The Laughter Prescription

5066327879 ceb9338556 The Laughter PrescriptionOn a recent trip to Indonesia I came across a temple, in a small village outside of Ubhud, where a group of local Balinese were rolling around on yoga mats in fits of hysterical laughter. The sound emanating from the temple walls was quite amazing and, intrigued, we went closer to see what they were doing. What we had stumbled across was a laughing yoga class run by a group called ‘Bali Happy’ who move around Bali promoting laughter as an exercise, with the aim of ridding the local people of their ailments. The lovely group leader invited us in, and explained the principles of the class; apparently there are different ‘sounding’ laughs to treat problems in different areas of the body, such as your gut, lungs, throat, head etc. He explained that the Balinese people were suffering from illness resulting from an unusual spate of weather which had left Bali wetter and colder than usual; and that they were helping people by focusing on the healing properties of laughter. He then invited us to join the class. This amazing experience left me questioning; aside from the psychological, emotional and communicative benefits, what are the biological principles underlying the healing properties of laughter, and could it really be of therapeutic value?

Norman Cousins The Laughter Prescription

Norman Cousins

The Western ideology for laughter as a medicine began in 1976, when Norman Cousin published his paper ‘Anatomy of an Illness’ which sparked a cascade of enthusiasm for health benefits of this innate, involuntary reaction. But is laughter really the best medicine? Well one thing’s for sure, it can’t hurt. Indeed, unlike many forms of prescribed medication, laughter certainly has no undesirable side-effects. Also a number of studies have highlighted its health benefits.

The act of laughing causes a series of physiological changes. These act rapidly and are often accompanied by many beneficial consequences; particularly to the muscular, respiratory and cardiovascular systems of the body. One of the most frequently reported benefits of laughter is that it exercises and subsequently relaxes many important muscles. In 1979, Cousins described laughing as “a form of jogging for the innards”; this is because when we laugh our whole body becomes involved, leading to the coordinated action of our facial, chest, abdominal, skeletal and even gastrointestinal muscles. Furthermore, after laughing we experience a period of muscle relaxation with assists in reducing tension in the neck, shoulders and abdominals.

Our cardiovascular and respiratory systems stand to benefit too. Laughter causes a prompt increase in heart rate and blood pressure, which can improve circulation. This, coupled with an elevated respiratory rate, respiratory depth and oxygen consumption, improves the rate of residual air exchange and ventilation. These physiological changes are followed by a drop in heart rate, respiratory rate and blood pressure. Indeed, research has identified an inverse association between the propensity to laugh and coronary heart disease. Laughter has also been suggested as an adjuvant therapy to reduce the risk of heart attack in high-risk diabetic patients. For a review of the health benefits of laughter, see here.

5515038358 09f4285956 The Laughter PrescriptionStudies have also identified that the muscle exertions involved in producing laughter may have a stimulatory effect on the production of endorphins. Endorphins are opioid compounds that stimulate feelings of euphoria and lower pain thresholds. It is widely accepted that a patient’s emotional state will often affect the course of a disease. Therefore any therapy which encourages positive emotions in patients may ultimately improve their prognosis.

Interestingly, laughter therapy it is one of the most frequently used complementary therapies in cancer patients worldwide. It’s success most likely stems from the observation that laughter can reduce stress levels. Any therapy which successfully reduces stress certainly can’t be a bad thing; especially since studies have correlated both laughter and reduced stress with improvements in immune function and increases in pain tolerance. Some studies even suggest that laughter may increase disease resistance. The precise mechanism of this is yet to be defined, but may be linked to attenuation of serum levels of the ‘stress hormone’ glucocorticoid. Glucocorticoids are known to suppress the immune system, making stressed individuals more susceptible to disease. So, in it’s action on the neuroimmune system, it seems that laughter can directly improve disease resistance, by manipulating our innate immune responses and reducing glucocorticoid levels.

Given the known psychological benefits of a positive emotional state, it’s not surprising that laughter therapy has also been suggested to have clinical applications for neurological diseases like dementia and schizophrenia. As with most serious illnesses, dementia can place both sufferers and their families under high levels of stress. Since stress is believed to negatively affect an individuals cognitive ability, this may exacerbate symptoms. Laughter therapy has been suggested as a way of reducing stress in both patients and their families. Indeed, when a positive attitude is shared by patients, families and staff, it can have a positive effect on the emotional-affective and cognitive functioning of the patients.

