Breaking the science silence on the blog to share a piece published over at The Sheaf Publishing Society. Read about the importance of science literacy, communication and why we need science in society.
Stay tuned for more science stories!
Breaking the science silence on the blog to share a piece published over at The Sheaf Publishing Society. Read about the importance of science literacy, communication and why we need science in society.
Stay tuned for more science stories!
Imagine you are at a cocktail party.
Some sort of creative kickstarter’s big reveal that includes an in-house DJ — some forty-year old guy named Craig with a receding hairline and reflective aviator glasses— set up in the corner next to some fiddle leaf fig plant. You clutch in your grip a cocktail that gives bourbon a bad name; some new spin on an Old Fashioned that’s replaced the bitters with wood smoke and orange peel with Rosemary twigs. In the corner, opposite Craig the DJ, there is a twenty-something in a three-piece suit with far too much pomade in his hair and the vague, nauseating smell of sandalwood.
There is cat hair on his collar.
“Hello,” He reaches out his hand “I’m Chad, entrepreneur”. He tells you with distilled enthusiasm and large white teeth. As you shake Chad’s hand and hold unblinking eye contact you come to the realization that staring back at you, through the echoing dot of his pupil is not Chad at all, but a gaping, dark abyss where Chad once resided.
Down inside the deep structures of his brain the parasite Toxoplasma Gondii sits on his intracellular throne with his parasitic fingers wrapped around the marionette strings used to control Chad’s corporal, entrepreneurial form
T.Gondii is really the business visionary here— the master mind— and Chad is merely the necessary meat sack for the mission. The vehicle of success and venture.
Except, this absurd Twilight Zone sequence can’t possibly be the reality of things. Can it?
A recent news story (HERE) thrusted the parasite front page and center, once again. It seems that every few months, Toxoplasma Gondii (Or T. Gondii to his friends. Also known as Toxo to those in his closest circle.) rears its head in popular science articles. This particular article told the tale of a sample of individuals who appeared to be both infected with T. Gondii and possessed the tendency to engage in business endeavors.
According to the article those that tested positive for exposure to T. Gondi were between 1.4 and 1.7 times more likely to go into business or entrepreneurship of some capacity.
The theory behind all this is that T. Gondii infections result in the human host being more likely to engage in risk taking behaviour. And since calculated risks are what being an entrepreneur is all about, it was speculated that Toxo gave these particular individuals a competitive edge.
Along with shaky business ventures, T. gondii has been theorized to have an hand in the greater frequencies of car accidents and incidences of unbridled behaviour that appear to pop up in those afflicted with the parasite This behavioural manipulation eventually pushes out into the periphery to include episodes of psychosis and even more complicated neuropsychiatirc disorders such as Schizophrenia.
It has been speculated that it may even be the culprit behind “crazy cat ladies” — the rare incidences where women hoard dozens of cats. Unusual behaviour that is neatly packaged into the guise of a mind controlling parasite that is seemingly driven by its reproductive cycle.
Something which can only be completed inside the body of a feline.
Do the three cats that I cohabitate with put me at risk for cat induced psychosis? Doubtful. They may put me at risk for enlarged lymph nodes, lethargy and the classic “flu-like” symptoms of the miscellaneous microbial infection. If I am really unlucky and/or immunocompromised, I could end up with a case of a brain abscess or some lovely collections of tissue cysts.
For all appearances, T. gondii’s mind control powers seem to be highly exaggerated in regard to human behaviour.
But, for curiosity sake, where does one begin to point accusatory fingers at this protozoa that happily hijacks the nervous system?
It all starts with a dopamine hypothesis.
Several papers have noted that T. Gondii may hijack the central nervous system by increasing dopamine production. Dopamine is our feel good neurotransmitter that is a heavy player of the pleasure pathway. It is released in sexual arousal and substance use — just to name a few stimulating and pleasurable events. Dopamine can be considered our reward for engaging in specific behaviours that elicit the release of the neurotransmitter. We feel GREAT and will seek out ways to engage in more dopamine release.
Sex, drugs and rock n roll. We will go to great lengths to achieve a little hit of dopamine.
It is possible that an increase in risk taking behaviour could result from an increase in the activity of dopaminergic neurons, specifically of the ventral tegmental area of the brain— the apparent center of our reward pathway. If our risky behaviour is rewarded by domaine release then we would likely engage in these behaviours more frequently in order to achieve that same pleasurable release.
The VTA has a hand in controlling motivation, orgasm and addiction. This area of the brain is also involved in some emotional cross-talking with the amygdala and other areas of the limbic system. When it comes to rewards and gains, we humans generally go out on a limb. We will often take a risk in fulfilling these cravings.
All for that dopamine hit.
Toxoplasma gondii has been found to encode genes for the synthesis of tyrosine hydroxylase, an enzyme involved in the catabolism (or break down) of amino acid tyrosine into L-DOPA. L-DOPA is then further broken down into dopamine, along with several other neurotransmitters. Theoretically, the presence of T. Gondii, inside a host’s brain could muck around with the level of catecholamines, such as a marked increase in dopamine. This, in turn, could lead to behavioural changes.
An Esquire article form 2007 (HERE) used incidences of female promiscuity as a particularly eyebrow raising example of the effects of T. Gondii’s chemistry hijacking.
Rest assured, if you have an insatiable sexual appetite for carnal pleasures, chances are you are not being controlled by a protozoan parasite. You can blame media and the rats for that interpretation.
And as we explore further, it all seems to come back to the rats.
While the debate of T. Gondii’s ability to muck about in our brain and navigate our behaviour is still on going, it appears that it does a fairly good job of controlling rodents.
It has been observed that rodents with a Toxo infection will suddenly lose their fear based aversion to cat urine. In fact, they appear to almost be aroused by the smell and are drawn, hopelessly, to the deadly cat.
Haven’t we all experienced that misguided sexual attraction? The sting of unrequited love with the wrong person? Helplessly drawn to them despite all logic and reason.
Dopamine. It’s a hella of a drug.
In this case, the rat’s behaviour appears to have a role in nature’s ultimate desire for procreation and gene propagation. Our friend T. Gondii can only reproduce inside the intestines of a feline. It must get back into the cat to continue its genetic lineage. All this to go forth and feast upon the brains of the unwilling for it’s day-to-day activities. As an obligate intracellular parasite, T. gondii needs mammalian cellular machinery to carry out its metabolic functions.
The fastest way to get into the intestine of a cat is through a tasty rodent treat.
It appears that T. Gondii hijacks the rat’s sexual arousal pathways in order to lure the rat to the cat. By stripping the rat of it’s natural aversion to the scent of cat it can position the rat close enough to complete its cycle. This type of behaviour manipulation is what originally sparked the theories of T. Gondii induced behavioral changes in humans.
All working through pleasure-reward systems and dopamine.
One can see why it may be thought to contribute to some neuropsychiatric behaviours.
Let’s take Schizophrenia, the popular example.
Schizophrenia is a neuropsychiatric disorder characterized by increased dopamine levels and an array pf positive and negative symptoms. These include: hallucinations and delusions (positive) to the very eerie waxy catatonia (negative). There has been speculation that when our friend T. Gondii is not making women more promiscuous or involved in an innovative start up, it is wreaking havoc in the brains of those with Schizophrenia.
Where does all this come from? Well, there appears to be a correlation between seropositive individuals (those testing positive for the parasite) and a Schizophrenia diagnosis.
Here you have a parasite that can manipulate dopamine levels and you also have a disorder that is characterized by the increase of dopamine. Easy to put two and two together, right? But it’s not that simple. Not all seropositive individuals have Schizophrenia and not all people with a Schizophrenia diagnosis are seropositive. There appears to be no causation here, meaning the cause of schizophrenia is likely not Toxoplasma Gondii.
And that’s where things can become confusing for media reports and the general population digesting the information.
Just because something exists along side something else does not mean that they have any effect or influence on each other. If there is no evidence to link the two —nothing describing influence, symbiosis or a connection — then you can not assume that they have any cause and effect relationship. Just because A is found in the presence of B does not mean that A created B or vice versa.
We like things to be neat and we possess the tendency to see patterns. Tidy explanations and seemingly causal events make us feel good (dopamine, again?) because it ties up loose ends. We come to a conclusion in a straight line and feel confident about the knowledge. In one glance we can see where all the puzzle pieces fit — all displayed for us to digest in a satisfying horizon line.
When things get complicated and messy, as most things in nature do, we tend to get a little agitated and anxious by all the busy, tangles before us.
T.Gondii is a good example of our misunderstanding of correlation and causation.
Is T. Gondii making you more entrepreneurial and a high-risk client for insurance companies? Is it the reason the older gentleman down the street from me smells like cat urine and has upwards of 10 feline friends? Is it the reason for your cousin’s schizophrenia diagnosis and paranoid delusions?
While we can’t say for certain, it appears that it is unlikely. The evidence just isn’t quite there.
