Take care: challenges medical relief teams after disaster

Take care: challenges medical relief teams face after disaster

As medical relief teams from Nepal and the rest of the world work to distribute supplies and care for survivors, it’s worth understanding how health workers handle extreme emergency situations.

As a trauma psychologist at the University of Florida I provide support to people coping with catastrophic injuries. I also assist in the training of health-care workers on preparing for extreme emergencies and mass causalities.

The painful truth is that it is impossible to be fully prepared for what to expect in a disaster situation. In training health and emergency professionals for these events, topics range from the ethics of triage to setting up safe practice locations to facilitating access to care. We initially cover safety and preparation factors, but we also focus on well-being and mental health needs for health workers and first responders.

People working in this field often view themselves with a “person-of-steel” mentality – placing themselves in peril by ignoring their own needs. This is why training focuses not just on the needs of survivors, but on the relief team participants as well.

In 2010, I was part of a medical relief team working in Haiti after a 7.0 magnitude earthquake devastated the nation. The parallels between the Haitian earthquake and the April 25 2015 Nepal earthquake are stark. Like Haiti, Nepal also requires emergency assistance from the world community. What, then, are the lessons we can bring forward from the earlier event that can assist relief teams today in Nepal?

Be prepared and take care of yourself

When we arrived in Haiti, we knew that food and fresh water would be an issue. Prior to departure, our team received advice that we should pack several days of supplies for ourselves. We did – and those supplies were either mishandled at the airport and given away to other volunteers, or given away to survivors who were begging for help.

So on day one, our primary mission was not to save lives, but to save ourselves. Right away we counted ourselves among the earthquake survivors who had no immediate source for food or water and it took several hours to locate a UN camp to help us out.

Aid teams must be prepared to change gears to ensure their own survival and prepare for the unexpected, even at the cost of delaying care.

Haitians wait in line for food and water distribution as a US Navy helicopter lands in Port-au-Prince January 22 2010. Thousands lined up at the first large distribution center outside a tent city waiting hours in line.
Hans Deryk/Reuters

Protecting others means protecting yourself

Without question, participating in disaster relief brings out the best in humanity. First responders to a crisis, including the earthquake in Nepal, are often neighbors and friends, running toward the emergency to dig survivors out of the rubble, even at the expense of their own safety.

But disaster can also bring out the worst in some. When a disaster has made it difficult for a government to provide services or basic assistance to its populace, people panic. And when relief workers arrive, that panic can turn otherwise peaceful people into a mob. Just as a drowning person might pull a rescuer underwater, survivors can threaten those who are providing assistance.

It’s easy for relief teams to become overwhelmed by the sheer volume of survivors in need of assistance. Resources may become strained and depleted, leaving countless people unserved and, potentially, unsaved.

In Haiti, relief camps were set up on the outskirts of tent cities that grew as temporary shelters for those displaced by the earthquake. When people learned of our medical relief center, hundreds of people began lining up.

Some were bleeding, some had broken bones, some were dying. Others had no medical problems but were eager for any assistance they could find. Security is needed for crowd control, to maintain order, and to ensure the safety of the relief workers and survivors themselves.

Early reports from Nepal suggest similar circumstances, with people rushing toward relief personnel, begging for any assistance including medical care, food and water, or just basic information. Aftershocks from the earthquake only serve to heighten the panic and make an already terrible situation that much more difficult to endure.

Nepal armed police personnel clear the debris of a collapsed building to search the trapped earthquake victims, in Kathmandu, Nepal April 30 2015
Adnan Abidi/Reuters

Psychological and physical toll on relief workers

The chaos that can result after a disaster can be traumatic for both survivors and relief workers. Few of us have witnessed death, and fewer yet have experienced a mass casualty scenario. It takes a psychological toll on survivors and on relief workers alike.

After a disaster, devastation assaults all of our senses. The sights of collapsed buildings, of bodies and gore; the sounds of crying out in pain, or the distant crack of gunfire; the acrid smell of rotting vegetation or the indescribable scent of decomposing bodies; the taste of our own sweat as we exhaust ourselves trying to make a difference; and the feel of the elements, such as pouring rain or unyielding heat, urging us to give up and go home.

In the face of trying to assist people in such dire circumstances, too often, relief workers ignore their own body signals suggesting that we need to rest, to eat, to hydrate.

In Haiti, our team was working in 100F weather with no shade, and by the end of the first day in our makeshift hospital I collapsed. When I came to, I was on a crude stretcher with an IV in one of my arms and one of my friends telling me how hard it had been to locate a vein due to my severe dehydration.

Even as a psychologist, and with specific training in disaster relief and psychological first aid, I found myself in harm’s way by trying to over-exert, over-extend, and, ultimately, over-spend my own body’s limited resources. Several of our team members had stress reactions ranging from breaking down into tears to experiencing psychotic symptoms and becoming hostile with each other.

As with the survivors themselves, the horrors aid workers endure persist long past the direct exposure to trauma. We bring our experiences home with us.

Recovery from bearing witness to such events is a process that can last days, weeks, months, or even a lifetime. It is not uncommon to experience sleep disturbance, nightmares, or withdrawal from friends and families.

As with soldiers returning for war, up to 30% of aid workers returning home may experience anxiety symptoms so severe that they meet criteria for a diagnosis of Post-Traumatic Stress Disorder, a condition requiring professional mental health assistance to manage.

At the end of the day it is easy to lose oneself in the scope and magnitude of the disaster. Even saving a hundred people might seem trivial when balanced against the thousands of survivors who still require assistance.

The devastation can weigh heavily and make us wonder if our presence mattered. The consolation is the reminder that for those we have saved and those we helped, our presence made a difference.

David Chesire is Associate Professor & Licensed Psychologist, College of Medicine at University of Florida.

This article was originally published on The Conversation.
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What works and doesn’t in disaster health response

Richard Bissell, University of Maryland, Baltimore County and Thomas Kirsch, Johns Hopkins Medicine

On Saturday, April 24 2015, a major (Magnitude 7.8) earthquake hit Nepal shortly after midday. Long-expected by seismologists, this large earthquake has left many of the older structures in this mountainous and economically challenged country of 31 million inhabitants in ruins. It has also released avalanches affecting mountaineers from all over the world.

As is the case of many mountain communities in developing countries throughout the world, Nepal is vulnerable to a trifecta of risk: a seismologically active landscape, slide and avalanche prone hillsides, and insufficient resources to construct modern earthquake-resistant structures. The country’s poverty also means that it will require outside help to mount an effective response to the widespread needs of an earthquake stricken population.

At the moment, the most important question is how can the global community best respond? What can and what should international relief teams be prepared to do when responding to such an event?

Research provides some well-documented evidence that many international health-oriented responses are poorly targeted and may be influenced by objectives that play well on the home front rather than what’s needed on the ground. Let’s look at this from the perspective of the still-unfolding Nepal earthquake response.

Assess damage and determine immediate needs

The first function in the response to any emergency, whether it is a multi-vehicle crash on the local interstate, or a massive earthquake in the Himalayas, is to conduct an immediate situation assessment.

