaries per this article. Estrogen therapy mitigates some but not all of the increased health risks of oophorectomy. But estrogen further reduces androgen levels increasing risk of osteoporosis and fracture. Nothing can replace the lifelong functions of the ovaries (and uterus).

The Uterus / Ovaries / Tubes Connection

The harms of ovary removal would also apply to ovarian failure that commonly occurs after hysterectomy and some other medical treatments. As previously cited, women who have had a hysterectomy have lower levels of testosterone. According to this 1986 publication, 39% of these women showed signs of ovarian failure. This study showed a nearly 2-fold increased risk of ovarian failure when both ovaries were preserved and nearly 3-fold when one was preserved. This likely explains the increased risk of heart disease and metabolic conditions as shown by multiple studies including this recent Mayo Clinic one. However, per this 1982 study, the uterus itself protects women from heart disease via the uterine substance prostacyclin. Loss of bone density is another harm of hysterectomy as shown by multiple studies such as this one.

Removal of even one ovary (unilateral oophorectomy) without hysterectomy is also harmful. Studies out of the Mayo Clinic showed increased risks of cognitive impairment or dementia and parkinsonism. Colorectal cancer is another increased risk according to this Chinese study and this Swedish one.

The Fallopian tubes appear to impair ovarian function to some degree as evidenced by Post Tubal Ligation / Sterilization Syndrome. This study shows an increase in Follicle Stimulating Hormone (FSH) after tube removal (salpingectomy).

Ovarian impairment after hysterectomy or salpingectomy is thought to be the mechanism of the reduced risk of ovarian cancer which is already rare.

The Uterus: Anatomy, Sex, Cancer Prevention

Hysterectomy is associated with other harms besides impaired ovarian / endocrine function. The uterus and its ligaments / pelvic support structures are essential for pelvic organ integrity as well as skeletal integrity. The effects on these structures and functions are detailed here and here. This article shows the many hysterectomized women lamenting their “broken bodies” – changes to their figures, back, hip and midsection pain, pelvic pain, bladder and bowel issues, and effects of severed nerves and blood vessels.

The uterus and associated nerves and blood vessels play a key role in sexuality and vibrancy. You can hear the desperation in women’s comments about the devastating sexual losses and feelings of emotional emptiness.

There is an increased risk of renal cell, thyroid, and colorectal cancers after hysterectomy. How ironic when cancer fear tactics are commonly used to market hysterectomy and/or oophorectomy.

Adhesions that commonly form after these surgeries can cause serious problems especially in the long term. Surgical complications – nerve injuries, bladder, bowel and ureter injuries, vaginal cuff dehiscence, a too short vagina, infections, hemorrhage – are more common than indicated by gynecologists.

Although “The Miraculous Uterus” article fails to mention the anatomical harms, it is otherwise “spot on.” It talks about the “ovarian conservation scam” and that “passion, love, ecstasy, the emotional essence that drives human achievement, forever after elude them.” This explains why “there’s no effective outrage against the barbarism of hysterectomy.”

Compelling Evidence of Harm

Clearly, there is compelling medical evidence that both hysterectomy and oophorectomy are destructive surgeries. Unfortunately, some hysterectomy forums censor negative posts giving a slanted view of the life shattering effects. Here is a sampling of women’s experiences on the Gyn Reform site.

The medical literature on the harms of these surgeries dates back over a century. Listed below are a small number of the numerous publications (minus the ovarian failure studies cited above). The Gyn Reform website has a fairly comprehensive list of resources on oophorectomy. Its Ovaries for Life sister site provides a good overview of the lifelong importance of our ovaries.

1912 – The Physiological Influence of Ovarian Secretion

1914 – Nervous and Mental Disturbances following Castration in Women

1958 – The controversial ovary

1973 – Osteoporosis after Oophorectomy for Non-malignant Disease in Premenopausal Women

“Oophorectomy before the age of 45 years was found to be associated with a significantly increased prevalence of osteoporosis within three to six years of operation.

