Can you die of a broken heart? Perhaps not, but heart attacks have been known to be triggered by intense emotion and mental stress. At a Packed Lunch event last month Malcolm Finlay, Senior Clinical Research Fellow at UCL, talked about investigating the electrical and physiological mechanisms behind this phenomenon. Nancy Wilkinson was there to hear how an increased understanding may help to identify those most at risk and reduce their chance of sudden death.
Valentine’s day. For some it is a romantic day filled with chocolates, flowers and teddy bears. For others it is an excuse to gorge on ice-cream whilesinging ‘All by myself’ in pyjamas. Whatever today means to you, it all revolves around our hearts.
Cynics may say that the heart has nothing to do with love, and is just the organ that keeps the blood pumping through our veins. But having a broken heart is real. Intense emotional stress is actually quite common in triggering heart irregularities I found out at a recent Packed Lunch event at Wellcome Collection.
Dr Malcolm Finlay, cardiologist at University College London, researches how the heart copes in stressful situations, and came to Packed Lunch to tell the audience all about it. Although a bad break-up can cause a broken heart, emotional stress can be caused by lots of things, and it all has an impact on our hearts.
Finlay told us about a few notable examples where during a stressful event the numbers of heart irregularities spiked. After an earthquake in San Francisco, there was a huge increase in the number of heart attacks, and during a football World Cup, there were spikes in the number of heart attacks in Germany every time their home team played a match.
The people who suffered these heart irregularities weren’t random; they were those who were pre-disposed to heart problems already. In each case there was a dip in the number of heart attacks following the event: the people who were going to have a heart attack, had it then.
To find out what happens when we are stressed, Dr Finlay and his team measure the heart when it is put in a stressful situation. The team find willing volunteers amongst patients who are already undergoing procedures on their heart. These patients have a catheter – a thin plastic tube, with a platinum end – leading from the upper leg, through a vein into a chamber of the heart. This platinum ended catheter can measure the electrical activity of the heart, and therefore if it is beating normally. Finlay brought along a catheter to show the audience, and I have to say it was a lot bigger than expected. He explained that veins don’t contain any nerves, and are extremely stretchy, so the patient doesn’t feel any pain at all.
To get the patients stressed, he first has to relax them. He dims the lights, gets them to think of themselves on a meadow or a beach and lie quietly for three or four minutes. Then “BANG”: the lights come on and Dr Finlay is saying, “wake up, we’re going to do some mental arithmetic”.
He then tries to crank up the pressure by asking the patients to imagine themselves in the most stressful situation possible. This often produces a heightened response: in one case, a woman actually suffered a heart irregularity right there on the operating table.
Finlay said he was surprised by the results he has seen: the heart exerts itself hugely, even when just imagining being under stress. It produces a similar response as it does when getting ready for some serious exercise, but then, of course, nothing happens. This can cause serious damage, particularly in these patients who already have heart problems.
The research aims to find out how and why our hearts react the way they do to these situations. Finlay wants to find out the mechanism of how the heart responds to stress, so it can be treated accordingly, rather than just treating symptoms. The research is still in its early days, but he has already seen more results than he thought. You never know, one day he could even find a cure for a broken heart.
Nancy Wilkinson is a graduate trainee at the Wellcome Trust.
How does a fish see where there’s no light? To find out, you have to join them in the gloomy nether reaches of the ocean. At a recent Packed Lunch, Professor Ron Douglas described his life as a visual science researcher, and Lydia Harriss was there to hear tales of the deep sea…
Out of the watery gloom, there comes a small, dark shape. It looks rather like a small fish. A tasty snack, perhaps? It’s definitely worth a closer look… Before you know it, something clamps on to you with sucker-like lips, digs in with razor sharp teeth, and twists to cut out a circular plug of flesh!
It sounds like the stuff of nightmares, but it’s not. It’s the cookie-cutter shark, and, as I discovered at a recent Wellcome Collection event, it’s real.
Speaking to Wellcome Trust’s Dr Daniel Glaser at a Packed Lunch session entitled ‘The Deep’, Professor Ron Douglas opened a window onto the secretive world of deep sea biology. He is Professor of Visual Science at City University and an expert on the visual systems of deep sea creatures.
The ‘deep sea’ describes the region from 200 metres below the surface down to the seabed, which can be 11 000 metres deep in some places. This means that his lab is the ocean and he does many of his experiments on board boats in warm and exotic locations. Costa Rica, Nicaragua, Samoa, New Zealand, Hawaii… his gleeful list of research destinations had me contemplating a dramatic change in career direction.
Although the locations sound idyllic, the research itself can be pretty tough. Catching the deep sea creatures that Professor Douglas studies is a “lucky dip” exercise. Despite dragging nets the size of a football goal behind the boat for up to ten hours at a time, a catch will often barely cover the bottom of a domestic-sized bucket.