The most important aspect of this process is called the “needs assessment,” which uses an initial damage assessment to predict what kinds of rescue, health, food and shelter needs exist at that time, as well as what will likely be needed going forward in the near- and midterm. As the needs are established, then the appropriate response can be directed to meet those needs.

International and United Nations-based organizations with previous experience in these kinds of assessments, and armed with the latest satellite imaging technology to estimate damage across the affected country, can provide assistance to local officials in setting response priorities.

Japanese rescue team members remove debris while looking for survivors at the site of a collapsed temple caused by a massive earthquake in Kathmandu, Nepal.
Kyodo/Reuters

Search and rescue needs to happen immediately

Earthquakes cause buildings to collapse, trapping people and causing massive amounts of injury. This was the case in the 2010 Haiti earthquake and now in Nepal. Fallen buildings make immediate search and rescue efforts critical to saving lives.

Unfortunately the nature of crush injuries necessitates rapid rescues and limits the amount of “saves” that external search and rescue (SAR) teams can accomplish. Crush syndrome, which occurs when blood circulation to a limb is cut off by heavy debris, can lead to kidney failure even if the victim is successfully extricated. And crush injuries can also lead to severe, and sometimes fatal, blood loss. In both cases, rapid extrication is necessary to save lives.

Decades ago, disaster epidemiologist Erik Noji and others demonstrated that up to 90% of successful rescue extrications after earthquakes are done by family members and local bystanders. People trapped under rubble are likely to die quickly without immediate rescue. We can’t expect much success from teams that arrive on-site 48, 72 or even 96 hours after the earthquake. Based on previous history, it is unlikely that the US SAR teams deployed to Nepal (some 72 hours post-earthquake) will save many people.

Past history has shown that international SAR teams rarely save many lives at the cost of millions of dollars that might have been better employed in other relief and treatment functions, such as water purification, emergency food supplies, and medications to replace those lost in the rubble.

What kind of health response is needed most?

Then the question is: what kind of health response would better target the needs of the Nepalese? Urgent trauma care is critical in the first days and even the first week, and well-trained and provisioned teams from the region that can set up in days can make a difference.

These teams would be capable of providing necessary amputations and surgical repairs. It is important, however, that such surgical teams not use technologies that are beyond local capacity to deal with once the international teams have left. Working closely with local medical practitioners is key.

Much of the injury-related care does not need surgical intervention, and can be provided in clinics and mobile health settings. This might include care for broken bones, cuts, and superficial injuries. The extent to which outside help is needed is not a function of how fast international teams can respond, but rather how the well the country or region is prepared before the earthquake.

For example, our research shows that Chile was well-prepared to provide injury-related and primary care after the huge Concepción earthquake (Magnitude 8.8) in 2010, because that nation had a string of earthquake resistant primary care clinics and hospitals. The lesson here is that international response teams need to know the resilience status of local health care facilities before embarking on a response.

People sleep as they wait outside the departure terminal at the airport in Kathmandu, Nepal, April 27, 2015, following the April 25 earthquake.
Danish Siddiqui/Reuters

Infectious disease risks

In some cases, earthquakes may directly or indirectly lead to increases in infectious diseases. Earthquakes can damage or destroy sanitation systems. They tend to disrupt the local environment and how people live, leading to changes in the behavior of both humans and disease vectors, such as mosquitos.

For example, there was a rise in malaria in Costa Rica after the 1991 Limón earthquake. We found that this was due to several factors. People were sleeping outside, thus increasing their mosquito exposure, and regular mosquito- and malaria-control programs were delayed until bridges could be rebuilt.

Nepal has a long history of both intestinal bacterial or parasitic diseases and malaria. The earthquake has destroyed or damaged buildings throughout the country. Powerful aftershocks have made people understandably reluctant to return indoors, which means that many are sleeping outside. A concerted public health effort with international assistance may go a long way toward mitigating an earthquake-related upsurge in these kinds of diseases by prioritizing the provision of mosquito netting, temporary shelter, and clean potable water.

There will be more Nepals and Haitis in our future earthquake experience. Back in the early 1980s Dr. Claude de Ville de Goyet noted that certain kinds of disaster health relief seem to be perpetuated because “they photograph well.” But we should shift the focus to things that actually work rather than what plays well on the news.

Looking forward to our next international earthquake responses, let us take into account what we have learned from past experiences, and, in coordination with our local hosts, provide the kinds of health assistance that are most likely to meet the needs of the people affected.

This article was originally published on The Conversation.
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The mystery of breast cancer

Richard Stevens, University of Connecticut

For most of the common cancers, a major cause has been identified: smoking causes 90% of lung cancer worldwide, hepatitis viruses cause most liver cancer, H pylori bacteria causes stomach cancer, Human papillomavirus causes almost all cases of cervical cancer, colon cancer is largely explained by physical activity, diet and family history.

But for breast cancer, there is no smoking gun. It is almost unique among the common cancers of the world in that there is not a known major cause; there is no consensus among experts that proof of a major cause has been identified.

Yet, breast cancer is the most common form of cancer in women worldwide. The risk is not equally distributed around the globe, though. Women in North America and Northern Europe have long had five times the risk of women in Africa and Asia, though recently risk has been increasing fast in Africa and Asia for unknown reasons.

Was it something I ate?
Supermarket aisle via www.shutterstock.com.

Is diet to blame?

Up until about 20 years ago, we thought it was all about diet. As people abandon their local food sources and begin to eat highly processed foods with lots of fats, the hypothesis went, breast cancer was thought to be more likely to develop.

This hypothesis was logical because when researchers analyzed countries’ per capita fat consumption and breast cancer mortality rates, they found a strong correlation. In addition, rats fed a high-fat diet are more prone to breast tumors.

By studying Japanese migrants to California, researchers found that the first generation had low risk like their parents in Japan, but then by the second and third generation, risk was as high as white American women. So, the genetics of race did not account for the stark differences in the breast cancer risk between Asia and America. This was also consistent with the idea that the change in food from the lean Asian diet to the high-fat American diet causes cancer. So it all made sense.

Until it didn’t.

Diet studies find that fat is not the answer

Starting in the mid-1980s, large, well-done prospective studies of diet and breast cancer began to be reported, and they were uniformly negative. Fat in the diet of adult women had no impact on breast cancer risk at all.

This was very surprising – and very disappointing. The evidence for other aspects of diet, like fruits and vegetables, has been mixed, though alcohol consumption does increase risk modestly. It is also clear that heavier women are at higher risk after menopause which might implicate the total amount of calories consumed if not the composition of the diet.

There is a chance that early life dietary fat exposure, even in utero, may be important, but it’s difficult to study in humans, so we don’t know much about how it might relate to breast cancer risk later in life.

If diet is not the major cause of breast cancer, then what else about modernization might be the culprit?

Some risk factors, like exercise, can be modified.
Runner via www.shutterstock.com.

