In the past few days, a great deal of media attention has been paid to Leanne Rowe, a Tasmanian woman who has lived eight years with a French accent she acquired after a car accident. This phenomenon is known as foreign accent syndrome, a rare disorder that usually arises after brain damage as a result of, for example, stroke or head injury.

Foreign accent syndrome has always been the source of much media interest and the stories often sound sensational. There has been, for example, an American who spoke with a British accent, a British Yorkshireman with an Irish accent and another British man with a Russian accent.

More spectacular are tales of people waking from strokes or comas speaking fluently in languages they hardly knew before. While there is no scientific verification of cases of speaking a new language, speaking with a foreign accent is well documented, as shown in the video below.

This is not just an English phenomenon – one of the first cases was of a Norwegian woman who suffered brain damage as the result of being hit by bomb shrapnel during an air raid in World War II. She acquired a German accent and was subsequently shunned by friends and neighbours who thought she was a German spy.

It is obvious how in this case the change of accent can have distressing consequences. But even in less extreme cases, the change in perceived identity can be hard to cope with, as Ms Rowe reports. However, better understanding of the cause of the problem often helps the sufferer and those around them.

What causes foreign accent syndrome?

Foreign accent syndrome is caused by brain damage which impairs the control of the muscles used to produce speech.

Speaking requires very precise control of the muscles of lips, tongue and jaw (the speech articulators) and the larynx (voicebox). If the placement of the articulators, speed or coordination of movements are slightly out of sync, then speech sounds will be altered. For example, when people are drunk the effects of alcohol on muscle control and coordination causes distortion of the speech sounds and leads to the perception of slurring.

Vowels are particularly susceptible: which vowel you say depends on where your tongue is in your mouth. Slight differences in where your tongue is – how far forward or back, how high or low in your mouth – changes the vowel you produce. Different languages have different vowels and within a language one of the main differences between accents is in the vowels. Aussies accuse Kiwis of saying “fush and chups” and Kiwis of Aussies “feesh and cheeps”!

Research has shown people with foreign accent syndrome nearly always have trouble producing vowels. Brain damage affects their ability to control their tongue movements. There may be too much or too little muscle tension and therefore they may “undershoot” or “overshoot” their target. This leads to the vowels sounding different, and sometimes they may sound like a different accent.

Another commonly reported feature of foreign accent syndrome is a problem with the stress pattern of words and rhythm and intonation of sentences (prosody). People with foreign accent syndrome may speak slowly, separate out syllables and say each one with equal stress – for example, “banana” as “bar-nar-nar” rather than “buhNARnuh”.

So, the problems with muscle movement and coordination cause in changes to the way the speech sounds. When the new speech sounds are similar to those of an existing accent, the speaker can be perceived to be speaking with a foreign accent. People with foreign accent syndrome don’t speak with all the features of a foreign accent, but there are enough things about the way they speak to make it seem as though they have a different accent.

In this case, why French?

Leanne Rowe describes herself as speaking with a French accent, and there have been other speakers with foreign accent syndrome also described as having a French accent. However, when these cases have been studied in more detail interesting observations arise.

One set of researchers found that for an English woman with a French accent the changes to her speech were not in fact only those associated with French speakers of English – there were changes that were typical of many different accents. Another study asked people to decide what accent they thought a person with foreign accent syndrome had: a quarter said French, a quarter African and others Italian, Chinese, Spanish, German, Welsh and more!

It seems then that there are features in the speech of people with foreign accent syndrome that remind listeners of other accents. There is evidence that once a listener has formed an impression of which accent it may be, then other features of the person’s speech which don’t fit with that accent will be ignored.

Which accent a listener thinks someone has may depend as much on their experience as the features of the speech itself. This is why many people with foreign accent syndrome are not described as having a single accent.

