In advance of the Society for Neuroscience conference in 2019, the Canadian Center for Behavioural Neuroscience (CCBN), located at the University of Lethbridge, is hosting a poster session to showcase the research of graduate students and postdoctoral scholars. My current research is showcased in the research poster below (I hope the text is large enough to read). Please feel free to contact me with any comments or questions. Enjoy!
We announced it at a family gathering, via a shirt on our two-year old son: I am being promoted to big brother. Little did we know, through the congratulations, celebrations, and inevitable wondering about what the sex might be, that the baby was already dead.
Technically, it was an embryo, but therein lies the dichotomy that I wrestled with throughout my miscarriage and beyond. Two versions of me responded to the same event. If I wasn't already (desperately) trying to finish my PhD thesis, I could write a thesis on this. But I'll try to keep it short.
Intellectual me recognized that at 6 ½ weeks of pregnancy, I was carrying an embryo. It had a functioning heart, paddles instead of hands, and was five millimeters across–about the size of a small blueberry. The fact that it was no longer alive was likely due to a lethal chromosomal abnormality.
Emotionally, I already loved it. I knew it was a girl. I called her blueberry.
The timing of the pregnancy was perfect: About five months after finishing my PhD, I would have my second child – a bigger age gap than I had wanted, but not a big deal. My husband would complete the house renovations, then we’d sell our house in the spring and move to the city where my postdoc was lined up.
It was almost too perfect–and it terrified me.
During the second dating ultrasound, the technician said blueberry seemed to be the same size as last time. I quietly thought about that, then suggested that was a bad sign. She agreed. As I lay on the table, waiting for her to return after consulting with the doctor, I let it sink in. This was happening to me. I was losing my baby. As soon as the doctor came into the room, his face perfectly sombre, my suspicions were confirmed. I would later wonder if the technician and the doctor told their partners, over dinner, about the poor woman who softly sobbed about losing her baby – or if it was just another day at the office.
I left the clinic as soon as I could. I remember a woman with two children held the door for me. She had what I had just lost: a second child. Despite the gratitude I felt for my son, that was part of the hardship. Because of him, I knew what was on the other side of a pregnancy: a little piece of my heart, wrapped in soft, warm baby chub.
It was a missed miscarriage. That means my body was in denial that the baby was dead. My placenta, still pumping out the hCG hormone, was firmly in place against the wall of my uterus, embracing the gestational sac that contained blueberry. For days, I waited for blueberry to make her exit – a private funeral march for a life that only a handful of people knew existed. But my body refused, such that pills were necessary to induce uterine contractions.
Intellectually, I wanted it to be over, so that I could restart the processes of ovulation and conception. Emotionally, however, I couldn’t bear the thought of blueberry leaving the warmth, safety, and love of her mother.
When the soft ball of tissues plunged, undignified, into the toilet bowl, I wanted to confirm the passage was complete. Being a biologist, I was curious about what it would look like. Emotionally, I couldn’t bear to flush blueberry into cold, dark, lonely waters.
Neither part of me was prepared for what I held: a dark red mass of tissue, attached to a transparent sac, that seemed heavier than it ought to be. Counter to my biological training, I didn’t poke, pop or prod. I wanted it exactly as it was: my blueberry safe in her gestational sac, attached to the placenta, the closest thing to a mother’s love she knew.
I have always hated being cold. Which is why I couldn’t bear to put blueberry in the freezer. So for that first night, swaddled in a white baby washcloth, tucked inside a Ziploc bag, blueberry remained by my bedside. I kissed the bag. Gooodnight, blueberry. The following day intellectual me made an executive decision to tuck blueberry in the freezer, but not before placing a rose from a bouquet my parents had sent me inside the bag. As I wrote this, that was 4 days ago.
A lifetime come and gone within two months.
About 20 per cent of pregnant women have a miscarriage in their first trimester, but thankfully one miscarriage is not a predictor of future fertility. Women aren’t supposed to talk about it, although I’m not sure why. Is it because being unable to carry an embryo to fruition is the ultimate shame – the antithesis of motherhood? Is it because the process of miscarriage is literally bloody, messy and by extension offensive to talk about? Is it because women are raised to avoid making others uncomfortable? It seems cruel, when a life has just ended, to have to go about life as usual as though everything is fine.
My husband, whom I love dearly, is stoic and logical. And while his response appealed to intellectual me, it wasn’t the only response I needed. I needed the emotional responses of my mother and sister. I needed the advice from friends who had gone through the same thing. I needed the support from other mothers in academia who had to keep working and mothering through it all. I am sad, but I am okay. I am not fine, but I am resilient.
The other day, as I was sifting through our son’s closet, I sadly showed my husband the shirt that had proclaimed his promotion to big brother and remarked that we would need to tuck it away. His response was a perfect blend of optimism and gratitude: It will just be a little tighter the next time he wears it.
Published in the Facts and Arguments column in the Globe and Mail, September 20th 2017
Are you an early riser, or a night owl? Given the timing of swim events at the 2016 Olympic Games in Rio, which frequently start at 10pm and don't wrap up until after midnight, the answer to this question may very well be on the minds of some athletes. It turns out the sleeping habits of these athletes might make all the difference in their performance.
Like animals, plants, fungi, and even some bacteria around us, humans have a built-in internal clock. These circadian rhythms guide many biological processes throughout the day, including our sleep cycles. Although humans are diurnal animals, there is a great deal of variation in our individual sleep preferences. Some of us are ‘morning larks’, who naturally wake up early to greet the day, while others are more ‘night owls’, opting for activities later in the evening. So do these ingrained preferences affect the performance of Olympic athletes in Rio, or our more modest workouts at the gym?
Researchers at the University of Birmingham sought to understand just that. For the study, 121 athletes were given a detailed questionnaire to gauge their ‘circadian phenotype’, or sleep patterns. Approximately 28% of subjects were early risers, 24% were night owls, and the remaining 48% were somewhere in between. The average wake-up times, bedtimes, and amount of sleep between each group was statistically different, suggesting that among this group of subjects, there were three unique circadian phenotypes.
From this group of athletes, 20 representative age- and fitness- matched subjects were selected to perform cardiovascular endurance tests at six different times during the day, all while keeping detailed sleep diaries. On average, the athletes performed best at 4pm and 7pm, and worst at 7am. But when the circadian phenotype was considered, the time of peak performance depended on whether the athletes were early, intermediate, or late risers. Early risers performed best at around 12:15pm, intermediates at 3:45pm, and late risers at 7:40 pm.
In the course of a day, the performance of the individual athletes varied. But do different circadian phenotypes suffer equally when they perform outside their optimal time? At most, early and intermediate risers suffered a 10% reduction in fitness scores. Late risers, however, faced up to a 26% reduction in fitness compared to their peak performance. It seems that night owl athletes face a potentially larger handicap than their earlier-rising counterparts, when they perform at sub-optimal times.
So is it just a matter of being awake for a certain amount of time to maximize your performance? According to the researchers, not so much. The peak performance time of early and intermediate risers was around 6 hours post wake up. The late risers, however, performed best about 11 hours post wakeup.
So the next time you're scheduling your workout, you might just want to consider if you're a morning lark, a night owl, or something in between. And if you find yourself competing at the Olympics, particularly if you're a night owl with an event early in the morning, perhaps some additional sleep training is in order.
Nearly two million years ago, an early hominid cooked the first steak, marking a turning point in our evolutionary history. Not only is cooked meat more easily digested and nutritious, but it is also sterilized of harmful pathogens. Nevertheless, there’s just something appealing about a rare steak, or fresh sushi. And when you’re shopping in climate-controlled grocery stores, it’s easy to forget that there are flesh-dwelling pathogens in the meat aisle. But sometimes, we are rudely reminded of their existence.
Recently, a 50-year old Calgarian man became the first Canadian known to be infected with anisakis, a parasitic nematode. An hour after eating homemade sushi, using raw, wild salmon from a large grocery chain, he went to the ER with severe abdominal pain and vomiting. An X-ray led doctors to send an endoscope to his stomach, whereupon they encountered numerous ulcers. At the center of each ulcer was a 1-2cm white, wriggling worm.
Once you’re finished being disgusted, maybe now you can be impressed. Within a single hour the worms were causing severe pain, presumably due to the formation of ulcers. While many other human parasites (like giardia, cryptosporidium, and the pork tapeworm for example) are eaten as cysts that must hatch before getting to work, anisakids are ready to go, already using their tooth to bore into the tissues of the gut.