Two kinds of risk factors: what we can modify, and what we can’t

The factors shown to affect a woman’s risk for developing breast cancer fall into two categories. First, those that cannot be easily modified: age at menarche, age at birth of first child, family history, genes like BRCA1. And second, those that are modifiable: exercise, body weight, alcohol intake, night-work jobs.

The role of environmental pollution is controversial and also difficult to study. The concern about chemicals, particularly endocrine disruptors, started after the realization that such chemicals could affect cancer risk in rodent models. But in human studies the evidence is mixed.

Because child bearing at a young age and breast feeding reduce risk, the incidence throughout Africa, where birth rates tend to be higher, and where women start their families at younger ages, has been lower.

Death rates, however, from breast cancer in sub-Saharan Africa are now almost as high as in the developed world despite the incidence still being much lower. This is because in Africa, women are diagnosed at a later stage of disease and also because there are far fewer treatment options.

The question is whether the known risk factors differ enough between the high-risk modern societies and the low-risk developing societies to account for the large differences in risk. The answer: probably not. Experts think that less than half the high risk in America is explained by the known risk factors, and that these factors explain very little of the difference in risk with Asia.

A related question is whether the high risk in America and Northern Europe is due to a combination of many known exposures, each of which affects risk a little bit, or mostly due to a major cause that has so far eluded detection. And maybe some of the known risk factors have a common cause which we don’t yet understand.

Are we just finding more cancer?

Since the 1980s, screening by mammography has accounted for some of the increase in incidence in the modern world compared to the developing world, but not nearly enough to explain the entire difference. About 20% of the cancers found by mammography are now believed to be of a type that would never have progressed beyond the very small early stage that mammography can detect. But the problem is that we can’t tell which are the benign ones and which are not.

Electric light and shift work may be factors.
Office worker via www.shutterstock.com.

What about electric light?

Electric light is a hallmark of modern life. So, maybe the introduction and increasing use of electricity to light the night accounts for a portion of the worldwide breast cancer burden.

This might be because our circadian rhythm is disrupted, which affects hormones that influence breast cancer development. For example, electric light at night can trick the body into daytime physiology in which the hormone melatonin is suppressed; and melatonin has been shown to have a strong inhibitory effect on human breast tumors growing in rats.

The theory is easy to state but difficult to test in a rigorous manner. Studies have shown that night-working women are at higher risk than day-working women, which was the first prediction of the theory.

Other predictions are that blind women would be at lower risk, short sleepers would be at higher risk, and more highly lighted communities at night would have higher breast cancer incidence. Each of these has some modest support though none are conclusive. What we do know is that electric light in the evening or at night can disrupt our circadian rhythms, and whether this harms our long term health, including risk of breast cancer, is not yet clear.

Whatever is going on, it’s important to find answers because breast cancer has become a scourge that now afflicts women all over the world in very large numbers, at almost two million new cases this year alone.

This article was originally published on The Conversation.
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How the brain reads music: the evidence for musical dyslexia

Jennifer Mishra, University of Missouri-St. Louis

Music education in the western world often emphasizes musical literacy, the ability to read musical notation fluently. But this is not always an easy task – even for professional musicians. Which raises the question: Is there such a thing as musical dyslexia?

Dyslexia is a learning disability that occurs when the brain is unable to process written words, even when the person has had proper training in reading. Researchers debate the underlying causes and treatments, but the predominant theory is that people with dyslexia have a problem with phonological processing – the ability to see a symbol (a letter or a phoneme) and relate it to speech sounds. Dyslexia is difficult to diagnose, but it is thought to occur in up to 10% of the population.

In 2000, Neil Gordon, a retired pediatric neurologist, proposed the idea of musical dyslexia (dysmusia), based on growing evidence that the areas of the brain involved in reading music and text differed.

The idea that dyslexia could affect the reading of non-language symbols is not new. For instance, dyscalculia is the difficulty reading and understanding mathematical symbols. Recent research supports dyslexia and dyscalculia as separate conditions with unique causes (dyscalculia is thought to be caused by a deficit in spatial processing in the parietal lobe). If the brain processes words and mathematical symbols differently, why not musical symbols too?

Reading music is a whole brain activity.
Flutist via www.shutterstock.com.

Music’s written system

Western music, like language, has a highly evolved coding system. This allows it to be written down and transmitted from composer to performer. But music, unlike language, uses a spatial arrangement for pitch. The page is divided into staffs of five lines each. Basically, the higher a symbol is placed on the staff, the higher the pitch.

Unlike letters in text, pitches can be stacked, indicating simultaneous performance (chords). Music also uses a system of symbols to indicate how pitches should be played. Symbols can indicate duration (rhythm), volume (dynamics) and other performance cues. Music also utilizes written words to indicate both the expressive features of the music and the lyrics in vocal music. Lyrics may be in languages not spoken by the performer.

Due to differences in the physical features of the written systems, it makes sense that the brain would read music and text differently. This appears to be the case – at least to some extent.

Reading music and reading text use different systems in the brain.
Violin and books via www.shutterstock.com.

Text and music reading in the brain

In the brain, reading music is a widespread, multi-modal activity, meaning that many different areas of the brain are involved at the same time. It includes motor, visual, auditory, audiovisual, somatosensory, parietal and frontal areas in both hemispheres and the cerebellum – making music reading truly a whole brain activity. With training, the neural network strengthens. Even reading a single pitch activates this widespread network in musicians. While text and music reading share some networks, they are largely independent. The pattern of activation for reading musical symbols and letters is different across the brain.

Composer Maurice Ravel.
Bibliothèque nationale de France via Wikimedia Commons

Brain damage, especially if it is widespread, as was the case with the composer Maurice Ravel, (perhaps best known for Boléro), will likely impair both text and music reading abilities. Ravel had a form of frontotemporal lobe dementia.

However, there have been cases where a more limited brain injury impaired reading of one coding system and spared the other.

Ian McDonald, a neurologist and amateur pianist, documented the loss and recovery of his own ability to read music after a stroke, though his ability to read text was unaffected. Oliver Sacks described the case of a professional pianist who, through a degenerative brain disease (Posterior Cortical Atrophy), first lost her ability to read music while retaining her text reading for many years. In another case, showing the opposite pattern, a musician lost his ability to read text, but retained his ability to read music.

Cases where music and language seem to be differently affected by brain damage have fascinated researchers for centuries. The earliest reported case of someone who was unable to speak, but retained his ability to sing, was in the 1745 article, On a Mute who Can Sing.

More recently, the Russian composer, Vissarion Shebalin, lost his language abilities after a severe stroke, but retained his ability to compose. Maintaining the ability to sing in the absence of language has led to the creation of a therapeutic treatment called Melodic Intonation Therapy that essentially replaces speech with song. This allows the patient to communicate verbally. These cases and many others demonstrate that music and language are to some extent separate neurological processes.

Differences in reading ability can occur even within musical notation. Cases have been reported where musicians have lost their ability to read pitch, but retained their ability to read rhythm, and vice versa. fMRI studies have confirmed that the brain processes pitch (spatial information) and rhythm (symbol recognition) differently.