Laughter has helped patients to withdraw from feelings of irritability, stress, tension, and counteract symptoms of depression; it elevates self-esteem, hope and energy, promotes memory, creative thinking and problem solving; increases aspects of self-efficacy and optimism and improves relationships and general quality of life. In other neurological diseases like schizophrenia, laughter has been shown to reduce hostility, depression and anxiety scores and encourage social competence.

Although complementary therapies such as this are not meant to replace mainstream treatment and are not promoted to cure disease. They may often be effective in controlling symptoms, improving well-being and quality of life. While laughter research is still in it’s infancy, there is much to be said for its numerous psychological and physiological benefits and the potential for it to become a very successful complementary and alternative therapy. With laughter as an exercise emerging into the main-stream, through clubs like laughing yoga, it appears that laughter-based interventions are gaining more acceptance, and hopefully further scientific study will follow as a result. As laughter medicine continues to generate more medical and public interest, it may be important to consider that along with eating your vegetables, exercising regularly and getting enough sleep, laughter is a wonderful way to enhance your health. Most importantly, as demonstrated here, there are more than a few reasons to conclude laughter is, and could in the future be, a widespread and effective complimentary intervention for many diseases.

Post by: Isabelle Abbey-Vital

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A pill to cure Alzheimer’s!?: Why science stories should be reported more carefully

On October 10th 2013, there were headlines on the front pages of several British papers claiming that “A simple pill may cure Alzheimer’s”. These papers included the Times (£) and the Independent, who both put the stories on their front pages, the BBC website and breakfast show. The story was also tweeted by these outlets as well as America’s Fox News:

As a scientist who has worked on Alzheimer’s disease, headlines like this always provoke my cynical side. I’ve seen stories proclaiming a cure many times before, yet no cure is forthcoming. My cynicism was somewhat rewarded when I researched the story further. The study did indeed find that a pill, which inhibits a protein called PERK, was able to prevent brain cell death in mice which showed symptoms of disease. However, the disease the mice had was not Alzheimer’s; they had a prion disease.

In order to understand the research, here’s a quick explanation. Prions are misfolded, infectious proteins which are linked to neurodegenerative diseases such as BSE (or “mad cow disease” as it was known in the 80s) and CJD in humans. Alzheimer’s is also caused at least in part by a misfolded protein, called amyloid-beta (Aβ). Both prions and Aβ are affected by something called the Unfolded Protein Response (UPR) in cells. The UPR detects the misfolded protein and stops the brain cell making any new proteins. This means that the cell cannot make proteins which are essential to its survival and so will eventually die, leading to neurodegeneration.

Don’t get me wrong, the results from the study are promising. However, the newspaper headlines are incredibly misleading. There are some key problems with interpreting the research as a “cure for Alzheimer’s”:

mouse 300x186 A pill to cure Alzheimers!?: Why science stories should be reported more carefully

    • This study only theoretically applies to Alzheimer’s disease as the authors note that Aβ is subjected to the same UPR as prions. The effects of the drug will need to be tested on Aβ before any definitive conclusion can be made about its effectiveness in treating Alzheimer’s. Furthermore, Alzheimer’s disease has other contributory destructive mechanisms not related to the UPR which also need to be assessed. The same is true before a link can be made to the other neurodegenerative diseases mentioned in the paper, such as Parkinson’s or ALS.
    • The research was conducted in mice rather than humans and there is no guarantee that the drug will be usable in humans. It may not have the same effects or the side effects may render the drug unusable.
    • The drug causes potentially serious side effects in mice such as mild diabetes and weight loss. This would have to be rectified before the drug can be administered to humans which could take a significant amount of time.
    • The weight loss side effect in mice means that they could not be used for a long time and it is unknown what the long term effects of the drug are. Something which targets both the brain and an essential cellular process such as the UPR may have detrimental effects if used over a long period of time.
    • The pill does not “cure” memory loss. The mice that were treated with the drug did not regain memories which were already lost. However, treating these mice did prevent the disease from progressing further. This pill will not help people who already suffer from mid to late-stage dementia.
  • Even if the drug is suitable for use in humans, it will have to go through clinical trials before being put to regular use. This will take years, possibly even decades.

Most of the newspapers covering this story did mention some of these problems. The Independent in particular made it very clear the study was in mice and a cure is “a long way off”. (However, in their tweet (above) they say that, “This breakthrough in treatment for Alzheimer’s could very soon pave the way for a simple pill to cure the disease.” showing the differences in these types of news communication). The Express, on the other hand, took seven lines to even mention that the study was in mice. Unfortunately, in this day and age, many people don’t read further than the headline, sub-heading and possibly the first two or three paragraphs.  Many people therefore may well get the impression that a cure for Alzheimer’s is imminent and misunderstand the point of the study.