To be clear, anisakid parasites want to end up in your stomach about as much as you want them to. Humans are a dead-end host. Here it is unlikely they will reach adulthood, instead remaining as pubescent larvae. Never mating, never laying eggs, and never passing along their genes.
Anisakids would much rather infect a marine mammal like a seal, dolphin, or whale. In the gut of these animals they develop into adults, mate, and lay eggs that are defecated into the water. When the eggs hatch into larvae, they make their way up the food chain. They are eaten by crustaceans, which in turn are eaten by squid or fish. Once the parasite migrates from the gut into the muscles, they develop into a stage that is infective to marine mammals-and potentially humans.
Prevention is, as always, the best medicine. While anisakids can live at refrigerator temperatures (4°C) for 2-3 weeks, they cannot survive when frozen at -20°C for 7 days, or -35°C for 15 hours. This is why reputable sushi bars will often freeze their fish before serving. If humans do become infected with anisakids, rather than prescribing anti-parasite drugs, doctors prefer to get rid of the parasite using an endoscope equipped with pincers at the end, much in the same way you use the claw crane to try and hook a stuffed toy at an arcade.
While North America has relatively few anisakid infections compared to the 2000 cases reported annually in Japan, experts predict infections will rise. Anisakids are well-travelled. They are found in all major oceans and seas, and their infective stage is found in many different commercially important species of fish—anchovies, salmon, and pollock, to highlight a few. Further, conservation efforts have led to rebounds in the populations of the marine mammals that serve as the final host for these parasites. Add in the increasing popularity of raw seafood delicacies like sushi, and it’s a perfect recipe for increased infection rates-even in the middle of the Canadian prairies.
Given the benefits of cooking, why are we drawn to rare and raw meat? From sushi to steak tartare, beef carpaccio to fermented herring, many countries boast raw meat delicacies, which are increasingly being exported beyond their borders. So if you still love sushi, but don’t want to host a parasite, perhaps best to learn about what might be lurking in your meat, and take a closer look at that piece of fish you’re about to eat.
I research inflammatory bowel disease. A few days ago I started a new experiment, using human cells from a cell line called THP-1. Not being very familiar with these cells, I was interested in where they came from. The results of a Wikipedia search left me speechless. They are derived from the peripheral blood of a one year old human male with acute monocytic leukemia. One year old.
My son had his first birthday less than two weeks ago. On that day he had his first taste of cake (red velvet with buttercream frosting). The cells I am using in my experiment came from a little boy whose first birthday was likely his last. These cells are identical to those that used to course through the circulatory system of a little boy the same age as my mine. Through the arms he used to hold his favourite toys, crawl up the stairs, and hug his mum.
Cell lines are a population of genetically identical cells that are all descended from a single individual cell. Normally, cells don’t live forever. However if they have mutations that prevent their natural cell death from occurring they will madly proliferate, and given the right conditions, live forever. For a cell line to exist, these mutations are necessary. But in a living organism, these cells are cancer.
Journalist Rebecca Skloot deserves monumental credit for investigating the human story behind immortalized cell lines. Her Pulitzer prize winning book “The Immortal Life of Henrietta Lacks” delves into the life of a woman whose cancerous cervical cells were used to establish the ‘HeLa’ cell line—the line used for most cancer research done today—without her knowledge or consent. The book humanized the woman whose cells have become immortalized in science, but also highlighted the ethical and legal complexities of using biological tissues in research.
It was in 1980 that the THP-1 cell line, established in a Japanese lab, was reported to the scientific community in a published paper. Based on some details in the paper, the cells were probably extracted from the little boy around 1977. Did his parents know his cells were cultivated into a cell line? Who owns the discarded biological tissues from patients and research participants? What level of control should donors have over their samples? Should we limit the rights of tissue donors in favour of the benefits of tissue-based research?
These are challenging moral and philosophical questions that legal experts are currently debating. I cannot comment on what ethical and legal frameworks were in place when the boy’s cells were extracted, and the THP-1 cell line established. I can tell you that in Canada, upon the parents’ request, the existence of THP-1 cell line would be disclosed. Additionally, the parents could withdraw their consent for the cells being used in research. Whether there is an obligation for researchers to disclose this information without the donor’s request is being debated. The profits from a commercial cell line would likely not be shared with the donor.
I can also tell you that in Canada, research involving human biological tissues involves intense scrutiny via the research ethics board, and similar protocols are in place in other countries. While it varies from country to country, human tissue-based research operates under the core principles of respect for human dignity, informed consent, patient privacy & confidentiality, minimizing harm, and maximizing benefit.
I can also tell you that THP-1 cells have contributed immeasurably towards our knowledge of the immune system, cancers, bacteria and viruses, and have played a key role in the development of drugs and vaccines. I can tell you that as a mother, I am conflicted about the thought of using the cells that killed my son for medical research. I can tell you as a scientist, I care both about the ethics of, and recognize the necessity for, tissue based research.
But I still wonder about that little boy with acute monocytic leukemia. According to WebMD, the survival rate for this kind of cancer is 24%. Did he survive? How was he feeling on that day his blood was drawn? Was he scared? Did his mum hold his hand? Did his parents know what happened to their son’s cells, that they inhabit research laboratories across the globe? Do they have any idea that the mother of a one-year old son is thinking about theirs?
You don’t want to let this one pass you by! Cozy and warm, with over 2700 square feet of living space. Comes fully furnished. Great place to raise a family, with on demand meal delivery services. Must be willing to contend with digestive juices, and bowel movements.
It’s no surprise that the gut is such an attractive piece of real estate for parasites. It’s a passive mode of entry. There’s no need to penetrate a thick epidermis, to access the circulatory system to get to the lungs, like the roundworm Necator americanus. You don’t need to migrate to the salivary glands of a mosquito vector, waiting to be injected into the bloodstream, like malaria-causing Plasmodium falciparum. You just need to be eaten.
Of course there are more than a few hurdles along the way. You need to be eaten by the right host(s), survive the acidic juices in the stomach, and withstand the immune responses directed towards you. But if you can make it to the small intestine of your final host, your dream home awaits. Nutrients are readily available, and when you’ve found a mate and reproduced, you can simply release your fertilized eggs along the gastrointestinal chute, where thousands of your babies are shuttled off into the outside environment.
Parasites possess some of the most remarkable examples of adaptation in the animal kingdom. Being a parasitologist myself, I will admit my bias, but let me take you through a typical lifecycle of one of the most successful gut-inhabiting parasites, the tapeworm, to illustrate my point. The operative word here is typical: there are hundreds of variations. These exquisite adaptations have allowed tapeworms to become one of the most successful colonizers of the gastrointestinal tracts of our planet.
STEP ONE: GET LAID
As a tapeworm egg, you won’t ever be lonely. Thousands of your siblings will keep you company through your journey down the gastrointestinal tract. Once you’ve been shuttled out the back end of your final host, there’s not much to do at this point but wait. Thankfully, you are equipped with a thick egg casing that keeps you safe from the cold, dry conditions in the outside world.
A single tapeworm can produce thousands of eggs every day. Tapeworm eggs are encased in proglottids, specialized segments of tapeworms. Once fertilized, these segments will become swollen with mature eggs, eventually detaching from the adult parasite.
Proglottids are then shuttled out the back end, into the external environment, where it disintegrates. In some species, the proglottid can actually expand and contract, wriggling its way along the intestine, and out of the anus, like an inchworm.
STEP TWO: FIND A RENTAL
You aren’t going to find a rental so much as the rental is going to find you. Parasitologists call this the ‘intermediate host’. Maybe you’ve been accidentally ingested by a grazing deer, alongside some lush grass. Perhaps you’ve been gobbled up by a field mouse. All you can do is hope that it’s a species you are compatible with (or the consequences, for both parasite and host, can be quite lethal).
After hanging around outside for a period of time, being inside the stomach of this animal feels so nice. It’s warmer. Darker. It’s time to hatch. You emerge from your protective casing as a tapeworm larvae.
Thanks to some nasty hooks and suckers, you burrow through the gut wall, and into the beetle’s body cavity. Or perhaps the body cavity of a fish. Or the muscle tissues of a pig. You absorb nutrients through your skin and grow. This can cause significant damage to the host, but there's no need to be too concerned. It’s only a rental. You secrete some molecules that suppress the host’s immune response against you. Eventually, you form a thick protective cyst, which will come in handy later on, and you settle in for a period of stasis, as a metacestode.