Musical dyslexia

The research starts to imply how a specifically musical dyslexia could occur. This deficit may be centered on pitch or musical symbols or both. No conclusive case of musical dyslexia has yet been reported (though Hébert and colleagues have come close) and efforts to determine the effects of dyslexia on reading musical notation have been inconclusive.

Children in western cultures are taught to read text, but not always taught to read music. Even when they are, inabilities to read music are not generally treated as a serious concern. Many gifted musicians are able to function at a professional level purely learning music by ear. Among musicians, there is a wide range of music reading proficiencies. This is especially apparent with sight reading (the first performance of a notated piece). Identifying musical dyslexia could help explain why some musicians read well and others don’t.

This article was originally published on The Conversation.
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Could Ebola mutate faster than we can develop treatments?

Peter White

As the worst known epidemic of the Ebola virus continues in West Africa, scientists around the world are trying to develop treatments for those infected. But a process of viral mutation, known as “genetic drift”, could potentially compromise their efforts.

Genetic drift is one reason why RNA viruses, such as influenza and norovirus, cause global epidemics of disease (pandemics) about every three years. To understand how it works, we need to go back to basics.

Ebola is an RNA virus, the fastest-evolving genetic entity we know. These viruses continually change their genetic sequence because the enzymes responsible for making more copies of their genetic code often make mistakes. The process is akin to photocopying a photocopy: the image changes slowly over time. And these changes are known as genetic drift.

Genetic drift lets the new viruses change the surface protection proteins that the immune system targets. This enables them to infect people who have immunity against previous versions.

The main candidates

The World Health Organisation’s November 2014 report Potential Ebola Therapies and Vaccines lists four classes of medicines for Ebola: i) immunomodulators, ii) antiviral drugs, iii) immunoglobulins and iv) antiviral small inhibitory RNA (or RNA therapies).

Drugs in the latter two classes are clinically the most advanced, but are only in the earliest of the three stages of human clinical trials. These types of drugs are among the forerunners of a new wave of exciting RNA-based therapies. But they have not previously been widely commercialised for the treatment of viral infections.

Immunomodulators

The first class of drugs – immunomodulators – are designed to stimulate the innate immune response (which has broad antiviral effects) by triggering the production of many hundreds of antiviral proteins in infected cells.

When tested in rhesus macaques soon after an exposure to a lethal dose of the Ebola virus, this class of drug increased survival time, but failed to stop the monkeys from dying. Other treatments have resulted in better outcomes in animal models.

Immunomodulators are, so far, perhaps the weakest of the four classes of drugs that could be used against Ebola.

Antivirals

The most common type of antiviral drug is called a nucleoside analogue. Chemically, a nucleoside analogue “looks like” a sub-unit of RNA (a nucleotide), the building blocks of viral genetic codes. The virus mistakes this “rogue” building block while replicating – to its own demise. Further genome copying is shut down, reducing viral disease or even, in some cases, curing viral infections by eliminating the virus from the host.

Originally developed to fight influenza, T-705 or Favipiravir (Toyama Chemical) is a nucleoside analogue with broad antiviral activity. While its potency against Ebola is low compared to how well it works against influenza, results from the latest clinical trial show it’s ineffective for people who are very ill but works for those with low levels of the Ebola virus in their blood.

Another nucleoside analogue, known as BCX4430 (Biocryst), has protected macaque monkeys from Ebola-related Marburg virus infection and death, when administered two days after exposure.

RNA therapies

RNA drugs could be the next big thing to treat viral disease. The viral genetic code is translated into proteins through an intermediate called messenger RNA (mRNA). Once the cell is infected, the viral mRNA tells the cell to make viral proteins. By using small RNA molecules that match the viral mRNA sequence, there are a few ways to prevent the viral proteins from being made.

UK army trainers teach health service medics how to put on Ebola safety suits.
DFID/Flickr, CC BY

It’s analogous to taking out the middle man in a business arrangement. One partner makes some cakes, the middle man transports them to a shop and the third person sells the cakes. If you take out the driver, then no cakes get sold, or in the context of mRNA and Ebola, the viruses don’t replicate.

Tekmira Pharmaceuticals is developing a triple combination RNA-based drug for fighting Ebola, which is probably the most advanced. It has now been through Phase 1 human clinical trials. Another company, Sarepta Therapeutics, has used an alternative RNA therapy to target the same three Ebola messenger RNAs to prevent replication.

Both Sareota and Tekmira’s RNA-base drugs have successfully protected monkeys from dying after Ebola infection.

Immunoglobulins

Immunoglobulins, an antibody class of treatment, target a surface protein that viruses use to enter cells. It’s an obvious target for an antibody-based drug because when antibodies bind to this Ebola protein, the virus’ entry into cells is blocked and infection is prevented.

But viruses can mutate or mask their outer protein coats to evade host immune responses, so using a single antibody will eventually result in viral evasion. One way to counter this is to use a combination of antibodies to target many different parts of the viral protein coat. This reduces the viruses’ ability to escape and become resistant.

The drug ZMapp, which is an immunoglobulin, uses a cocktail of three antibodies to stop the viruses evading cells. It protects Ebola-infected monkeys from death and has been used on two people infected with the virus, who survived. Although it is not known whether they survived because of the drug, there are strong indications it has an impact.

Where to now?

Immunoglobulins and RNA therapies could both become less effective if Ebola mutates because they are based directly on viral genetic sequence. Both RNA therapies were designed against the original 1976 virus, while Zmapp was designed from the version of the Ebola virus circulating in 1995.

A recent paper evaluating the impact of genetic drift since these dates has found the Ebola genome has mutated by around 3% compared to both the 1976 and 1995 Ebola predecessors. This mutation rate is lower than for other RNA viruses, such as HIV, hepatitis C virus and influenza, but not by much. All RNA viruses mutate a lot and this poses a danger to the effectiveness of immunoglobulins and RNA therapies.

The good news is that genetic drift would be unlikely to result in viral resistance against nucleoside analogues. For this to occur, mutations within the “viral engine” (the polymerase gene), which copies the genome, are needed. And this type of mutations renders the virus weak compared to their non-mutated brethren. So a virus that could evade the drug through genetic drift wouldn’t be very virulent in the first place.

But drug resistance could occur in people who are treated with these medicines. That’s because the presence of the drug creates pressure for the virus to mutate its engine to survive as only resistant viruses will be able to replicate.

Genetic drift is unlikely to render newly developed drugs ineffective. The three most advanced therapies we have were formulated on older versions of the virus but their developers don’t seem concerned. This is because each company has three separate versions of the drug in its formula.

For the virus to become resistant, three viral mutations would need to occur simultaneously, and this is very difficult. Given what’s at stake here, we should be comforted by the fact that drug developers have taken genetic drift into account.