Later on in the day when things had calmed down a bit many newspapers did write editorials (for example in the Independent and the Guardian). These mostly highlighted some of the points above and clarifying that there is still a long way to go in curing Alzheimer’s.  But this is after the damage had been done, the headlines had been seen and the tweets had been sent. The point is that the story should never have been given so much prominence in the first place.

It’s quite easy to assess how people are reacting to a story by use of Twitter. A quick search of “Alzheimer’s” on the day the story broke showed a lot of people re-tweeting the story from various news sources, some with a link, some without. The misleading nature of the headline can be seen by the nature of some of these tweets, including one which said “They’ve found a cure for Alzheimer’s. This is big”. One of the big tweeters was the comedian Jimmy Carr, who tweeted this (rather lame) joke:

With no link to the story, how are people supposed to know where he got the information from? Another problem with today’s microblogging news delivery system is that there isn’t a lot of room for details and so the story can easily get mutated.

There were some expressing cynicism. The Alzheimer’s Society stated “This is a promising development as it shows this biological pathway is a potential target for new treatments.  However, it is important to note that this study was carried out on mice with prion disease and so it is not clear how applicable it is to humans with diseases such as Alzheimer’s.”

But it’s not the users of Twitter who I am concerned about. The problem with misleading story reporting like this is the effect it has on sufferers of the disease or their relatives. The reason this particular story has got me angry is because I have seen the effects that this sort of reporting can have. Long-term readers will be aware that my grandmother suffered from Alzheimer’s Disease, which took a huge toll on my grandfather.

I still clearly remember a day when a national tabloid newspaper carried the headline “Vaccine for Alzheimer’s Disease!” My grandfather read the headline, turned to me and said “Does this mean they’ll be able to cure your grandmother?” My cynicism piqued, I read the article and had to gently tell him no. That story held many of the same points as this one; it was a study done in mice and no human trials had been conducted. It is five years later and there is no news on that subject; whether it failed at clinical trials or is still being tested I don’t know. But the false hope it gave to my grandfather, and the countless others who read these headlines and think their disease may be cured soon, is a sad and dangerous thing.

newspaper 300x202 A pill to cure Alzheimers!?: Why science stories should be reported more carefullyWho is to blame for this misinformation spreading? It’s probably a subtle combination of the scientists who wrote the paper, the journal who published it and the reporters who wrote the newspaper stories. For scientists, having work published in national newspapers is a huge coup; national reports result in interest in your work and so you’re more likely to secure funding  to continue with your groundbreaking research. Unfortunately, newspapers and by extension their readers will mostly respond to “interesting” stories, which translates to “treating a disease that people have heard of”.

Alzheimer’s is big news now, as it is predicted to affect 1 million people by 2021. Therefore, the scientists probably put Alzheimer’s as the key point of the findings to increase interest in their research. This is a common practise amongst researchers desperate to secure funding from a dwindling pot. I noted when researching this post that every single headline said the more evocative “Alzheimer’s” rather than “Parkinson’s Disease” or “ALS” which were also mentioned in the research paper as potential beneficiaries of the drug. Curiously, CJD isn’t even mentioned by the researchers as a disease which can benefit from the treatment despite being the best-studied prion disease in humans. However, CJD is much rarer than Alzheimer’s (causing 1 death per 1-2 million of the population) and the media storm that happened around it in the 90’s has died down. It is not a “sexy” enough disease to sell research or newspapers on such a grand scale.

How is this problem going to be solved? Is it possible to make research interesting if it’s not linked to a disease? I would like to think it would, but them I’m biased. It’s a real bugbear for me as a biologist that an “interesting” story about biological research has to be about curing a disease. Research which just explains how a system works can be fascinating.

Certainly taking out a small, speculative point and blowing it up to the key part of the story doesn’t work.  However an accurate headline such as “There’s a drug which prevents brain cell death in mice that have something similar to Alzheimer’s disease; won’t be used in humans for a decade or so” is hardly catchy. But it should be made crystal clear in the very first reading points of the article exactly what has been found and its relationship to the disease; the authors and journalists at least owe that to the people affected. As a reader, it’s probably best to take headlines involving the words “cure” and a deadly disease with a pinch of salt until you’ve read the full article. Unless they involve the words “repeated successful human trials” then it’s probably best to treat the information with caution.

Post by: Louise Walker (in rant mode)

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Are we on the verge of an era of personalised medicine? Ten years on from the Human Genome Project.