STEP THREE: FIND A HOME
Once again you wait. All you can do it hope the right predator comes along to consume your rental host, with yourself inside, much like a trojan horse. Although this time, it’s a bit different. You may be able to stack the deck in your favour.
Not all parasites are able to modify the behaviour of their intermediate host, but many do. Scientists are identifying more and more examples of such parasite modifications all the time. The key is to try and make it a little bit easier for your rental host to get into the belly of your final host. But how?
The bird tapeworm Schistocephalus solidus drives its host, a stickleback, to seek warmer waters. These higher temperatures make it possible for the tapeworm to grow as large as possible, eventually outweighing the host. Ultimately parasitized fish become bolder, more solitary, and less likely to avoid predators. This makes them easy targets for the fish-eating bird for whose guts the tapeworm longs for.
Brine shrimp, often translucent, turn a bright red when parasitized by several species of tapeworm. Infected shrimp swim closer to the surface, making them more likely to be eaten by a wading bird. The tapeworm sterilizes the shrimp, which might account for the behavioural changes. Alternatively this might be a way to ensure that shrimp energy resources aren’t diverted to the costs associated with reproduction, but remain with the shrimp (and thus the parasite) instead.
When the rat tapeworm Hymenolepis diminuta develops a fully mature cyst within its beetle host, infected beetles are more attracted to light, are no longer attracted to sex pheromones. Remarkably infected beetles live longer than their uninfected counterparts, which may increase the likelihood that the beetle is ultimately eaten by a hungry rat.
STEP FOUR: MOVING DAY
Congratulations on your new home! You've been eaten by your definitive host! But first, you must survive a churning, acidic compartment. The mammalian stomach has evolved to be a hostile environment for many organisms, for good reason. Luckily, the cyst you developed when you were still renting protects you. This is why the timing of parasite-mediated host changes are so important. Immature stages of tapeworms are in the process of developing this cyst, and if they reach their final hosts’ stomach too soon, the consequences are lethal.
This tapeworm was cruelly evicted from the intestine of my cat.
Once you’ve passed into the intestine, intestinal juices containing trypsin, a digestive enzyme produced by the pancreas, wash over you. This signals that it’s time to emerge from your cyst, as a juvenile tapeworm. After a big stretch, you wrap yourself around an intestinal villus. You use some suckers to secure yourself against the rhythmic muscular contractions in the intestine that propel food forwards. Since you don't have a mouth or an intestine, you simply absorb nutrients across your skin, and grow.
STEP FIVE: MAKE SOME BABIES
It's time to start a family. While you have both male and female reproductive organs, they mature at different times, so you’ll have to find a mate. This is for the best anyways, as sexual reproduction makes for genetically diverse, and thus more adaptable and resilient organisms. Luckily as a hermaphrodite, any tapeworm you encounter of the same species is a potential mate. You exchange sperm with your partner, and both of you become egg-producing machines. Swollen proglottids, teeming with eggs, detach from your proximal end, leaving the safe comforts of home. The cycle continues.
Slow dancing tapeworms!
It's a long journey for these tapeworms. Many will never find a rental, let alone a permanent home. In some cases, the host immune system can thwart the tapeworm, cruelly evicting it from a warm safe place to eat and reproduce.
The complex life cycles of parasites pose an interesting question: why undergo such an arduous journey, only to end up back in the gut of the same species you started in? You have to admire the tenacity of these tapeworms. Maybe they don't deserve their maligned status. They're just looking for a place to hang their hat, and it's a tough market these days. Come to think of it, do you have any vacancies?
The last thing you might expect to greet your senses when you enter an art gallery is the pungent smell of feces. But that’s exactly what artgoers experienced when encountering conceptual artist Wim Delvoye’s exhibit, “Cloaca” in 2000. Cloaca is a digestive machine of impressive design; it was nearly a decade in the making, involving extensive consultation with gastroenterologists, computer scientists, and engineers. A series of pipes, tubes, and pumps transport food through a mechanical grinder and into a series of large glass vats bearing digestive enzymes and bacteria. Over the course of 27 hours and over 30 feet, the product is ultimately extruded onto a conveyer belt as feces. Cloaca makes a subversive statement on the pointlessness of modern life; to Delvoye, a machine that could be so expertly constructed to produce something as worthless as excrement was the pinnacle of uselessness.
As it turns out, such a machine might not be so useless after all. Or, more specifically, it’s fecal output may not be such a useless product. By weight, 60% of feces is made up of bacteria. In our gut there are more than 100 trillion bacteria, representing over 1000 species. These bacteria play a vital role for us: they aid in digestion, nutrient absorption, help develop immune responses, and they actually protect us from pathogens. Together, these groups of commensal bacteria form an intricate community collectively called the gut microbiome, or gut microbiota. Like any complex ecosystem, however, minor perturbations can have profound effects on the whole, leading to imbalances among the different types of bacteria. This condition, termed microbial dysbiosis, is believed to play a key role in certain diseases of the gut.
Robogut, the brainchild of Dr. Emma Allen-Vercoe of McMaster University, is a bioreactor designed to mimic the complex conditions of the large intestine. Through Robogut, Dr. Allen-Vercoe has been able to develop a synthetic stool substitute containing specific types of bacteria found in human stool samples. Cloaca and Robogut certainly bear some similarities in their design. Both machines mirror the incredible complexity of our digestive systems, from the enzymatic and bacterial components, to the specific temperature, pH and anaerobic conditions found in the gut. As well, both machines produce an unmistakable odour that cannot be masked. But the intent behind these two machines couldn’t be more different. While Delvoye’s machine is a statement of pointlessness, Robogut explores the potential of our gut bacteria as a treatment for patients with severe infections caused by Clostridium difficile.
In healthy people, the spore-forming bacteria C. difficile, also known as C. diff, does not pose a significant health risk. For those with weakened immune systems and the elderly however, C. diff can be a serious health concern. C. diff has emerged as the most common cause of infectious diarrhea in hospitals and long-term health care facilities in developed countries, including Canada. Infection occurs when the bacterial spores, which are found in feces and on fecal-contaminated surfaces, are accidentally ingested. Because C. diff spores are long-lived and resistant to routine cleaning procedures, they are readily transmitted between beds and rooms in health care settings. Once these highly resistant spores germinate and establish in the colon,C. diff bacteria produce inflammation-inducing toxins that can cause disease. Symptoms include watery diarrhea, abdominal pain, fever, and potentially life-threatening complications; an exceptionally virulent outbreak in Quebec in 2004 resulted in the death of over 1000 hospital patients.
C. diff follows what clinicians refer to as the 20-40-60 rule: contracting C. diff once renders a person 20% more likely to get the infection a second time. With each subsequent recurring infection, the risk increases to 40% and 60%, and symptoms become increasingly severe. Patients are typically treated with specific antibiotics, but those patients with recurring infections usually find that once the round of antibiotics are complete, the infection returns. Researchers believe that recurring infections are indicative that microbial imbalances are never properly restored, allowing C. diff to easily establish itself again. Indeed, inducing microbial imbalances through the prolonged use of certain antibiotics has been implicated as a risk factor for contracting an initial infection, as some antibiotics can wipe out good bacteria, giving C. diffthe opportunity to colonize the intestine.
The cost of antibiotic treatment is staggering, especially given the likelihood of recurrent infections. This is to say nothing of the emotional and physical pain facing patients living withC. diff infections. Estimates suggest that in 2012, there were over 37,000 cases of C. diff in Canada, with a socio-economic price-tag of over 280 million dollars. Management of this disease has proven exceptionally challenging for physicians, as current treatments are falling short. Therapies with long-lasting effects are needed, and researchers believe that requires the restoration of microbial balance in the gut. But how can you get back the good bacteria, to keep the bad ones at bay?
The use of fecal microbiota transplant as a therapy was first reported in the scientific literature in 1958. Sporadic case reports involving this curious therapy were published since then, but it was not until 2011 that a group of researchers at McGill University in Quebec, led by Dr. Amee Manges, published a systematic review in Clinical Infectious Diseases that examined all known case reports involving this type of therapy. The study included a total of 27 previously published case reports involving over 300 patients with recurring C. diff infections. Dr. Manges reported that in an astonishing 92% of cases, patients receiving fecal transplants had resolution of disease. The need for properly controlled trials that compared the effects of fecal transplant therapy with standard antibiotic treatment were clearly needed.