In essence, the strategies that people use to try to overcome their problems with muscle coordination and movement result in speech changes that overlap in some ways with those of non-native speakers. For Ms Rowe, some of those features are similar to those of French speakers of English. So even though it might sounds like Ms Rowe spent years in France, her acquired accent is an accident, produced by problems with movement and coordination of her lips, tongue and larynx.

References:
David Stehling (2009). Foreign Accent Syndrome (FAS): The Speech Characteristics of Foreign Accent Syndrome Grin

Dio, C., Schulz, J., & Gurd, J. (2006). Foreign Accent Syndrome: In the ear of the beholder? Aphasiology, 20 (9), 951-962 DOI: 10.1080/02687030600739356

This article was originally published at The Conversation, by Lyndsey Nickels

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Preliminary studies of a research carried out by the University of Melbourne on 500 Australian minors confirm: member of same-sex families are closer to one another –the research suggests- since they have to face attacks that come from society, digest them and give them an explanation.

They live with two mums or two dads, and they are on the same level as their school friends regarding self-esteem, emotional behavior and time spent with their parents. But they seem to have the edge over the average regarding overall health and familiar cohesion. Kids that grow with homosexual couples grow up as good as in traditional families, and even better in some aspects. This seems to be confirmed by a study conducted by a group of researchers of the University of Melbourne on 500 minors living in Australia: member of same-sex families are closer to one another –the research suggests- since they have to face attacks that come from society, digest them and give them an explanation.

The Australian Study of Child Health in Same-Sex Families is the widest research that has been conducted on this theme in the world. It started in 2012, it will end in 2014 and it involves 500 minors aged between 2 months and 17 years old, and 315 parents (80% women, 18% men, and 2% of other gender) among gays, lesbians, bisexuals and queers that have completed an online Child Health Questionnaire recognized by the international scientific community. The aim is to measure the physical, psychological and social wealth of those kids who grow in this environment: according to the Australian Bureau of Statistics, in 2011 in Australia there were 33 thousands homosexual couples living together with 6120 sons aged under 25.

Among the objectives of the research there is also that of “studying the role of discrimination” on the basis of their developments. Five indicators have been used: self-esteem, emotionality, time spent with parents, health and familiar cohesion. The first results suggest that “that these children are doing well in many aspects of their lives, however they are often affected by the discrimination that their families may experience due to parental sexual orientation”. This may explain why, compared to their peers, they score higher points, regarding health and familiar cohesion.

According to the research, the way in which same-sex families have to face homophobic phenomena would have an impact on how their members relate to one another. “Because of the situation in which they live- Dr. Simon Crunch, responsible for the project, explains- these kids tends to communicate more and they are more willing to face with their relatives topics such as bullying”. The research is also about the relation between the general wealth of the children and the discriminations that families may overcome at school, in hospitals and through the media. “A discrimination that can vary from uninformed comments to teasing, from bullying to overt homophobia, up to rejection”, Dr. Crunch says. The way these attacks are metabolized in the family would have positive effects: discussion on these topics “develops openness  and makes kids stronger”. On the other hand, this is a probable objection, this factor could then become an element of self-exclusion or partial isolationism of social life.

In Australia gay marriage is not legal (in 2012 the parliament voted against and the topic will not be touched before next elections in fall), but the law recognizes civil partnerships between same-sex couples as well as traditional couples.  Moreover, rights are granted to lesbian co-mothers in the same manner as to parents of sons born with an in vitro fecundation or artificial insemination. Kate and Susan live together with their sons Hannah (8 years old), Xavier (6) and Anouk (5), conceived with the semen of the same donor. “We talk about everything- Kate (39) tells the newspaper The Age – from the way in which babies are conceived to the different relationships that human beings may have. Our sons are very open to diversity”.

There is a wide range of scientific literature regarding the topic. According to the Australian researchers, there are 40 relevant studies that have been conducted between January 1990 and March 2011. The last influential pronouncement in favor was made on March 21^st: that day the American Academy of Pediatrics, that represents 99% of the pediatricians currently active in the United States, gave their consent to homoparental families. In the document Promoting the Well-Being of Children Whose Parents Are Gay or Lesbian, the 60 thousands members of the Academy voted in unanimity in favor both for “civil wedding for same-sex couples” and for “full adoption and rights of Custody, independently of the sexual orientation”.