As boats cost £25 000 per day to hire and run, scientists work as close to non-stop as they can manage, on trips that last for four to six weeks. In vision research, it’s important to minimise the amount of light that the animals come into contact with, so they usually fish at night and try to persuade the captain to switch off the deck-lights (captains are normally reluctant to oblige, as “people tend to fall off the back”). Weather conditions can also be very rough, so good sea legs are a must. And then there are the other scientists…
To spread the research costs, a single boat may carry 20 scientists from, say, 10 different labs. Living and working at such close quarters with collaborators, and perhaps potential rivals, is bound to be difficult at times. Although cruises are carefully planned to avoid having multiple scientists with the same research focus, there’s likely to be competition over who gets first dibs on what’s in the bucket.
This is where Professor Douglas has the advantage, as his experiments require the animals to be kept in the dark. Thus, the first port of call for the bucket and its contents is his dark room. “I get to see what’s there first, and then I hand the bucket out into the light and I say ‘no, there’s nothing of interest in there’”, he jokes. His particular expertise is finding out what colours animals can see, by extracting and analysing the chemicals found within their eyes.
There’s an intriguing and rather enchanting alternative to fishing for “a few mangled creatures in the bottom of a bucket” (Professor Douglas’ choice of words). Namely, going down to observe these animals in their natural environment.
The conversation between Professor Douglas and Dr Glaser carried us into a submersible and down through clear blue Caribbean water. The deeper we went, the darker and bluer it became, as though we were descending through a cathedral of blue light. This is because water more readily absorbs light of longer wavelengths, such as red and yellow, than light of shorter wavelengths, such as blue. The blue component of sunlight therefore penetrates further into the ocean than other colours of light and is the last to fade out.
By 700 metres, we were beyond the reach of sunlight, but it was not completely dark. Many of the creatures living in the deep sea make their own light through a chemical process called bioluminescence. This light is almost always blue, probably because it can travel further through water than light of longer wavelengths. The chemical reactions that produce it are similar to those found in fireflies or glow sticks (the sort that you activate by bending, which breaks an internal glass separator and allows different chemicals to mix and react).
Bioluminescence occurs in tiny pits known as ‘light organs’, which may be covered with filters that are used to expose or hide the light. Often located under an animal’s eyes or on their forehead, light organs can help to illuminate the way ahead. They are also distributed across the bodies of some fish, in characteristic patterns that may help the fish to identify each other.
In the case of the cookie-cutter shark, which can migrate between the surface and depths of as much as 3700 metres on a daily basis, light organs act as camouflage. They produce a glow that helps the cookie-cutter to blend in with sunlight from the surface, rather than appearing as an ominous silhouette likely to scare away its prey. Light organs are absent from a dark patch around the shark’s neck, which is shaped roughly like a small fish. It’s thought that this may lure the shark’s prey, who are themselves hunting for food. Many fish, whales and dolphins have been found with circular ‘crater wounds’ characteristic of cookie-cutter bites. Although these sharks have been known to attack humans, they are not usually considered a serious threat.
The majority of the deep sea creatures that we know about only see blue light, enabling them to detect most bioluminescence and any residual sunlight from the surface. Single-colour vision is also more sensitive than multicolour vision, which is a real advantage where light levels are so low.
In this mostly monochrome world, there is at least one animal exploiting the evolutionary niche of multicolour vision. Dragon fish, named for their monstrous teeth, are able to bioluminesce and see both red and blue light. A large light organ beneath their eyes produces red light, effectively giving these fish their own private wavelength. The potential advantages are huge. Imagine being able to flash your lights as a signal to potential mates without drawing unwelcome attention from your predators, or hunting with a bright searchlight that you can see but your prey cannot.
Unlike dragon fish, the humans investigating the deep sea are far less stealthy. Professor Douglas likens going into the deep sea with a submersible to going into the savannah with a Land Rover to see lions. At night. With the headlights on, the stereo blasting, and a blue flashing light on the roof. “All you really see are the deaf, the blind, the stupid and the old. In other words: the things that can’t get out the way.” Despite this, researchers reckon that roughly one in three dives find an entirely new animal that no one has ever seen before. “Deep sea biology is one of the few fields where you really can just be an explorer.”
At present, submersibles can go down as far as about 4000 metres. As we develop technology that will take us further into the depths of the ocean, allow us to stay down there for longer and enable us to switch off the metaphorical stereo, we are likely to discover more incredible creatures. Creatures that are already lurking out there in the deep, just waiting to be discovered…
Lydia Harriss is a graduate trainee at the Wellcome Trust.
With the flu season upon us, at the first Packed Lunch talk of 2012 in Wellcome Collection, Professor Wendy Barclay – Chair of Influenza Virology at Imperial College – discussed her current research. Penny Bailey was there to hear about the race against a constantly changing virus.
We think of flu as a human disease, but its main hosts are birds (particularly wild waterfowl), with whom the virus enjoys a very successful relationship. It causes few symptoms in birds and passes easily from one host to the next, courtesy of the waterholes where large flocks of migratory birds gather to defecate and drink. Infected birds shed the virus in their gut into the water, which others then imbibe.