Does T. Gondii affect rat behaviour in a way that is evolutionarily favourable for the parasite? Well, yes, there is evidence that appears to suggest this.
The thing is, you can’t just jump from rats to humans. What’s good (or in this case, bad) for the rat is not good (or bad) for the human and vise versa. We just can’t extrapolate from a rodent model to a human model.
What’s to be learned from all this?
Cook your meat well, wash your hands after changing the litter box, correlation does not equal causation and just because it’s proven in a tiny rodent does not mean it’s going to perform the same inside the complicated biological system in the meat sack that is you.
Science is messy. It intersects and it turns in on itself. It expands beyond what we can observe in one quick glance.
We have to search for the answers. We have to keep asking questions.
Ah, light. The ubiquitous radiation that bombards our humble human bodies. Multiple wavelengths of vibrating photons that illuminate our world. The wonderful, yet minute, visible spectrum that we can detect and the invisible, hidden ranges that slip past our primitive senses.
Light is all around us.
From the incandescent glow of city street lights to the blue glow of our electronic screens — light follows us throughout the day and into the night. Something so commonplace and pervasive lulls us into a sense of safe serenity.
Light is warm and comforting. Light is our friend.
Of course, we are aware of the devastating effects of the sun’s blitzkrieg of unforgiving UV rays. The ones that ravage our skin — causing our epithelial cells to make mistakes, mutate, and replicate unchecked —often leading to proliferation as the common carcinoma or the insidious melanoma.
Light kills. Light destroys.
Light giveth and light taketh it away.
Let’s start with the sun— the gaseous orb sizzling in the sky above our heads.
An assortment of energy is currently raining down upon the earth.
Plants absorb it and cultivate their own energy from it and it warms our skin as we bask in it.
There, in our skin, a little molecule awaits the sun’s light to change its shape. This is the precursor to vitamin D — the “sunshine vitamin”— necessary to maintain many biological functions. Our immune system and equilibrium of the minerals within our bone rely on this molecule.
Without it, we begin to crumble.
Rickets — a disease characterized by softening and degradation of the bones— occurred frequently in 19th century urban children of Europe who, with industrialization, had infrequent exposure to the sun. Weakness, pain and decreased density of the bones lead to a debilitating disease that caused poor mobility and deformities.
Incidence of rickets declined over the 20th century when a correlation between sunlight and the disease was drawn by the medical community. (Although, not gone nor forgotten, rickets still lurks and lingers in populations to this day.)
Sunbathing soon became the prescription to cure and prevent ill health.And to this day, the beguiled nature of the sun’s warmth still leads many to bask in it’s glory.
What is better than the beautiful warmth of ultraviolet light catching our skin a blaze.
Ultraviolet light—the wavelength needed to get the vitamin D precursor vibrating —along with, X Rays and infrared light, are part of the electromagnetic radiation that is emitted from the sun. Radiation that is constantly raining down on our skin, lulling us to sleep with its warmth.
In our sunscreen culture, it is widely known that UV light can be dangerous. It gets its sunlit fingers inside our DNA and mucks about — supercharging the molecules with it’s gooey golden energy.
Our DNA can take quiet the wallop of additional energy without any real repercussions but, if exposed for long enough, things can start to falter.
It gets tired. It gives in.
DNA consists of a sugar backbone, phosphate molecules and a very important nitrogenous base — either a pyrimidine or purine. If two pyrimidines are next to each other —thymine or cytosine — an extended barrage of UV light can lead to the two molecules fusing together.
Something called dimerization.
The two bases become linked to each other, creating a ringed structure. This contributes to an unstable intermediate molecule which can put a literal kink in the transcription of proteins— a key part of cellular processes— by changing the shape of the DNA’s backbone.
UV light can also indirectly affect DNA, with the creation of reactive oxygen species, better known as free radicals. Free radicals, act a little bit like a Viking horde — raiding and ravaging molecules for electrons. leading to mutations that can add up during DNA replication.
Tiny infractions lead to the swapping of base pairs and create a mess of the once pristine code, often producing nonsense sequences. Nonsense sequences lead to nonsense (defective) proteins which, in turn, lead to phenotypic mutations and often times disease.
Fortunately, we have repair mechanisms that scan the length of our DNA. They remove and replace the mistakes before the wound is sealed behind it. Sometimes, however, these mutations are missed or go unchecked and the result can lead to some serious, prolific consequences.
Light, itself can also change gene expression, leading to substantial changes in our body’s regulation.
And it’s not just sunlight tickling the melanin cells within our skin long enough to produce monstrous melanoma. It occurs on a much smaller, more subtle scale that we are only beginning to understand.
And most of it starts in the palm of your hand or the comfort of your lap.
The light your phone or computer emits is unique compared to the sunlight that trickles in through your windows. The wavelength is shorter and this is the reason for that familiar blue tint.
This has a direct effect on specific genes. The ones that regulate the production of melatonin and put “the rhythm” in our circadian rhythm.
The circadian rhythm is a network of interconnected mechanisms working together to influence specific, timed functions inside your body. It controls the cycle of hormone production and release, metabolic pathways and maintenance of proper cellular function.
The circadian rhythm is not unique to humans, in fact, even bacteria have a circadian system. It appears to be an important, well conserved mechanism across both eukaryotes and prokaryotes.
However, unlike bacteria, humans have a circadian pacemaker hidden inside our hypothalamus called the suprachiasmatic nucleus. It has its hand in signaling the production of the hormone melatonin and for sending out neural signals in response to light and other inputs.
It keeps everything in line and on time
Many important physiological functions rely on this train conductor — and its well timed, 24 hr pocket watch —for things to run smoothly.
Although there may be several factors that have an influence on the clock, light is one that plays an incredibly important role.
It is critical at keeping the rhythm from oscillating and It all starts with your eyes.
Taking a deep dive inside the vitreous humour, towards the very back of your eye, you can find your retina.
The retina is home to many light sensitive neurons called ganglion cells. These cells are particularly excited by blue light and they send crackling messages blazing straight to your hypothalamus.
There, they poke at that little pacemaker in charge of keeping everything in order.
This bombardment of light and excitation disrupts melatonin production which, in turn, throws the rhythm from the tracks — effectively derailing the clock.
Now, the beguiling blue light may be quite innocuous when you assault your retinas with glowing screens in the day time hours. However, when you stare at glowing pixels in a darkened room at night, you find yourself actively sabotaging your rhythm and sending a big, glaring stop light to hormone production.
A decrease in melatonin is not just detrimental to your ability to sleep and your mood regulation, it has systemic implications on physiological functions throughout the tissue and cells of your body. Like the methodical tumbling of a set of dominos — the effects are compounding.
Metabolism is negatively affected and there are discrete endocrine implications. This is especially apparent in altered glucose metabolism and insulin sensitivity. This may put an individual at increasing risk for obesity, type two diabetes and metabolic dysfunction.
Studies on circadian rhythm disruption also found elevated blood pressure and increased risk for cardiovascular disease and stroke. This seems to be related to modifications of neurotransmitters, lipid metabolism and a increase in oxidative stress due to sleep deprivation.
The body does not work insolation. It is an interconnected, intertwined system — an elegant ballet that requires rigorous, finely tuned footwork from all its players.
It does not function alone and cannot survive alone.
When things fall out of sync and the orchestra is suddenly out-of-tune, a cascade of failures tend that occur.
And It all comes back to light. The photons of light that bounce off our skin and beam into our eyes directly affect the tiniest mechanisms in our body.
It can turn a gene on or turn one off.
These simple switches of transcription factors — molecules that bind to lengths of our DNA and control the information that is transcribed — have huge physiological impacts.
Artificial light, streaming from our devices in the darkness of the night, appears to have a direct influence on the smallest molecules in our body. It has the power to influence our genetic and phenotypic expression, our metabolism, our cell cycles and, in turn, our health. It appears we are ever unaware of the power and influence our environment has on our fallible bodies.
Light— pulsating invisible atoms— can alter us in ways nearly unimaginable.
I am a big subscriber to the thought that “you are your brain”.
That the very things that make you who you were, who you are and who you’ll become lie inside the squishy sulci of this gelatinous organ. You rely on the thing staying intact and with all systems firing. If something comes along and mucks about inside of it — injury, microbe, mutated proteins, etc. — you cease to be you.
However, it’s appears to be more nuanced than that. That something as ubiquitous as light, can reach inside and play around with our DNA — effectively changing our physiological functions and phenotypes — with some fair reaching and sometimes negative consequences.
It illustrates the balance of the entire system. That everything needs to be in rhythm, on time, flowing and tumbling together. That who you were, who you are and who you’ll become depends on the synchronicity of a trillion molecules.
Ones that are both inside you and outside of you— tumbling through the great, wild and indifferent universe.
This is a blog about science and storytelling. It’s about science writing and communication. Science and writing.
This post is a personal reflection of writing, of striving to be a storyteller — a half-ass decent communicator. This is a sharp departure from the science focus but I believe it’s equally important to examine the writing side. We are dynamic, after all, and behind science and stories are the humans engaging in these activities. Both are about satisfying curiosity and attempting to explain the world around us.