References
Crouch SR, Waters E, McNair R, Power J, & Davis E (2012). ACHESS–The Australian study of child health in same-sex families: background research, design and methodology. BMC public health, 12 PMID: 22888859

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Gene therapy’s had a bad reputation over the years, but some gene-based treatments have been successful. One type of therapy, for degeneration of the retina, has been somewhere in the middle: Injecting a gene directly into the retina that can aid against eye disease. This procedure requires a hospital stay and general anesthesia, and can often damage the retina itself (thus defeating the point of the therapy).

But other eye drugs are often delivered into the eye’s vitreous humor (the fluid inside the eyeball), which is a much safer procedure that can be conducted in a doctor’s office. So, what if the gene for retinal degeneration could be delivered that way?

The problem was that the virus that usually delivers to the gene to its destination, called an Adeno-associated virus or AAV, was never very good at puncturing through dense tissues like the retina. It works fine for thin lung tissue, or even other areas, but not the retina. So, researchers at the University of California, Berkeley, started looking for versions of AAV that could penetrate into the retina.

And as they reported in Science Translational Medicine, they found those versions. Testing several types of AAV on mice, a tiny percentage made their way into mouse retinas. By collecting those versions and amplifying the growth of them in the lab, they finally isolated about 48 AAV variants for genetic sequencing (up to now, by the way, is now traditionally breeding for traits is done). Two thirds of those variants, it turns out, were the same. Now, thanks to what they called “directed evolution,” the scientists had their viral delivery system for retinal gene therapy.

The scientists still don’t know how or why these variants work better at penetrating the retina. Perhaps the gene sequencing studies will provide clues.

Sources: The Scientist

Dalkara, D., Byrne, L., Klimczak, R., Visel, M., Yin, L., Merigan, W., Flannery, J., & Schaffer, D. (2013). In Vivo-Directed Evolution of a New Adeno-Associated Virus for Therapeutic Outer Retinal Gene Delivery from the Vitreous Science Translational Medicine, 5 (189), 189-189 DOI: 10.1126/scitranslmed.3005708

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A violent attack by someone who is mentally ill quickly grabs the headlines. And it’s usually implied that mental illnesses are a preventable cause of violent crime. Tackle that and we can all sleep safer in our beds. But by pressuring mental health services to focus on the risk of violence we are in danger of actually increasing it.

Most of the debate around risk and offending has centred around schizophrenia – the bread and butter of community psychiatry. But what is the evidence relating to the risk of violence in those diagnosed with schizophrenia? It’s tricky because schizophrenia varies so much in character and severity. And other factors known to have an association with violent crime, like migration and social disadvantage, are often also implicated as a part of the cause or consequence of schizophrenia.

To assess the risk of someone with schizophrenia attacking others, we’re basically trying to work out the risk of a rare event happening in a bunch of people with a mixed bag of symptoms with the “schizophrenia” label – and with multiple other factors confounding and perpetuating the issue. No wonder it’s nigh on impossible to work out the risk from just the schizophrenia.

Other factors in play

Researchers put different emphasis on the importance of these other factors. This might explain the wide variation in the figures for how much more likely violence is in someone with schizophrenia. The largest study to date, conducted in Sweden, compared more than 8000 people with schizophrenia with control groups using hospital and criminal records. They found that much of the increased rate of violence in those with schizophrenia was confined to those who also abused drugs.

Controlling for other factors, those with a diagnosis of schizophrenia who did not abuse drugs were only 1.2 times more likely to have committed at least one violent offence than control subjects. But even for those with a diagnosis of schizophrenia who did abuse drugs, the comparison lessened when the researchers considered early environment and genetics – they were only 1.8 times more likely to have committed at least one violent crime than their siblings (who didn’t have schizophrenia).