In 2013, the first randomly controlled trial was published in the New England Journal of Medicine by a group of researchers from the Netherlands and Finland, led by Dr. Josbert Keller. Feces were collected from multiple donors, diluted and strained, and a single fecal infusion was delivered to one group of patients with recurring C. diff infections, while a second group received the standard antibiotic treatment. Ten weeks later, physicians unaware of treatment groups assessed the patients for disease. They reported that 94% of the patients receiving fecal microbiota transplants -including two patients that required a second infusion of feces- were cured. Less that one third (31%) of the patients that received standard antibiotic treatment had resolution of their disease.
Recently, as reported in Microbiome in 2013, the synthetic stool produced by Dr. Allen-Vercoe’s Robogut was tested in two patients with recurring C. diff, and both patients were cured. Moreover, the researchers confirmed their hypothesis: that synthetic stool treatment resulted in an altered microbiome in patients that was maintained even 6 months after initial treatment. This technology paves the way for the production of reproducible batches of microbiota, and the identification of which bacteria, or which combination of bacteria, can restore microbial balance in the gut.
Delvoye used his synthetic digestive machine to explore the futility of the human condition. But futility, it seems, is a matter of perspective; Robogut’s synthetic stool explores the utility of gut bacteria as a treatment. While the synthetic production of poop likely appears a worthless enterprise to most of the population, Robogut’s output represents liquid gold to scientists, generating species of bacteria that have never before been cultured in a lab. The potential benefits of these bacteria are not limited to recurring C. diff infections; researchers see hope for treatment in a wide range of gut diseases including ulcerative colitis, Crohn’s disease, and irritable bowel syndrome. And to the millions of people that suffer such chronic diseases, such an endeavor is anything but futile.
Based on the success of House of Cards and other political dramas, it’s no secret: humans love their politics. But is it for the birds as well? In a new study published in Current Biology, researchers at the University of Vienna have found that ravens play politics too.
Ravens are social creatures, travelling in flocks with dynamic social structures. Within a flock there are kinship bonds, but there are also male-female bonds with varying degrees of strength. Pair bonds between established breeding pairs are the most powerful, while the bond between breeding ravens without established territory is weaker. Loosely bonded pairs are ‘dating’ so to speak- still in the process of establishing a bond, while some ravens fly solo, remaining unbonded.
In the raven world, the strength of a bond is related to dominance in the flock: the stronger the bond, the stronger the alliance, and the greater the rank within raven hierarchy. Not only do ravens remember these alliances for years, but remarkably, they follow the dominance ranks between other individuals.
So what does a raven bond look like? Bonds are both created and maintained through what researchers call affiliative behaviours. Sitting side by side, feather preening, touching beaks, or playing with objects together all help form and maintain bonds. Over time as the bond deepens, these interactions become more intense, more reciprocal, and an alliance develops.
Forming strong alliances is one surefire way to raise your stature in the raven hierarchy. But are there other strategic ways to ensure power? This was the question posed by researchers at the University of Vienna, in Austria. When researchers studied the behaviours of a population of wild ravens, they found that about 20% of the time a raven will try to interrupt the alliance-building behaviours of other ravens. And about half of the time, that raven is successful.
As you can imagine, interrupting a pair of happily grooming/playing ravens does not always go well. A raven risks starting a fight-with the potential to be outnumbered-when it puts its beak where its not wanted. That’s why ravens are very strategic when it comes to the type of alliances they target.
Researchers found that interrupting ravens largely ignored ravens without alliances, likely because they aren’t considered much of a threat. And ravens were not likely to discourage the bonding behaviours of ravens with strong alliances because, the authors conclude, it’s not worth the cost to try and break up a well-established alliance. But those ravens that are just ‘dating’ –without an established bond– are an ideal target. Preventing a potential future alliance may be the best way for a raven to ensure its current dominance. Overall, ravens with the strongest alliances were most likely to intervene in alliance-building behaviours.
What is remarkable is that throughout the 6 month study, the authors never once saw an immediate benefit, such as food, territory, or breeding partners, for the interrupting raven. This suggests that the ravens are in it for the long-term benefits, and truly are playing politics. Who knows? Maybe you've encountered the Frank and Claire Underwood of the raven world on your morning commute.
We have all heard that ‘breast is best’, for a variety of reasons. It provides infants with an ideal source of nutrition, and breast-fed babies have fewer cases of illness than their formula-fed counterparts. Benefits extend to the mother as well; breast feeding helps reduce risk of post partum depression, aids in uterine contraction, helps mothers to return to pre-pregnancy weight, and promotes bonding with baby. As the research evolves and the benefits of breast milk keep adding up, there are even more remarkable things researchers are discovering about the white stuff. Here are five things you may not know about breast milk.
1. Breast milk may influence infant behaviour
Cortisol, a stress hormone that has been found in breast milk, can act on receptors in infants and trigger hormonal signaling cascades. In turn, these cascades have direct and indirect effects on behavior.
A study of 253 women found that mothers with higher blood cortisol concentrations, which reflects the levels of cortisol in breast milk, described their infants as more fearful than mothers with lower levels of cortisol. This effect was not observed in those mothers who formula-fed their babies. This suggests that the fearful behaviour is linked to ingestion of this stress hormone through milk, rather than maternal cortisol levels affecting infant care, (which could impact baby fearfulness), or the how mothers might report the fearfulness of their baby.
The same research team later assessed breast milk cortisol levels and found a positive correlation with the degree of ‘negative affectivity’ of the infant-the tendency towards sadness, fear, and discomfort. Interestingly, this association was only observed in breast-fed daughters, not sons.
Although these studies are certainly intriguing, the relationships between breast milk hormones and infant personality are still in their infancy. Given the complex nature of personality, which involves a wide variety of both genetic and environmental components, a great deal more research is needed in this emerging field of study before any conclusions can be drawn. So breast-feeding mothers, relax. You've got enough to think about as it is.
2. Breast milk contains bacteria-and lots of it.
But don’t worry, it’s the good kind. Studies suggest that a single millilitre of breast milk can contain 1000-10 000 colony forming units of bacteria, encompassing over 700 species.
Researchers believe these bacteria may contribute to the development of the infant's gut microbiome (all the commensal bacteria in the gut). When the species of bacteria in the breast milk of 16 women was analyzed, researchers discovered that half of the bacteria in each sample contained the same 9 species-representing a ’core’ microbiome within breast milk- while the remaining half varied from woman to woman.
Interestingly, the weight status of the mother (normal versus obese), and the mode of delivery (vaginal versus planned caesarean) influences the composition of the breast milk microbiome.
It’s hypothesized that specialized immune cells, called dendritic cells, transport bacteria from the mother’s gut to the mammary glands, where they are then passed on to the infant via breast milk.
3. Breast milk is full of 'good bacteria' food
Although it was originally believed that the guts of developing fetuses were sterile, many researchers now believe that the gut microbiome is first seeded in the womb. The microbiome, however, is anything but stable. It adapts to a variety of environmental factors, including diet.
Research suggests that breast milk can influence the infant microbiome. The third most dominant nutrient in human breast milk, after lactose and lipids, are human milk oligosaccharides. These oligosaccharides are the sugars in breast milk that are a food source for bacteria, but can't be digested by babies. Commensal strains of ‘good’ bacteria, such as Bacteroides and Bifidobacterium, are happy consumers of these sugars. Pathogenic strains-like Clostridium, E. coli, Enterococcus, and Streptococcus- are either poorly adapted to consuming these breast milk sugars, or unable to metabolize them altogether.
This is a positive feedback loop- the more ‘good’ bacteria that establish in the infant gut, the more difficult it is for pathogenic strains to compete for limited space and resources.
4. Breast milk contains decoys to fool bad bacteria
There are a whole slew of ways in which breast milk components protect infants from bad bacteria. Breast milk contains a variety of immune cells: neutrophils, macrophages, and white blood cells that can target and destroy bad bacteria. Or take lactoferrin, a protein that binds to iron, which makes this essential nutrient unavailable to the many kinds of pathogenic bacteria that thrive on iron.
A more recently discovered line of defence in breast milk are human milk oligosaccharides. Like using a key in a locked door, many harmful gut bacteria must first attach to receptors on the surface of the epithelial cells that line the gut in order to invade them. Among these pathogens include a strain of E. coli that is responsible for severe diarrheal diseases in infants. Studies on mice have determined that breast milk oligosaccharides serve as a decoy, as they possess the identical receptors that the pathogen uses to invade cells. These harmless sugar-bacteria complexes are then flushed from the intestine.