Occasionally the virus crosses to pigs and chickens on nearby farms. From pigs it can pass to humans – not through pork products, but through contact with the live animals. It can also pass directly from birds to humans, as the H5N1 virus did in Southeast Asia in 2007. This ability to move around in lots of different ways is crucial both to its ‘success’ and to the threat it poses to people.
Influenza’s new clothes
Like many viruses, the flu’s genetic material is made of RNA. RNA is much more mutable than the DNA in our human chromosomes, the extreme stability of which restricts our evolution to a leisurely pace over millennia. The flu virus, by contrast, swaps bits of RNA around to change its coat of surface proteins within months – that rapid evolution allowing it to elude the host’s immune system, and any new vaccines aimed against it.
The flu virus is too small to see without an electron microscope, but Wendy brought along a model – a sparkly, remarkably symmetrical ball with spikes sticking out of it – to demonstrate how it changes its protein coat. The spikes (or surface proteins, or ‘antigens’) are shaped like lollipops, each comprising a head on a stalk that sticks out of the body of the virus. Our immune systems detect these antigens and generate specific antibodies against them that target the virus for destruction.
The flu virus ‘wears’ two main types of spike or antigen, labelled ‘H’ and ‘N’. Each of these has a number of subtypes: there are 16 known ‘H’ antigens (H1 to H16) and nine ‘N’ antigens (N1 to N9). Combining the two gives the names of particular strains of the virus, such as H1N1 (the strain responsible for the 2009 swine flu and 1918 Spanish flu pandemics), H5N1 (the 2007 avian flu pandemic) and so on.
The numerous possible combinations of ‘H’ and ‘N’ – plus the fact that an antibody against any one subset of either won’t protect against another subset – pose a challenge for vaccine makers, who have to design a new vaccine each year to target the most prevalent strains circulating.
The dream is to develop a once-only, one-size-fits-all vaccine that will protect us from all possible strains of the virus. In a bid to realize it, researchers are attempting to design a vaccine that will target the stalks, rather than the heads, of the lollipop-shaped antigens because these are structurally similar across all different types of H and N antigens. At present our immune systems don’t readily make this type of antibody, so it’s a question of finding a way of persuading them to do so.
Until we can do that, our bodies will be constantly running to keep up with the flu virus’s rapidly changing genome and ‘coats’.
Altruism and silence
It’s not a battle to the death. In fact, Wendy points out that it’s in the interest of the virus not to kill its host. If it only makes 100 copies of itself, that’s still enough to pass on to a new host. A million copies would overwhelm our bodies and kill us (as probably happened in the 1918 flu pandemic), effectively making the virus ‘homeless’. The most successful viruses are ‘silent’ and cause few symptoms in the host, like those living in wild waterfowl or the numerous viruses all of us humans harbour but are unaware of because they don’t make us ill – the herpes virus, for example.
Our bodies compromise in turn. When we catch a flu virus, some of our cells die an ‘altruistic’ death, to protect the rest of the cells in our bodies by limiting the number of copies the virus can make of itself.
We also have to keep a balance between by releasing inflammatory chemicals (such as cytokines and chemokines), which push up our temperature and destroy the virus, and damaging our own tissues with those same chemicals: a ‘cytokine storm’ can be fatal. The jury is still out on whether we should take paracetamol to lower our temperature during flu or let it take its course.
The 2009/2010 H1N1 swine flu turned out to be far more harmless than we first feared, and most people infected didn’t even notice they had it – but it did kill some people. Wendy believes the different impact of the virus on different people may be due to subtle changes in our genomes that protect some of us from infection (like mice, nearly all of whom have a gene that prevents them getting flu).
Alternatively, some people who got off lightly may only have received by a low dose of the virus that their body could deal with efficiently, generating antibodies against it (the basis of vaccination). Or they may have better innate barriers to infection, such as mucus and cilia. They may even have been First Defense users. Apparently it does work – Wendy confessed to using it herself on occasion. It’s very acidic (and viruses are sensitive to low pH), so it kills them in our nose and throat when they first infects us. But, she warned, we would have to ‘sniff a lot’ for continuous protection.
Since mice have a protective gene that rules them out as models for human flu, the ferret is the gold standard model for laboratory studies. Ferrets and humans have the same molecules on their respiratory tract that allow the virus to stick to and invade the cells there. And ‘ferret flu’ follows the same course as human flu: two to three days of fever, 12–24 hours after infection, followed by coughing and sneezing two or three days later (the virus denudes the protective layer of mucus and cilia in our respiratory tract).
Wendy used a ferret flu model during the 2009/2010 swine flu pandemic to try and answer a question numerous journalists were phoning her to ask: at what stage of the illness were people most infectious? And when could they return to work without risk of infecting their colleagues?