This article was originally published on The Conversation.
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Chromosome errors cause many pregnancies to end before they are even detected

Rajiv McCoy, Stanford University and Dmitri Petrov, Stanford University

Given the fact that there are seven billion people on Earth, one might conclude that human beings are pretty good at reproducing. But fewer than 30% of all fertilization events result in successful pregnancy, even for young, fertile couples.

The remaining 70% of conceptions result in pregnancy loss, with most of these losses occurring before the mother misses a menstrual period. This means that many pregnancies begin and end before the mother even notices. These early pregnancy losses are one reason why it generally takes several months for couples to achieve a successful pregnancy. But why is pregnancy loss so common?

The pregnancy loss iceberg.
Larsen et al. BMC Medicine 2013 11:154

Current evidence suggests that both the process of egg formation (this is called meiosis) in the mother’s ovaries and the initial embryonic cell divisions (called mitosis) just after fertilization are extremely error-prone, producing embryos with too many or too few chromosomes.

What happens after fertilization?

During fertilization, the sperm and egg fuse so that the resulting embryo will have 23 chromosomes inherited from the father and 23 chromosomes inherited from the mother. If all goes well, the subsequent cell divisions in the embryo (called mitotic divisions) simply replicate this 46-chromosome set as new cells are formed.

An example of aneuploidy formation: a cell with mis-segregating chromosomes.
Stefano Santaguida and Angelika Amon, MIT

Chromosomes contain genes, the blueprints for human development. When processes go awry in meiosis or mitosis, chromosomes can go into the wrong cell or get lost completely, drastically altering this blueprint. The resulting cell will not possess the standard 46-chromosome set – an imbalance that is the defining feature of aneuploidy. This means that many genes will either be missing or present in extra copies, placing cells under stress.

Embryos with many aneuploid cells rarely survive. Trisomy 21, the genetic cause of Down syndrome, is one of the rare forms of aneuploidy in which the baby can survive to live birth. The vast majority of embryos affected with other aneuploidies perish in early development.

What causes aneuploidy?

Aneuploidy is associated with maternal age. Female meiotic errors (these are errors in the eggs themselves) increase from a frequency of less than 20% in mothers younger than 30 years old to greater than 60% in mothers older than 45. Errors in sperm, called paternal meiotic errors, are comparatively rare, affecting fewer than 5% of sperm cells.

But age isn’t the only factor influencing aneuploidy. Our recent work in collaboration with the genetic testing company Natera, published in Science, suggests that risk is also influenced by a common genetic variant in the mother’s genome.

Embryonic cell division.
Henry Vandyke Carter via Wikimedia Commons

Even when the egg and sperm are normal, aneuploidies often arise after fertilization, during the first three embryonic cell divisions. These initial cell divisions of the embryo are controlled by maternal machinery pre-loaded into the egg.

Unlike meiotic errors in the egg, mitotic errors do not increase with age, but affect all age groups.

A maternal genetic variant influences aneuploidy risk

Using data from in vitro fertilized (IVF) embryos screened by our collaborators at Natera, we found that mothers with a particular genetic variant on chromosome 4 tend to produce embryos with more mitotic aneuploidies – the aneuploidies that arise during post-fertilization cell division.

This effect was observed for mothers of all ages and from diverse ethnic backgrounds. This genetic variant is surprisingly common; approximately half of all people carry at least one copy of this risk variant.

The most likely suspect is a gene called Polo-like kinase 4 (PLK4), which is known to be a master regulator of the centrosome cycle. The centrosome is molecular machine that is responsible for proper cell division and distribution of chromosomes.

We estimated that each copy of the risk variant increases the rate of aneuploidy by about 3%, regardless of the mother’s age. Having two copies doubles this risk. This increased risk could be especially important for older mothers who are already more prone to aneuploidy. It is likely that there are other genetic variants that contribute to aneuploidy risk to a lesser degree, and further work will be required to determine if this is the case.

Because of the established link between aneuploidy and pregnancy loss, we hypothesized that the aneuploidy risk variant might also affect embryo survival. We found that mothers with the high-risk genotypes had fewer embryos available for testing, suggesting that their embryos are less likely to survive very early developmental stages due to aneuploidy.

Given these results, it seems like this genetic variant could influence the average time it takes to achieve successful pregnancy, an idea that we are hoping to investigate further.

A signature of natural selection: comparison to the Neanderthals

Normally, natural selection weeds out damaging variation, reducing it to very low frequency. But the aneuploidy risk variant is very common. Hoping to learn more about the evolutionary history of this variant, we compared human genomes to Neanderthals and Denisovans, our ancient hominin relatives.

Comparison of a modern human skull and Neanderthal skull in the Cleveland Museum of Natural History.
hairymuseummatt (original photo), DrMikeBaxter (derivative work) via Wikimedia Commons, CC BY

Despite the fact that the harmful genetic variant is relatively common in humans, it was absent in these close relatives, meaning that it likely rose rapidly in frequency in an ancestral population of humans. If this is true, it means that this version of this gene was actually somehow beneficial (and maybe still is) while simultaneously being harmful in the context of early development.

So what could possibly have been the benefit?

We aren’t sure at this point, but we speculate that for ancient humans, there might have been a benefit to having a reduced probability of successful pregnancy per intercourse. Maybe the benefit had to do with infanticide – men may be less likely to kill a baby if there is a chance it is their child, and not that of a rival. Likewise, lower probability of pregnancy per intercourse might encourage repeated mating with the same female, fostering pair bonding and paternal investment. This hypothesis was first proposed by Alexander and Noonan in 1979 to help explain the human-specific trait of concealed ovulation and continuous sexual receptivity – women do not externally signal or limit intercourse to the fertile portion of their cycles as do some other primates.

Another idea is based on the fact that PLK4 is often mutated in human cancers. Could there be a beneficial effect of the risk variant in the context of cancer? PLK4 plays yet another role in testes development. Could the aneuploidy risk variant have a beneficial effect in this context?

We are hoping that additional data and future research can shed more light on this signal of human-specific adaptation. Is it real or simply an artifact of chance events in human evolution? Did our ancestors have lower rates of aneuploidy? What about Neanderthals, Denisovans, and living non-human primates? And perhaps the most basic question: why is human aneuploidy so common? Armed with modern genomic technologies, we can continue to chip away at these questions to understand not only the medical aspects of aneuploidy risk, but also the broader evolutionary basis of this intriguing trait.

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What is going on in your brain when you sleep?

Padraic Monaghan, Lancaster University

Sleep has profound importance in our lives, such that we spend a considerable proportion of our time engaging in it. Sleep enables the body, including the brain, to recover metabolically, but contemporary research has been moving to focus on the active rather than recuperative role that sleep has on our brain and behaviour.

Sleep is composed of several distinct stages. Two of these, slow-wave (or deep) and REM sleep, reflect very different patterns of brain activity, and have been related to different cognitive processes.

Slow-wave sleep is characterised by synchronised activity of neurons in the neo-cortex firing at a slow rate, between 0.5 and three times per second. The neo-cortex comprises the majority of the cerebral cortex in the brain which plays a role in memory, thought, language and consciousness. In contrast during REM sleep, when most of our dreaming happens, neuronal firing is rapid and synchronised at much higher frequencies, between 30 to 80 times per second.