But a recent Australian study showed that people with schizophrenia – even without substance abuse – were twice as likely as control subjects to have a violent conviction.
 Most researchers recognise that there is an increase in violent offending in those diagnosed with schizophrenia. But the studies don’t tell us how much violent offending is actually caused by the mental disorder itself.

And we tend to forget about how uncommon it is to have these kinds of incidents (though shouty headlines can make us think otherwise). Even if it could be proved that the disorder actually caused an increased rate of violence, completely taking all of those with major mental disorders out of society would only reduce violent crime by about 5%) – less than for drugs and alcohol.

Is our obsession with risk making it worse?

So what worries me is the interpretation and outcomes of these findings and their adoption into policy, legislation and clinical practice.

The real danger here is that the focus is on risk, and decisions based only on that risk at the expense of the illness itself, could even increase that risk. The main problem is that we’re not actually very good at predicting violent events. This isn’t because mental health professionals are rubbish but mainly because they’re so rare in the populations we’re looking at.

A concept that just doesn’t seem to be that well understood, even among doctors, is that the predictive ability of any risk assessment depends on the rate of the event in the population we’re looking at. The lower the rate, the less able the assessment is to correctly predict it. If something happened frequently, it would be easier to predict.

Although the rate of violence may be slightly higher in those with schizophrenia than Jo Public the absolute rate of violence in those who suffer from schizophrenia is still very low – too low to predict with any accuracy.

Our worst fear?

Let’s look at the worst case scenario – murder.

If we use the MacArthur instrument – one of the well evaluated tools for measuring the risk of violence – to classify people as a high or low-risk of committing murder then, as Australian psychiatrist Christopher Ryan put it: “4117 patients would have to be detained or otherwise managed for a year in a homicide-proof fashion to try to prevent just one of those patients committing a homicide. And yet one in every 22,421 patients assessed to be ‘low-risk’ would commit a homicide in that period.”

Most people who suffer from schizophrenia would correctly be classified as low risk. Because of this, they would have resources diverted away from them despite suffering from a debilitating but treatable condition. And a very few of those classified as low risk would actually go on to commit a violent offence.

We currently have different legislation for those with mental health problems. It is hard to imagine any other group of people being subject to different laws based on a higher statistical rate of violence. Men are more likely to be violent than women but aren’t subject to legislation that allows us to more easily detain them against their will.

Not that we should just shrug our shoulders and say that risk just isn’t our thing. A comprehensive assessment that includes a risk component should allow people to make informed decisions about their treatment, based on their capacity to do so ([which, incidentally, is something we are good at assessing]). Decisions should rely on the characteristics of the illness and evidence for treatment, not just the enforcement of short-term and inadequate interventions as a nod to risk at the expense of treating the illness itself.

We know there is a higher rate of violence in those who’ve developed schizophrenia before they even seek help from services. I’m pretty sure that if I was suffering from schizophrenia I would be more likely to go to services that offered help for my illness rather than those seen as punitive and risk-obsessed. Sadly, the over-emphasis on risk of violence is a grave disservice to many suffering from a debilitating but treatable illness.

Reference:
Fazel, S. (2009). Schizophrenia, Substance Abuse, and Violent Crime JAMA: The Journal of the American Medical Association, 301 (19) DOI: 10.1001/jama.2009.675

Short, T., Thomas, S., Mullen, P., & Ogloff, J. (2013). Comparing violence in schizophrenia patients with and without comorbid substance-use disorders to community controls Acta Psychiatrica Scandinavica DOI: 10.1111/acps.12066

This article was originally published at  The Conversation, by Rebecca Syed

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Pesticide levels considered environmentally friendly in Europe and Australia are, in fact, having a devastating effect on invertebrate insect biodiversity in nearby creeks and streams, a new study has found, showing the need for an urgent overhaul of the way pesticide risk is assessed. Water-dwelling invertebrates like worms, snails, crustaceans, mites and insects play a crucial role in regional ecosystems because they provide food for fish, birds and platypuses.