1974 – Endocrine Function of the Postmenopausal Ovary: Concentration of Androgens and Estrogens in Ovarian and Peripheral Vein Blood

1978 – The emotional and psychosexual aspects of hysterectomy

1981 – Premenopausal hysterectomy and cardiovascular disease

1981 – Sexual response after hysterectomy-oophorectomy: Recent studies and reconsideration of psychogenesis

1981 – The role of estrogen and oophorectomy in immune synovitis

1982 – Prostacyclin from the uterus and woman’s cardiovascular advantage

1989 – The effects of simple hysterectomy on vesicourethral function

“The results show that simple hysterectomy is associated with a significant incidence of post-operative vesicourethral dysfunction and that there is an identifiable neurological abnormality incurred at operation which is pertinent to the subsequent disordered voiding.

1990 – Effects of bilateral oophorectomy on lipoprotein metabolism

1994 – The climacteric ovary as a functional gonadotropin-driven androgen-producing gland

1996 – Urinary incontinence in older women: who is at risk? Study of Osteoporotic Fractures Research Group

“Urinary incontinence is a common problem in older women, more common than most chronic medical conditions. Of the associated factors that are preventable or modifiable, obesity and hysterectomy may have the greatest impact on the prevalence of daily incontinence.

1997 – Bladder, bowel and sexual function after hysterectomy for benign conditions

1998 – Ovaries, androgens and the menopause: practical applications

1998 – Impairment of basal forebrain cholinergic neurons associated with aging and long-term loss of ovarian function

1998 – Influence of bilateral oophorectomy upon lipid metabolism

1999 – Estrogen and movement disorders

2000 – The hypothalamic-pituitary-adrenal and gonadal axes in rheumatoid arthritis

2000 – Risk of myocardial infarction after oophorectomy and hysterectomy

2000 – Hysterectomy, Oophorectomy, and Endogenous Sex Hormone Levels in Older Women: The Rancho Bernardo Study

2005 – Ovarian conservation at the time of hysterectomy for benign disease

Ovarian conservation until age 65 benefits long-term survival…. There is sustained, but decreasing, benefit until the age of 75, when excess mortality for oophorectomy is less than 1%.

2007 – Ovarian conservation at the time of hysterectomy for benign disease

Approximately 78% of women between the ages of 45 and 64 years have prophylactic oophorectomy when hysterectomy is performed for benign disease. Therefore, the decision to perform prophylactic oophorectomy should be approached with great caution for the majority of women who are at low risk of developing ovarian cancer.”

2009 – Ovarian conservation at the time of hysterectomy and long-term health outcomes in the nurses’ health study

In no analysis or age group was oophorectomy associated with increased survival.

2010 – Current indications and role of surgery in the management of sigmoid diverticulitis

A previous history of hysterectomy is a valuable clinical clue to the correct diagnosis as colovaginal and colovesical fistulas are rare in females with their uterus in place, as the uterus becomes a screen interposed between the inflamed colon and the bladder and vagina.”

2012 – Oophorectomy for whom and at what age? Primum non nocere

2016 – Study: Remove ovaries, age faster

2017 – Cardiovascular and metabolic morbidity after hysterectomy with ovarian conservation: a cohort study

A Harmful Practice That Won’t Die

Ovary removal / castration was introduced by Robert Battey in 1872 and “was practised widely for several decades….. Better insight into female physiology and ovarian function finally pushed the sinister operation of Robert Battey from the scene.” This publication refers to Battey’s operation as “barbaric.”

Despite the long-standing and compelling evidence of harm, these surgeries continue at alarming rates. Publications are misleading in that they report inpatient surgeries despite the large majority being outpatient (70% in 2014). This 2008 article reported that oophorectomies “more than doubled in frequency since the 1960’s.” According to results of a FOIA request by Ovaries for Life, there are over 700,000 oophorectomies every year despite there being only ~22,000 cases of ovarian cancer. Hysterectomy figures obtained by Ovaries for Life are also shocking at 830,000 in light of less than 70,000 cases of endometrial and cervical cancers.

Many media reports have questioned the high rate of these surgeries since gynecologic cancers are rare. The oldest one I could find was dated 1969. I found about three articles per decade in the mainstream media since then. According to the Athena Institute, half of U.S. medical schools in 1986 “had changed their suggestions and were now recommending a reconsideration of the common practice of ovariectomy.” Evidently, that never took hold.

