In the US, birthdays peak in early September, but in Northern states — and Scandinavia — the peak comes earlier, in the summer or even spring. Although many factors likely go into the popularity of birthday months (a spike in November is popularly attributed to Valentine’s Day), seasons themselves may play a role in how easy it is to conceive, according to a new Boston University School of Public Health (BUSPH) study.
The first-of-its-kind study, published in the journal Human Reproduction, finds that, although couples in North America and Denmark are most likely to start trying in September, it’s in late November and early December that they have the best chances of conceiving, especially at lower latitudes.
“There are a lot of studies out there that look at seasonal patterns in births, but these studies don’t take into account when couples start trying, how long they take to conceive, or how long their pregnancies last,” says study lead author Dr. Amelia Wesselink, postdoctoral associate in epidemiology at BUSPH. “After accounting for seasonal patterns in when couples start trying to conceive, we found a decline in fecundability in the late spring and a peak in the late fall,” she says. (“Fecundability” refers to the odds of conceiving within one menstrual cycle.) “Interestingly, the association was stronger among couples living at lower latitudes.”
But, after taking those patterns into account, season affected fecundability for North Americans by 16 percent, while Danes got only an 8% seasonal boost in the fall and dip in the spring. In southern U.S. states, the seasonal variation was even stronger, at 45%, with a peak in quick conceptions in late November. Meanwhile, the relationship between season and fecundability turned out to be about the same in Denmark and in northern states and Canada.
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With 855 reviews counted, we at the Reproductive Science Center of New Jersey are proud to report an average rating of 5 out of 5 stars!
We want to thank everyone who took the time to post their reviews of our care and service. And we invite anyone looking for fertility care in the region to see what our patients have said. You can find our reviews on our web page.
Most cells in the tissues of most organisms proliferate through somatic cell division (mitosis). This is a continuous cycle where a single cell doubles its genetic information (chromosomes) and divides equally to create two copies of the original cell. In contrast, egg and sperm cells are produced through a special type of cell division called meiosis, which takes place in the gonads.
This process begins like normal mitosis but switches after some time to create four genetically dissimilar germ cells that have half the original cell’s genetic material. The mechanism that causes this switch has been a longstanding research problem and controlling it is an important, yet challenging, global issue in reproductive medicine.
Recently, a group of researchers from Kumamoto University in Japan set out to assess the proteins involved in meiosis to clarify its development. Using mass spectrometry, the group was able to identify a gene that acts as a meiosis on-switch, labeling it “Meiosin” (for meiosis initiator). The Meiosin gene has the extremely rare property of becoming activated only at a specific time — just before the beginning of meiosis in the gonads.
In animal experiments, the researchers found that both male and female mice became infertile if the Meiosin gene was artificially inhibited. Further analysis of the mouse male and female gonads clarified that the gene plays an essential role in meiosis activation. The Meiosin gene acts as a control tower that simultaneously switches on hundreds of genes for germ cell formation, and appears to be involved with infertility. The group expects that the discovery will be a big step forward for reproductive medicine.
“Our work shows that the Meiosin gene is the switch that turns on meiosis, the special type of cell division that creates eggs and sperm, and this includes the turning-on of hundreds of other genes in the process. However, the functions of those genes have not yet been fully elucidated,” said Associate Professor Kei-Ichiro Ishiguro of the Institute of Molecular Embryology and Genetics at Kumamoto University. “We have high expectations that the processes involved in germ cell formation will be greatly clarified as the role each of these genes plays is discovered. If it eventually becomes possible to control meiosis, the benefits would be far-reaching for reproductive medicine.”
Researchers have lifted fertility rates in older female mice with small doses of a metabolic compound that reverses the aging process in eggs, offering hope for some women struggling to conceive.
The University of Queensland, Australia, study found a non-invasive treatment could maintain or restore the quality and number of eggs and alleviate the biggest barrier to pregnancy for older women.
A team led by UQ’s Professor Hayden Homer found the loss of egg quality through aging was due to lower levels of a particular molecule in cells critical for generating energy. “Quality eggs are essential for pregnancy success because they provide virtually all the building blocks required by an embryo,” Professor Homer said. “We investigated whether the reproductive aging process could be reversed by an oral dose of a ‘precursor’ compound — used by cells to create the molecule.”
The molecule in question is known as NAD (nicotinamide adenine dinucleotide) and the precursor as NMN (nicotinamide mononucleotide). Professor Homer said fertility in mice starts to decline from around one year of age due to defects in egg quality similar to changes observed in human eggs from older women.
“We treated the mice with low doses of NMN in their drinking water over four weeks, and we were able to dramatically restore egg quality and increase live births during a breeding trial,” Professor Homer said.
This study was published in the journal Cell Reports.
There’s more to fertility care than just doctors. Your experience depends on everyone at our clinic, and our staff also receive high praise for their compassionate care. As one patient wrote recently:
“Domenica has been so kind and helpful during our second go at IVF and FET. She emails me right back, answers all my calls and many questions! She goes out of her way to make sure the appointment schedule works best for me.”
You can read more reviews like this, of our physicians and staff, at our web site.
From plastics to pesticides, it seems like every week delivers fresh news about the dangers of endocrine disruptors — chemicals in the environment that alter the body’s hormones and can lead to reproductive, developmental, neurologic and immune problems and cancer. Industry regulation and individual consumer choice can reduce exposure to such chemicals, but there are few options to counteract damage that has already occurred.