One ferret (the ‘patient’) received a dose of flu on a known day and then had two ferret ‘visitors’ – one on the first day before the infected ferret was symptomatic, and one on day five when fever had abated and the animal was coughing and sneezing. Unexpectedly, the first ‘visitor’ developed a worse case of flu, pointing to the unfortunate conclusion that we’re most infectious when we don’t even know we have the flu yet.
Genetically engineered flu
Wendy also gave her opinion on the controversial study published in November 2011 showing that five tweaks to H5N1 (that has killed 500 people) make it more contagious. She believes the scientists were trying to answer a very vital question – how likely is H5N1 to jump from birds to humans, or to another species? – by anticipating the mutations the virus would need to jump from birds to ferrets, then ferret to ferret.
We spend vast amounts of money globally stockpiling vaccines and drawing up plans to protect people from a possible H5N1 pandemic. But there are 16 (or more) types of bird flu virus – any one of which could mutate and jump species to humans. If the research showed that H5N1 would never pass to humans, we might want to change our priorities and look at other strains.
The researchers also used the genetically engineered virus to look at whether the drugs and vaccines we’ve developed against H5N1 actually work – something that hasn’t yet been tested on a real human virus.
Living on the edge
We talk about the behaviour of the flu virus, its ‘success’ and its ‘relationship’ with its host. Does this mean it is actually alive? Wendy’s take on that (still hotly debated) question is ‘almost’. The flu virus is, she believes, on the brink of life.
Finally, how worried should we really be about a possible global flu pandemic? That it will happen is a certainty, she says. There are so many viruses in the wild, in pigs and birds, more of which will definitely emerge and jump to humans, and overcrowded populations of people offer perfect conditions for a new strain to take off and spread rapidly. On a brighter note, however, not all strains will be deadly.
Packed Lunch is not just about science; it is also about the lives of scientists. At a recent event, Lydia Harriss found that happenstance plays a part not only in scientific discoveries but also in scientific careers…
History is littered with stories of great scientific discoveries happening by chance. The haphazard drifting of mould into a dish of bacteria that led to the discovery of penicillin. The sloshing bath water that inspired Archimedes’ principle of displacement. A pocket full of melted chocolate hinting that microwaves could be used to cook food. But the one about the monkey and the peanut? I confess that this particular example of scientific serendipity had passed me by, until I went to a Wellcome Collection Packed Lunch event in which Dr Zarinah Agnew spoke about her research on mirror neurons.
It turns out that mirror neurons, nerve cells found in the brain that are activated when an individual carries out an action or sees someone else performing the same action, were also discovered by chance.
In 1992, researchers in a lab in Italy had just finished their experiments. They had been looking at the electrical activity of a particular neuron inside a monkey’s brain as the animal picked up a peanut. While clearing up, one of the researchers picked up a peanut, causing the same neuron to activate in the monkey’s brain, even though the animal stayed still and was only watching the researcher pick up the peanut.
This ‘mirror’ response was totally unexpected, and since then mirror neurons have generated a great deal of excitement. It’s been suggested that they are able to match an observed action to an executed action, and could be responsible for our ability to understand, recognise and imitate actions. Wilder speculations have included proposals that mirror neurons may play a role in autism, where a person’s ability to understand other people’s actions is affected. For example, ‘broken’ mirror neurons might prevent a person from mentally simulating an action that they’ve seen someone else perform, stopping them from correctly understanding the reason behind it.
Dr Agnew was quick to point out that although these theories linking mirror neurons to autism might be true, they are a massive leap from the evidence we currently have. No direct evidence of mirror neurons has yet been found in humans, as we can’t readily be experimented on with the electrical recording technique used to identify these neurons in monkeys.
During her PhD, Dr Agnew was able to show that human brains do produce a mirror response similar to that seen in monkeys, using magnetic resonance imaging (MRI). MRI is a technique that can measure brain activity by showing which parts of the brain require increased levels of oxygenated blood. She found that a particular region of the human brain becomes active when people both perform and watch an action, such as a hand-wave.
She also discovered that this system is more complicated than previously thought, by showing that mirror responses vary for different kinds of action. This intriguing finding indicates that the brain does not simply simulate every type of action in the same way, but encodes different actions in different ways.
Curiously, Dr Agnew’s first encounter with mirror neurons also happened by chance, when, after finishing her undergraduate degree in neuroscience and frantically looking for a PhD, one of her housemates showed her an article about mirror neurons in a copy of the Economist. Inspired, she scrambled off to write the proposal for her PhD project straight away. It took Dr Agnew a year to search for funding and a supervisor, but once she got her PhD underway, she went on to do exactly what she’d described in her initial proposal. Impressive stuff, given that the path of a PhD is often winding (my own certainly took a few twists and turns), and very few people actually achieve what they set out to do at the start.
Since finishing her PhD, Dr Agnew has moved on to using MRI to look at the links between action and perception in relation to speech, as it’s been suggested that mirror neurons might also be involved in understanding sounds made by the mouth. Describing her research as “a lot more fun than I thought [it would be]… a real adventure”, she shows every sign of continuing on her terrifyingly directed career path.