The study, published in Proceedings of the National Academy of Sciences (PNAS), found that invertebrate biodiversity, mostly insects, was slashed by up to 42% in the streams studied. The international research team, which included scientists from the University of Technology, Sydney, examined data on levels of pesticide toxicity in 48 and 24 sampling sites in Europe and Southern Victoria respectively.

The researchers selected creaks and streams that were close to crops of grape vines, orchards, berries, vegetables, corn, sugar beet or oil-seed. The sites selected had no wastewater treatment plants, industrial facilities, or mining drainage upstream, allowing the researchers to rule out the possibility that pollution was from non-agricultural sources.

“Current use pesticides in southern Victoria and regions in Germany and France is reducing the number of different types of animals without backbones, or invertebrates, living in streams and rivers. The animals most affected were mayflies, stoneflies, caddisflies and dragon flies,” said ecotoxicologist and aquatic ecologist from the University of Technoligy, Sydney, Dr Ben Kefford, who co-authored the paper. “Importantly, the reduction in the number of different types of invertebrates occurred at the regional scale.”

Pesticide regulation

The findings also show that pesticide regulation in Australia and Europe may be flawed. Pesticide regulation is intended to prevent threats to biodiversity or collateral elimination of insects that are not pests. “The regulation in both these continents is probably failing because they are both based on determining the effect of pesticides in the laboratory […] without studying the effects pesticides have in real streams and rivers,” Dr Kefford said.

Dr Jon Brodie, Senior Principal Research Officer at James Cook University, who was not involved in the study, said the findings did not surprise him. “We already know the current pesticide regulatory regime in Australia, at least, is not up to the mark for protecting aquatic biodiversity.”

Dr Brodie said that the results highlight a need for better pesticide use evaluation.  “The results could be used to show the inadequacy of the current protection regime and to improve it by doing more sophisticated analysis and addressing the cumulative nature of pesticide exposure,” he said.

Crop protection

Dr Richard Roush, Dean of Melbourne School of Land and Environment at the University of Melbourne, said the new findings were unsurprising. “I don’t think this paper makes a particularly strong case that the risk assessment needs to be across regional scales. To be used in practice, the new standards and methods in risk assessment do need to measure risk at biologically relevant concentrations and identify the specific pesticides that need to be better regulated, which are likely to be the insecticides rather than some of the other pesticides listed,” said Dr Roush, who was not involved in the study. “Before this is somewhat underway, the immediate implications for aquatic biodiversity are limited, because there is still huge demand for crop protection.”

However, Dr Kefford, who co-authored the paper, said that while pesticides were often regulated at a national level, the risk is mostly assessed by its effect on individual organisms rather than on real ecosystems. “Indeed, if pesticides kills some aquatic invertebrates it is not a major environmental problem but it is if it reduces biodiversity across a region,” he said.

“What is undeniable is the need for regulation to consider the effects of pesticides in real ecosystems and not be confined to effects in the laboratory and semi-natural ecosystems.”

This  article was originally published at The Conversation, by Michelle See-Tho

References:
Beketov, M., Kefford, B., Schafer, R., & Liess, M. (2013). Pesticides reduce regional biodiversity of stream invertebrates Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1305618110

Archaeopteryx’s claim to fame is that of the first true bird in the fossil record. It was the first dinosaur known to be able to fly, and it lived during the Jurassic, roughly 150 million years ago. It also helps to link birds to the dinosaur line itself, more specifically to a family of dinosaurs called Theropods (Greek for ‘beast-like foot’, due to their feet looking like the feet of predators).

First feathers
It begins in 1999, from China, with the discovery of Sinornithosaurus , a member of the Dromaeosaur line of theropod dinosaurs –  better known to most people as Raptors (after Velociraptor).