Congress held two hearings on hysterectomy, one in 1976 and one in 1993. The 1993 transcripts state that the hysterectomy rate increased 250% in women ages 15 to 24 and 186% in ages 25 to 34 from 1965 to 1984! Despite these shocking statistics, it appears that no action was taken after either hearing.

According to this “Reassessing Hysterectomy” article, the Agency for Healthcare Research and Quality sponsored research and conferences on the overuse of hysterectomy in the 1990’s. This article is packed with information on the prevalence and harms of hysterectomy and oophorectomy as well as alternative treatment options. Yet, the high rate of hysterectomy has continued such that 45% of women will end up having one. Citing 2006 data, the oophorectomy rate was 73% of the hysterectomy rate.

How to End the Harm?

I’ve been researching this subject for over 10 years and sharing my experience and knowledge on various websites. It’s shocking how many women are misled and deceived into these surgeries. Age doesn’t seem to matter; younger and younger women are undergoing these surgeries. This appears to be the biggest surgical racket and women’s healthcare con as discussed here.

There are a number of issues that perpetuate the gross overuse of these harmful surgeries. These include:

  1. These surgeries and “forever after” care are very lucrative.
  2. The public has been led to believe that the female organs are disposable after childbearing is complete.
  3. Medical education and decades of practice have made these surgeries “a standard of care.”
  4. Informed consent is seriously lacking.
  5. Gynecology consent forms are open ended giving surgeons “carte blanche” to remove organs unnecessarily.
  6. We still live in a climate of gender disparity / male dominance.

As you can see from the list of publications above, some study authors have called out the practice of ovary removal as unethical. Numerous professional societies have issued guidelines discouraging its use in most women. But most have been silent on the overuse of hysterectomy despite its many harms.

Why has our government not stepped in to address this egregious harm? Women who have contacted their legislators have been met with indifference. Gyn Reform reported on their experiences with legislators and other authorities who can effect change. The non-profit HERS Foundation has been educating women and advocating for informed consent legislation since the 1980’s.

Why do insurance companies approve so many of these surgeries that are rarely necessary? Not only are the surgeries themselves expensive, treatments for the chronic after effects are costly. Reining in unnecessary treatments especially those that cause lifelong harm would go a long way towards making healthcare more affordable.

Why has Graduate Medical Education (GME) not changed their surgical requirements to favor organ preservation? Each resident must do at least 70 hysterectomies but there is no requirement for myomectomy (fibroid removal). Residents don’t need to do any cystectomies (cyst removals) either which is partly why so many women lose ovaries for benign ovarian cysts. Here are the GME ob/gyn requirements.

A popular mantra at Tufts in the 1970’s – “There’s no room in the tomb for the womb” – reflects this culture of the disposable uterus and gynecologists’ obsession with its removal. Insurance reimbursement rates are also to blame as they incentivize hysterectomy and oophorectomy over myomectomy and cystectomy. In many cases, medical management versus surgery is the appropriate course. The “Reassessing Hysterectomy” article cited above lists a number of treatment options for gynecologic problems. Revamping reimbursement rates to strongly favor organ preservation should eventually force GME to change their requirements. But how do we make that happen?

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Lucas Cranach the Elder, Public domain, via Wikimedia Commons

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From DES to the Pill: Are We Doomed to Repeat History?

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“The doctor wouldn’t have given it to me if he thought it was dangerous, right?”

My wife asked this salient question as we discussed the pros and cons of The Pill. It sent us both into deep reflection. Everything we read said The Pill was dangerous, but the doctor had acted like they should come in a Pez dispenser. To this day, I’m not sure where the cognitive began and the dissonance ended.

The DES Debacle: Origins of Obstinance

Doctors are generally dogmatic, but their nearly universal laissez-faire attitude toward The Pill seems particularly paradoxical when you study the scope and seriousness of its side effects. How can doctors believe that The Pill is safe, when tomes of studies suggest otherwise? Research links The Pill to everything from breast cancer and strokes, to Crohn’s Disease and lupus. To understand where we are and how we got here, it’s important to study the journey that brought us here.