My eyes opened into the morning light that leaked out from behind the brown curtains. The open window let a cool 7:00 am breeze filter through the room. It whispered across my bare leg — exposed through the tangles of sheets, quilts and faux fur blankets that served as the bedding on this seven-year-old mattress. I blinked a bit, my eyes puffy from the tears I had found myself shedding all week.
The night before was a particularly catastrophic waterfall that lead to this residual inflammation of the soft tissue around my eyelids and cheek bones; my nasal passages and their mucosal membranes swollen and congested.
It had just been an ambiguously rough week.
Research suggests that emotional tears have a different chemical composition than your every day lubrication or reflexive tears. They have higher amounts of hormones, a neurotransmitter and cations. Vaguely, I remembered a neuroscience prof lecturing about an obscure experiment. Male volunteers viewed porn inside an MRI machine while cotton balls, soaked in the tears of sad women, were pressed to their nose.
They subsequently lost interest in the porn.
The chemical composition of a sad woman’s tears changed their neuronal responses. The areas that blaze brightly when aroused now darkened. The tears may have even dropped the testosterone levels in these men, enclosed in these lonely MRI machines that recorded their brain activity while porn danced across their retinas.
(I can’t find the appropriate reference to this particular study. Perhaps, he embellished it. Perhaps, I dreamt it. I am guilty of having some bizarre dreams.)
“Anthony Bourdain is dead”, he stated from the pillow behind me.
“What?” I gasped out in a voice coated thick from sleep. I didn’t turn to look at him. I keep my eyes fixed on the wall — a pale aquamarine I painted years earlier.
Heart attack? No, that didn’t feel quite right. It was something else.
“He killed himself”, he clarified without my asking.
“What?” I repeated, a little breathlessly “What the fuck?”
I was shocked, but I was not surprised by the news. It made sense. I saw it in his social media posts. I saw it in his episodes. I heard it in his words. It was familiar. I recognized it.
I’ve looked into someone’s eyes as they shouted senselessly about killing themselves. I’ve spent hours negotiating and attempting to talk them through it. I spent hours waiting in a busy emergency room. I spent hours listening as a rotation of medical professionals asked them to explain their plan.
A belt and a door knob.
Before that incident I would have never guessed at this thoughtful design. It was something I would have never anticipated, despite my fairly vivid imagination.
It is June 9th, 2018. Yesterday Anthony Bourdain died, the belt from a bathrobe wound tightly around his neck. Yesterday I started to write again after a severe bout of writer’s block left me struggling to form sentences of any substance.
Whether these sentences have substance now is up for debate, but they are coming easier and that is something.
I have always wanted to be a writer.
Nearly eleven years ago I sat in a dimly lit grocery store cash office, in ill-fitting khakis, counting out nickels from a cashier’s tray. On the cusp of nineteen years old with flat-ironed chestnut hair that hung down to my scapula and the same sardonic humour I have now. Perhaps it was slightly less refined. It still has room to mature — we are always a work in progress.
I made small talk with the meat manager who sat next to me in the cramped closet that housed the safe. He was a tall, quiet, intellectual — finishing his master’s degree in some esoteric interdisciplinary study that involved new media and philosophy. He was a little mysterious, smoked cigarettes and drank black coffee.
“What do you want to be when you grow up?” he asked during a smirking bout of small talk.
“I want to be a writer” I said, as I leafed through wrinkled twenty-dollar bills, laying them down in neat piles to be double counted by his hands.
My answer rendered him speechless for a moment. I can’t recall what we spoke of after that.
He read some of my pieces — poorly written fiction that went no where and reflected my age. I wanted to be a writer but I had nothing to write about then. I hadn’t found the right story to tell
He thought I had talent. He said I made him nervous.
I ended up marrying him.
And then I stopped writing. I stopped seeking out stories. I went dormant — mimicking the elegant process of endospore forming bacteria.
I packaged up everything that I contained and drew inward. Staying in this liminal state for years. Resistant. Persistent. Silent.
It was only within this past year I stumbled across the stories I wanted to tell. Carve out a space where I could explore my curiosity. Tell a tale with substance.
Anthony Bourdain was a storyteller. He was a writer, a communicator, an astute illustrator of the grittiness reality had to offer.
He explored the humbleness of humanity.; examined the beauty contained within the ugliness and the seemingly mundane scenes that most people wander through absentmindedly. Existing — blissfully unaware or simply focused to far inward.
He was a food writer — a food and travel host — but it wasn’t about the food.
The food was merely a vehicle for storytelling. It was an access or reference — a vantage point for the human story he desired to tell. The unique stories of individuals that revealed the small, familiar tales everyone could identify with.
He was a master at showcasing the non-discriminatory nature of the human condition.
What was really compelling about Bourdain’s work is that he was not afraid to explore people and places. He was certainty not afraid to explore emotions and the deep ethos that makes us human.
He got his hands dirty. He immersed himself in it.
He was ravenously curious — questioning things, seeking to understand all that was around him. He deeply desired to understand people and the nuance of the things that comprise the world.
A voracious reader and consumer of music and film, Bourdain sought to understand himself and others in different contexts and settings. The human condition and human experience is subtle and dynamic. One needs a knowledge base, an understanding, or simply a platform to leap from.
Read — devour those books. Consume all you can. Attempt to satisfy your curious cravings. Explore from there. Never stop learning.
As a curious person myself — as an aspiring writer and storyteller — I understand his insatiable curiosity. I deeply identified with it. I recognized it.
The loneliness too.
A permeating sadness that crests and breaks like waves. A dull hum.
Thinking and writing are often very insulating activities. Sometimes you may get lost in observing the world and others. Most of the time it’s a deeply comforting feeling. Sometimes it can be overwhelming.
I was able to understand the voracious determination to accurately represent the tales one tells and the sheer desire— the need— to share them with others. In stories, you can actively engage with various ways of explaining the world and explaining ourselves. Ways of describing and understanding. However isolating the act of observing and writing can be, the end product must be a communal experience.
It must be shared —like a meal.
There is no honesty in storytelling without the vulnerability. You must have the narrator — the guide— asking questions, seeking truths, giving a voice to things that would otherwise have none. It leaves the narrator exposed.
Writing opens you up in ways that can be torturous. It’s a revealing and deeply personal act, that leaves you liable. You reveal small truths about yourself in your words — a deeply intimate gesture that is not always well received.
What Tony did with food writing I can only aspire to do with science writing. That ability to seek out the humanness within the subject. To tell a tale that piques the interest of others. To do it all honestly and accurately. To do it well.
Science, like food, is a very human activity — one that brings out the many facets of our nature. One that may assist in explaining it.
It quenches curiosity and satiates the mind. At the same time, it opens us up for conversation, thought, and exploration.
We can find all the parts previously unknown over a bowl of food and a beer with strangers or with friends. We can do the same over plates of media, microscopes, data and gels. We can learn about one another, we can catch glimpses of people and their origins. It opens up dialogue and discussion.
They are both ways for us to describe, discover and explain our nature and our existence. Food and science are merely vehicles for us to explore our humanity.
It isn’t about the destination, is it? You must be compelled to stop and collect the stories along the way. Observe. Write. Communicate. Share.
Thanks for inspiring us, Tony.
As the cliché goes — one man’s garbage is another man’s treasure.
And also, perhaps, a viable buffet of tasty, tantalizing delights.
Bacteria are notorious for eating our waste. They attack, devour, proliferate and thrive in all kinds of unseemly matter. They colonize rotting food and break down the organic matter into usable material for their biological functions. Within our own intestines they happily congregate within the cozy folds, breaking down the last remnants of food and synthesizing Vitamin K — which helps prevent us from bleeding to death. Thanks, bacteria.
They happily monopolize our fecal matter as it journeys through us and out into the great unknown.
We need bacteria. In a world without bacteria dead things would linger indefinitely. Dead leaves and vegetation would pile up on top of each other, wildly taking over every square inch of land. And so would we after our death — or, to be more specific, the void shell that was once us would linger.
One way of reaching immortality, I suppose. In a world without bacteria our empty bodies would essentially exist forever.
It would appear that our planet would be in some trouble without our bacteria buddies.
And yet, despite all of bacteria’s ravenous ways, we are still in a predicament. Plastic is set to overrun us and reign supreme. A true immortal, plastic may out last all of us — piling up increasingly, choking the life out our oceans and littering our lovely beaches.
In response, we halfheartedly try to limit our plastic consumption. But honestly, scrapping your drinking straws is really a last-ditch effort here. One that is not likely to save us, despite all our good intentions.
Enter Ideonella Sakaiensis, an unassuming rod-shaped bacteria that was discovered, only a hand full of years ago, feasting on plastic outside a bottle recycling facility.
Up until then, it was assumed that biodegradation — or the breaking down of material through biochemical means — was not a viable option for dealing with our plastic problem.