“Ten years ago, James Watson testified to Congress that once we had the genome sequenced, we would have the language of life. But it turns out that it’s a language we don’t understand.”         Robert Best, 2013

In April 2003, at a cost of $2.7bn, the human genome was announced to great pomp and ceremony. This would reveal the deepest secrets of biology, give us the blueprint to create a human and disclose how diseases develop. But 10 years on, has the Human Genome Project been a true medical breakthrough and what role does it play in medical treatment today?

The Human Genome Project was headline busting. This was an international collaboration like no other, which would be the shining peak of human endeavour. Being able to look into an individual’s DNA would give us new knowledge about what caused diseases. What’s more, this would herald a new era in medicine whereby we could use this to diagnose diseases years before a patient felt any symptoms and tailor their treatment to their own personal needs.

Unfortunately, passionate headline-filling coverage has waned recently. The human genome is sadly a lot more complex than we had hoped. The quote above, from geneticist Bob Best, sums up the current state of genome sequencing. Speaking to the Guardian’s Carole Cadwalladr in her excellent first-hand account of how it feels to get your own genome sequenced, Dr. Best hits the nail on the head. We can now sequence a whole human genome for $5,000. That part of the technology has accelerated forward. What remains however, is the pining question of what it all means.

DNA Double Helix 300x226 Are we on the verge of an era of personalised medicine? Ten years on from the Human Genome Project.

The first problem is that the most common diseases seem more complicated than we had hoped. Instead of being one disease caused by one gene, these diseases seem to be lots of smaller diseases caused by many different genes, conspiring to produce similar results. This is the most evident in cancer. People like to group cancers together into one disease but in reality, there are many, varied faulty processes that can cause a cancer to develop.

One can now do an experiment whereby you measure the genomes of a group of cancer patients and compare them to the genomes of a group of healthy volunteers. Unfortunately, this gives you many, subtle deviations and not one Holy Grail ‘cancer gene’.

Despite this disappointment, there are great success stories emerging from this area. Angelina Jolie nobly led the way earlier in the year with the announcement that she had had a preventative double mastectomy. Jolie had a genetic test which revealed she carried a faulty copy of a gene known to increase women’s chances of breast cancer to 87%. Having a complete code of the cells in your body can only increase the likelihood of finding similar preventable risks of your own. Whether you would want to is another matter entirely.

Genome sequencing has given rise to the potential for personalised treatments. We know that the best treatments we currently have do not work for all patients. This fits with the knowledge that these diseases are actually different diseases all showing similar symptoms. By understanding which small subset of disease a patient is showing and how a patient might deal with a drug, we can tailor the treatment accordingly. The way this technology can be used is explained excellently in this animation. At this stage, we have increasing numbers of great success stories from rare genetic diseases, but limited success in the most common diseases.

This could be because the genome only tells us what may be happening in a living organism. Genes contain the instructions to make life; on their own they do nothing. It is the proteins that are made from these instructions that are the true machines of the living world. Proteins are made from genes via processes known as transcription and translation (see picture below). How a protein is made from the instructions in a gene can be impacted by many lifestyle and environmental factors. This is exactly why lifestyle and environmental factors play such a huge part in disease.

Gene Protein1 Are we on the verge of an era of personalised medicine? Ten years on from the Human Genome Project.

One’s genes do not tell us everything, they only contain the instructions. It is the proteins they make that are the true workhorses of the living world. Genes contain the instructions to make proteins via processes known as transcription and translation. These are impacted by environment, lifestyle and disease.

There are leaps and bounds being made in the field of proteomics. This is the process in which proteins, as opposed to genes, are measured. By measuring the proteome (all the proteins in a cell) we can now see what the genes are doing. We can see which genes are more active than others by seeing how much of the respective protein is being made. The vast complexity of this comes when people can have very similar genes, but widely different combinations of proteins they make from them. The human genome contains roughly 21,000 protein-encoding genes. These are responsible for the production of an estimated 250,000 – 1 million proteins. Measuring someone’s genome alone will not tell you exactly what is going on within their bodies.

Albeit technically difficult, analysing the proteome of patients has the potential to tell you which subset of disease patients may have, it can tell you which faulty genes are the most harmful, and can give you possibilities for new treatments. We hope that what goes on beyond a person’s genes will unlock further understanding of disease and truly bring in the era of personalised medicine.