By 1970, the current dogma that ‘The Pill is safe’ was well rooted in the medical community. However, enough doctors expressed concerns that Senator Gaylord Nelson decided to hold Congressional Hearings on the matter. The big three networks covered the hearings extensively, which caused great anxiety among women taking The Pill — and even greater anxiety among pill proponents, who subsequently demanded more ‘pro-pill’ doctors be included.

Senator Nelson took umbrage with their complaints, noting that all but one of the previous doctors had actually been ‘pro-pill’ to some extent, but all had reservations about its complications. Nonetheless, many of the doctors in the second round of hearings seemed more decidedly ‘pro-pill,’ including Dr. Kenneth Ryan, who stated,

I know of no information that indicates that biological properties of the estrogens used in the contraceptive pill are any different than stilbesterol for which we have at least 30 years of clinical experience…(Competitive Problems in the Drug Industry, Ninety-First Congress, Second Session, Page 6541)

Very reassuring… Unless you were actually familiar with the 30-year history of stilbesterol, also known as diethylstilbestrol (DES). Sir Charles Dodds discovered DES in 1938, and rushed it to market in the public domain. The English doctor bypassed the patent process hoping it would discourage the Nazis from further tests on women prisoners in their development of ethinyl estradiol (Barbara Seaman, The Greatest Experiment Ever Performed on Women; page 36).

From DES to the Pill

Despite his noble intentions, Dodds soon regretted the decision. Without a patent, drug companies around the globe were free to produce DES. He never expected that synthetic hormones would be given to healthy women, and was horrified that doctors were prescribing it as hormone therapy for natural menopause.

You Can’t Put the Hormones Back in the Tube

Even worse, Dodds soon learned that an American doctor named Karnaky had begun blazing a new trail – doling out DES to ‘prevent miscarriages’. Alarmed by the news, Dodds sent him a study he had personally performed, which showed that the drug actually caused miscarriages in animal subjects. It didn’t deter Dr. Karnaky or the many doctors who followed his lead. (Robert Meyers, D.E.S. The Bitter Pill; pp. 56-73)

Dodds began to feel like he was fighting a monster that he himself had unleashed. He was most concerned about how his discovery could affect certain cancers. He sent DES samples to the newly formed National Cancer Institute in the United States, and urged them to conduct tests and notify doctors.

Dodds wasn’t alone. The Council on Pharmacy and Chemistry warned,

…because the product is so potent and because the possibility of harm must be recognized, the Council is of the opinion that it should not be recognized for general use at the present time…and that its use by the general medical profession should not be undertaken until further studies have led to a better understanding of the functions of the drug. (Barbara Seaman, The Greatest Experiment Ever Performed on Women; page 44)

The concerns sent murmurs through the medical community, and many doctors began experimenting with lower doses of DES. By 1940, the editors of the Journal of the American Medical Association (JAMA) felt compelled to add theirs to the litany of warnings:

“It would be unwise to consider that there is safety in using small doses of estrogens, since it is quite possible that the same harm may be obtained through the use of small doses of estrogen if they are maintained over a long period.” (JAMA, April 20, 1940)

In 1959, the FDA determined the link to side effects (including male breast growth) was sufficient to ban poultry farmers from using DES as a growth hormone. However, the widespread use of DES in humans continued. In fact, it had become standard medical practice by the time Dr. Ryan assured Congress that The Pill was just as safe as DES – showing how medical dogma often trumps scientific evidence.

The greater irony of Dr. Ryan’s statement materialized one year after his testimony, when researchers first linked a rare vaginal cancer to the daughters of women who received DES during pregnancy. The FDA reacted strongly, listing pregnancy as a contraindication for DES use.

Consumer Groups Take the Lead

You would expect this to be the beginning of the end for DES. Shockingly, the medical community responded with indifference, continuing to prescribe DES for a variety of ‘off label’ uses, including as a morning-after pill, to catalyze the onset of puberty, and the old faithful, hormone replacement therapy. (Robert Meyers, D.E.S. The Bitter Pill; page 185)

It took nearly a decade of passionate effort from consumer movements like DES Action to convince doctors to (mostly) abandon DES. Dozens of lawsuits were filed; some were settled; and some are still pending. There is evidence that the harmful consequences could now be affecting a third generation of DES victims.

