Unsuccessful Pregnancy: experiencing Secondary Infertility…

Maybe your family is okay as it is…

Shifting our idea of the perfect family: Experiencing secondary infertility
Personal stories

My name is Theresa and my husband’s name is Matteo.
We have a beautiful little girl named Malia who just had her third birthday.
Matteo and I started trying for a baby when I was 35 years old – once we both finished school, got our careers established and did some of the travelling we both love to do.
Time seemed to fly by and suddenly when I hit my 35th birthday we realized we better get moving on starting our family.

Continue reading Shifting our idea of the perfect family: Experiencing secondary infertility
on MyFertilityChoices.comPersonal Stories – also on Twitter

An Estimate of Five Million IVF Babies born!

Fertility Breakthroughs…

Five Million IVF Babies Born Since 1978
Frozen embryos ‘more successful than fresh’ for IVF pregnancies

The five million figure was announced last month at the annual meeting of the European Society of Human Reproduction and Embryology (Eshre) taking place in Istanbul, Turkey.

Dr David Adamson, chair of the International Committee for Monitoring Assisted Reproductive Technologies (ICMART), which made the calculation, said: “Millions of families with children have been created, thereby reducing the burden of infertility. The technology has improved greatly over the years to increase pregnancy rates. The babies are as healthy as those from other infertile patients who conceive spontaneously. The technology is available globally in many different countries. IVF is firmly established now in the mainstream of medicine.”

Read Five Million IVF Babies Born Since 1978
The HuffPost LifeStyle, 02/07/2012.

Infertility among Daughters either exposed or not exposed to DiEthylStilbestrol

Higher infertility rate and abnormalities found in the DES Daughters

Infertility among daughters either exposed or not exposed to diethylstilbestrol
Higher infertility rate and abnormalities found in the DES Daughters

Infertility was examined among 343 diethylstilbestrol-exposed and 303 unexposed daughters whose mothers participated in an evaluation of diethylstilbestrol use during pregnancy 35 years ago. Of the married individuals who were not using contraception and who were actively trying to conceive, a greater proportion of diethylstilbestrol-exposed women than unexposed subjects experienced primary infertility (33% versus 14%, p less than 0.001). Among those with primary infertility, abnormal hysterosalpingograms were observed in 46% of the diethylstilbestrol-exposed group and in none of the unexposed group (p less than 0.02), while tubal abnormalities were found in 42% of the exposed and in none of the unexposed (p = 0.02). First pregnancies were achieved by 40 (58%) women exposed to diethylstilbestrol and 18 (64%) unexposed subjects. Twenty-four (60%) of the exposed women and 15 (83%) of the unexposed individuals who conceived had a live-born infant who survived. The estimated cumulative rate of first pregnancy was 16% for the exposed group and 36% for the unexposed group at 12 months after the diagnosis of primary infertility (p less than 0.05).

Sadly for many DES daughters having their own children is not possible! Many of us who have experienced miscarriages, want to have kids but are struggling or unable to…
More about DES pregnancy risks – our posts tagged pregnancy

Sources: Infertility among daughters either exposed or not exposed to diethylstilbestrol, NCBI, Dr Herbst A, Mar 1988

More DES DiEthylStilbestrol Resources

Urogenital Abnormalities in Men exposed to DiEthylStilbestrol in Utero

Prenatal exposure to DES increases risk of male urogenital abnormalities

DES Follow-up Study Summary

National Cancer Inst logo image
Prenatal exposure to DES increases risk of male urogenital abnormalities.

One of the most frequently asked questions from DES exposed families is whether the sons have had any adverse health effects. For that reason, our collaborative follow-up has included over 1,000 DES-exposed sons and over 1,000 other men of the same ages who were never exposed to DES. These men have been completing mailed questionnaires on the same schedule as women in the study, in 1994, 1997, 2001, and 2006. Some of the questions are the same and some are different. The men were asked whether they had ever been diagnosed with any of a list of urogenital abnormalities. These abnormalities were studied more than 20 years ago in both the offspring of mothers from the University of Chicago DES clinical trial and in a group of sons born to mothers at the Mayo Clinic. The two studies reported different findings, with the University of Chicago follow-up finding a higher prevalence of abnormalities in the DES-exposed sons and the Mayo Clinic study finding no difference between DES-exposed and unexposed sons. We thought we might be able to clarify this question with data from the entire collaborative cohort – including the Mayo sons, the Chicago sons, and additional sons from women who gave birth in Massachusetts.

