Beating the Odds after being diagnosed with Premature Ovarian Failure
” My name is Cole. I’m writing this today because I feel it is important to get my story out there to as many women as possible. To give inspiration to those wanting a family but are suffering from infertility and encourage them to not lose hope. I am 34 years old and had come off of birth control last summer after seventeen years. When I didn’t get my period back after four months my OBGYN recommended I see a reproductive specialist. Upon doing so I was given a battery of blood tests to measure my hormone levels. When the test results came back I was given the shock of my life. The numbers indicated I was POSTmenopausal with diminished ovarian reserve. ”
Could a ‘Fertility Switch’ Save Women From Pain Of Infertility Or Miscarriage?
Scientists from the Imperial College London have discovered an enzyme in the body that determines infertility and the chances of miscarriage, as it acts like a ‘switch. The SGK1 protein discovery could pave the way for new treatments and/or be used before women undergo IVF…
Mistaken beliefs about “test-tube” and “designer” babies
Despite 5 million births due to IVF and other assisted reproductive technologies worldwide since the first “test-tube baby,” Louise Brown, was born in July 1978, there remain some “myths” and common misperceptions about “test-tube” and “designer” babies:
Your fertility is mostly determined by genetics, which influences how many eggs you are born with Doctors believe that the number of eggs you have at birth determines the length of time you will remain fertile. At birth, women have about two million eggs in their ovaries. For every egg ovulated during your reproductive life, about 1,000 eggs undergo programmed cell death. Other things, such as smoking cigarettes and certain types of chemotherapy, can accelerate egg cell death and promote an earlier menopause.
Regular menstrual cycles are a sign of regular ovulation Most women have regular cycles lasting between 24 and 35 days. This is usually a sign of regular, predictable ovulation. Women who do not ovulate regularly have irregular menstrual cycles. Those who do not ovulate at all may have a genetic condition called polycystic ovarian syndrome (PCOS).
Basal temperature charting does not predict ovulation An older method of tracking ovulation involves taking your oral body temperature each morning before getting out of bed. This is called basal body temperature. This method is used to spot a rise in basal temperature, which is a sign that progesterone is being produced. The main problem with using this method is that your temperature rises after ovulation has already occurred. This makes it more difficult to time intercourse at an optimal time for conception. A better method is to use over-the-counter urine ovulation predictor test kits such as Clearblue Easy. These kits test for the hormone that prompts ovulation, which is called luteinizing hormone (LH).
Most women with blocked fallopian tubes are completely unaware they may have had a prior pelvic infection About 10 percent of infertility cases are due to tubal disease, either complete blockage or pelvic scarring causing tubal malfunction. One major cause of tubal disease is a prior pelvic infection from a sexually transmitted disease such as chlamydia. These infections can cause so few symptoms that you may be completely unaware your tubes are affected.
In most cases, stress does not cause infertility Except in rare cases of extreme physical or emotional distress, women will keep ovulating regularly. Conceiving while on vacation is likely less about relaxation than about coincidence and good timing of sex.
By age 44, most women are infertile, even if they are still ovulating regularly Even with significant fertility treatment, rates of conception are very low after age 43. Most women who conceive in their mid-40’s with fertility treatment are using donated eggs from younger women.
Having fathered a pregnancy in the past does not guarantee fertility Sperm counts can change quite a bit with time, so never assume that a prior pregnancy guarantees fertile sperm. Obtaining a semen analysis is the only way to be sure the sperm are still healthy!
For the most part, diet has little or nothing to do with fertility Despite popular press, there is little scientific data showing that a particular diet or food promotes fertility. One limited study did suggest a Mediterranean diet with olive oil, fish and legumes may help promote fertility.
Vitamin D may improve results of fertility treatments A recent study from the University of Southern California suggested that women who were undergoing fertility treatments, but had low vitamin D levels, might have lower rates of conception. This vitamin is also essential during pregnancy. At Pacific Fertility Center, we recommend our patients take 2,000-4,000 IU per day.
Being either underweight or overweight is clearly linked with lowered levels of fertility The evidence in recent years is that obesity is clearly linked with a longer time to conception. Having a body mass index less than 18 or over 32 is associated with problems ovulating and conceiving, as well as problems during pregnancy.
A new government study shows the percentage of married couples having trouble conceiving has actually dropped slightly in recent years. The percentage of married women aged 15–44 who were infertile fell from 8.5% in 1982 to 6.0% in 2006–2010. Among married, nulliparous women aged 35–44, the percentage infertile declined from 44% in 1982 to 27% in 2006–2010, reflecting greater delays in childbearing over this period.
” 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. ”
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.”
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).
Prenatal exposure to DES increases risk of male urogenital abnormalities
DES Follow-up Study Summary
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.
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.
The vast majority of assisted reproductive technologies fail…
” 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. ”
The orphan nuclear receptor small heterodimer partner mediates male infertility induced by diethylstilbestrol in mice
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.