5. Caloric content of breast milk depends on infant sex. Maybe.
Is all breast milk created equal? Not so, say researchers at Harvard and Boston University. In a2010 study, the energy content of breast milk in 25 healthy mothers with babies aged 2-5 months was assessed. They found that the breast milk of mothers with baby boys had 25% more calories than the milk produced by mothers with baby girls. One possible explanation is that baby boys have higher energy requirements than baby girls, and their increased demand drives milk production.
However, it might be more complicated than that. A more recent study of 83 women similarly revealed differential breast milk quality for sons and daughters. In Northern Kenya, the sex of the infant that received the more fattier, richer milk depended upon the economic status of the mother. Wealthy mothers produced more calorically dense milk for their sons over daughters, while breast milk from poorer mothers was richer for daughters over sons.
The authors state that according to evolutionary theory, mothers should invest more in their sons than daughters, since sons can ultimately produce more offspring than daughters. In times when resources are scarcer, however, it may be prudent to for mothers to invest in the sex that will produce fewer offspring. In this case, the authors suggest that daughters have a greater chance of increasing their status through marriage than sons do, making daughters a more wise investment when times are rough. The biological mechanism driving this effect, however, remains unknown.
Author’s note: It is my intention to highlight some of the amazing features of breast milk. While breast milk is amazing stuff, not all women are able to breastfeed for a variety of reasons. Formula is a lifesaver in these cases, and its use as a supplement to, or in lieu of breastfeeding, shouldn’t be maligned or judged.
Let’s talk about sex. That’s what Dr. Kelly Suschinsky, a post-doc researcher at Queens University in the SageLab has been doing since 2005, when she began researching human sexual arousal.
"Because sexuality can be such an important component of people’s lives, it is crucial to better understand various aspects of it, including basic information such as the sexual response." says Suschinsky. "Until very recently, models of sexual response which have informed decisions about what is "healthy" versus "dysfunctional" have been based mostly on research conducted on men."
It turns out that when it comes to human sexual arousal, it isn’t black and white, especially for women. The story for heterosexual males is pretty straightforward. Overall, researchers have found that straight men are aroused by sexual stimuli that involves their preferred partners: women. In contrast, heterosexual women are less specific, responding to straight, gay, or lesbian sex.
Why are straight women, but not straight men, aroused by a wide variety of sexual stimuli? This is a question that has long intrigued Dr. Suschinsky. It turns out a dark reality may have played a role in driving this response. Sexual arousal is accompanied by physiological genital responses, such as increased lubrication. These responses evolved in women to help reduce the risk of injury during sex. Being sexually aroused to a wide variety of stimuli could help protect female genitalia against injury incurred during sex-whether consensual or not. Dr. Suschinsky explains: "The preparation hypothesis suggests that women’s genital responses….. should occur in the presence of any sexual stimulus, functioning to prepare a woman for a sexual encounter." Dr. Suschinsky sought to test the preparation hypothesis when she was studying at the University of Lethbridge.
She recruited healthy heterosexual participants who listened to consensual or non-consensual, violent or non-violent, and sexual or non-sexual stories. Two measurements were taken in response to the stories. Subjective emotional arousal was assessed by simply asking participants how turned on they felt while listening to the stories. Assessment of genital arousal required a different approach. For males, genital arousal was measured using penile plethysmography, a technique where a rubber gauge is placed mid-shaft on the penis, and changes in circumference are measured (above right). Female genital arousal is assessed using vaginal photoplethysmography, which measures blood flow changes as a function of changes in light (above left). The participant inserts the device into the vagina, similar in shape and size to a tampon.
“The results of the study do support the preparation hypothesis." Dr. Suschinsky concludes. "Women showed relatively similar levels of genital response to a variety of sexual stimuli, including consensual and non-consensual sex, whereas men showed their greatest genital responses to consensual sexual stories."
Men stated they were most turned on by the consensually sexual non-violent story, and this was reflected in their genital arousal as well. While women reported the same story to be the most arousing, their genital arousal was similar among all the stories that contained sexual content-whether violent, consensual, or otherwise. This suggests that women’s subjective sexual arousal and genital arousal don’t always go hand in hand, like men’s do.
Dr. Suschinsky believes her research will have far-reaching implications for women's sexual health. "More and more research is showing that women and men respond differently, and that there is even substantial variation within each gender…. [T]his variation is important to consider when we define what is a sexual dysfunction and when we try to develop effective treatments for such difficulties."
Sexuality being such an important part of the human condition, its remarkable how little research has focused on women's sexuality, Dr. Suschinsky remarks. Happily, she reports "...that this is changing. It's exciting to study something that is so important to so many people. "
The idea first arose in the mid-eighties. Imagine what we could do if we knew what it looked like? We could understand where we came from. What makes us tick. What makes us sick. We could revolutionize the field of medicine. Forensic science. Biotechnology. Anthropology.
Therein began the quest to sequence the human genome.
Bear with me for a brief lesson on genetics. All the genes within an organism make up a genome. The human genome contains about 20,000 genes, which is neatly packed into 23 chromosomes, and resides within the nucleus of our cells. Genes are a specific region of DNA that contains the instructions to make a specific protein. There are only 4 subunits of DNA; these subunits, called nucleotides, are often denoted as A, C, G, and T (adenine, cytosine, guanine, and thymine). It's all about the sequence of these nucleotides. The sequence of a gene's DNA determines what protein that gene will make. On average, about 1000 of these nucleotides will produce a single protein, and one gene will produce about 3 proteins. (Variation, obviously).
By figuring out the order of these nucleotides, scientists can understand what genes make what proteins, and ultimately the function of those genes and their proteins. If you were a reductionist, you might say that the human genome is a recipe for people.
The Human Genome Project began in 1990, and the first representative human genome was successfully sequenced 13 years later in 2003. It was the world's largest collaborative scientific endeavour.
Whose genome had the honour of being the first to be sequenced? No one knows. The white blood cells of two men and two women were randomly selected from a pool of 20 male and 20 female volunteers. Thus, the first human genome to be sequenced was actually a composite of four men and women. As it turned out, most of the genome (70%) came from a man from Buffalo, New York, known as 'RP11',
As humans, we share 99.99% of our genomes with each other (unless you are an identical twin, like myself, which means that our genome is 100% identical). The remaining 0.01% of genomic difference accounts for the entire variation that exists within the human species. This means that the human genome project has successfully sequenced a representative human genome. It's available online, and it's free for everyone to access.
In 2001, the cost to sequence the human genome was about $100 million dollars. Eight years ago, it was still a substantial $10 million. Currently, it costs a relatively mere $1000 to sequence a human genome. I always find this graph to be an optimistic reminder of how advances in technology can render a seemingly insurmountable task possible.
The time it takes to sequence the genome has also been drastically reduced. The first round of human genome sequencing took 13 years. New sequencing technology like the MinION (pictured right), can plug into a laptop, and spit out the sequence of a human-sized genome in about 24 hours. Analyzing the data, however, requires about 10 graduate students working day and night for a week.
Both the cost and time to sequence the human genome has been greatly reduced. So what? Haven't we already sequenced the human genome? Or at least a representative human genome? Isn't the genome that represents 99.99% of everyone's genome enough?
The human genome includes many different versions of the same genes. These versions of genes (allelles) are represented by different nucleotide sequences in a given gene. Where 70% of the population might have an "A" in the 208th nucleotide of gene X, the remaining 30% of the population might have a "C". Such 'single nucleotide polymorphisms' (SNPs) could account for the fact that I have blue eyes, while my son has brown. Or it might account for the fact that while one patient with Crohn's disease responds well to the drug inflixamab, another does not.
Better predicting what kind of medicine to prescribe to a patient is just one of many benefits of identifying these variations in the human genome. I've heard it touted many times in the seminars I attend as a graduate student: the future of medicine will be personalized to your genome.
I will leave you with a fun fact: we share about 50% of our DNA with bananas. Think about that the next time you make a batch of banana bread. It's practically people!
I won’t forget the phone call. At the time, my brother, sister and I were engaged in an epic battle of monopoly. My mum answered the ringing phone, and when we heard the heart-wrenching sobs, we realized something was terribly wrong. I was too young to know what a cervix was, but I did know that cancer of anything was bad. My mother’s only sister would pass away in her arms, 4 years later.