Since then, a bunch of other, new, raptor fossils have popped up also showing evidence of having borne feathers. Most notably Microraptor and Velociraptor. Though not all raptor species have been proven to have worn a coat of feathers, many of the raptors found so far that were originally thought to be without feathers have now been shown otherwise. Thus, it is now speculated by palaeontologists that the entire raptor line could have been feathered, including the big-and-bad Utahraptor .

But wait, it gets even fluffier…

In 2009, a feathered theropod named Anchiornis was found in China. Anatomy places the little guy in the same line as Troodon, another theropod originally thought not to possess feathers.

Fun fact: Troodon (pictured on the right) has been called the smartest of the dinosaurs, with an intelligence thought to equal that of your common chicken.

While it’s still not proven yet whether Troodon itself possessed feathers, it is in the same line as Anchiornis, and so some palaeontologists also depict Troodon with feathers.

Now for the grand finale:
Two other dinosaur fossils were found in China that belonged to a rather infamous line of theropods.

They are Dilong  and Guanlong , and both of them were feathered precursors to… Tyrannosaurus Rex.

Think about that for a moment: T-rex, with feathers.

No need for T-rex to worry yet, as no such feathery evidence has thus far been found. However, as with the raptor and troodon lines, the tyrannosaur line is populated with feathered, Jurassic ancestors to the more well-known, Cretaceous descendants. Palaeontologists, nonetheless, now think that it was likely that Tyrannosaurus young were feathered, with those feathers being lost as they grew into adulthood.

No need for dinosaurs in general to worry yet, either, as all the current feathered finds are of theropods only. I’m sure some people can rest easier on that fact.

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Justin Beckerman, an 18-year-old student and inventor from New Jersey, has made a submarine that can dive to 30 feet below the water’s surface. Check out this video to see how it did it, and how the submersible works.

Source: NJ.com, JustinBeckerman.com

Photo: JustinBeckerman.com

Antelope Canyon, Arizona, U.S.

Cappadocia, Anatolia, Turkey

‘Door to Hell’ , Derweze, Turkmenistan

Dragon’s blood trees, Socotra, Yemen

Giant Buddha, Leshan, China

Grand Prismatic Spring, Yellowstone National Park, U.S.

Hitachi Seaside Park, Hitachinaka, Japan

Odle Mountains, Italy

Red beach, Panjin, China

Rice terraces, Bali, Indonesia

Salar de Uyuni, Bolivia

The Wave, Arizona, U.S.

Sossusvlei, Namibia

Travertines, Pamukkale, Turkey

Tunnel of Love, Klevan, Ukraine

Giant’s Causeway, Antrim, Northern Ireland, U.K.

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For half the population, it comes three to five days each month, 12 months each year, for 40 years of our lives. Menstruation can be debilitating, relieving, disappointing, or simply an inconvenient fact of life.

But why do humans menstruate, when most animals don’t? When you shake the tree of life, you find that only a handful of mammals aside from us – primates, a small number of bat species, and the elephant shrew – have opted for the monthly bleed.

Each month the uterus prepares a thick and luxurious lining in preparation for the arrival of a fertilised egg – an embryo that will develop into a fetus and after nine months, a full-term baby. If no embryo arrives, there will be no pregnancy and menstruation sheds the thickened lining.

Evolution is often viewed in terms of a cost-benefit ledger: if something is costly, it must have some benefit. Women lose over half a standard glass of wine’s worth in iron-rich blood and tissue – about 90 millilitres – each time they menstruate, so the process does seem quite costly. And in the predator-filled environs of our early ancestors, leaving a trail of blood was presumably not advantageous.

So how did menstruation arise? Over recent decades, evolutionary biologists have come up with three key theories to explain human menstruation.

Cleansing mechanism

One controversial theory, proposed in the 1990s by self-taught biologist Margie Profet, suggested menstruation was a cleansing mechanism. Being the amorous species that we are, human females require a mechanism to regularly flush out the infection-laden sperm that gathers from our sexual conquests.