Now new research conducted in worms suggests a path toward changing that. A naturally occurring antioxidant known as Coenzyme Q10, or CoQ10, reversed most of the reproductive harms caused by exposure to the plasticizer BPA (bisphenol A) in Caenorhabditis elegans worms, according to a study led by the lab of Monica Colaiácovo, professor of genetics in the Blavatnik Institute at Harvard Medical School.
The findings, published in Genetics, provide the first evidence that at least some BPA-induced fertility damage can be undone.
Nevertheless, humans are not big worms, and people should not rush out and start taking CoQ10 as an anti-BPA agent without consulting a doctor, the study authors said. For one thing, the researchers used “very pure,” quality controlled CoQ10, while store-bought supplements vary in CoQ10 content and do not always contain the amounts stated on labels, previous analyses have found.
For the authors, though, the findings offer a glimmer of hope amid a flood of concerning findings. “When we uncover evidence of toxicity from yet another chemical, often there is a feeling of ‘Here we go again,'” said Colaiácovo. “But it’s important to see what we can learn from it. I want us to figure out solutions.”
Black History Month, each February, raises awareness of issues important to African Americans. One of those issues you may not know about is infertility.
A 2019 study in Conception and Reproductive Medicine reports that African American (AA) women are disproportionately affected by infertility in terms of prevalence, utilization of treatment and access to care. Even after adjusting for socioeconomic status, risk factors and pregnancy intent, a US population-based study showed that AA women ages 33–44 years are still two times more likely to experience infertility in comparison to Caucasian American (CA) women. And statistical trends have shown that infertility rates were increasing among AA women while simultaneously decreasing among CA women.
This racial disparity persists when it comes to pursuit of infertility care and success rates of Assisted Reproductive Technology (ART). “It is well documented in the literature that AA women usually have a longer duration of infertility before seeking care and they also pursue medical care for infertility significantly less often than CA women,” the study says.
Why not use Black History Month as a prompt to take care of your fertility health? If you are struggling with getting pregnant, give us a call. Our first phone consultation is free.
Infertility likely stems from age-related decline of the ovaries, but the molecular mechanisms that lead to this decline have been unclear. Now, scientists have discovered, in unprecedented detail, how ovaries age in non-human primates. The findings, published in Cell, reveal several genes that could be used as biomarkers and point to therapeutic targets for diagnosing and treating female infertility and age-associated ovarian diseases, such as ovarian cancer, in humans.
“This is the first in-depth analysis of ovarian aging at a single-cell resolution in a non-human primate model,” says Juan Carlos Izpisua Belmonte, one of the co-corresponding authors, professor in Salk’s Gene Expression Laboratory and holder of the Roger Guillemin Chair. “We found that oxidative stress, the cellular stress that damages cells, is a key player in ovarian aging. This discovery provides valuable insight into the mechanisms by which ovaries age and eventually become infertile.”
The scientists compared 2,601 ovarian cells from young and old non-human primates, and identified gene activity patterns for every type of primate ovarian cell including ooctyes and granulosa cells, which surround the oocytes as they develop. The scientists then compared the primate data with granulosa cells from healthy women ranging in age from 21 to 46 years.
Two key antioxidant genes (IDH1 and NDUFB10) showed decreased function, as seen in the non-human primate cells. To better understand the connection between ovarian aging and the antioxidant genes, the scientists tested what happened to the human cells when the antioxidant genes were made non-functional. They found that without IDH1 or NDUFB10, the cells appeared old and similar to the old non-human primate cells. The results suggest that IDH1 and NDUFB10 play a critical role in protecting both human and non-human primate ovarian cells from cellular stress during aging.
“This study provides a comprehensive understanding of the specific mechanisms of primate ovarian aging at single-cell resolution,” says Guang-Hui Liu, co-corresponding author, professor at the Chinese Academy of Sciences and former Salk research associate. “Our results will hopefully lead to the development of new tools to aid in the rejuvenation of aged ovarian cells.”
At least one in five cases of infertility remains unexplained. Male factors contribute to about half of these cases and, much of the time, men lack a specific causal diagnosis for their infertility. Researchers estimate that genetics could explain up to 50 percent of these cases, but many of the genes involved in male infertility remain unknown. A new study led by investigators at Brigham and Women’s Hospital identifies a genetic abnormality that may be at fault.
Investigators have found that a genetic rearrangement and variants affecting a gene known as SYCP2 are associated with low sperm count and report the first cases implicating the gene in four men with infertility. The team’s findings are published in the American Journal of Human Genetics.
We hope that our evidence will contribute to this gene being in panels for diagnosis of male infertility,” said corresponding author Cynthia Morton, PhD, medical geneticist at the Brigham. “Infertility is a big problem for young people, and 40 to 72 percent of men lack a diagnosis. This means that we have a lot of gene finding to do.”
Morton notes that while the discoveries about SYCP2 may help inform diagnosis, implications for treatment remain to be determined. “A diagnosis can be therapeutic in itself — even if there isn’t something that can be done to correct it. It ends the search for the underlying issue and opens the door for enrolling in clinical trials,” she said. “And I believe there is good reason to be optimistic; we now have better tools for discovery and can begin on the path toward therapy.”
William Ziegler, DO, FACOG
Alan Martinez, MD