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Pregnant Women Recognize Baby Expressions Differently Depending On Mental Health History

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A pilot study has found that pregnant women who have suffered from depression or bipolar disorder (i.e. both mania and depression) recognise babies’ faces and how babies laugh or cry, differently to healthy controls. This happens even if they are not currently experiencing depressive or manic symptoms and may represent an early risk-factor for children of these women, although the authors stress that research would be needed to confirm any long-term effects. This work is presented at the ECNP Congress in Barcelona.

Figures show that nearly 8% of Europeans (EU) have suffered from depression in the previous 12 months, with the rate of depression in women (9.7%) being around 50% higher than the rate in men. Around 1% of Europeans have suffered from bipolar disorder in the previous 12 months. With over 5.1 million births in the EU every year, a significant number of the women who become pregnant will suffer from depression or bipolar disorder.

Researchers compared 22 pregnant women, currently well but with a history of depression, and 7 with bipolar disorder who were also currently well, against 28 healthy pregnant women. They also tested 18 non-pregnant women, as controls.

Between the 27th and 39th weeks of pregnancy, all the women were tested for how they responded to a series of happy or sad faces, and to laughter and crying, of both babies and adults. Specifically, the women were asked to rate how happy or distressed the infants were based on infants’ facial and vocal displays of emotion (including smiles, laughter and cries). They were also asked to identify adult facial expressions of emotion (including happiness, sadness, fear and disgust) across varying intensity levels

According to lead researcher, Dr Anne Bjertrup (Rigshospitalet, Copenhagen), “In this study, we found that pregnant women with depression or bipolar disorder process infants’ facial and vocal signals of emotion differently even when they are not currently experiencing a depressive or manic episode. These differences may impair these women’s ability to recognise, interpret and respond appropriately to their future infants’ emotional signals.”

The researchers found that, compared to healthy pregnant women:

  • Pregnant women with bipolar disorder had difficulty with recognising all facial expressions and showed a “positive face processing bias,” where they showed better recognition of happy adult faces and more positive ratings of happy infant faces.
  • In contrast, pregnant women with previous depression showed a negative bias in the recognition of adult facial expressions and rated infant cries more negatively.

Anne Bjertrup continued:

“This is a pilot study, so we need to replicate the findings within a larger sample. We know that depression and bipolar disorder are highly heritable, with up to 60% of children of parents with these affective disorders more likely to develop a mental disorder themselves. Genes play a role, but it is also likely that the quality of the early interaction with the mother is important. The different cognitive response to emotional infant signals in pregnant women with a history of mania and/or depression may make it more difficult for them to relate to their child and could thus confer an early environmental risk for the child.

It’s worth emphasizing that this work does not say that the affected women are “bad mothers.” It simply means that because of their health history, they may experience difficulties interpreting and responding appropriately to their infants’ emotional needs and that we as clinicians need to be more aware of these possible difficulties. These are early days; this is the first research to show this link in both depression and bipolar disorder, so we need further studies to design and test early screening and intervention programs possibly involving ways which will train mothers to interpret the signals from their children better.

But above all, we need evidence of any effect on children; our group have an ongoing study of mothers with affective disorders and their infants, to see if what we have found does indeed make a difference to the mother-infant interaction, which has an impact on the child’s psychological development — this is something the work presented here does not address.”

Commenting, Professor Eduard Vieta (Institute of Neuroscience, University of Barcelona) said:

“This study adds to the growing scientific literature showing emotional bias in people with mood disorders, even when they are in remission, and for the first time shows the difficulties mothers have in identifying emotions in their own newborns. The results, however, do not imply at all that women with such conditions would not be able to raise a child properly and it does not prove any risk for their children since longitudinal data are lacking. This work may help us identify targets for pharmacological and psychological treatments, which in turn may help people with depression and bipolar disorder.”

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Paternal Transmission Of Epigenetic Memory Via Sperm

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Studies of human populations and animal models suggest that a father’s experiences such as diet or environmental stress can influence the health and development of his descendants. How these effects are transmitted across generations, however, remains mysterious.

Susan Strome’s lab at UC Santa Cruz has been making steady progress in unraveling the mechanisms behind this phenomenon, using a tiny roundworm called Caenorhabditis elegans to show how marks on chromosomes that affect gene expression, called “epigenetic” marks, can be transmitted from parents to offspring. Her team’s most recent paper, published October 17 in Nature Communications, focuses on transmission of epigenetic marks by C. elegans sperm.

In addition to documenting the transmission of epigenetic memory by sperm, the new study shows that the epigenetic information delivered by sperm to the embryo is both necessary and sufficient to guide proper development of germ cells in the offspring (germ cells give rise to eggs and sperm).

“We decided to look at C. elegans because it is such a good model for asking epigenetic questions using powerful genetic approaches,” said Strome, a distinguished professor of molecular, cell, and developmental biology.

Epigenetic changes do not alter the DNA sequences of genes, but instead involve chemical modifications to either the DNA itself or the histone proteins with which DNA is packaged in the chromosomes. These modifications influence gene expression, turning genes on or off in different cells and at different stages of development. The idea that epigenetic modifications can cause changes in gene expression that are transmitted from one generation to the next, known as “transgenerational epigenetic inheritance,” is now the focus of intense scientific investigation.

For many years, it was thought that sperm do not retain any histone packaging and therefore could not transmit histone-based epigenetic information to offspring. Recent studies, however, have shown that about 10 percent of histone packaging is retained in both human and mouse sperm.

“Furthermore, where the chromosomes retain histone packaging of DNA is in developmentally important regions, so those findings raised awareness of the possibility that sperm may transmit important epigenetic information to embryos,” Strome said.