This argument was soon found to have more than a few flaws. For a start, women are more susceptible, not less, to infections such as chlamydia and gonorrhoea during menstruation, as the cervical mucus thins out.

The iron-rich blood also serves as an attractive food source for Staphylococcus aureus, of tampon-associated toxic shock syndrome notoriety.

And there is no correlation between level of promiscuity in us and our close primate relatives and heaviness of bleeding, as the theory predicts.

Invasive embryos

A more plausible explanation for menstruation is that it evolved to accommodate the peculiar way in which human embryos embed into the lining of the uterus – the endometrium – during pregnancy.

In some mammals with a placenta, a fertilised embryo attaches to the endometrium only superficially. In humans and other menstruating species, implantation is deep and invasive, and requires an especially luxurious lining to develop in preparation for implantation.

While other mammals are able to reabsorb the lining that adorns their fertile womb, the volume of tissue in humans is too great, so if no pregnancy ensues, it is expelled instead.

In the evolutionary cost-benefit analysis, building up the lining only when a pregnancy is on the cards – only when we ovulate once a month – could be less costly than maintaining this expensive lining indefinitely.

Another key difference between menstruators and non-menstruators is in the impetus for uterine thickening. In non-menstruating mammals, the final thickening of the endometrium (a process called decidualisation) only occurs once the lining senses the bleating signals from the embryo saying, “I’m here, now make my bed!”

Somewhere along the human evolutionary path, the dialogue between embryo and uterus shifted, so that the signals causing the endometrium to thicken came not from the embryo, but from the mother herself. Instead of being linked to the presence of the embryo, uterine thickening became linked to ovulation and the choreographed hormonal up-and-down that each woman cycles through on a monthly basis.

Maternal self-defence

But what’s with all this pre-emptive pampering? Not all mammals prepare for pregnancy so hopefully each month. Rabbits, for example, only ovulate and thicken their endometrium when they copulate.

American evolutionary biologists Deena Emera, Roberto Romero and Günter Wagner argue that the spontaneous thickening of the uterine lining is in fact a defence mechanism. Except the defence is against our own parasitic offspring, rather than sperm-borne infection.

Since mother and child do not share identical genes, their purposes are at odds. From the embryo’s perspective, the maximum benefit is gained from squeezing as many resources from its mother as possible. It even dampens its mother’s response to insulin, ensuring that a greater slice of the circulating sugar pie is placenta-bound during its nine-month residence.

The embryo tries to squeeze as many resources from its mother as possible. Image from shutterstock.com

The mother, meanwhile, prefers to be frugal with her resources, so that she can survive this pregnancy and go on to populate the next generation with additional children endowed with her unique genetic contribution.

There are two reasons that this maternal–fetal tug of war could have resulted in spontaneous thickening of the uterus. First, with implantation already invasive in humans and other menstruating species, the pre-thickened lining could be an evolutionary push-back to prevent the embryo from burrowing even deeper into the uterine wall.

The second reason is to protect the mother from expending valuable resources on faulty fetuses. The thickened lining could be an efficient way to sense – and if necessary, jettison – any tainted, and therefore unwanted, embryos. Around 30% to 60% of all human embryos are unceremoniously discarded in this way, before any signs of pregnancy occur.

While its evolutionary origins are firmly rooted in what takes place during pregnancy, the reality is that for most menstrual cycles, no embryo arrives. The decidual cells that have thickened the uterine lining pack up shop, the extracellular matrix keeping them all together breaks down, and the lining becomes as deciduous as the autumn leaves.

For Western most women who bear few children, this menstrual cycle is repeated 450 to 480 times over.

References:

Emera, D., Romero, R., & Wagner, G. (2012). The evolution of menstruation: A new model for genetic assimilation BioEssays, 34 (1), 26-35 DOI: 10.1002/bies.201100099

Blanks, A., & Brosens, J. (2013). Meaningful menstruation BioEssays, 35 (5), 412-412 DOI: 10.1002/bies.201300022

This original article was published by Dyani Lewis at The Conversation.

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