It seems that the ‘right place, right time’ variety of chance certainly has its part to play in research, but success takes much more than mere luck. From hearing Dr Agnew talk about her own career, it’s clear that determination, ability and passion are essential for making the most of those tantalizing moments of serendipity when they do come along.
Lydia Harriss is a graduate trainee at the Wellcome Trust.
Psychologist and sceptic Chris French, of Goldsmiths, University of London, has spent his career subjecting paranormal claims to scientific scrutiny. When he came to our regular Packed Lunch event to talk about parapsychology, Sarah Allen went to find out whether scientific truth is indeed even stranger than fiction.
The scene is set with the offering of apples and the opportunity to absorb scientific information while enjoying a sandwich. With standing room only and a BSL interpreter at the front, this packed lunch on the topic of parapsychology had certainly whet the appetite of the incurably curious.
As part of a series of Miracles and Charms events, Chris French, Head of the Anomalistic Psychology Research Unit at Goldsmiths, talked about why our belief in ‘weirdy stuff’ is so enduring. His credentials and his role of self-titled sceptic is grounded in his constant questioning and gathering of scientific evidence to ascertain whether paranormal events are in fact true phenomenon or a fabrication of the mind.
So what is parapsychology? For Professor French it is the ‘psychology of the weird and wonderful’ and when asked what could be classified as such, examples of telepathy, life after death, feng shui, UFOs, reincarnation and angels made the cut. These beliefs can depend not only on personal sensibilities but can also be due to social and economic factors, such as where you live and what the beliefs of your nearest and dearest are.
In Professor French’s typical experiment we are watching a film of a spoon bender in action. Once bent, the spoon is placed on a table. One set of people are then told that the spoon keeps on bending whilst others just watch the spoon without any additional suggestions. The film finishes and participants are asked ‘did the spoon keep on bending?’: 60% of those with the additional suggestion said ‘yes’ compared to only 40% without any additional input.
Anomalistic psychology is a branch of psychology which in layman’s terms could be classed as the psychology of paranormal belief. It is the use of science to test whether paranormal forces exist. In experiments you work on the hypothesis that nothing exists and try to challenge it by producing evidence to support the event. Alien abduction is an interesting area as it looks at the psychology of false memories (like the suggestive spoon bending!).
When the podcast finished the audience was asked to pose questions. Professor French was asked about his view of the role of forensic psychics in the USA and who he would class as the ancestors of parapsychology. Ancestors lie with those who seek the scientific basis for these phenomena such as Susan Blackmore, Bob Morris and Richard Wiseman and for forensic psychics – well, let’s say that the media does its job well and any information can be investigated.
Professor French’s view of psychics is that there is a difference between the ‘genuine article’ and those with a more sinister agenda. Those who believe that they have the gift are always sincere about helping others, and many different factors may affect why we believe that people have a gift, including our emotional dependence on information, and feelings of guilt twinned with a willingness to accept.
Talk of forensic psychics led to the rise, fall and subsequent re-emergence of faith healer Peter Popoff and the reality that even though he was proved a fraud and claimed bankruptcy he has rebranded himself and is making his abilities work for him again.
People like Derren Brown use the skill of cold reading and convincing others that they have a gift. Yet we are all believers in something – whether that be that the new face cream really will prevent people asking you if you want to take their seat on the Tube or if indeed you have to be in it to win that lottery prize on Saturday.
But is there any room for the believer in the mind of Professor French? There is no direct answer however it appears he has a ’box’ for those things that still remain a mystery – one instance being experiences of reincarnation by children. One example is Cameron Macauley, a 6-year-old boy with memories of another life and family in Barra.
Sarah Allen is Communications and Operations Officer in Science Funding at the Wellcome Trust.
I had a bone to pick as I walked into the Forum for this Packed Lunch on breastfeeding. In January, while on maternity leave, I remember quite clearly reading an article about how it could be harmful to breastfeed babies for too long. There I was in my pajamas, breastfeeding my six-month-old, reading this on my iPhone. Incidentally, I had started introducing fresh fruit and vegetables – actually on Christmas Day – but that was more out of my baby snatching a carrot and a parsnip off my plate than anything else.
The article’s ideas questioned government advice and WHO recommendations, both of which I took quite seriously. At the time, I had enough to worry about without these unknown scientists undermining something I felt proud to have accomplished – giving my baby the best start to life. It wasn’t helped by reading the study had industry funding – I imagined greedy formula and baby food manufacturers rubbing their hands with the publication of this article.
Now, as I sit down, I look around to see if there are any other fuming mothers, ready for a fight. I spot only one mother – breastfeeding happily, I note – and two (visibly) pregnant women. The researcher, Mary Fewtrell from the Institute of Child Health at UCL, sat – somewhat nervously, I thought – waiting to be grilled, no doubt.