When her lab looked at C. elegans sperm, they found the sperm genome fully retains histone packaging. Other researchers had found the same is true for another commonly studied organism, the zebrafish.

“Like zebrafish, worms represent an extreme form of histone retention by sperm, which makes them a great system to see if this packaging really matters,” Strome said.

Her lab focused on a particular epigenetic mark (designated H3K27me3) that has been well established as a mark of repressed gene expression in a wide range of organisms. The researchers found that removing this mark from sperm chromosomes causes the majority of the offspring to be sterile. Having established that the mark is important, they wanted to see if it is sufficient to guide normal germline development.

The researchers addressed this by analyzing a mutant worm in which the chromosomes from sperm and egg are separated in the first cell division after fertilization, so that one cell of the embryo inherits only sperm chromosomes and the other cell inherits only egg chromosomes (normally, each cell of an embryo inherits chromosomes from both egg and sperm). This unusual chromosome segregation pattern allowed the researchers to generate worms whose germ line inherited only sperm chromosomes and therefore only sperm epigenetic marks. Those worms turned out to be fertile and to have normal gene expression patterns.

“These findings show that the DNA packaging in sperm is important, because offspring that did not inherit normal sperm epigenetic marks were sterile, and it is sufficient for normal germline development,” Strome said.

While the study shows that epigenetic information transmitted by sperm is important for normal development, it does not directly address how the life experience of a father can affect the health of his descendants. Strome’s lab is investigating this question with experiments in which worms are treated with alcohol or starved before reproducing.

“The goal is to analyze how the chromatin packaging changes in the parent,” she said.

“Whatever gets passed on to the offspring has to go through the germ cells. We want to know which cells experience the environmental factors, how they transmit that information to the germ cells, what changes in the germ cells, and how that impacts the offspring.”

By demonstrating the importance of epigenetic information carried by sperm, the current study establishes that if the environment experienced by the father changes the epigenetics of sperm chromosomes, it could affect the offspring.

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Father’s Nicotine Use Can Cause Cognitive Problems In Children And Grandchildren

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A father’s exposure to nicotine may cause cognitive deficits in his children and even grandchildren, according to a study in mice publishing on October 16 in the open-access journal PLOS Biology by Pradeep Bhide of Florida State University in Tallahassee and colleagues. The effect, which was not caused by direct secondhand exposure, may be due to epigenetic changes in key genes in the father’s sperm.

Exposure of mothers to nicotine and other components of cigarette smoke is recognized as a significant risk factor for behavioral disorders, including attention deficit hyperactivity disorder, (or ADHD) in multiple generations of descendants. Whether the same applies to fathers has been less clear, in part because in human studies it has been difficult to separate genetic factors (such as a genetic predisposition to ADHD) from environmental factors, such as direct exposure to cigarette smoke.

To overcome this difficulty, Deirdre McCarthy, Pradeep Bhide and colleagues exposed male mice to low-dose nicotine in their drinking water during the stage of life in which the mice produce sperm. They then bred these mice with females that had never been exposed to nicotine. While the fathers were behaviorally normal, both sexes of offspring displayed hyperactivity, attention deficit, and cognitive inflexibility. When female (but not male) mice from this generation were bred with nicotine-naïve mates, male offspring displayed fewer, but still significant, deficits in cognitive flexibility. Analysis of spermatozoa from the original nicotine-exposed males indicated that promoter regions of multiple genes had been epigenetically modified, including the dopamine D2 gene, critical for brain development and learning, suggesting that these modifications likely contributed to the cognitive deficits in the descendants.

Nicotine and cigarette smoke have been previously shown to cause widespread epigenetic changes, Bhide said.

“The fact that men smoke more than women makes the effects in males especially important from a public health perspective. Our findings underscore the need for more research on the effects of smoking by the father, rather than just the mother, on the health of their children.”

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Nutrition Has A Greater Impact On Bone Strength Than Exercise

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ANN ARBOR—One question that scientists and fitness experts alike would love to answer is whether exercise or nutrition has a bigger positive impact on bone strength. University of Michigan researchers looked at mineral supplementation and exercise in mice, and found surprising results–nutrition has a greater impact on bone mass and strength than exercise. Further, even after the exercise training stopped, the mice retained bone strength gains as long as they ate a mineral-supplemented diet.

“The longer-term mineral-supplemented diet leads to not only increases in bone mass and strength, but the ability to maintain those increases even after detraining,” said David Kohn, a U-M professor in the schools of dentistry and engineering.

“This was done in mice, but if you think about the progression to humans, diet is easier for someone to carry on as they get older and stop exercising, rather than the continuation of exercise itself.”

The second important finding is that the diet alone has beneficial effects on bone, even without exercising. This surprised Kohn, who expected exercise with a normal diet to fuel greater gains in bone strength, but that wasn’t the case.

“The data suggests the long-term consumption of the mineral-supplemented diet could be beneficial in preventing the loss of bone and strength with age, even if you don’t do exercise training,” he said.

Combining the two amplifies the effect.

Most other studies look at effects of increasing dietary calcium, Kohn said. The U-M study increased calcium and phosphorous, and found benefits to increasing both.

This isn’t to suggest that people run out and buy calcium and phosphorus supplements, Kohn said. The findings don’t translate directly from mice to humans, but they do give researchers a conceptual place to start.

It’s known that humans achieve peak bone mass in their early 20s, and after that it declines. The question becomes how to maximize the amount of bone when young, so that when declines do begin, people start from a better position, Kohn said.

In addition to testing bone mass and strength, Kohn and colleagues performed a full battery of mechanical assessments on the bone, which is important because the amount of bone doesn’t always scale with or predict the mechanical quality of the tissue.

They tested the mice after eight weeks of training and supplemented diet or normal diet, and then after eight weeks of detraining.

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