However, it appears this bacterium had found a way to utilize all of this plastic potential. To quote my childhood crush, Dr. Ian Malcolm —Jeff Goldblum’s character in Jurassic Park — “Life, uh, finds away.”
Little Ideonella uses a couple different enzymes to break down polyethylene terephthalate or PET. PET is catabolized (fancy biochemistry word for” breaking down big things into smaller pieces”) into two molecules—terephthalic acid and ethylene glycol— which the bacteria then use as a major energy source.
Recently, it appears scientist have been able to harness the power of Ideonella’s enzymes and even improve on their potency.
Meaning, the ability to break down plastic may potentially be at our finger tips. Potentially.
Plastic eating bacteria are a product of evolution. Bacteria are brilliant and resilient — able to reinvent themselves in the harshest of environments. When the going gets tough the bacteria get going (Groan). In the presence of antibiotics, the strongest bacteria pass on the keys of survival to select others in their colony. This “resistance” gene or plasmid is a passed on again and again through a process called horizontal gene transfer. The end result is the very familiar, yet still terrifying, antibiotic resistance.
Bad news for us.
Much of this resistance arises from the bacteria’s ability to change how it utilizes resources or alter various faculties it already processes. From using heavy metal pumps to pump out the antibiotics to manufacturing an enzyme that attacks its very attacker — bacteria can MacGyver their way out of many a situation.
So, when bacteria show up outside of a recycling facility, you know they have adapted to and have utilized their environment to their advantage.
They are not the first organism to alter themselves in the face of adversity.
The peppered moth pulled a similar trick over a hundred years ago.
Before the nineteenth century, the peppered moth was a delicate little white creature with black speckles that were —uhh—”peppered” across it’s wings. This allowed them to camouflage on lichen covered trees. A safety feature that helped to protect them from being picked off by their natural predators
Now, in nature you have a few naturally occurring mutations. The white, or light coloured, peppered moth is something called a “wild type phenotype” meaning it is the most abundant version of its kind to be found among the lichen covered bark. One mutation, however, gives rise to a very dark peppered moth.
This dark moth exists in far fewer numbers because:
a) it’s a mutant
b) the dark wings make the moth stand out — signaling to predators that lunch is served.
But, this moth’s dark wings proved to be an advantage over our wild white friend centuries ago
With the rise of the Industrial Revolution in Europe, smoke and soot from coal fires filled the air and settled on the streets. This thick black dust coated buildings and trees, killing off the lichen and painting the bark a shade too dark for the lightly speckled wild type moth. Soon the delicate little white moth was dying at a rapid rate— their white wings, now in stark contrast against the new dingy backdrop, made them vulnerable.
The darker moth, on the other hand, thrived. It’s population soon surpassed the lighter moth, usurping the throne to become the dominate phenotype.
The darker moth was able to pass on it’s version of genes in more numbers than ever before, allowing these black sheep of the bug world to proliferate and happily exist among the soot and the smoke-filled air of progress.
The story of the peppered moth is a specific type of natural selection called directional selection — where an extreme phenotype, or physical appearance, is favoured over another. This leads to a shift in the population.
Once the coal fires died down and industrialization’s pollutants were brought under control by legislation, the tables once again turned on the dark moth — leading to a ebb in population and the restoration of the white winged moth to their rightful wild type throne.
The resilience of the natural world is incredible and, occasionally, unsettling. Nature manages to alter itself in the harshest of circumstances and sometimes, even thrive in these less than ideal situations. This has implications and impact on us. It can be detrimental (antibiotic resistance), beneficial (plastic eating enzymes) or neutral (different flavours of moths) to us lowly humans.
Life, uh, really does find a way, doesn’t it?
Moths and Microbes
We left off on our brainstem’s foibles in it’s sleep induced regulation over our bodies. We are merely slaves to the humble pons — our brainstem’s envoy in charge of applying the break to our motor neurons when necessary. Sometimes, the pons gets a little overzealous. I can relate.
Sleep paralysis is a phenomenon experienced for centuries and gave rise to the word nightmare itself. Before we ever had an inkling about the squishy pink mass in our skull and the functions it may control, this inability to move upon waking was attributed to demons. Reasonable, right? Of course, demons.
These demons put the “mare” in “nightmare.” And they were not any ol’ demon coming to haunt and torment one in the vulnerability of sleep. These night visitations, by the Succubus and Incubus, were for one thing — sex. These demons had come to straddle your chest and take advantage of your human body while you lay helpless to their demonic desires.
Puts your most horrific sex dream to shame, really.
It is much more likely that your brain has been distracted by your dreams and failed to take its foot off the break than it is for a demon consort to be visiting you for some sexual deviancy and demon baby making.
Drifting away from demon babies and back into the murky contents of your brain, we find that your usual dreams are just as bizarre as these folklore visitations. Such strange and curious images conjured up from the depths of our brain.
We have all had dreams that range from the horrifying, to the bizarre, to the downright embarrassing.
And for the sake of the narrative, I guess I will divulge a few of my own.
In one recent disturbing dream of mine, I came across the eviscerated body of someone known to me (I blame my Netflix binge of Hannibal episodes). Before that, I dreamt I had a steamy secret rendezvous in a hotel room — twisting in white sheets with a delectable individual (A scenario I will never experience in my waking life). Most recently, I dreamt I was an electron bouncing around in the electron transport chain, sacrificing myself for oxidative phosphorylation and the synthesis of ATP.
The latter was the most disturbing of the three, I must admit.
In short, our dreams tend to be messed up. It’s the nature of them. Your brain, floating inside it’s secluded dark home, is generating fantastical images conjured from bits and pieces it finds stuck in its darkened corners.
When we dream, an area of our brain linked to our visual cortex — the occipital lobes’ extrastriate cortex — lights up in a wild fire of activity. During this light show our primary visual cortex, where we interpret visual stimuli, is oddly quiet. This strange pattern of activity suggests to us that the brain believes it is seeing something.
This something is, quite eerily, internally generated.
Dreams tend to get your stomaching turning and your palms a little sweaty. You can thank your emotional and often hysterical limbic system for that uneasy queasy feeling. All the emotional players in the game are highly active during your dreamy state. Usually, emotional responses are routed to the frontal lobe for us to assess. In our waking life, our rational frontal lobe helps us attribute meaning and context to those gut-wrenching feelings. While awake, we are often able to lesson or intensify emotional significance — depending on the situation.
When we dream, our frontal lobe — like our visual cortex — also appears to be on break from its general duties. This suggest that there’s limited interpretation of the visual information we are internally generating and the emotions they are provoking. This is the root cause for the sometimes terrifying, non-linear and incredibly bizarre movie projected nightly inside your skull.
If you awake from a dream that involved yourself in a compromising position with an impossible individual or one that involved you riding a tricycle down a hallway in your underwear — rest assured you are not alone in your brain’s freakish, fetish visuals. It’s simply a collection of found images pasted together by your extrastriate cortex with the emotional soundtrack courtesy of your limbic system.
But, now we come to the strangest part — what happens to our brain when we can’t sleep?
Insomnia — the word itself has a dreaded weight to it. Insomnia can be a chronic condition or a fleeting one. We can go through periods of insomnia when we are stressed, anxious or have ingested too many stimulating substances. Our autonomic nervous system betrays us — ramping up our sympathetic response — trapping us in a hyper-aroused state. For others, insomnia can be more familiar; a shadowy companion constantly with us
Insomnia, like most sleep related conditions, is still fraught with mystery when it comes to its mechanism and its origins. One insomniac may have difficulty falling into the depths of sleep while another has no problem relaxing into her open arms. For the latter, insomnia creeps in shortly after to rip them from sleep’s embrace — leaving them to spend the many remaining hours staring at a shadowed ceiling.
We can’t last too long without sleep and we are not alone. Experimental rats, kept awake by a rotating platform, quickly loose ability to regulate their body temperature. Despite consistent food intake, our furry rodent friends lose massive amounts of body weight before succumbing to death — roughly a month after they stopped sleeping.
A whole new take on the phrase “I’ll sleep when I’m dead”.
This is not all that different from the horrific (yet intriguing) prion disease, Fatal Familia Insomnia. FFI rises from a genetic mutation resulting in misfolding proteins within the brain. In FFI’s case, the area of the brain affected is our mighty thalamus— our stoic sleep regulator.
Like a bomb, hidden in the brain — ready to let loose a cascade of terror and tragedy — these proteins will eventually mutate and wreck havoc. They decimate the brain and lead to progressive sleep loss, stupor and atrophy.
I have thought of worse ways to die and I have not been able to find one more horrifying than these neurodegenerative harbingers of death. Hemorrhagic viruses may be a close second, but I morbidly digress.
The onset of FFI is insidious and usually occurs around an affected individual’s fiftieth year of life. The afflicted’s pupils constrict to pin points and they begin to profusely sweat. Increased salivation, heart rate and blood pressure follow suit. They are no longer able to reach the depths of sleep they need — instead falling into a catatonic like stupor. Slowly they lose control over their bodies and succumb to their fate, less than a year after onset.