We found that urogenital abnormalities were fairly rare among DES-exposed sons, as is true for the general U.S. population. However, DES-exposed sons did have a higher prevalence of both undescended testicle and epididymal cyst. They were two times as likely to have had one of those conditions as were unexposed men. For both of these conditions, the prevalence was highest if son was exposed during the first 10 weeks of gestation. In men born at the Mayo clinic, DES exposure was not significantly associated with these conditions overall, but there was a significant association with undescended testicle and epididymal cyst for sons exposed early in gestation. In the University of Chicago clinical trial, the protocol was to give DES as soon as a pregnancy was identified and for use to continue until the last weeks of pregnancy. This same protocol was typical in Boston and in some other regions of the U.S. It was not the usual protocol at the Mayo Clinic, however, where women usually began DES later in pregnancy and took it for only a few months. Differences in patterns of use may explain the conflicting findings in earlier studies of urogenital abnormalities in sons. Our conclusion is that DES-exposed sons do indeed have a higher risk of certain urogenital abnormalities particularly if they were exposed in the early months of fetal development. Fortunately, we and others have already shown that prenatal DES exposure does not affect fertility in men, even in those men with these urogenital abnormalities.

Because the sons are now adults, they were also asked if they had ever been diagnosed with infection or inflammation of the urogenital organs. Prenatal DES exposure was not associated with occurrence of infection or inflammation of the prostate, urethra, or epididymus, or with benign prostatic hypertrophy (enlarged prostate). DES-exposed sons were approximately two and a half times more likely to have had an infection or inflammation of the testes. We do not know the reasons for such an increase. It is possible that minimal structural abnormalities, such as minor obstructions, could explain the increase in infection and inflammation. We will continue to investigate these conditions, especially benign prostatic hypertrophy, as men in the study grow older.

2009 Study Abstract:

BACKGROUND:
Diethylstilbestrol (DES), a synthetic estrogen widely prescribed to pregnant women during the 1940s70s, has been shown to cause reproductive problems in the daughters. Studies of prenatally-exposed males have yielded conflicting results.

METHODS:
In data from a collaborative follow-up of three U.S. cohorts of DES-exposed sons, we examined the relation of prenatal DES exposure to occurrence of male urogenital abnormalities. Exposure status was determined through review of prenatal records. Mailed questionnaires (1994, 1997, 2001) asked about specified abnormalities of the urogenital tract. Risk ratios (RR) were estimated by Cox regression with constant time at risk and control for year of birth.

RESULTS:
Prenatal DES exposure was not associated with varicocele, structural abnormalities of the penis, urethral stenosis, benign prostatic hypertrophy, or inflammation/infection of the prostate, urethra, or epididymus. However, RRs were 1.9 (95% confidence interval 1.13.4) for cryptorchidism, 2.5 (1.54.3) for epididymal cyst, and 2.4 (1.54.4) for testicular inflammation/infection. Stronger associations were observed for DES exposure that began before the 11th week of pregnancy: RRs were 2.9 (1.65.2) for cryptorchidism, 3.5 (2.06.0) for epididymal cyst, and 3.0 (1.75.4) for inflammation/infection of testes.

CONCLUSION:
These results indicate that prenatal exposure to DES increases risk of male urogenital abnormalities and that the association is strongest for exposure that occurs early in gestation. The findings support the hypothesis that endocrine disrupting chemicals may be a cause of the increased prevalence of cryptorchidism that has been seen in recent years.

Sources:

  • Urogenital abnormalities in men exposed to diethylstilbestrol in utero: a cohort study,NCBI, PMID: 19689815, 2009 Aug 18;8:37. doi: 10.1186/1476-069X-8-37. Full text PMC2739506.
  • NCI, DES Follow-up Study Published Papers.
More DES DiEthylStilbestrol Resources

My IVF Treatments: learning the hard Way that Science has Not outsmarted Mother Nature…

The vast majority of assisted reproductive technologies fail…

Learning the hard way that science has not outsmarted mother nature
Personal stories

My name is Miriam. I am one of those women who delayed motherhood until the age of 40. I was fit and healthy, ate well and practiced yoga. I had no idea that trying to become pregnant would be so difficult. Since I was a teenager I had been bombarded by cultural and media messages that said it was okay to postpone childbearing. I wasn’t aware that women’s fertility declined so rapidly after the age of 35, and dramatically more after the age of 40. ”

Continue reading Learning the hard way that science has not outsmarted mother nature
on MyFertilityChoices.com, Personal Stories – also on Twitter

Nr0b2 Molecular Mechanism underlying many of the Harmful Effects of DES on Male Mice