Such patterns of brain activity during REM sleep are reminiscent of those observed during wakefulness, and for this reason REM sleep is often referred to as “paradoxical” sleep.

Cognitive functions

There is growing evidence that slow-wave sleep is related to the consolidation of memory and is involved in transferring information from the hippocampus, which encodes recent experiences, and forging long-term connections within the neo-cortex. REM sleep has been linked to processes involving abstraction and generalisation of experiences, resulting in creative discovery and improved problem solving.

Though there are substantial similarities between wakefulness and REM sleep, numerous studies have explored differences in the activity of brain regions between these states, with the cingulate cortex, hippocampus and amygdala more active during REM sleep than wakefulness. These regions are particularly interesting to cognitive neuroscientists because they are key areas involved in emotional regulation and emotional memory.

However, which sub-regions are active within these broader cortical and limbic areas – the pathways in the brain that produce these patterns of activation – and the precise function of the activity in these regions during REM sleep is currently under-described.

Cortical activity in rats

A new study published in Science Advances studied the physiology and functionality of REM sleep in a group of rats and provides insight into the cortical activity and the sub-cortical pathways that result in this activity. The level of detail of this study provides a major step forward for our understanding of the effect that REM sleep has on our brain and cognitive behaviour.

Rat sleep.
Tomi Tapio K, CC BY

The authors studied groups of rats who were allowed to sleep, but prevented from entering REM sleep for three days. Six hours before assessment, half of the rats were allowed to sleep normally, and half continued to be deprived of REM sleep. The rats that were permitted to sleep normally then demonstrated raised levels of REM sleep within those six hours. This enabled a comparison of the effect of recent REM sleep between groups. An additional control group of rats were allowed to sleep normally throughout the study.

Gene expression analysis involves tracking the presence of particular mRNA or proteins that can be identified as the consequences of certain genes operating. The rats who underwent substantial REM sleep before testing were found to demonstrate greater expression of several genes that are associated with syntaptic plasticity (how quickly their synapses can adapt to changes in a local environment) and which affects the efficiency of neural transmission in the hippocampus.

In the neo-cortex, the gene expressions related to how well our synapses adapt also increased following REM sleep, but those related to neural transmission were reduced compared with the group that was prevented from REM sleep. So, the function of REM sleep appears to be due to changes in the way that neurons communicate. This is consistent with the view that REM sleep allows the brain’s memory processing systems to re-balance, which enables effective responses to experiences the next day.

Where in the brain?

Stained neurons from somatosensory cortex in the macaque monkey.
Brainmaps.org, CC BY

In a further study, the same group determined the precise location of where these changes actually occur in the brain. In the neo-cortex, there was a general increase in plasticity throughout several areas, including sensorimotor regions that bring together sensory and motor functions. In the hippocampus, it was generally confined to the dentate gyrus, which is thought to contribute to forming new episodic memories among other things. REM sleep was also associated with reduced neuro-transmission throughout many regions of the neo-cortex, indicating that REM sleep likely results in a general weakening of the connections between synapses, which may enable brain networks to better learn from multiple experiences rather than be affected only by single instances.

The claustrum: consolidating emotion and memory.
Was a bee

The final studies the group conducted determined the source of the cortical changes in plasticity and neuro-transmission during REM sleep. By tracking signal transmission between different brain areas together with chemical lesioning (in which brain areas are temporarily inactivated), they identified two further areas called the claustrum and the supramammillary nucleus as having key roles during REM sleep.

These two areas have been identified as involved in integrating emotion and memory. The claustrum is a very thin layer of neurons that are found underneath the inner neo-cortex. It is known to link to and from very many regions of this part of the brain. As such, the claustrum has been implicated in integrating stimuli from several senses and is involved in linking areas involved in emotional processing and attention.

The supramammillary nucleus, within the hippocampus, is also known to interconnect to multiple areas of the brain, several of which are associated with emotional processing.

The implications of this work provide converging evidence that REM sleep modulates activation and synaptic processing in areas of the brain that contribute to the processing of emotion. This is also consistent with previously untested accounts that suggest REM sleep is important for encoding memories (but without their emotional content). While the role of dreaming during REM sleep is still yet to be linked to observed effects from neuro-chemicals in the brain, understanding what is happening in our brains when we dream could yet prove to be key to processing of emotion and memory.

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What is cognitive behaviour therapy?

Explainer: what is cognitive behaviour therapy?

Peter McEvoy, Curtin University

If you or someone you care about experience an emotional problem it won’t be long before you hear that cognitive behaviour therapy, or CBT, is probably the treatment of choice.

Research over the last 40 years or so has found CBT to be helpful for all manner of problems, including anxiety, depression, insomnia, pain, anger, sexual problems, and the list goes on. But what exactly is it?

CBT is probably best understood by what it is trying to achieve. The main premise of CBT is that problems develop as a consequence of learnt ways of thinking (cognition) and behaving, and that learning new ways of thinking and behaving will have more helpful impacts on emotions and well-being.

Cognition: the C in CBT

The cognitive element of CBT refers to our thoughts, mental images, self-talk and core beliefs about ourselves (I’m ok, or I’m not), other people (they are generally friendly or they’re not) and the world around us (the future is bright or it’s not).

The more threatening our thoughts (I’m going to be criticised), the more anxious we will feel. The more hopeless we believe the future is (there’s no point), the more depressed we will feel. The more strongly we believe things should be different (the world must not be this way!), the more frustrated and angry we will feel.

The way we think is guided by what we pay attention to (a tendency to focus on negative things?), the way we interpret what is happening around us (seeing the glass half-full?) and the experiences we are most likely to remember (such as the times things went bad rather than the times things went well).

We all use particular styles of thinking from time to time that can get us into trouble. We are “catastrophising” when we blow things way out of proportion (things are rarely that bad). Using words like “never” and “always” is a good sign we’re thinking in an overgeneralised way (most bad things happen somewhere between never and always).

It’s important to remember that thoughts are, well, just thoughts. They are not immutable facts.

Most of the thoughts we have throughout the day are random streams of consciousness that are simply the output of creative minds. And many people can interpret exactly the same situation in many different ways.

Behaviour: the B in CBT

The behavioural aspect of CBT is based on learning theory. If you’ve heard of Pavlov’s dogs then you know about classical conditioning. Pavlov rang a bell just before he gave his dogs some food. Eventually the dogs started to salivate when they heard a bell ring (even if no food was given). They learnt that the bell signalled food. (Voila! Classical conditioning.)

Emotional responses can be classically conditioned in a similar way. As a simple example, someone with a dog phobia might recall being bitten as a child (perhaps by one of Pavlov’s dogs?). A cognitive behaviour therapist might speculate that the child developed a classically conditioned fear response to the dog.

Just like the bell triggered Pavlov’s dogs to salivate, an image or thought of a dog can trigger fear (even if the dog has no intention of biting).