The Human Genome Project has and will continue to open up new realms of possibility for understanding more about life. It has given us the basis to build on our knowledge of how we are made and the beginning to personalised medicine. However, there is still a very long way to go. It is the proteins inside you that truly define health and disease. Until we understand more about how specific genes make specific proteins and how this is impacted in common diseases, we will only be scratching the surface of the potential personalised medicine has to revolutionise treatment.

Post by Oliver Freeman


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Printing human organs – is this the answer to solving the transplant shortage?

There are approximately 10,000 people on the UK transplant list waiting to receive an organ. Statistics show that, due to a shortage in organs available for transplant, every day 3 of these people will die before receiving their transplant. Unfortunately, we have not yet found a way to address this shortage. However, with this in mind, money is being poured into investigating new technologies aimed at tackling this problem.

But how? Well, the answer may have been under our noses all along. Using a popular everyday technology, we may be able to use printing with a modern twist to generate these desperately needed organs. Imagine being able to print out a new liver, or a lung, or in fact whatever organ you needed.

Kidney 1 300x230 Printing human organs – is this the answer to solving the transplant shortage?In 2011 Dr. Anthony Atala, director at the Wake Forest Institute for Regenerative Medicine, received a standing ovation when, on stage during a presentation, he printed out a prototype kidney made from living cells. Although far from perfect, the kidney was able to break down toxins and produce a waste-like product, just like the genuine thing. Despite their diminutive size, these ‘miracle organs’ have the potential to revolutionise medicine as we know it.

And these aren’t the only organs to have been produced using 3D printing. Scientists at Organovo, a bioprinting specialist, have now created miniature livers. These tiny livers are just 4mm wide and ½ mm in depth, but are still able to produce the proteins essential for carrying hormones and drugs. Importantly, the livers produce cytochrome p450, which is vital for breaking down drugs in the body. What’s more, cells from blood vessels can be incorporated into the livers to supply them with oxygen and other nutrients.

printer 1 277x300 Printing human organs – is this the answer to solving the transplant shortage?3D printers work by printing out layer upon layer of ink (or any other substance) until a 3D object is achieved.   All we have to do is tell the printer what to print with a computer aided design program, hit the print button and let the magic commence. Hey presto- there you have a real-life 3D object.

When printing organs, layers of living cells are laid out in sheets upon each other and a scaffolding material called hydrogel is spread between the layers providing nutrition to the cells and helping them fuse together. The cells are able to survive for as long as four months in these conditions. Images of the patient’s original organs are generated using a CT scan which forms a template that instructs the printer on how to to produce a life-like replica of the organ.

Although 3D printing may seem ultramodern, it has actually been used in the medical field some time to produce things such as hearing aids and braces.  This technology has astonishingly also been used to create an entire lower jaw for an elderly women who was deemed too fragile to undergo reconstructive surgery. The jaw was designed to be realistic, with cavities and grooves in the mould to allow for the re-attachment of jaw muscles and nerves.

We are now at a stage where we are able to print sheets of living cells, but only on a small scale. Researchers have surmounted a massive hill, and have finally found a way to pass human embryonic stem cells through a 3D printer without sustaining any significant damage to the cells.

Researchers are hopeful that over the next few years we will be able to use these tissue strips to test the toxicity of new drugs before exposing living patients to these potentially dangerous substances, saving not only time and money but also reducing risks to patients. Using the so-called mini organs, researchers will be able to watch the progression of diseases in life-like organs outside of the body.

Over the course of the next 10 years we will most likely see 3D printing being used to assist in regeneration such as bone and skin grafts, patches for heart conditions, regeneration of sections of blood vessels and replacement cartilage for joints.

As for producing entire organs, there is still a long way left to go. The problem lies with being able to produce a fully functioning organ on a full-size scale with the ability to maintain its own oxygen supply via a vascular system, and to remove its own waste.           The hope is that researchers will be able to devise a way that will allow a printer to produce a full scale organ without any damage to the cells, and that is sufficiently supplied with oxygen and nutrients. If we manage to achieve this, then using ‘printed’ organs may cease to be something of a dream and become a reality. Over the next 10 or 20 years, the thousands of people likely to need a transplant could be lucky enough to receive an organ almost immediately instead of waiting months or even years as is the case now.

Post by: Sam Lawrence

For more information on organ donation or to join the organ donor register visit:

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The Komodo dragon: how this foul-mouthed fiend feasts

“Meddle not in the affairs of dragons, for you art crunchy and good with ketchup.” ― Anon

Komodo1 300x190 The Komodo dragon: how this foul mouthed fiend feasts

A wild Komodo dragon

The fearsome Komodo dragon (Varanus komodoensis) is the world’s largest living lizard, weighing in at an average of 150 lbs, and measuring 3 metres in length. It is native only to five of Indonesia’s islands, including its namesake, Komodo.