The orphan nuclear receptor small heterodimer partner mediates male infertility induced by diethylstilbestrol in mice

cropped-Black-Lab-mouse-sma
The sexual function of male rodents can be impaired by in utero and/or neonatal exposure to external molecules that disrupt normal hormone functioning, giving rise to concerns that low-level exposure to such molecules might cause similar effects in humans. Examples of such molecules include the synthetic nonsteroidal estrogen DES, which was used as a treatment for various diseases until the mid 1990s, and BPA, which is found, among other places, in some plastic containers. “

2009 Study Abstract

Studies in rodents have shown that male sexual function can be disrupted by fetal or neonatal administration of compounds that alter endocrine homeostasis, such as the synthetic nonsteroidal estrogen diethylstilbestrol (DES). Although the molecular basis for this effect remains unknown, estrogen receptors likely play a critical role in mediating DES-induced infertility. Recently, we showed that the orphan nuclear receptor small heterodimer partner (Nr0b2), which is both a target gene and a transcriptional repressor of estrogen receptors, controls testicular function by regulating germ cell entry into meiosis and testosterone synthesis. We therefore hypothesized that some of the harmful effects of DES on testes could be mediated through Nr0b2. Here, we present data demonstrating that Nr0b2 deficiency protected mice against the negative effects of DES on testis development and function. During postnatal development, Nr0b2-null mice were resistant to DES-mediated inhibition of germ cell differentiation, which may be the result of interference by Nr0b2 with retinoid signals that control meiosis. Adult Nr0b2-null male mice were also protected against the effects of DES; however, we suggest that this phenomenon was due to the removal of the repressive effects of Nr0b2 on steroidogenesis. Together, these data demonstrate that Nr0b2 plays a critical role in the pathophysiological changes induced by DES in the mouse testis.

Sources and more information
More DES DiEthylStilbestrol Resources

Poisoned by every Day Life: PLOS One Landmark Study

Plastics Derived Endocrine Disruptors (BPA, DEHP and DBP) Induce Epigenetic Transgenerational Inheritance of Obesity, Reproductive Disease and Sperm Epimutations

Chemicals found in every home may cause breast cancer, asthma, infertility and birth defects, global health chiefs said yesterday

Poisoned by every day life: Landmark study warns gender bending chemicals in your home, food and car ARE linked to a huge range of diseases  Read more: http://www.dailymail.co.uk/news/article-2281394/Poisoned-day-life-Landmark-study-warns-gender-bending-chemicals-home-food-car-ARE-linked-huge-range-diseases.html#ixzz2LfOpgG2J  Follow us: @MailOnline on Twitter | DailyMail on Facebook

  • Phthalates is used to soften plastic and improve consistency of cosmetics
  • Chemical commonly found in children’s toys, make up, cars and PVC flooring
  • Could cause breast cancer, asthma, infertility and birth defects, WHO says

Read Poisoned by every day life: Landmark study warns gender bending chemicals in your home, food and car ARE linked to a huge range of diseases.

PLOS One Study Abstract

Environmental compounds are known to promote epigenetic transgenerational inheritance of adult onset disease in subsequent generations (F1–F3) following ancestral exposure during fetal gonadal sex determination. The current study was designed to determine if a mixture of plastic derived endocrine disruptor compounds bisphenol-A (BPA), bis(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) at two different doses promoted epigenetic transgenerational inheritance of adult onset disease and associated DNA methylation epimutations in sperm. Gestating F0 generation females were exposed to either the “plastics” or “lower dose plastics” mixture during embryonic days 8 to 14 of gonadal sex determination and the incidence of adult onset disease was evaluated in F1 and F3 generation rats. There were significant increases in the incidence of total disease/abnormalities in F1 and F3 generation male and female animals from plastics lineages. Pubertal abnormalities, testis disease, obesity, and ovarian disease (primary ovarian insufficiency and polycystic ovaries) were increased in the F3 generation animals. Kidney and prostate disease were only observed in the direct fetally exposed F1 generation plastic lineage animals. Analysis of the plastics lineage F3 generation sperm epigenome previously identified 197 differential DNA methylation regions (DMR) in gene promoters, termed epimutations. A number of these transgenerational DMR form a unique direct connection gene network and have previously been shown to correlate with the pathologies identified. Observations demonstrate that a mixture of plastic derived compounds, BPA and phthalates, can promote epigenetic transgenerational inheritance of adult onset disease. The sperm DMR provide potential epigenetic biomarkers for transgenerational disease and/or ancestral environmental exposures.

Read Plastics Derived Endocrine Disruptors (BPA, DEHP and DBP) Induce Epigenetic Transgenerational Inheritance of Obesity, Reproductive Disease and Sperm Epimutations, PLOS one, January 24, 2013.