And interestingly enough, not five minutes in, she mentions that she wasn’t entirely happy with the billing for this talk – and the representation in the media. She fully supports breastfeeding, she says, and is a member of the NCT and has been a breastfeeding counselor. And as for industry funding, she says apparently that’s quite a normal thing to have – they have no say in experimental design or publication. I still don’t know how I feel about that, to be honest. I’d rather the money come from elsewhere.
So then, what was her motivation for the article, published in the BMJ? If you only read the news, you’d think she was out to undermine all breastfeeding mothers. But Fewtrell says actually, she’s trying to address the lack of data supporting these recommendations. She points out that WHO’s stance, taken in 2001, was based on a systematic review by scientists, who actually also called for more randomized trials. She says she’d rather get more people to even try breastfeeding – because of the very strong evidence over the reduction of risk of infection, in addition to other lesser-supported benefits in brain development, for example – than try and make mothers feel guilty for not meeting a goalpost of 6 months. This makes sense to me.
Fewtrell also made an interesting point in that she says she feels pressure to say the ‘right’ thing when she publishes, to interpret the data in a way that supports something ‘good’. That’s not the way science should work, she says – the data needs to speak for itself, and she can’t bias it. All she can do is try to add to a body of evidence. This makes sense too.
She’s now undertaking a randomized trial, based in Iceland (where breastfeeding rates are higher). The trial involved women who were still breastfeeding at 4 months, who were then asked to either continue breastfeeding exclusively until 6 months or begin introducing solids alongside breastmilk.
By the end, I felt somewhat mollified. I still have concerns about the way that science can be twisted in the media. In the case of breastfeeding (which isn’t easy at the best of times!), it can be extremely undermining to hear conflicting advice all the time. My baby’s now 14 months, and I feel confident I did the right thing by her – at least on that point. Now I can move on to worrying about her university tuition fees…
Drug resistance to malaria is a huge deal. The battle to stay ahead of the parasite has been fought for decades. But how does drug resistance arise? What can be done to prevent it? We sent Benjamin Thompson to find out…
Each time a new drug has been introduced to combat malaria, the parasite that causes the disease has quickly become resistant. Fun fact: the drug resistant strains of the parasites all came from the same place – the Cambodia/Thailand border. What is it about the environment there that aids the evolution of drug resistance? What can be done about it?
The talk began with Dr Yeung describing her travels by boat, foot and ox-cart through the jungles of Cambodia, visiting remote villages to find out what people did when they caught malaria. What treatment did they seek? What drugs did they buy? How much did they cost?
This work was undertaken to get a snapshot of what is actually occurring in Cambodia. We learnt that anti-malarial drugs are freely available in local shops. Current research is trying to find out what these drugs contain, very important to stem the tide of resistance.
Dr Yeung’s study used a ‘mystery shopper’ approach, where research staff went into shops and clinics pretending to have malaria, to discover whether they were offered a diagnosis and what drugs they were given. Generally shopkeepers and medical professionals all claim to offer the correct treatment, although the reality is often very different.
The talk moved onto the biology of malaria (helpfully illustrated in this Wellcome Trust animation). This disease remains one of the world’s biggest killers and is in the top three causes of death for children in sub-Saharan Africa.
It turns out that malaria can be caused by four separate parasites. Plasmodium falciparum causes the most severe form of the disease and is the most common strain found in Africa. In Asia both P. falciparum and P. vivax are prevalent. P. vivax has an extra developmental stage that allows it to lie dormant in the liver for months before going on to infect red blood cells.
But why study malaria in Cambodia specifically? Dr Yeung explained that the P. falciparum strain of malaria found in the region of the Cambodian/Thai border has always been quick to develop drug resistance, while African P. falciparum is still relatively drug sensitive.
By studying the way people take anti-malarial drugs we can better understand what causes resistance to develop. Often in Cambodia people only take a single anti-malarial drug when they become ill – not finishing the course of treatment. This can easily lead to drug resistance occurring. To combat this, people need to take a decent dose of a drug for long enough – ideally in combination with other drugs.
Malaria is not a health priority in Cambodia: it doesn’t really affect those that live in cities, only those that live in remote areas – disproportionately affecting the poorest people. Globally, however, Cambodian malaria is a huge problem. Already strains of the disease have been discovered with tolerance to artemisinins, fantastic drugs that have only been used for a decade or so.
Artemisinin combination therapy (ACT) should be the weapon of choice against the malaria for the foreseeable future – if resistance develops and spreads, there are very few new compounds in the drug development pipeline, and those do exist are years away from clinical use.
The reasons for this enhanced ability for Asian P. falciparum drug resistance are being intensely studied. Some believe that resistance occurs in this region first is a self-fulfilling prophecy. In the 1950s, the drug chloroquine was added to salt in an early example of a mass drug administration (MDA).
People eating the salt consumed a low-level of the drug with the aim of killing all the parasites and breaking the human-parasite-mosquito cycle. Sadly all this did was create an evolutionary pressure that selected for parasites resistant to chloroquine. New drugs had to be used to kill the chloroquine resistant strain, which of course had more time to develop resistance to the new drugs, meaning that yet again they were the first to develop resistance to the new drugs.