The Dragon is both a scavenger and an ambush predator; capable of lying in wait for hours at a time until prey, such as buffalo, come close enough for it to attack. Of course, not all kills are clean and quick. Animals injured in attacks by Komodo dragons can survive only to die days or weeks later from their wounds. Dragons have even been known to follow wounded prey for days until they die in order to enjoy an easy meal.

Interestingly, being the dominant predator in their habitat, it is likely that a member of the species will benefit from a delayed kill; even if it isn’t the individual that caused the death. This is very possibly a demonstration of ‘altruistic’ behaviour whereby an individual’s actions benefit the population as a whole.

But what exactly do these injured animals die from? Certainly Komodo dragon bites can be sufficiently deep to cause fatal blood loss but this is not always the case. Something else must come into play. The nature of that ‘something’ has caused a lot of controversy in recent years as different studies have produced contradictory results. There are currently two major theories, the oldest of which is coming under increasingly heavy fire from supporters of its more contemporary rival:

The Original Theory: Harmful bacteria live in the mouth of the Komodo dragon and infect wounds the dragon inflicts upon its prey

This particular theory originated in Walter Auffenberg‘s book, ‘The Behavioral Ecology of the Komodo Monitor’, published in 1981. In order to understand why Dragon bites sometimes resulted in delayed fatalities, Auffenberg swabbed the gums of captured Komodo dragons and identified four bacterial species from the samples. Three were described as being common causes of infections in animal bites.

Around 20 years later, Joel Montgomery’s group repeated this test, but on a much larger scale and with far more sophisticated screening techniques. They identified 58 species, with considerably more seen in wild Dragons than captive ones. The group also injected Dragon saliva directly into the abdomens of mice in the hope that they might recover a bacterial culprit from any mice that died from these simulated ‘bites’.

Some, however, consider their results contentious. All of the bacterial species the group found are pretty common in soil, plants or on animals’ skin. One species – Pasteurella multocida – present in some of the infected mice, was assumed to play an important role in prey infection, since the Dragons themselves were immune to it. Unfortunately, the species was only present in 5% of Dragons’ mouths and it turns out it isn’t actually capable of causing fatal septicaemia at the rate seen in Dragons’ prey.

Komodo2 300x201 The Komodo dragon: how this foul mouthed fiend feasts

Young Komodo Dragon feeding at a water buffalo corpse on Rinca

 It is now increasingly thought that the bacteria found in Komodo dragons’ mouths are simply the bacteria that were growing on/in the reptiles’ most recent meals. This may explain why captive Dragons, which are fed fresh meat, have fewer bacterial species in their mouths than their wild relatives, which will eat rotting carcasses. This all makes for a conspicuous lack of compelling evidence to support the idea that Dragons have evolved to use bacteria as a ‘weapon’.

The Modern Theory: The Komodo dragon uses venom to incapacitate its prey

This idea arose from a 2009 study by Bryan Fry’s group in Australia. They noticed that prey wounded by bites from Komodo dragons show common symptoms; namely being subdued, bleeding heavily and finally going into shock. Interestingly, these are the same symptoms caused by venom released by members of a related genus of lizards called the Helodermatids.

With this in mind, Fry’s group performed a Magnetic Resonance Imaging (MRI) scan of a preserved Dragon’s head and discovered a large venom gland in the lower jaw. The gland was divided into 6 compartments, with separate ducts leading from each compartment into the mouth, opening out between the Dragon’s serrated teeth.

The team discovered that the venom contained 2,000 proteins, around a third of which were known toxins in related reptile species. Indeed, the Dragon’s venom composition was similar to that of snakes, containing anticoagulants and toxins that lower blood pressure, causing persistent bleeding and weakness.

Interestingly, unlike other venomous lizards, Dragons do not have teeth specially adapted for chewing and working venom into their unlucky victims’ wounds. Instead, Fry suggests that the Dragons, who don’t have particularly strong bites, use their serrated teeth to “grip-and-rip” flesh, forming deep wounds into which venom could easily flow.

Continuing controversy:

The venom theory has more convincing evidence behind it than its predecessor and has become a far more widely accepted theory since its conception in 2009. It seems far more feasible that Dragons could have evolved effective venom, rather than evolving a co-dependent relationship with a variable bacterial population. The next steps in proving this theory may be to find evidence of Dragon venom in a prey animal, as well as physical proof that these venom glands actively work.