The current Director of Epidemiology and Biostatistics at the National Cancer Institute, Robert Hoover, M.D. oversees the DES Follow-Up Study to track the ongoing repercussions. With identifiable problems now affecting the grandchildren of women who took DES, the disaster hasn’t yet moved into the past tense of our nation’s history. Despite that, Dr. Hoover says:

There’s essentially a whole generation of medical students who don’t know the story. The story has such powerful lessons that I think that’s a tragedy…For about 20 years now, when I standardly ask in my general epidemiology lecture… how many of you have heard of DES, nobody raises their hand.

Sidney Wolfe, M.D., who headed up Ralph Nader’s Health Research Group offered this perspective,

DES is an excellent example of how drug companies behave, how they take advantage of the ways doctors act, and how they make millions of dollars by ignoring evidence of a drug’s harmfulness, by failing to get evidence that it is effective, and then by marketing a product that plays on fears and misconception. (Robert Meyers, D.E.S. The Bitter Pill; page 208).

In just 20 years, the American Medical Association moved from “It would be unwise to consider that there is safety in using small doses of estrogens…” to embracing the release of insufficiently tested hormones as birth control for millions of women. I’m leery of trusting a dogma founded on such an erratically moving target. In their defense, the dogma really hasn’t moved much in the decades since.

Today, the medical community assures us The Pill is the most researched drug ever. Sorry doc, that reassurance just doesn’t ring true. At this point, it feels more like a phrase learned by rote than a statement based on any kind of empirical evidence. Unfortunately, it’s not the only hollow mantra that should raise a red flag when it comes to hormonal contraceptives. I will discuss how the medical community responds to scientific studies in my next post, The Spin Doctor’s Prescription for Birth Control.

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DES – The Drug to Prevent Miscarriage Ruins Lives of Millions

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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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Weight Gain and Hormonal Contraceptives

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Once upon a time, a 26-year-old woman went to her doctor and asked to be put on the new birth control pill that allowed women to only have four periods a year. She had seen it advertised on television. Four months later, 15 pounds heavier and suffering from mild depression, she returned to the doctor feeling miserable. The doctor told her the weight gain and depression were not from the pill because those were not side effects of hormonal birth control. This left the young woman feeling like it was her fault she had gained weight. Needless to say, that didn’t help with the depression. But she switched back to her original birth control pill and lived happily (but heavily) ever after. Well, until it gave her a stroke two years later.

I’ve written a lot about my stroke and about blood clots and birth control pills, but there are many other side effects from hormonal birth control. More often than not, we are told that these side effects do not exist; that they are all in our heads. Are they? Or are we simply being ignored and lied to?

What Does The Research Show?

When researching my thesis, I was interested in finding out what women knew about the risks associated with birth control pills. I created a survey based on a published study by researchers in this field. The original study outlined which side effects were and were not associated with birth control pills. The survey used in my thesis demonstrated the following:

“When the women were asked to select which risk factors were associated with birth control pills, most women, 76.7% of the 313 who answered the question, selected blood clots. Weight gain, which is not considered a health risk or even a side effect of birth control pills, was the selection most chosen (79.9%).”

The number one answer most women chose was weight gain, yet all the research I read said that weight gain was not a side effect of birth control pills. My own doctor had told me it wasn’t a side effect when I stood before her 15 pounds heavier after switching pills. Even as I wrote my thesis, I wondered how we could all be so wrong. Well, it turns out we weren’t. The pill can cause weight gain. And they knew it could, even back in 1970. The following is testimony from the Nelson Pill Hearings.

Dr. Francis Kane (page 6453): [In a Swedish study of 344 women] Of the 138 women who stopped using the medication, weight gain and emotional disturbances were the most frequently reported, 26.1 percent and 23.9 percent.

Dr. Louis Hellman (page 6203): My private patients… come off the pill because of a host of minor reactions. The most prevalent one is weight gain. The modern American girl just does not want to gain 5 or 10 pounds if she can help it.

What About Today’s Birth Control Pills?

I took another look at what I could find out about weight gain and hormonal contraception now. According to WebMD:

“When birth control pills were first sold in the early 1960s, they had very high levels of estrogen and progestin. Estrogen in high doses can cause weight gain due to increased appetite and fluid retention. So, 50 years ago they may indeed have caused weight gain in some women. Current birth control pills have much lower amounts of hormones. So weight gain is not likely to be a problem.”