Cervical cancer: so prodigious in one woman, Henrietta Lacks, that it has been proliferating for over 60 years after her death as an immortal cell line used in biomedical research. While the incidence of cervical cancer has been reduced through Pap Smear screening techniques, it remains the fourth leading cause of death by cancer (following breast, lung, and colorectal cancer) in women, globally. Out of the 1 in 150 women that are expected to develop the disease, more than 1 in 500 will die from it.
Human Papilloma Virus (HPV), the culprit of nearly all cases of cervical cancer, has many faces. There are over a hundred ‘types’ of the virus, 40 of which can be sexually transmitted. Estimates suggest over 70% of sexually active Canadians will have a sexually transmitted HPV infection at some point in their lives. Two of these types (HPV-16 and HPV-18) are particularly high risk in their ability to cause cancer: they are responsible for over two thirds of cervical cancer, the vast majority of anal cancers, and one in three cases of eosophageal and penile cancers. There is no cure for HPV infection, only treatment of the physical symptoms of infection, namely precancerous and cancerous lesions. In the case of HPV, prevention is indeed the best medicine. Such preventative measures were first licensed for use in 2006, over ten years prior to my aunt’s diagnosis.
There are two licensed prophylactic vaccines available: both Cervarix and Gardasil offer protection from the most high-risk types of HPV. Gardasil has the added benefit of being licensed for use in both males and females, and offers protection against HPV types 6 and 11, the major cause of genital warts. To make these vaccines, yeast are engineered to produce massive amounts of virus proteins: the same proteins that make up the empty shell (capsid) of the virus. Because only these proteins, not virus DNA, are purified for use in the vaccine, there is no risk of infection. These proteins are introduced into the human body through intramuscular injections. After 3 doses over a 6-month period, specific and long-lived antibodies are generated against these harmless proteins. If the real virus rears its head, the body’s antibodies immediately recognize the same virus capsid proteins, and mounts the most efficient and effective immune response possible.
My aunt was scheduled to begin treatments about 4 months after her initial diagnosis, however that schedule was accelerated after she hemorrhaged on her kitchen floor. She lost nine pints of blood that day, and flat-lined en route to the hospital. She survived, and was given radiation treatment that consisted of radioactive material sewn nearby the tumor. Her doctor’s described this as her “life insurance policy". After several rounds of chemotherapy, the cancer had gone into remission.
Two years later: in the kitchen, the remnants of the Christmas turkey were being carved away for soup. Once my grandfather pried the wishbone free from the carcass, I was the lucky grandchild selected to hold on the opposite end and make a wish. I still remember the childish disappointment I felt when I my end snapped only a few centimeters above my fingers. And I still feel the shame of my (now forgotten) childish wish when my grandfather, once prompted to share, quietly said he wished his eldest daughter would survive. It was discovered several months earlier that the life insurance policy had failed. The cancer had returned, and she would never recover.
As the data rolls in, comparisons betweenpre-and post-vaccine rates of HPV reveal that the vaccine is a success. Markowitz and colleagues report in the Journal of Infectious Diseases that the prevalence of the most high-risk types of HPV was significantly reduced in girls aged 14-19 once HPV vaccines were introduced into routine immunization schedules in late 2006. Prior to routine HPV vaccination, between 2003-2006, 1 in 10 women were HPV positive for high-risk strains. Post-vaccination, that number has fallen to 1 in 20.
One of the most contentious issues surrounding the HPV vaccine is timing. The reality is, vaccination before or at the onset of puberty is critical for protection for three main reasons. First, for a protective strategy to be effective, it needs to be in place when the risk is greatest, and the risk of contracting HPV is highest within 5-10 years of a first sexual experience. Second, benefits of vaccination are greatest in children aged 9-15: the virus-killing antibodies generated in this age group are over twice as high compared to 15-26 year-olds. After the age of 26, clinical trials demonstrates limited, if any, protection is offered to women. And third, these vaccines are not effective as a treatment, as the virus-killing antibodies induced by vaccination are not found in the epithelial cells where the cancer lives. So once HPV is established, no amount of vaccine-induced antibodies will eliminate the virus.
I try to understand the discomfort of parents who are asked to consider vaccinating their children against a sexually transmitted infection. Such vaccinations are as close as parents can get to making informed sexually educated decisions for their children. One thing is for certain: the discomfort of such a decision is a luxury, one that wasn’t afforded to my parents, or my grandparents. And hindsight being what it is, had such measures been available to my grandparents, my mother might be one sister richer today.
- Asiaf et al. 2014 European Journal of Cancer Prevention.
- Markowitz et al., 2013. Journal of Infectious Diseases.
- Public Health Agency of Canada, Canada Communicable Disease Report, Update on HPV Vaccines
Ammendum: Canada has a publicly funded HPV immunization strategy in place, that varies from province to province. To date, Alberta and Prince Edward Island offer the HPV vaccine to both boys and girls, which makes an awful lot of sense.
Who is this little critter, and why is he so happy?
This is Hymenolepis diminuta, the rat tapeworm. It doesn't look much like a tapeworm just yet, because it's in an intermediate stage of development, called a cysticercoid. This larval stage of tapeworm lives in beetles.
We raise flour beetles in our lab to serve as a host for these larval stages of tapeworm. The beetles find the eggs pretty tasty. Once they've been eaten, the eggs hatch in the beetle gut, and the parasites use hooks to migrate into the beetle's body cavity. There, they undergo some changes (including the development of a protective cyst), and become a mature larval tapeworm. Our current lab record is 35 of these cysticercoids in a single beetle.
In a non-lab setting, some of these infected beetles would be eaten by a rat. In fact, the parasite modifies the behaviour of the beetle to help increase the odds of that happening. While the infected beetles don't look any different than the uninfected ones, they act very differently. The infected beetles move more slowly, are less fearful of the light, don't respond to sex pheremones. These changes in behaviour are only present when the larval stage of parasite is fully developed (it takes about 2-3 weeks), suggesting that these behavioural changes are mediated by the parasite.
In our lab, we squish up the infected beetles in a petri dish with water, and hunt down the little cysticercoids that pop out. We carefully count them out, and place 5-10 of them in a little tube, filled with salt water. The larval parasites, along with the salt water, are fed to mice or rats (depending on the experiments being done). The parasites are swallowed, and when the pH levels are nice and high, they hatch out of their cysts. This ensures they hatch in the small intestine -which has a high pH thanks to the digestive enzyme trypsin-where they want to be, rather than the stomach, which would mean certain death. They stretch, find a nice intestinal villi to snuggle up to, and bathe in a seemingly never ending supply delicious nutrients.
Maybe it can sense that's where it's headed. Maybe that's why it looks so happy.
To my loyal readers (hi mom!), I have a few changes to announce.
I have returned to what researchers call 'the bench'. It's been 15 months. One media internship and one maternity leave later, I'm back in the lab. I had two goals during my maternity leave: publish my first research article from my PhD work, and develop a website devoted to my foray into science writing. I'm happy to say that I was able to accomplish both of those things-although it was not nearly as easy as I thought it would be. Parenthood is a time consuming affair, and that third reviewer is a ball buster.
I have so many ideas for articles: Five things that improve a baby's immune system. How lentils from Saskatchewan are combatting arsenic-contaminated groundwater in Bangladesh (this story is incredible). The cold remedies you should ignore, and the ones worth trying. Everything you ever wanted to know about psychopaths. How estrogen cycles affect willpower. Why the gut is a hot piece of real estate. Not water, nor land: the third environment, and who lives there. The science of birdsongs.
While it kills me to have to leave these stories temporarily untold, my writing focus has to be on my PhD thesis. I'm hoping I can still find time for creative writing here and there, but I'm also being realistic: the articles are going to churn out a lot slower.
This brings me to the changes in my website posts. First, I'm going to provide links to great science stories and science writing (via the 'sci du jour' link), but on a monthly basis instead of a weekly one. Second, I'm going to focus mainly on my blog, with postings related to my work. Stay tuned for photos, descriptions, and self-involved diatribes about life in the lab.
I hope that you find it informative, entertaining, and interesting enough to keep stopping by.
When it was discovered that adopted 3 year old twin girls Binh and Phuoc had a potentially fatal genetic disorder, Michael Wagner did what any father would do: he donated a portion of his liver to his child. Unfortunately, there was only enough tissue for one of his daughters, and their mother was not a match. The gut-wrenching decision of which daughter would receive the liver tissue was given to the doctors. A devastating plea to the public ensued: is anyone willing to donate a portion of his or her liver to help a complete stranger?