Pavlov found that if he repeatedly rang the bell without providing food eventually the dogs stopped salivating when they heard the bell. They learnt that the bell no longer signalled food.

Similarly, if we repeatedly expose someone with a dog phobia to dogs without them being bitten, then they will learn that dogs are not dangerous and the fear response will stop being triggered. It turns out that repeated exposure to any feared object or situation (in the absence of the fear coming true) can effectively diminish the fear response.

When someone learns from experience that dogs are not dangerous, the fear response will stop being triggered.
Uwe Mäurer/Flickr, CC BY-NC-SA

A cognitive behaviour therapist is interested in all the things we do (or avoid doing) to manage the difficulties life throws our way. This might include unhelpful behaviours such as always avoiding the things we fear, excessively using drugs or alcohol, being controlling or violent towards others, and the list goes on.

Avoidance denies us any chance to challenge our fears and build confidence that we can cope. Alcohol and drugs might feel good and distract us in the short term, but ultimately our problems still exist and might be even worse in the longer term.

Being controlling towards others might help us feel powerful and in control in the short term, but this can conceal an underlying core belief of vulnerability (if I don’t control my environment, then perhaps it will control me).

These problems are only likely to be resolved when the fears driving these unhelpful behaviours are directly challenged and modified.

Therapy: the T in CBT

Cognitive behaviour therapists help clients better understand why they might have developed particular problems and, more importantly, what vicious cycles are maintaining them.

The most important questions for treatment are:

How do our thoughts, behaviours, physiology, interpersonal relationships and emotions interact to maintain problems in our lives?
How can we break these cycles?

Here are some things you can expect from a competent cognitive behaviour therapist.

A strong therapeutic relationship: Cognitive behavioural therapists appreciate that therapy can be emotional and difficult. They know their client needs to trust them before they will be able to work effectively together. Empathy, genuineness, unconditional positive regard and warmth need to be there in spades.

Collaboration: CBT involves a close working relationship between the client and therapist. The client is seen as an expert in their lives and the therapist is seen as an expert in evidence-supported treatments. Both forms of expertise are equally important to achieve a good outcome.

Goal-setting: CBT aims to be an efficient and time-limited form of therapy. A cognitive behavioural therapist will be very interested in what you would like to achieve from therapy. Together you will plan how to get there and how long it should take.

There is some flexibility if progress is slower than expected, but for most problems the therapist thinks in weeks or months rather than years.

Monitoring and evaluation: Cognitive behavioural therapists don’t rely on their own judgement about when clients’ problems have resolved; the therapist might be wrong. Rather, they measure change from the client’s perspective.

The therapist might ask the client to complete some monitoring or questionnaires during therapy so that progress can be tracked.

Cognitive behavioural therapists don’t blame the client if the problem isn’t improving. The therapist takes responsibility for changing what is done in therapy to ensure things get back on track.

Practical skills: CBT aims to teach clients to relate differently to their thoughts, physical sensations, emotions and behaviours so that they don’t get caught up in them in problematic ways.

One technique might involve identifying negative thoughts and challenging them by recognising when they are overly catastrophic and generating more realistic and helpful alternatives.

The techniques covered in CBT will depend on the nature of the problem, but you can expect to leave therapy with a toolkit full of helpful skills.

Between-session tasks: Clients never come to therapy just to feel good for the hour they are in the therapists’ office. They come to improve their lives out in the real world. For this reason, cognitive behaviour therapists encourage clients to apply their new skills between sessions and report back on how it went. This is where much of the hard work, learning and changes occur in CBT.

Here and how focus: CBT acknowledges the role that past experiences play in shaping who we are, but at the same time recognises that little can be done to change what has already occurred.

Instead, CBT focuses on identifying what is left behind from these experiences in the form of core beliefs about ourselves, others, and the world, and how these beliefs impact on present-day experiences.

Modifying these core beliefs can change our emotional responses to memories of earlier negative experiences, and can change the way we respond to challenges in our lives now and into the future.

The process of therapy is challenging and takes courage. A cognitive behavioural therapist’s role is to guide, support and cheer-lead when required. CBT’s overarching aim is to increase clients’ coping self-efficacy – their confidence in their own ability to manage their problems on their own.

If a cognitive behavioural therapist has done a good job, the client should leave therapy knowing that they are responsible for the benefits they have achieved from therapy and that they can continue to build on these gains well into the future.

This article was originally published on The Conversation.
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What is placenta?

Explainer: what is placenta?

Astrud Tuck

An incredibly complex and important organ in its own right, the placenta is only found in mammals. And how it functions has the potential to have profound effects on the lifelong health of the developing foetus.

The placenta exists solely during pregnancy, and plays a crucial role in nurturing and protecting the foetus throughout gestation. It’s connected to the foetus via the umbilical cord and attached to the wall of the womb, allowing for essential exchanges of nutrients, gases and waste with the mother’s circulation.

Placenta is composed of maternal and foetal parts, which are known as the basal and chorionic plates, respectively. Nutrients are exchanged through the maternal blood entering the foetal section, but maternal and foetal blood don’t actually mingle; they’re separated by arteries and capillaries.

Interestingly, the placenta has a gender matching that of the foetus, indicated with the presence of either XX or XY sex chromosomes. But placental sex is not used to test fetal gender as that would require invasive surgical tests and add unnecessary risk to the pregnancy.

In the beginning

The placenta begins developing once the embryo is implanted into the wall of the uterus. During the nine months of pregnancy, it increases in size and performs several vital functions. It regulates the exchange of nutrients for foetal growth and development, the exchange of gases including oxygen and carbon dioxide, and hormone secretion.

It also protects the foetus from toxins and infections as well as the mother’s immune system, which would otherwise regard it as a foreign invader. This is a critical aspect of placental physiology; if the mother’s immune system rejects the foetus, it will spontaneously abort.

In order to prepare the developing foetus for the world it will inhabit after pregnancy, the placenta is very sensitive to the mother’s environment. It’s able to adjust its functions in response to external cues, such as the mother’s diet or environmental pollutants, which can then alter foetal development.

The placenta begins developing once the embryo is implanted into the wall of the uterus.
Louise Woodcock/Flickr, CC BY-NC

Maternal diet plays a major role in foetal development; studies show eating a balanced diet of fruit, vegetables, and lean meat helps reach a good birth weight. But exposure to pollutants, such as car exhaust fumes, can have a negative impact and may increase the risk of the child developing asthma.

Permanent changes to the developing foetus’s physiology during development is known as foetal programming. And variations in the development of organs and systems within the foetus may increase lifetime susceptibility to cancer, heart disease, allergies and other diseases.

The mechanisms underlying these susceptibilities are incredibly complex and we’re only now beginning to understand them. One of them is epigenetics, which changes foetal gene expression, altering the physiology and functioning of the foetus throughout life.

What can go wrong

Placental disorders can cause serious health complications during pregnancy for both the foetus and mother. They can result in abnormal foetal development, growth restriction, malformations, miscarriage or stillbirth, and may even endanger the mother’s life.