For those of us who experience a milder affliction of sleeplessness, the symptoms and consequences may not lead to our horrifying end, but they can be detrimental to our health and well being.
Being sleep deficient puts us on edge. It makes us emotionally labile. It impairs our memory and reduces our ability to preform cognitively complex tasks.
We also have a tendency to lose our shaky grips on reality.
We have a propensity to hallucinate.
It’s a lot more common than one may think
Our brain is a master of filling in the blanks and connecting the dots. What we see, what our brain interprets and what is in front of us may all be very different. We are filling in gaps in our vision daily. Smack dab in the middle of our visual fields is our blind spot, a hole in our perception, where thick neuronal fibres exit our retina and send their electrical signals off for higher processing. Our brain fills in this void with what it expects and predicts will be there. And most often, it is correct. But not always.
Again, for the sake of narrative, I might as well tell a tale of my blind spot revelations.
One afternoon, while waiting to turn onto a highway from a side road, I looked out to my right and then to my left to survey for vehicles and assess the safety of my crossing. I could see for half a kilometer in both directions. All appeared to be clear to my right but, as I was about to begin my turn onto the highway, a vehicle suddenly appeared before me. The highway was clear only second earlier and yet a truck was suddenly a few feet away. Makes one question the accuracy of their perception. Is it congruent with reality?
Now, think about this with me for a moment and keep in mind I could be wrong. I can only make an education assumption that, at the time I gazed down the road, the vehicle in question had reached my blind spot ( Although, I’d be interested to see the statistical odds of that…). This would have attributed to my brain’s failure to add it into the interpretation. To my brain, it simply did not exist. My brain was not expecting that vehicle because it had no information to suggest that there was a vehicle to anticipate. It had missed the truck and failed to integrate it into the landscape. Once the vehicle had passed my blind spot that information was relayed through those thick neuronal tracts all the way back to my visual cortex. My brain was able to correctly identify the vehicle’s presence, but the continuity was off. It was as if the truck materialized out of a void.
This idea of the brain’s anticipation and interpretation of our surrounds also accounts for the additions to our visual and auditory survey of the world — the ever misunderstood hallucination.
Hallucinations are more common than one would be led to believe. Their existence does not signify a psychotic break from reality. Sleep deprivation and sensory deficits are among the common contributors to hallucinatory experiences. Charles Bonnet syndrome is common among the elderly population who have rapidly deteriorating vision. They experience vivid visual hallucinations without any contributing cognitive abnormality.
And I am talking vivid. Animals and people tromping around in bright coloured clothes in your kitchen, kind of hallucinations.
Now, visual hallucinations can be lumped into one of two unimaginative categories— simple or complex.
Simple hallucinations generally involve shadows in the periphery. These are flashes of light or things that take on no complicated shape or form. Complex visual hallucinations tend to be…well…complex. They have substance and shape — often taking forms of a human or animal.
I know an insomniac who has frequent visual hallucinations that become especially terrible when he goes days without a good night’s sleep.
Generally, his visual hallucinations come in the form of shadowy figures and bugs. Movement from the corner of his tired eyes has his brain conjure up flying insects or ones that skitter soundlessly by. Often, they are spiders crawling inwards from the periphery only to disappear when they draw too much attention.
Oliver Sacks, neurologist and beautiful human, once had a complex philosophical conversation with a spider in his kitchen. He was high as a kite and, in hindsight, recognized that spiders should not be so well versed in philosophy and certainly should not speak. Regardless, he was not phased by this event.
The thing that is so remarkable about visual hallucinations from sleep deprivation is that there are no drugs acting upon receptors and mucking about in the chemistry of your brain. It is simply you. Organic, GMO free hallucinations.
My friend, the hallucinator, can experience some fairly complex hallucinations if his sleep habits become horrendous.
He once saw a bear come to life from the side of a highway. It ran up the ditch to barrel down the road towards his vehicle. The ghostly bear evaporated upon impact.
(The bear was brown, in case you were wondering.)
Another time, he saw a woman materialize from the ground between two parked cars, wearing a dirty lacey shawl. She too faded into a vehicle.
In both cases my hallucinatory friend knew almost instantly that they were not real. It took him a minute to get over the fear of a bear in the road but, once it evaporated into the ether before him, it became clear what had occurred. Much like Dr. Sacks and his philosophical spider friend.
If we make ourselves vulnerable when we pull back the sheets — naked within their cool folds— to drift into blissful unconsciousness then it becomes astoundingly clear that we are just as vulnerable, if not more so, when we stay awake.
We can lose sight of ourselves — quickly and spectacularly.
Our brains can only keep the congruent narrative of our every day life going for so long before things start to unravel at the edges and split at the seams.
The ground begins to shift like we are walking across sand. Our emotions begin to slip from the control of our frontal lobe and become lost to the whims of our limbic system.
We have lapses in our judgment and flares of irrationality. Without the enveloping embrace of unconsciousness and the depths of sleep we begin to slip away — piece by piece, we erode like ground glass under the pressures of insomnia.
It’s little at first— broken down bit by bit. A chip away here, or a tatter there, until we are left as a fragment. A specter of the person we truly are. Becoming, I suppose, much like the ghost of another’s hallucination.
Not much is more important than sleep and yet nothing quite as eluding. For the chronic insomniac, sleep is much like a lost lover. One night she slipped out of bed, pulling the sheets around her thin frame, and floated out of the room leaving you awake. There you lay, blinking at the shadows that drift across the ceiling.
Sometimes, when the light is just right and the waking hours have slowly accumulated, the shadows of the ceiling may just blink back.
“A hallucination is a fact, not an error; what is erroneous is a judgment based upon it.” Bertrand Russell
“One does not see with the eyes; one sees with the brain” – Oliver Sacks
“One does not see with the eyes; one sees with the brain” – Leonard Cohen
Neuroscience: Exploring the Brain, Fourth edition. M. F. Bear
Hallucinations Oliver Sacks
As the late and ever lovely Oliver Sacks said, “Waking consciousness is dreaming – but dreaming constrained by external reality.”
Dreaming — that fantastic, frank and, sometimes, quite fu—bizarre activity that we engage in on a nightly basis and yet we know so little about our unconscious conjured visions. Forget what Freud has disseminated into the winds of the zeitgeist about the images that are projected across our dancing eyelids. It’s much less about our unconscious desires and sexual lust for our paternal and maternal figures and more about our neurons oscillating between the humming hive like collective and the rolling waves bringing in the tide. Our brains are synching in and out of varying depths of unconsciousness and neuronal activity and we, helplessly, are along for the often-horrifying ride.
But dreams and their emotional provoking, fantastical narratives are only a small portion of the very absurd activity of sleep. We, generally speaking, attempt to avoid vulnerability at all cost while we are awake. We are vigilant of our surroundings, with a tendency to assess the likelihood of danger or disaster.
We look both ways before we cross the street. We may keep secrets shoved down deep in our throats, to avoid revealing ourselves in what would likely be a disastrous outcome. We evaluate the minute ways the body of a stranger moves when they approach and assess what this reveals about their intentions. Perhaps, we simply avoid public speaking at all cost. In everything we do, during our waking hours, we avoid putting ourselves in a compromising position.
And yet, when the sun goes down on the horizon and darkness inches his long fingers across the sky, we feel the strong, siren call from our beguiled bed. We shed our armoured day clothes and crawl beneath the cool sheets to stretch our limbs out across mattress and pillows. We tangle in blankets and, perhaps the arms of our lovers, relaxing our spines into the softness beneath. We close our eyes and the darkness of our bedrooms floods into the darkness of our skull. Our breathing becomes deeper and less guarded — that unmistakable heaviness of breath that comes when sleep crests and crashes over our bodies, sweeping us away in the undertow of unconsciousness.
Keeping with this watery theme, let’s explore a little deeper into the science of sleep and dreams.
Following, in Part Two, will be a look at what happens when the two become unattainable.
Think of you brain like a free diver in the middle of the Pacific. We start at the surface, head above the waves, treading water with slow even rotations of one’s leg. We are awake and focused — surveying the horizon and the emptiness of the water that surrounds. This is an activated cortex — beta waves of unsynchronized neurons, crackling away at all the stimulus you are taking in.
Now our diver has perhaps pulled her goggles down over her eyes and secured the snorkel between her lips. She takes one last look out to the horizon as she slowly sucks air into her lungs until they reach their limited capacity. She slips beneath the waves and begins her descent. This is your brain, still awake, but relaxed. Here, alpha waves — deeper oscillations and less neuronal chatter.
It is in this state that you will, at some point, slip passed consciousness and into the arms of sleep. This is stage one, and our alpha rhythms will slowly give way to deeper waves, as our eyes roll from side to side beneath their lids.