Maybe larger doses of hormones cause more weight gain. But I don’t think that means that smaller doses cause none. And what about taking that smaller dose for a decade or more?

Most current medical information dismisses weight gain completely. On the Mayo Clinic website’s FAQ page for birth control pills it says:

“Do birth control pills cause weight gain? Many women think so. But studies have shown that the effect of the birth control pill on weight is small — if it exists at all.”

That’s right, ladies. Just like your menstrual cramps, weight gain on the pill probably doesn’t exist. But wait, the Mayo Clinic says there are studies that show hormonal contraceptives don’t cause weight gain. Where are these studies?

Inconclusive? Or Incorrect?

A recent meta-analysis (2014) conducted by Cochrane (an independent group that reviews randomized controlled trials and organizes medical research information) found the following:

Available evidence was insufficient to determine the effect of combination contraceptives on weight, but no large effect was evident. Trials to evaluate the link between combination contraceptives and weight change require a placebo or non-hormonal group to control for other factors, including changes in weight over time.

You mean to tell me in the 40+ years since the Nelson Pill Hearings we haven’t been able to conduct one conclusive study to determine how hormonal contraception affects weight? Perhaps it’s time to start asking why. All those studies that provided insufficient evidence, who funded them and who might stand to lose if they were conclusive? I don’t know for sure but I do know that one of the few things women fear as much as an unintended pregnancy is weight gain. Even the staunchest feminists among us often fret over our figures.

According to Naomi Wolfe’s The Beauty Myth, “thirty-three thousand American women told researchers that they would rather lose ten to fifteen pounds than achieve any other goal.” Setting aside how disturbing that is, we can easily see how the fact that hormonal birth control can cause weight gain might adversely affect the pharmaceutical industry’s bottom line (pardon the pun).

At the Nelson Pill Hearings, there were at least a half dozen experts–doctors specifically chosen to testify before Congress–that mentioned weight gain as a side effect of the birth control pill. Including ones who admittedly worked for the pharmaceutical industry. But now, nearly five decades later, the research is inconclusive. Doctors are telling patients that hormonal contraceptives are not responsible for weight gain, yet 80% of women surveyed thought that weight gain was a side effect. Like so much surrounding the pharmaceutical industry, something doesn’t add up here. And who is paying the difference? Women. Yet again we are being told that it’s all in our heads. Have you had experience gaining weight on hormonal birth control?

Further Testimony on Weight Gain

This testimony from the Nelson Pill Hearings just scratches the surface of the side effects caused by hormonal contraceptives. I’ll be expanding more on a lot of this testimony in future articles. But perhaps Dr. Victor Wynn explained most succinctly how these side effects manifest when he testified (page 6303):

When I say these changes occur, I mean they occur in everybody, more in some than in others, but no person entirely escapes from the metabolic influence of these compounds. It is merely that some manifest the changes more obviously than others.

Dr. Robert Kistner (page 6082): I tell her about the side effects plus a weight gain edema and I may even give her a prescription for this.

Dr. John Laragh (page 6165): We do not have any firm clues. But it does look as though those who accumulate salt and water and gain weight on the oral contraceptives might be especially vulnerable [to increased hypertension].

Dr. Francis Kane (page 6449): Complaints of moodiness, being cross and tired, alterations in sexual drive, weight gain, edema, and insomnia were commonest in the group using the estrogen-progestin group.

At the hearings, Dr. Herbert Ratner (page 6737) was asked by James Duffy, minority council:

Mr. Duffy: You use the word “disease” here. Disease to me seems to be a pretty strong word and I am just curious why you would consider weight change to be a disease?

Dr. Ratner: You realize that obesity is one of our major problems in this country.

Real Risk Study: Birth Control and Blood Clots

Lucine Health Sciences and Hormones Matter are conducting research to investigate the relationship between hormonal birth control and blood clots. If you or a loved one have suffered from a blood clot while using hormonal birth control, please consider participating. We are also looking for participants who have been using hormonal birth control for at least one year and have NOT had a blood clot, as well as women who have NEVER used hormonal birth control. For more information or to participate, click here.

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