This is a perfect example of altruism. In a biological context, altruism is a behavior that is detrimental to that individual, but benefits another. Evolutionary biology typically explains such behaviours as a form of kin selection (helping out someone who shares some of the same genes as you). More broadly, as a cultural concept altruism is the concern for the welfare of others; selflessness.
Donating a piece of yourself is certainly the definition of selflessness. But what are the chances someone might be willing to undergo a potentially life-threatening surgery to donate an organ to someone they’ve never met? That level of altruism is simply remarkable.
Marsh and colleagues certainly thought so, and the team sought to better understand what’s going on in the brain of such extraordinary altruists. Are there neurological differences in people that engage in extreme acts of life-saving altruism? Ironically, the authors developed their hypothesis based on what research has taught us about psychopaths.
Psychopathy is a condition characterized by antisocial behaviours, including a lack of compassion, empathy, guilt, and remorse. The authors hypothesize the existence of a social spectrum, with psychopathy on one end, and extreme altruism on the other.
In psychopaths the amygdala, a region of the brain associated with emotional reactions, is both smaller and less responsive to the facial expression of fear. Being able to identify fear in other people is a marker of sensitivity, compassion and empathy towards others.
This suggests a potential neural mechanism that might explain some of the behaviours characteristic of psychopaths. Perhaps the amygdala of extreme altruists, the authors hypothesized, is larger and more responsive.
A group of altruistic kidney donors and matched controls were shown angry, fearful, and neutral facial expressions. Subjects were administered a functional MRI, allowing researchers to examine levels of activity in specific regions of the brain. The amygdala of extreme altruists was both significantly larger, and more responsive to fearful facial expressions than controls.
Marsh and colleagues take care to point out that these neurological differences only partly explain extreme altruists; personality, social, and cultural differences are also important components.
Two months after her sister received her father’s liver tissues, Binh Wagner successfully underwent a liver transplant after receiving tissue from an anonymous donor. Nearly 500 people contacted the Toronto General Hospital to offer a portion of their liver. It’s nice to know that such people exist, to balance out the psychopaths.
The MMR vaccine causes Autism. Barack Obama was not born on American soil. Man-made climate change is a fallacy and while we’re at it, the moon landing wasn’t real either.
There’s a psychological phenomena as to why people may hold onto such beliefs in the face of indisputable evidence. When we have a strong belief, we have an instinctive and unconscious need to protect it. Unsurprisingly, we welcome information that reinforces our beliefs. We love this kind of information so much that we will, often unconsciously, seek out new information that supports our current position. This is called confirmation bias.
It’s never been easier to confirm your bias in the age of the Internet. One of the most egregious examples I’ve encountered was a website (that I'd rather not link to) with a custom search engine that procures scientific studies with whatever conspiratorial results you seek. However, confirmation bias can be more subtle. Facebook employs algorithms to modify your newsfeed in such a way that your feed becomes biased towards the friends’ opinions and articles you agree with. Your google searches are tailored to your internet browsing history.
You can't always control the information that comes your way. So what happens when we are presented with information that directly contradicts our belief systems?
We all like to believe we are thoughtful rational people, capable of critical thought and the ability to learn new things. However psychology has found that often the opposite is true: in the face of contradictory information, we may defend our positions with even more vigor.
To those of us who can’t resist a futile facebook argument, this is not a surprise. No amount of evidence to the contrary will convince anti-vaxxers that vaccines do not cause autism. Man-made climate change deniers do so in the face of a 99% consensus among climate scientists, and no amount of time listening to Bill Nye will convince a creationist that the earth is more than 6000 years old.
In 2010, psychologists Nyhan and Reifler conducted a study to understand how people process factual information contrary to their political beliefs. Subjects with a range of political ideologies were given one of two articles to read. The fake news article suggested there were weapons of mass destruction (WMD) in Iraq prior to the US invasion. A 'corrected' news article outlined the absence of WMD stockpiles or an active WMD program, as concluded by the Duelfer Report.
After reading the article, subjects were then asked how much they agreed that Iraq possessed, or had an active program to develop, WMD prior to the US invasion. Comparisons were made between how subjects responded to the fake article and the corrected article, based on their political ideology.
Generally, liberals did not believe there were WMD in Iraq, while conservatives tended to support Bush’s claim that there were.
Very liberal subjects that read the corrected article disagreed that there were WMD in Iraq even more strongly than very liberal subjects that read the fake news article. This isn’t surprising, as the corrected information supported the political ideologies of liberals. Those with a more centrist ideology felt similarly about the statement, regardless of which article they read.
However, conservatives that read the corrected article believed more strongly that WMD were in Iraq than conservatives that read the fake article. So in the face of contrary evidence, these subjects held onto their convictions with greater intensity. Presenting new, corrected information had the opposite intended effect-it backfired. Hence, Nyhan and Reifler coined this phenomenon the backfire effect.
This effect extends to other belief systems as well. In 2015, Nyhan and Reifler sought to understand how misconceptions about the flu vaccine might be corrected.
Subjects were divided into three groups. One group was given information that either highlighted the danger of influenza, another group was given ‘corrective information’ (information that corrected common misconceptions about the flu vaccine), while a third control group received no additional information to read. The participants were ranked as either having low or high levels of concern over the side effects of the flu vaccine. Finally, subjects were asked if they intended to get vaccinated against the flu.
Overall, corrective information did successfully reduced false beliefs about the flu vaccine. However, it did not increase the likelihood that subjects would actually get vaccinated. In fact, among those subjects who had high levels of concern over the vaccine’s side effects, their intent to vaccinate actually dropped when given corrective information. Again, the effect backfired.
Why do people subconsciously resist evidence that contradicts their beliefs? How might such behaviours be beneficial? When I asked a few of my behavioural biologist and psychologist friends (of which I have a disproportional amount) for their opinions about this, they all indicated that such behaviours would have evolved to increase fitness in some way, shape, or form.
According to Dr. Danny Krupp, a research associate with the SALT lab at One Earth Future, belief systems exist as a way to further one’s fitness. That is, people value things that they believe will benefit them. Through defending your position, even in the face of contradictory evidence, you are defending the perceived benefits to yourself that your position supports.
Dr. David Logue, an assistant professor at the University of Lethbridge, highlighted that in the animal kingdom, increases in social standing often translate to an increase in fitness. Assuming this is true for humans, losing an argument can diminish one’s social standing. Consequently stubbornness may be a viable strategy.
In the same vein Dr. Sandeep Mishra, an assistant professor at the University of Regina, suggested that if the beliefs held by an individual represent those held by that individual’s social group, publicly maintaining the group’s position-especially in the face of contradictory evidence-may be a way to demonstrate allegiance to one’s social group.
We may never know why the backfire effect exists. But understanding its implications can offer insight into how we can better inform an electorate, or promote measures of public health, for example. The uncomfortable truth is that we are all susceptible to obtuse thinking. It begs the question: what corrective information has backfired on you?
I am a woman in science. Most of the times, the ‘woman’ part is a non-issue. But sometimes, it is.
“Let me tell you about my trouble with girls. Three things happen when they are in the lab: You fall in love with them, they fall in love with you, and when you criticize them they cry.” The musings of not just any scientist, but Nobel Laureate Tim Hunt at the World Conference of Science Journalists in South Korea last week. Most definitely not the conference where one should be making headline-grabbing controversial statements.
When the proverbial shit hit the fan, Mr. Hunt explained that he was speaking from personal experience, and he had meant the comments to be funny. He apologized for what he said, but when prompted to explain about women crying in the lab, he dug himself deeper:
“It’s terribly important that you can criticize people’s ideas without criticizing them and if they burst into tears, it means that you tend to hold back from getting at the absolute truth. Science is about nothing but getting at the truth and anything that gets in the way of that diminishes, in my experience, the science.”
Sure. In science, criticism is important. The truth is important. And while I believe Mr. Hunt deserves better than the rush-to-judgement he's received, these comments reveal a not-so-hidden truth about women and STEM (the traditionally male-dominated disciplines of science, technology, engineering and math).
Julie Beck wrote an excellent piece in The Atlantic that illustrates why Mr. Hunt’s attempt at humour was met with stone-cold silence. Social media erupted with legitimate fury: twitter’s #distractinglysexy conversation was equal parts hilarious and inspiring.