The smooth strong kicks from our diver’s legs leaves a trail of bubbles as the rubber fins cut through the heaviness of water. Her movements are graceful, choreographed and designed to get her to where she needs to be. We have entered true unconsciousness and stage two of our sleep journey. Our neurons begin to synch up and start to generate something called a sleep spindle. This is produced by a structure buried in our deep brain– the master of sleep regulation– the mighty Thalamus.
The sleep spindle might be the most whimsical name for the electrical charge that ushers in sleep. It conjures to mind Sleeping Beauty, reaching her pale finger out to touch the cursed spinning wheel — pricking her porcelain skin on the sharp spindle and plunging herself into the supernatural unconsciousness.
The sleep spindle seems to be involved in looping through the landscape where our memories are consolidated — laid down and packed away for safe keeping. It is with these sleep spindles that our brain thumbs through all the activities of our day and stashes them away between sulci and gyri of the cortex. Tucking our day into folds and hiding events and newly learned skills in to hidden grooves, to be retrieved later when they are needed.
Back to our diver, she moves silently pass stage two and into stage three where we find very high spikes of electrical activity — it is here that we find our neurons are all humming together, and our body is absent of movement. She presses on, swimming towards the sea floor and entering into stage four. Large, slow delta waves roll across our skull as we lay still, silent and heavy in our beds. This can last for just over a half hour.
And then, just like our diver — when her lungs begin to yearn for air and the crushing pressure of the ocean becomes too great — we begin our ascent, passing through each stage again until we reach stage one. Our diver is here, just beneath the surface of the water; the tip of her snorkel crests through the lazy waves to draw in the oxygen from the world above. She stays here, in a liminal space between sea and sky.
This is the breast stroke of REM sleep. It is eerily similar to our waking physiology. Our blood pressure and heart rate had decreased as we descended into the depths of sleep. Our breathing slowed and our temperature dropped. Our metabolic rate followed suit.
With REM, all of these increased dramatically — mimicking that which regulates our waking form. But appearances are deceiving. Our body does not behave as though it is awake. In fact, despite our increased respiration rate and our eerily rolling eyes from behind their hooded homes — we are no longer in control of our bodies.
We are no longer capable of deliberate movement, or any movement for that matter. We are paralysed — if all the mechanisms are in working order.
When we are reach REM sleep there is increased activity in the cluster of neurons in your brainstem — specifically a little ancient area called the pons. Within the pons there is a series of neurons releasing their specific neurotransmitters. These chemical messengers defuse from arm like projections, sending precise signals to other neurons. The net result of all this chemical chatter is the shutting down of the neurons in your spine that produce movement. Our brain wraps our muscles in restraints every night, preventing their activity.
Like a straight jacket, your brainstem prevents your limbs from flailing around as you reach your nighty destination in your mind’s dreamy landscape.
Of course, like nearly every mechanism within our fallible bodies, nothing is fool-proof. Mechanisms fail, pathways breakdown and the results can be far worse than any dream we can conjure up from the depths of our grey matter.
REM sleep behaviour disorder is one such example of how when shit goes wrong, it fails spectacularly. If something disrupts the conversation within our brainstem while it is in the process of shutting down our motor neurons, the inhibition fails, and the paralysis doesn’t stick.
We are no longer locked-in prisoners of our brain — hapless immobile limbs frozen in place.Our motor neurons are now in charge of this show and they cannot be trusted. Producing violent, hyperbolic movements we become catastrophic marionettes, doomed to act out our dreams with our motor neurons tugging blindly on the strings.
People have succumbed to this physiological failure by either gravely injuring themselves or the ones they love. Take the Welsh man who murdered his wife in 2009, while having a dream that he was battling with intruders (found HERE). Horrifyingly, his story is not unique — you can find dozens of ones quite similar all over the world.
Of course, there are occasions when our brainstem’s vise-like paralysis is too heavy handed and continues on after we have broken the surface of the water, our aching lungs gasping for air. This second failure of our clumsy brainstem will be explored in the depths of part two — which you can find HERE
“Sleep that knits up the raveled sleave of care” – Macbeth
“The death of each day’s life” – Macbeth
“I love sleep. My life has the tendency to fall apart when I’m awake, you know?” – Hemingway
Neuroscience: Exploring the Brain, Fourth edition. M. F. Bear
There is a scenario that many of us have had the painful privilege of experiencing. That moment when your eyes flutter open and you glance around while your heart picks up a few beats per minute and your muscles twitch with a sudden increase of adrenaline. Confused, your inner monologue shouts out, “Where the hell am I and how did I get here?”
Perhaps, this is the first waking moment after a night of too many drinks on an empty stomach that led to a swirling vortex of blackness. Maybe it’s the first eye opening moments after anesthesia was withdrawn from your veins.
How ever you got there and where ever you were, after the brief wave of confusion and mild anxiety rushed across your body, you were aware of a few things:
Chances are you woke up not too far from where you started and a moment of reassurance floods over you.
Now, if you are familiar with the aforementioned scenario, lets take a minute to journey into the horrifying thought experiment I will present to you.
Imagine your eyes fluttering open to survey the unfamiliar world around you and you end up asking yourself, “where am I, how did I end up here and who the hell am I?” In addition to this terrifying scenario, imagine waking to find yourself half way across the country or in the case of one man – who may or may not have known who he was or how he got there – all the way to another continent on your bare feet (Read that HERE).
There was a news story that surfaced a few weeks ago about a Toronto firefighter who disappeared from a New York state mountain side during a ski trip and re-emerged in a Sacramento California airport – an astonishing 4,500 kilometers away. He had gotten himself a spiffy new hair cut, withdrew 1,000 dollars in cash and purchased a new iPhone which he used to call his wife. He was picked up by police and medical personal who believed he had suffered a head injury (you think?). He was still wearing ski gear in the California winter and had a vague recollection of riding in a big rig at some point on his journey. He, however, had no idea how he made it halfway across a country that was not even his own. Furthermore, his nonchalant demeanor appeared to unnerve the first responders that snagged him from the California airport. One would anticipate panic in a situation such as this, and yet he was cool as a cucumber. ( HERE).
So what happened to our firefighter friend?
Well, the jury is out of that one. The media states that he was not a victim of a crime and had possibly obtained a head injury. But how did he wander so far away from home?
Now, I am asking you to follow me on a little weird theory here. Pure speculation, let me remind you.
How about we call it a dissociative fugue state brought on by a bump to the head after a fall from his skis during his mountain decent.
Dissociative what, you say?
Let’s suspend our disbelief for a moment and explore this hypothesis.
You bump your head, discharge some electrical impulses and end up kilometers from where you started without any recollection of how you got there.
Sounds implausible? Did he need a little breather from his firefighter buddies? Was he pulling a Walter White naked at the grocery?
Let’s jump into the disorienting world of amnesia and dissociative fugue states.
Tabula Rasa, Latin for “Blank State”, is a philosophical stance that views the mind as empty and pure. Individuals are born as a blank page awaiting the ink from our perception and experience of the world. We are merely subjected to that which we encounter; there is no inherent narrative to our life, no underlying monologue, no free will.
We are all subjected to fate and his fountain pen.
Tabula Rasa could be a way to view the blank slate of the brain when there is a radical disruption that leads to amnesiac states. Something jams the signal and certain things are wiped clean – like chalk being brushed off a board.
There are various types of amnesia and varying conditions, or disease states, that involve loss of memory. To complicate the matter further, there are a multitude of things that influence these states in varying magnitude. This list includes: seizures, physical trauma, pharmaceuticals and high states of emotion.
Let’s define and break down amnesia in to easily digestible components for us to choke, er, swallow down.
Amnesia is pretty straightforward and really quite the dauntingly broad term. It is an umbrella word meaning “pathological loss of memory.”
How delightfully vague.
It gets more specific when you start adding in phrases, such as the very descriptive “retrograde” and “anterograde.”
Retrograde, or traveling backwards in time, describes the inability to retrieve the memories that you laid down before whatever event left your squishy friend rattled and in tatters. This can include a wide time frame and even extend into core pillars of your personhood—such as the inability to remember your name and very self.
Who the hell are you even?
Anterograde, or traveling towards the future, is the inability to lay down new memories. You remember who you are and where you came from. You may even remember how you got to the point where you experienced the damage that shook some connections loose. Unfortunately, if you venture too far passed those trees you enter woods so dense that there are places sunlight can no longer touch.
For a much lighter example, perhaps you remember the awful early 2000 Rom-Com 50 First Dates? That is a very apt example (also quite annoying).
However, things start to drift further from away Adam Sandler and into Twin Peaks territory after those two major categories.
Transient Global Amenesia involves both these amnesia subtypes. Like a chocolate and vanilla swirl ice cream cone of forget. The heaviest element at play is the anterograde amnesia. The afflicted will have difficulty remembering what occurs during the event. Retrograde is still a player. The past is vague and fuzzy– especially the moments leading up to the state.
Generally, people still remembered who they are and hold on to more core memories, such as a childhood memory of petting their dog or the time they cried at their ninth birthday party.