Benjamin Thompson is a writer at the Wellcome Trust.
Vitamin D, pretty in the sun by Perfecto Insecto, on Flickr
The sun’s been shining a lot recently, but do we get all the vitamin D that we need from natural light? And what good does the vitamin do us anyway? Benjamin Thompson spent his lunchtime indoors finding out…
On a beautifully sunny spring day this April I sat in Wellcome Collection listening to an excellent talk about vitamin D, ‘the sunshine vitamin’ (oh, the irony). The speaker was Dr Adrian Martineau, Senior Lecturer in Respiratory Infection and Immunity at Barts and The London Medical School. He spoke about the ways in which vitamin D is made and how it may have many unexpected health benefits.
Dr Martineau trained as a doctor in Newcastle and Liverpool and spent time working in a rural hospital in South Africa. Given the high prevalence of HIV in South Africa, there are also high levels of TB (find out more about TB and World TB Day on the Wellcome Trust blog).
On his return he became interested in an article written by his future PhD supervisor detailing how patients with latent (dormant) TB infections have a higher level of vitamin D in their bloodstream than those with active TB.
Dr Martineau’s PhD involved a randomised study to determine whether it was the TB that made patients vitamin D deficient, or if having a low level of the vitamin increases the risk of developing TB. The results showed that in fact, a higher level of vitamin D in the blood enhanced the ability of the immune system to fight the infection.
The talk was not just about bacterial infection, with Martineau explaining much about how vitamin D is made and why we need it.
The major source of the vitamin is made in a chemical reaction in the skin in response to UVB light from the sun. This light causes a chemical reaction to occur, converting (wait for it) 7-dehydroxycholesterol into 1,25-Dihydroxyvitamin D.
When sunlight is weak, such as in the UK in autumn and winter, we can’t make any vitamin D so need to get it from the food we eat – particularly oily fish. However, to entirely supplement our diet in this way we’d need to eat fish three or four times a day, which is simply not possible. This means that most of us during the colder months have sub-optimal levels.
The childhood disease rickets is caused by severe vitamin D deficiency, and the role the vitamin plays in the absorption of calcium and hardening of bone is well understood. Less well understood is why else it may be important. Over the past 20 years it has been discovered that a wide variety of cells, not just those in the skin, can make vitamin D – with an equally diverse number of cells having chemical receptors to accept the molecule. This is an indicator that the vitamin is important and affects many parts of the body.
Population studies have shown that those with lower vitamin D levels tend to have higher incidences of a number of diseases, including diabetes and cancer. However, given that it can be linked to so many diseases, are these low levels the cause of the problem, or are other factors such as an unhealthy lifestyle to blame?
As many of us in the UK appear to have low levels of vitamin D in our blood, Dr Martineau suggested it was time that nationwide food fortification or dietary supplementation are investigated. Will raising the overall levels of the vitamin improve the nation’s health? Some foods, like breakfast cereals, are already fortified, and studies in other countries have shown that it is a safe practice. Thankfully it’s very difficult to take an overdose by mistake, with the body able to break down any excess when present.
The speaker himself explained that he takes vitamin D pills to supplement his diet. We also learned how these pills are made. It turns out that the most common form (vitamin D3) we can buy is made from sheep’s wool. The molecule lanolin from the wool is extracted and exposed to UV light to make the vitamin D.
With the weather getting better, and learning all I did from this Packed Lunch, I can’t wait to get outside and top my vitamin D levels up (sensibly, of course – getting burnt is dangerous). It’s certainly given me something to think about over the winter months too.
Benjamin Thompson is a writer at the Wellcome Trust.
You’re listening to this Packed Lunch podcast, but how are the sound waves converted into what you hear? And how could understanding their amplification help those who can’t hear? UCL’s Ifat Yasin has been researching the inner ear, and Benjamin Thompson was there to hear what she said…
The final Packed Lunch event of March saw Dr Ifat Yasin, Lecturer in Auditory Anatomy and Physiology at the UCL Ear Institute, come and discuss her research and the science behind hearing to a room full of interested guests.
A new addition trialled during the talk were two large speech-to-text screens allowing those with lower levels of hearing to follow all the details. Dr Yasin talked us through her work, and explained what can go wrong within the ear and how it can lead to hearing difficulties.
Yasin described the current focus of her work. Picture yourself sitting in a sound-proofed room, in front of a computer monitor showing two lit squares. With a set of headphones on you’d have to listen carefully and press a button when you think you hear a ‘peep’ sound between two ‘shhh’ sounds.
These experiments can be very long: an hour, ten hours, 60 hours. That’s a lot of listening time. Thankfully the volunteers get lots of breaks! Yasin explained that many of the volunteers find the downtime really relaxing. These volunteers have hearing levels within normal limits – important given the subtle differences in volume and duration between the ‘peeps’ and the ‘shhh’s. By manipulating these parameters, Yasin can map out how the ear amplifies sound.