Because the placenta keeps forming throughout pregnancy, abnormalities in its structure and implantation into the uterine wall can happen at any time. Placental abruption, for instance, occurs in approximately one in a 100 pregnancies. Abruption is either the partial or full detachment of the placenta from the uterine wall. And it can deprive the foetus of oxygen and nutrients, potentially leading to preterm birth or stillbirth.

One of the most common disorders of pregnancy is pre-eclampsia, which occurs in 3% to 7% of all pregnancies; it’s the leading cause of maternal health complication and death. Characterised by high blood pressure and protein in the urine, pre-eclampsia can lead to permanent vascular and metabolic damage in the mother.

The exact cause of the disorder is unknown, but it’s thought several factors including poor diet, high body fat, a history of high blood pressure and genetics may all play a role. Abnormal placental development and function is thought to be another major contributing factor.

If left untreated, pre-eclampsia can develop into eclampsia, which is characterised by cerebral fluid build-up and seizures. Once the placenta is removed, pre-eclampsia and eclampsia end.

Out of the several thousand mammalian species, humans are among only a handful that don’t regularly consume the placenta.
Kom bo/Flickr, CC BY

The placenta can become infected by bacteria, viruses or parasites which can lead to abnormal foetal development, preterm birth or foetal death. This occurs mostly in developing countries such as Africa, where the malaria parasite contributes to 100,000 deaths annually as a result of severe foetal growth restriction.

Finally, cancer of the placenta, known as choriocarcinoma, occurs in approximately one in 20,000 to 40,000 pregnancies. This cancer usually spreads to lungs and while it can be life-threatening, the cure rate is over 90%. It’s very responsive to chemotherapy, which is given after the baby is born.

Cultural significance

The placenta has little cultural value in Western countries; it’s often unrecognised by parents as being fundamental for a healthy and successful pregnancy. So, it’s usually discarded after childbirth.

But some other cultures hold great respect for this uniquely temporary organ, and have the mother eat it, in a practice known as human placentophagy. According to traditional Chinese medicine, for instance, the placenta is thought to rejuvenate the body after childbirth.

This practice has recently become more popular in Western culture but remains highly controversial, mostly due to the cannabalistic nature of the act. There are few scientific studies examining the benefits of placentophagy, but it’s worth noting that out of the several thousand mammalian species, humans are among only a handful that don’t regularly consume the placenta.

Different cultures hold a variety of beliefs about the placenta. Indonesian and Malaysian cultures consider the placenta to be a sibling of the newborn, for instance. And, in China, it’s thought to be its first and finest clothing. They all have a deep reverence and appreciation for the placenta and its ceremonial role in the birthing event.

The placenta plays a critical role in pregnancy, foetal development and health throughout life. It may only be a temporary organ, but plays some of the most important roles in sustaining early life.

This article was originally published on The Conversation.
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Don’t judge pregnant women, give them good nutrition advice

Karen Charlton, University of Wollongong and Catherine Lucas, University of Wollongong

At no other point in life is good nutrition more important than while the foetus is developing. But women in Australia often don’t receive adequate reliable information about how to ensure what they eat is best for both themselves and their developing baby.

Early nutrition is the key to lifelong health. The “developmental origins of adult disease” hypothesis first proposed by David Barker in the late 1980s drew attention to the role of intrauterine nutrition on the later health of the child. The Barker hypothesis states inadequate nutrition results in permanent changes in the foetus’ physiology and metabolism. These adaptations, it’s thought, equip the foetus for postnatal life in an environment of nutritional deficit.

So, low birth weight (but not pre-term) babies, who are later exposed to excess – as is the case of most economically developed societies – are more prone to developing diabetes, hypertension and heart disease in adulthood.

But eating too much during pregnancy is not recommended either. Maternal obesity is also associated with the risk of chronic disease in the offspring.

Medicalisation of pregnancy

But advances in scientific knowledge like this one have sadly meant pregnancy has moved from being considered a natural life stage to a state that requires medical management, with strong parameters around risk reduction. This shift has been accompanied by societal judgement that considers women responsible for the poor health of their children.

Popular media perpetuates this with headlines such as “Obese pregnant women risking babies’ health”. And then there are non scientifically-trained celebrities, who nonetheless get to air their opinions. Consider chef Pete Evans who attributes autism to maternal diets, even when the diets comply with relevant guidelines.

There’s plenty of pressure on women to do all the ‘right things’ during pregnancy to have a healthy child.
Sami Taipale/Flickr, CC BY-NC-SA

All this places pressure on women to do all the “right things” during pregnancy to have a healthy child. It also results in women feeling judged about their decisions and becoming extremely risk averse.

Mixed messages

You’d think all this pressure stems from the fact that women receive lots of good nutrition-related advice during pregnancy so they can make informed decisions and limit risk. But this is not the case. Pregnant women receive conflicting information about nutrition, and are often confused by the mixed messages they get from health-care providers, the media and the internet.

Fish and seafood, for instance, are good sources of several nutrients, including protein, omega 3 polyunsaturated fatty acids and iodine, all of which are important for foetal development. Australian dietary guidelines say:

maternal consumption of fish during pregnancy is likely to have a number of health benefits for women and their children.

But research shows many women may be avoiding fish and seafood during pregnancy because of concerns related to food safety and the detrimental effects of mercury. Although both can be eaten as long as they have been well cooked and served hot, and when larger species (shark, marlin, swordfish) are limited, women report avoiding these foods altogether.

Advice about fish and seafood is one example of how women are not getting the right guidance about what to eat during pregnancy.
IamNotUnique/Flickr, CC BY-NC-SA

Much of the educational material given out in antenatal clinics emphasise the risks of fish and seafood consumption also, without highlighting their nutritional benefits. This is just one example of the kind of coupling of risk aversion and limited advice that work together to promote less than ideal nutritional outcomes in pregnancy.

The right way forward

All in all, the causes of poor nutrition in the preconception and pregnancy stages are complex and multifactorial. They may be related to poor education and low income, inadequate access to proper health care, and a general lack of awareness about nutritional requirements. To address it, we need an approach that encompasses both individual education and “upstream” public health initiatives.

In Australia, pregnant women are not routinely referred to allied health professionals such as dietitians, which means it’s often left to midwives to provide them with nutrition-related advice. But midwifery degrees are not required to include nutritional content, so midwives are clearly ill-equipped for this task.

General practitioners, who are often the first point of call for women when they get pregnant, and who may continue caring for them throughout their pregnancies in shared-care models, are also failing to provide essential nutrition information.

If we’re going to help pregnant women ensure they’re eating right for themselves and their babies, we will need to start by educating health professionals who they encounter throughout their pregnancies to provide clear nutritional advice. This guidance should address myths about food risks and emphasise trustworthy sources of information. And whatever else they do, it’s vital our messages aren’t about blaming soon-to-be mothers.

This article was originally published on The Conversation.
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