This weird state of memory loss lasts for several hours, perhaps a day, before mysteriously disappearing back into the ether. Good news, people in this state aren’t destined to date Adam Sandler over and over again like poor Drew Barrymore.
Transient global amnesia is characterized by its eerily and insidious nature. Its cause is generally quite subtle in nature and can come on in an instant.
A quick dip in a cold water, overwhelming negative emotions or a routine medical procedure, such as an endoscopy, have been cited as possible instigators of a TGA attack.
And of course we must also include physical exertion.
And by that, I mean sex.
There have been a few transient global amnesia attacks brought upon after some vigorous sheet disturbing activities. Many of the poor individuals affected where between 50 and 75 years old and recovered from their event in the expected period of time. No need to panic.
My personal favourite anecdotal piece is the story of one man from several decades ago. Upon orgasming he was struck with a TGA attack which caused him to shout out during the throes of passion, “Where am I? What’s happened?”
Not the words you expect to hear.
Now that I have filled my sex quota for this post (this is becoming a reoccurring theme), let’s recap what we know about amnesia.
It comes in many shapes and sizes – subtypes and specific pathological conditions included. It can be caused by trauma (both physical and emotional), brain injury, seizures, drug use (including anesthesia or ketamine) and (apparently) orgasms.
What ever happens, the brain is not a fan of it. The cause, however, is still not well understood.
So where in your brain is this strange storm of forgetting occurring?
Generally, it’s the temporal lobe, specifically a snug little corner of the hippocampus (CA1 and CA3 regions) that is the most affected during these memory loss events. Remember this lobe, we will come back to it soon.
Now what makes run of the mill amnesia differ from that which the Toronto Firefighter experienced?
It’s the tendency to wander.
He ended up a very long way from where he started with no idea how he got there. And he isn’t the only story like this.
Dissociate fugue is a much more descriptive term than those we explored previously. Dissociation refers to the removal of one’s self. “Fugue” has its origins the romantic languages as meaning to “flee” or “flight”.
Dissociate from myself and flee. It’s vaguely poetic.
You don’t remember who you are, where you come from or even what is happening right at that very moment. This is coupled with the urge to go somewhere, any where, any how.
Sounds like a past Saturday night filled with regret.
But how does this happen?
Drugs like anesthesia (or if you are looking to party, ketamine) can cause dissociative states and memory loss.
If you have ever had the pleasure of experiencing general anesthesia, there is really nothing quite like the feeling that over comes you right before you check out. A sudden sensation that is both hot and cold travels through your veins and every trepidation you had about what was about to occur suddenly has vanished. You are a compliant, happy little clam staring up at a OR light that, with all of its light bulbs inside one circular ring, is the spitting image of a giant fly’s eye.
Right before you lose consciousness there is a vague feeling that you are floating away like a piece of paper in the wind.
And then you are awake again. If you are lucky you will even vaguely feel the strange sensation of being extubated – or having a breathing tube removed from your throat. It’s a little like a collapsible straw.
Not unpleasant because you are still high as a kite.
You don’t usually remember too much surrounding the event or even that time has passed.
High intensity emotions can also cause dissociative states. The physiological mechanism behind this is a little hazy but the psychological reasoning is that the brain is trying to protect itself so it removes itself from the event hoping that, when things calm down, it will all be fine. Brilliant!
Spoiler alert. It generally is not fine.
One of the common conditions associated with dissociative states are seizures and, most notably, those that occur with in the temporal lobe.
Did you remember?
The temporal lobe houses the hippocampus which is a memory hub of sorts. Now the hippocampus is generally heavily involved with your spatial memories. This means he takes note of the layout of your house or how you get to one place and then get back to your original destination. He is great at creating and reading a personalized map. There is evidence, however, that he also has a hand in general memory formation.
Memory formation does not have one specific brain structure and it is known to occur in a lot of different places within the brain. Neurons buzz and spark, sending off the packaged components of a memory to various structures and liminal spaces of white and gray matter to consolidated it where it belongs.
This can be anywhere.
The hippocampus is thought to have a role in keeping short term memories, but long term or consolidated memories, are said to become independent of the hippocampus and are stored else where in the neuronal beehive of your brain.
Temporal lobe epilepsy is characterized by seizures and electrical discharges resonating from the (you guessed it) temporal lobe. This is the one that is located snugly on either side of your ears.
The state that follows a seizure is the funny little word “postictal”. Think “icky”. During this time many epileptics are confused, exhausted and nauseated — just to name a few unpleasant sensations. Some are disoriented while others suffer from episodes of dissociative states.
In fact, one statistic stated that a third of clinical case of temporal lobe epilepsy will experience a dissociative event.
Let’s look at a story, shall we?
A man with temporal lobe epilepsy found himself in a hotel half way across the country. He had driven his car, fueled up and checked himself into a hotel while his brain had checked itself out of his skull. Anyone that encountered him hadn’t the slightest idea that anything was unusual. He was able to operate complex tasks, like driving or signing his name, and yet he had no idea any of those events were occurring.
He is not alone, I read about a surgeon who was on call over night. He was paged for surgery, scrubbed up, completed the task and left. The nurses noted he seemed a little off but not enough to really think twice about. The next day, the surgeon had no recollection of coming in to the hospital. He could perform the complex task of cutting into a person and not killing them essentially with his eyes closed.
(I can not, despite my greatest efforts find the link to this story online. It is merely from the depths of my memory and, as we know, memories can be liable to error. It was too good not to mention. Temporal lobe epilepsy hotel is a tale for Sam Kean’s book on the history of neurosurgery).
Although the media has no idea what happened to the fleeing firefighter, after a quick peek into amnesia and dissociative states it is not hard to speculate that one falls down while they ski. This brings the risk of knocking a few neurons loose and wanders away from his friends and family before waking up in an airport with a questionable new hair cut and the wrong outfit for the climate
Pure speculation. Full stop.
But wasn’t that a little fun thought experiment?
Our brain is simply a big, black box filled with electricity and chemicals. When something misfires the result can have very considerable consequences. It’s just once big chemoelectrical roll of the dice.
Reproduction, biologically speaking, is the motivation for us all. As Shakespeare said, “all the world is controlled by the propagation of our genes and all the men and women merely players”. Or, something like that, right?
Anyway, from an evolutionary point of view, on this lovely planet we call home, the be-all and end-all of all life is to procreate. It’s what drives large mammals to tiny protozoa.
We all are just a slave to the ambition for immortal transcendence that only our genetic material can give us.
But, as in all of life, we humans like to think we are superior to the mindless drone of existence. We create art, we feel things. It’s an overwhelming ache –one that can be compared to that which Marburg victims feel when their intestinal epithelium sloughs off.
I have just finished reading The Hot Zone and have gotten a little carried away. (Pick up a copy, you will not be disappointed.)
In short, we human beings, with all our complexity and diversity, do not obey by the laws of nature.
We laugh in the face of them.
And perhaps we do.
More and more women forgo having children in the age of IUDs and autonomy over our bodies. More and more individuals on this planet are engaging in non-traditional relationships where the transfer of genetic information (to the end result of viable mini-humans) is not a reality — at least in the organic sense of the word.
But does that mean that the lonely cry from our DNA is not still echoing in the dank chamber of our cells?
Or, in the end, is it that elusive sexual gratification is our master and not this depth of our biological nature?
Are we in it for the momentary fleeting orgasm and not that lasting genetic immortality?
(Are you an aspiring science writer when you default type “organism” instead of “orgasm”? Yes, the answer is yes)
So, if we take a look at the sex drive of our species– away from the existential nature of continuing our lineage– what makes us hot under the collar? (Not lame sentences like that, that’s for sure.)
Let’s tip toe away from evolutionary factors by taking a look at the structures in our brain that create our reality.
The Hypothalamus, the Thalamus’s smaller naïve brother, is a brain structure that is known for the oldest joke in biology, psychology and neuroscience a like.
It controls the Four “F’s” of evolution (stop me if you have heard this before) – Fighting, Fleeing, Feasting and Fu…Sexual intercourse.
The hypothalamus is part of our diencephalon – one of those fancy neuroscience words that describes our forebrain. This is a hop, skip and a jump away from our “Reptilian brain” or the seat of our basic autonomic functions – the brainstem. The hypothalamus, the wizard behind the curtain of our sexual desires, sits above the master of hormone secretion, the pituitary gland. (The pituitary gland happens to be the doppelganger of another hormone secreting organ that hangs much lower on the bodies of select individuals).
Now that we have oriented ourselves to this area of the brain – let’s turn our attention to an adjacent region – the basal ganglion. In the front seat of our basal ganglion we have the ventral striatum which houses the nucleus accumbens
All you are seeing are words and no meaning, right? I will break it down for you, don’t fret.
This whole area, of the Russian nesting doll that is our brain, is responsible for making up our so-called reward system. This area is often implicated in addictions and the neurobiological basis behind what makes people strive for another fix of their drug of choice.
Although, it is not all about outside substances. Certain stimuli can lead to a release of a cascade of chemicals in our brain. For example, that pleasure or reward system lights up like Christmas trees in December when one views porn inside an MRI machine. Yeah, you read that correctly.