Despite all of this, however, the original theory still has a lot of supporters and has not yet been entirely ruled out. It is likely that the scientific community will remain split on the issue for some time to come. One thing we can all agree on, though, is that this fascinating beast has evolved a highly effective killing mechanism, which makes it both a powerful and intimidating predator.

Guest post by Ian Wilson

Learn a little more about Ian:

IanWilson 234x300 The Komodo dragon: how this foul mouthed fiend feasts“I’m currently about to enter my fourth and final year of a PhD studying the genetics of the human parasite Entamoeba histolytica. I’m based at the University of Liverpool, which is also where I completed my undergraduate degree in Microbiology. I’m really passionate about improving the public’s relationship with science and I aim to become a full-time science communicator when I finish my PhD so I can really get stuck in!”

You can follow Ian on twitter @Science_Gremlin and for more top-notch science writing, including an answer to the question: Just how scientifically possible are Gremlins?: Visit his blog:

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Science of the bloody brain

mosso 300x205 Science of the bloody brain

One of Mosso’s experiments. Each of the four traces on the right compares brain blood flow (red) and pulsations in the feet (black) simultaneously, during 1)resting 2)listening to the clock and church bells 3)remembering whether Ave Maria should have been said and 4)’8×12’?

Luigi Cane literally had a hole in his head. A brick had unforgivingly fallen on the back of it, smashing a section of his skull like a spoon knocking the shell off the top of a hard-boiled egg. And so, after surgery, part of the surface of his brain was left precariously unprotected except for a layer of skin. Peering through this accidental window into his head, Dr. Angelo Mosso was able to measure the pulsations of the brain’s blood supply. Cane sat in Mosso’s lab with pressure gauges strapped around his feet and a handmade instrument resting delicately on the skin over his vulnerable brain. This was to be the world première of neuroimaging.

972 Science of the bloody brain

Angelo Mosso, a 19th century physiologist and first brain imager

“What is 27 times 13?” Mosso inquired. Cane thought deeply and silently while the various contraptions simultaneously showed his feet shrinking while his brain swelled with blood flow. This experiment was the first to reveal that when our mental ‘cogs’ turn, a boost of blood is directed to the brain. Mosso confirmed this in individuals with intact skulls with what was essentially a wobble-board bed. When people lying down on the balance thought about tricky or even particularly emotional questions, it would tip down towards the head end with the weight of the extra blood.

The brain is an extremely greedy part of the body when it comes to blood. While it only makes up about a fiftieth of the body’s mass, it consumes up to a fifth of the total energy and oxygen carried in the bloodstream. Charles Roy and Charles Sherrington later proved that the blood rushing to the head was actually being diverted specifically to the parts that were most active – like a bonus for the busiest brain cells. Over twelve decades later, neuroscientists are still using this same principle to observe brain activity and the accompanying ‘rush of blood’ to the head.

The brain imaging technique functional magnetic resonance imaging (fMRI) works on the principal that deoxygenated haemoglobin (the protein that carries oxygen in red blood cells) has magnetic properties. In essence, fMRI can measure how well-oxygenated or deoxygenated different parts of the brain get when the person in the scanner performs a task, for example reading, writing, or thinking about chocolate. But information collected from this kind of experiment needs to be handled very carefully.

Face recognition Science of the bloody brain

Computer-enhanced fMRI scan of a person who has been asked to look at faces. The image shows increased blood flow in the part of the visual cortex that recognizes faces.

Firstly, fMRI is not a direct measure of brain activity per se; rather, it’s the triggered oxygenated blood flow response to brain activity. Secondly, no one really knows what a larger blood flow response means, especially in parts of the brain that have several jobs. Lots of blood in a specific part of the brain while doing sums might mean that a person can do sums easily because their blood supply is so efficient. Alternatively, it could be interpreted as suggesting that person struggles with mental arithmetic and needs more blood in their head to cope. Thirdly, fMRI data needs to be stringently tested to avoid seeing activity that isn’t there. Researchers at the University of California found that using different statistical tests they could see a blood flow response in the brain of a dead salmon while it was looking at different human faces – and won an IgNobel Prize for highlighting the dangers of shoddy stats.