But because this is a blog post, let me tell you about my trouble as a woman in science. For the most part, it’s no trouble at all. For the most part, I am surrounded by extremely supportive mentors. The majority of my colleagues in my current lab are women-and this trend is on point with many other labs in our research group. However, when I look one step above my current position as a PhD candidate to the post-docs, most are male. And if I look one step further, out of the twenty-two principle investigators in the Gastrointestinal Research Group, two are female.
This is part of a larger trend: that women disproportionately drop out of scientific careers. Nature magazine has a comprehensive write-up about the lack of women in science, and a lack of identifiable role models is, in frustratingly cyclic fashion, a primary reason.
So getting back to my experiences as a woman in science, I'll limit my blatherings to a single example.
When I first was exploring various PhD positions, I met with a potential male supervisor who told me (and while I am paraphrasing, I'm not paraphrasing that much), that if I wanted to embark in a PhD program I shouldn’t get pregnant. I didn’t even know if I wanted children at the time, but here I was, being told to consider what I wanted the state of my uterus to be throughout the next 4+ years of a PhD program. I doubt that the men interested in entering his lab were told they should refrain from impregnating anyone.
Although this was relatively recent, I choose to believe that such schools of thought are fading. Case in point: contrast the above scenario to my current supervisor, who actually encouraged me to consider having a child during my PhD, as maternity benefits are better for graduate students than post-docs.
Well I took his advice to heart, and as I write this I am on my last few months of maternity leave. And I am equal parts optimistic and terrified about my future as a scientist. Optimistic because it’s my nature. Because with hard work, ambition, and a supportive partner, there’s no reason not to be. Because I believe I somehow owe it to myself and other women in science to at least give it a try. Terrified because it’s also my nature. Because I have witnessed so few examples of women in science with successful careers and a family. Because my lab tech has outright told my colleagues that since I had my son, I have become more stupid (not paraphrasing), and losing my science-edge to motherhood has always been one of my fears.
I truly believe that very few people (Mr. Hunt excluded) think that STEM wouldn’t benefit from more women. What discipline wouldn’t benefit from increased diversity within its ranks? But as I said before, I'm an optimist.
Every year the University of Calgary puts on an intensive one-day Leadership Exchange conference that seeks to motivate and inspire young minds. It focuses on leadership: what it looks like, how it’s achieved, and what it takes to be a leader. This year, the Leadership Exchange conference focused its message on how individuals can be a catalyst for change. When I was approached to sit on the Leaders in Sciences panel I was honoured, but quite surprised to be considered a leader in my field. As a graduate student, I am constantly aware of how much more I need to learn, so it’s difficult to imagine myself as a leader. However, as scientists, we are in a constant state of learning, so I’m sure I’m not alone in feeling this way.
I sat on the panel with two other very accomplished women, and we fielded questions from a large audience of eager undergraduates. Students were interested in how we came to be in our chosen fields, what kinds of obstacles we’d encountered, and what life as a scientist was like. Finally, we were asked to share lessons on leadership. For me, two things came to mind.
First, you need to both embrace and create opportunity. Careers are forged over time, by knocking on (or kicking in!) the doors you find along the way; they aren’t just something you apply for. Networking is a big part of this. I am still in contact with a professor I worked for in 2003, and recently contacted him for an article I’m writing about hummingbird foraging behaviours for my website. Another part of embracing opportunity is thinking outside your field. I’ve always loved CBC radio, so when an opportunity presented itself to apply as a research intern for the Calgary Eyeopener, I jumped at it, poured everything I had into the application, and a new door opened. While I have no idea where these opportunities might lead in the future, I know the regret of not trying to open doors is greater than the effort it takes to try and open them.
The second lesson I imparted was the importance to recognize failure. Science is blood, sweat, and tears. If you include the few times a mouse has bitten me and drawn blood, this can be taken literally. Consequently, it can be challenging to recognize when you need to keep persevering, and when you’ve hit a dead end and its time to move on. The first research avenue of my PhD was a dead end. Instead of recognizing this sooner, I attributed these failures to my own ineptitude as a scientist-for twelve long months. It was a hard lesson, but I’ve learned the importance of trusting in your own abilities and instincts.
Overall, the conference forced me to take some time and think about where I started as a scientist, where I am now, and how I’ve navigated the trials in between. What makes a good leader, and how can one be a catalyst for change? My final conclusion is that is comes down to passion, and the passion of scientists to satiate their curiosities. Passion is contagious; it can motivate and inspire. Passion gets you through the first nine failed experiments, and makes that tenth successful experiment worth the first failures. I think that passion might just be the ultimate leader.
In the summer of 2014, I was awarded a position as a research intern with CBC radio through a program sponsored by Alberta Innovates Health solutions-the same folks that fund my PhD. I was stationed with The Calgary Eyeopener, CBC Calgary's flagship program, and Calgary's most popular radio program.
Immediately I was enveloped into the daily routine involved in producing and directing the show; discussing the quality of the previously aired show, assessing what stories needed to be followed, and pitching story ideas for the next day’s program. There was no probation period. Two things struck me: how relaxed the atmosphere was, and how impeccably stylish the women of Calgary CBC radio are.
Within the week I was trained on the Dalet Media Program, learned how to operate the portable Marantz recorder, and was familiarized with the protocols for conducting pre-interviews, confirming guests, and writing scripts. From conducting ‘streeters’ to get local Calgarian’s opinions on controversial topics in the news, to preparing ‘packs’ (mini documentaries) on a variety of topics, and recording the ‘downtimes’ that promote musical acts coming through Calgary, I had the opportunity to try my hand at a variety of different elements that make up the radio programming at CBC.
It’s difficult to pinpoint the most rewarding part of my internship experience. Listener feedback via twitter and voicemail from stories I’d pitched was always validating. My first successful story pitch, in which a bee ecologist voiced his concerns over how urban honeybee keeping could have unforeseen costs on native pollinators, prompted an industrious 13 year-old listener to send our host, David Gray, one of the beautiful houses he designs and builds for native mason bees.
It was also gratifying to witness how beloved the Calgary Eyeopener is within the community, a testament to the relationship that can exist between media and the audience. The CBC’s Annual Stampede Breakfast brought in hundreds of revelers, who were not shy about voicing their support for their beloved CBC radio.
On Neighbour day, devoted to recognizing the community spirit that Calgary demonstrated when the floods ravaged through dozens of communities in 2013, many Calgarians stopped by to take in some doughnuts and coffee, and chat with the staff like old friends.
The infectious enthusiasm of many guests was similarly a highlight. It was difficult to not be inspired by Chris Koch’s quest to get a drivers license at age 35, despite his lacking arms and legs since birth. The members of the Masonic Lodge that hosted an open house on Calgary’s inaugural ‘Mason’s Day’ were exceptionally welcoming to my questions. And the mussel-sniffing conservation dogs (pictured below) working to keep invasive zebra and quagga mussels out of Alberta’s lakes and rivers stole my heart.
I was assigned to the summertime “Big Ideas” series, which showcased some incredible, often unusual innovations developed to address a variety of problems. This led to a hunt for the perfect idea and guest to match. The weekly series brought to light some fascinating projects, from the intriguing collaboration between the ketchup connoisseurs at Heinz and Ford automobiles, to the technology that converts your old bike into an efficient electric hybrid. We heard from the engineers piloting flying wind turbine projects, learned how cell phones can save the Amazon rainforest, and discovered the latest trend in dating: sniffing out pheromones on unwashed t-shirts. These guests were consistently engaging, enthusiastic, and always grateful to share their stories with me.
The AIHS Media Fellowship provides an incomparable opportunity to develop the skills necessary for effective media communication first-hand. The Calgary Eyeopener team was welcoming, patient, skilled and very accessible team to work with. As friendly off-air as they sound on-air. The hands-on approach and length of the internship gave me the opportunity to identify the skills I needed, and the time I needed to develop them. Radio is a unique medium, and I came to understand that the narrative for radio has a pace and style unique from other forms of media, with a strong focus on voices and soundscapes
The societal benefits of a scientifically literate and well-informed public are immeasurable. Understanding the scientific process, herd immunity, and disease risk factors, for example, are just some of the ways in which effective communication can impact the health of communities and individuals. The need for effective science communicators is well evident, given the misinformation that is so easily spread via the internet. Ultimately I hope to embed science communication and writing within my career as a medical science researcher. I will always be grateful to AIHS and the Calgary Eyeopener team for the once in a lifetime opportunity to participate in this internship!