The talk moved on to discuss how amplification occurs. This happens inside an organ found within the inner ear called the cochlea. This is a snail-shell-shaped structure filled with liquid. Sound waves picked up by the ear cause the liquid to move. In turn this causes a membrane within the cochlea to vibrate. Very fine ‘hair’ cells detect these vibrations and turn the movement energy into electrical energy, sent to the brain via nerves attached to the cochlea. These hair cells only look like microscopic hair, but it turns out they’re not made of the same stuff as those on the top of your head.
Dr Yasin is investigating how the cochlea is able to act as an amplifier. Cleverly, it can amplify quieter sounds more than mid-level sounds. It turns out that low-level sounds make the membrane within the cochlea vibrate more than mid-level sounds. The response to rising noise levels is known as ‘nonlinear’ and is important for normal ear functioning.
‘Auditory illusions’ were also discussed. These aren’t quite illusions in the sense of hearing things that aren’t there, but are very useful for us day-to-day. When we’re in a noisy environment it can be difficult to pick out individual sounds. Thankfully our brains help to collate sounds of a similar pitch or loudness – helping us pick out relevant sounds within noise. This is known as the ‘cocktail party effect’.
Dr Yasin’s current round of experiments will take another three years. She hopes by understanding how a healthy ear is able to amplify sounds, the tests (when drastically reduced in length) can be used to diagnose those with cochlear problems.
Benjamin Thompson is a writer at the Wellcome Trust.
Greenwood Space Travel Supply Co. by WordRidden, on Flickr
Space travel might sound glamorous, but it’s not all playing golf on the moon. For a start, in zero gravity your bone and muscle start to rot. February’s Packed Lunch featured a scientist whose speciality is keeping spacemen healthy. Benjamin Thompson found out more…
Fong discussed a variety of topics, including why being in space is bad for our health, whether astronauts really do have ‘The Right Stuff’ and why humanity needs to continue exploring the heavens.
The lunch began with Dr Fong describing an experiment he participated in at the Johnson Space Centre, Houston. It involved being strapped to a plank and spun at 45 rpm for an hour, watching a Harry Potter film. The point of this? To experience an artificial gravity. Being spun like this forces the blood to your feet, making you feel bent over for the time you’re spinning. The reason for Harry Potter? That was the only DVD available.
While this might seem a bit daft, it’s all preparatory work for sending people to Mars. It turns out that over long periods of time, weightlessness is very bad for our bodies. As humans we are entirely designed to live under the Earth’s gravitation pull of one g (what are the chances?), so as soon as we encounter zero gravity, Fong explained, we basically we begin to rot. This might sound extreme, but it makes sense. When weightless our skeleton and muscles no longer need to support our weight so they begin to degrade. Add to this an inability to sleep or eat healthily (no refrigerators in space) and the astronaut has a multitude of problems to deal with both in space and when re-acclimatising after returning home.
Health maintenance of astronauts is very important and this is the role of a space doctor, or flight surgeon. Space is not an easy place to practice medicine, with many of the procedures we take for granted on terra firma not working under zero g. There’s not much spare room in a rocket to take medical supplies with you on a mission, and everything has to be thoroughly tested in weightless conditions on Earth using the delightfully titled ‘vomit comet’, an aeroplane that through clever flying can provide short periods of zero g.
Thus far, doctors haven’t been specifically sent on space missions. Fong explained that given the relatively short distance between here and the International Space Station, if you are taken ill, you can be home in a few hours and cared for by the cream of the US Army Medical Services. Currently the biggest danger from spaceflight is the travelling. Either everyone returns safe, or no one does…
This will all change, though, if/when humans are sent to Mars. If you’re a year and a half away from home, becoming seriously ill is bad news. Fong explained that risk analysis from activities carried out in extreme environments, such as Antarctica, or in submarines, suggests that it is more likely than not that something will go wrong. This suggests it’s best to send a doctor on the mission. But what if the doctor gets sick? Do you send one or two? The debate is raging, and is likely to for a while.
Fong was asked if, in today’s testing economic climate, he thought that space exploration could still be justified. He wondered whether space travel be viewed in future times in the same way as we do the pyramids now, a one-off project achieved at massive cost, both human and economic? Or will commercial bodies step in, reducing the cost and boosting the speed of knowledge creation?
He explained that although expensive and dangerous, manned space travel can teach us things that robotic missions simply can’t. For example, we only know how old the rocky planets in the solar system are by studying and ageing moon rocks brought back from the Apollo missions and counting the numbers of craters seen on the other planets to extrapolate their ages. In total, all the robotic missions have brought back a sum total of 37 grams of rock, whilst manned missions have brought back around 500 kilos. If we truly want to look for evidence of life – extinct or otherwise – beyond our own planet, we’re going to have to send people.
Benjamin Thompson is a writer at the Wellcome Trust.