With all this to bear in mind, it’s perhaps unsurprising that poorly carried out fMRI experiments have been dubbed the modern phrenology – the practice of comparing measurements of peoples’ skulls to infer personality traits. What is perhaps more surprising, though, is that despite the speculations on the validity and accuracy of fMRI, it is being used for things besides its more traditional remit. ‘No Lie MRI’ is a company in the U.S. that advertises the use of brain imaging to detect liars or untrustworthy individuals, whether they be potential politicians, investments or romantic interests. Brain imaging techniques including fMRI have even controversially been used as evidence in Indian courts of law.

pain 300x80 Science of the bloody brain

Example of fMRI responses to painful heat to the forehead in a cohort of 12 subjects. ACC, anterior cingulate cortex; PCC, posterior cingulate cortex (Moulton et al., unpublished observations). Borsook et al. Molecular Pain 2007 3:25

There are, however, other emerging uses for fMRI that may improve its reputation. By watching live feedback of the blood flow going to the anterior cingulate and insula, two pain centres deep within the brain, sufferers of chronic pain can consciously train these parts of the brain to receive more blood. Christopher deCharms and his colleagues at Omneuron have found that people who were given the real, live feedback from their insula and cingulate and successfully learnt to train the blood flow within these parts said they experienced less pain than usual. Conversely, people unwittingly shown a dummy feedback (random fluctuations or blood flow levels from an unrelated part of the brain) didn’t report any substantial pain relief.

Brain imaging techniques that rely on measuring blood flow around the brain should be carefully interpreted; fMRI is heavily-used in research and is still fashionable in brain research. Technology has come on a massively long way since the days of wobble boards, so we should probably count ourselves lucky that we don’t need a hole in our heads to unlock the further mysteries of the blood in our brains.

Post by Natasha Bray


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Hope for new MS drug which could repair damaged cells.

Researchers from the private biotech firm ENDECE Neural have just announced the development of a new compound they believe may have the potential to repair damage caused by multiple sclerosis (MS).

MS is the most common neurological disorder affecting young adults in the western hemisphere. Although scientists are still unsure of what causes the disorder, it is known that symptoms stem from damage to the fatty covering surrounding nerve cells, known as the myelin sheath. It is believed that in the early stages of the disease the body’s own immune cells (cells usually primed to seek out and destroy foreign agents within the body, such as viruses and parasites) mistake myelin for a foreign body and launch an attack. Since myelin is essential for fast neural communication and cell protection, the symptoms of MS stem from a slowing of neural communication and ultimately nerve cell damage.

oligo 253x300 Hope for new MS drug which could repair damaged cells.The myelin surrounding cells in the brain and spinal cord is provided by cells called oligodendrocytes. These cells reach out a number of branching arms which wrap around segments of surrounding neurons, forming the myelin sheath. The majority of drugs available for treatment of MS aim to reduce initial damage to this sheath. However, researchers from ENDECE are now investigating treatments which can increase the number of oligodentrocytes in the central nervous system, thus leading to remyelination of damaged cells. Dr. James G. Yarger, CEO and co-founder of ENDECE notes, “For decades, researchers have been seeking ways to induce remyelination in diseases such as MS that are characterized by demyelination,”. And now this dream may be becoming a reality.

ENDECE’s work revolves around their pipeline drug NDC-1308. Although the name isn’t likely to turn any heads, its properties just might. Following the observation that pregnant women typically do not experience the symptoms of MS during their third trimester, a number of researchers have been exploring a possible role for estrogen in the treatment of MS. ENDECE researchers created 40 separate estradiol analogues (substances similar in structure to estradiol but with a range of key modifications) and assessed their biological effects. From this work they found that one analogue (NDC-1308) had a particularly potent effect on oligodentrocyte precursor cells (OPCs – cells with the ability to become mature oligodentrocytes), causing them to differentiate into mature oligodendrocytes. In follow-up studies researchers found that treatment with NDC-1308 led to remyelination in a mouse model of MS, specifically showing a 20% increase in myelination in the hippocampus (a region of the brain known to experience demyelination in this model). NDC-1308 was also found to cause remyelination in the rat and to induce cultured OPC cells to differentiate into mature oligodendrocytes. Taken together, these findings suggest that NDC-1308 may prove effective in restoring the lost myelin sheath on damaged axons in patients with MS.

Dr. Yarger states, “We envision NDC-1308 being administered either alone or in combination with current therapeutics that target the immune response and/or inflammation associated with MS. By inducing remyelination, it may be possible to restore muscle control, mobility, and cognition in patients with MS. Therefore, a drug that induces remyelination, such as NDC-1308, can potentially double the size of the current market for MS therapeutics.”

NDC-1308 is still in late preclinical development, and has yet to go through rigorous safety screening and clinical trials. However, as a drug that potentially stimulates remyelination, it represents a whole new strategy for the pharmaceutical treatment of MS patients in the future.

Post by: Sarah Fox

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