A lot of that light show has to do with an endogenous chemical – a little neurotransmitter called Dopamine.
Dopamine is an excitatory neurotransmitter—meaning he likes to get the neurons aroused. Once excited, these neurons rain down action potentials, which are (to quote a neuroscience prof of mine) “the only currency we have.” Action potentials are what help us make sense of the world inside the sealed darkness that is our skull.
Dopamine is merely the messenger and he is responsible for a lot of other things beyond our reward system — like movement. A less than adequate amount of dopamine is responsible for movement disorders like Parkinson’s diseases and Parkinsonian like symptoms. (Perhaps dopamine’s greatest claim to fame is through L-DOPA and the lovely Oliver Sacks in the book and film Awakenings).
However, I am betting we are all familiar with dopamine’s dirty reputation in our reward system.
I like to refer to it as “The Dopamine Hit”.
That lovely, warm and satisfied feeling you get when excess dopamine is released inside your squishy friend. This often occurs when you have a positive encounter with someone you are attracted to. There is that one person (or perhaps multiple people) that really lend you a helping hand in that dopamine release. It is a tough animal to pin down, as that rewarding release can come in many forms: A dark glance from behind fluttering eyelashes or an unexpected touch – that brief fleeting moment of skin to skin contact. It could be something small, like a smile from across the room. Watching the smooth movement of their body as they walk away or hearing their voice at the other end of a line can get your dopamine buzzing. Hell, even a response to a message that draws a smile to your lips – it does not take much to secure your fix.
Dopamine is insidious; his release can happen anywhere…even if we aren’t expecting it.
But it isn’t Dopamine’s fault – he has a job to do and that is it. The rest is our interpretation of his chemoelectrical Morse code. You perverts.
Now that we have explored the curves and cavasses of the reward pathway, lets touch on the limbic system– where we meet our friend the almond once more. ( I have spoken about him HERE)
The amygdala is a key player in the strange tingling feelings that we often try to ignore. Our emotional almond plays a role in associating emotional responses to key stimuli, along with stimulating some specific organs involved in arousal.
Ahem, is that your cell phone in your pocket or is your amygdala just happy to seem me? (I am so sorry. I could not help myself)
Back to porn and MRI machines. Studies have found that men respond more heartily to sexually explicit visual stimuli (the porn industry had the keys to that golden information for decades now) and that little almond may be the reason behind that.
The bigger the better it seems — even in terms of our brain structures. The amygdala has been found to be much larger inside the brains of males. It has also been noted that, when viewing sexually stimulating images, the activity measured by both the amygdala and our friend the hypothalamus was significantly greater in men than in women.
Much brighter fireworks went off inside the MRI machine of love.
Now, that we have a rough grasp of the structures and chemicals that play a role in our sexual responses, it appears that we are of more a slave to our neurotransmitters and grey matter than anything else.
It seems that we are compelled to seek out the attention of those people that provide us with that dopamine dump but what makes us attracted to these certain individuals in the first place?
It just might be microbes and compatible immune systems. Sexy, right?
Attraction is a funny thing. We tend to be attracted to other people in a response to specific attributes they possess – so called “types.” This can be based upon visual and physical attributes or more esoteric traits like humour or intelligence. Sociology and Psychology has packaged attraction into neat little boxes and labels for us to consume.
You can be an sapiosexual and find intelligence overwhelmingly sexy. Perhaps you dig brunettes or people with a taller stature.
You could be heterosexual, homosexual, bisexual – sexual orientation we are all familiar with – but you could also be into mesophilia, or the attraction to middle-aged individuals.
As Lana Del Rey elegantly puts it in her masterpiece of musical composition, Cola, “I gots a taste for men who are older, it’s always been so it’s no surprise”
But, is there any biological or scientific explanations for our sexual preferences? Well, it might all go back to our desire to find the perfect vessel to secure the continuation of our genetic lineage – in the case of heterosexual attraction, at least. (I tired so hard to get away from evolution, but he keeps pulling me back in).
In one study, woman expressed attraction to men that possess broad shoulders and muscular torsos, as apposed to more feminine looking male bodies. It was noted that even huskier individuals were marked higher on the attraction ladder. It came down to woman finding the illusion of strength an attractive quality. You can read that study, full of scientific rigour and bursting with robust quantitative data (so kidding) HERE.
Now let’s leave strong, masculine torsos behind for a minute and take a look at the cellular level.
There is another theory behind women’s attraction to a male mate – the immune system.
Remember the woman who can smell Parkinson’s? (HERE for your viewing pleasure) Well, in the same nostril as that idea, can we unconsciously pick up on immunochemical signals?
Seems a little out there, I must say, but let’s take a look at the literature.
Major histocompatibility complex, MHC, is a genetic component of the immune system across many species. The animal kingdom prefers mates with differing make up than their own. It’s all about that “securing the best possible progeny” thing I keep mentioning.
Variety is the spice of life and key to the successful continuation of your kind.
Animals pick up these kinds of things through olfactory cues and there is evidence that human’s can too.
In humans the MHC is referred to as the HLA (for human leucocyte antigen) and the jury is out on whether it is an aspect of our sexual behaviour. Women are the key players in the HLA game and appear to be more sensitive to picking up HLA related peptide ligands (fancy word for “molecules that bind to things”). Even though we humans lack the vomeronasal organ that other animals use to pick up on pheromones, it appears our olfactory cells are able to pick up on the subtle hints of the HLA. Like a fine wine.
In one study, the authors found that partners who had few similar HLA markers reported a more satisfied sex life than partners who had many HLA markers in common.
OK… So, those HLA related peptide ligands are what’s really responsible for that tachycardia I get when I see a man I am attracted to.
Some weird fetishes you have there Biology, but who am I to judge?
And lastly, we have fruit flies and microbes. Oh humble Drosophila, what wisdom can you bestow on us today?
Apparently, the microbes inside the fruit fly influence their sexual preference and can be manipulated through food. Flies given molasses diets prefer other molasses flies and this preference could be further manipulated with antibiotics. Once the flies’ bacteria were destroyed by the antibiotic treatment their sexual penchants disappeared and they became more promiscuous – choosing to mate with flies outside of their former food circle. This all came down to smell once more. The theory is that the presence of a specific bacteria altered sex pheromone production in the flies, creating their sexual quirks.
Remember the torsos? Well, that might not have been the out-of-place quirky anecdote it appeared to be. The illusion of strength tends to go hand-in-hand with higher testosterone levels in men. The higher the testosterone the theoretically more attractive the male. This, despite the fact that high testosterone levels can lead to some interesting traits — like anti-social behaviour and a higher rate of divorce.
The heart wants what the heart wants. And it appears to want, as my friend Vanessa so appropriately describes, “a vision of masculinity.”
Now, lets tie it all together – high testosterone levels in men are supposedly linked to stronger immune systems. The stronger the immune system, and the more diverse the HLA complex, the better the offspring.
We have come full circle and our hearts have been crushed by evolution once more.
But what about orgasms, you ask? Ok, well maybe you didn’t..but I sure did. The ever so sought after orgasm… truly this must be the reason we engage in the limb tangling activities we actively seek? Well, if you do a literature search on orgasms (please do) there is an exhaustive list of studies done involving its evolution.
Yeah, evolution again. Sorry.
The male orgasm plays an obvious role in this evolutionary affair, but the female orgasm is a little more esoteric. Theories range from mate selection to vestigial left-overs of our evolutionary journey.
Perhaps, we have all been tricked by our genes. As THIS ARTICLE so aptly put it:
“What possible incentive could you offer your host to bring about that union? Try a somatic blitzkrieg of ecstasy, courtesy of the limbic system, the pleasure (as well as the pain) center of the brain. That’s orgasm.”
“Blitzkrieg of ecstasy” is the only way I am referring to orgasms from now on.
But what about love? We fall in love with people and this feeling can endure regardless of the expectation of our genes transcending through space and time. Right?
While you may be strongly attracted to someone, and possibly engage in physical fantasies when that dopamine hits your brain, chances are the appeal of that person extends beyond that. Perhaps you like what they have to say or how they think and just want to be around them.
Their presence makes you feel warm and tingly – and not in the way we have explored earlier.
As I said, we are humans.
We feel things.
We engage in partnerships for many different reasons, with many different kinds of people, because sometimes you just like being near them.
We will end with the story of Thomas, a blind goose, who fell in love with Henry a male swan. The couple lived together for nearly two decades before Henry partnered up with Henrietta, a female swan. But that did not discourage Thomas, who entered into a polyamorous relationship with the two swans. After another decade or so together Henry the swan died and Thomas was left alone. He went on to forge a relationship with a female goose and procreated. Thomas’ sham marriage to the female goose feel apart and his goslings were adopted by another male goose. Thomas was left to face the world alone again before succumbing to his increasing age (and perhaps a broken heart). You can read about Thomas HERE
Love is a hell of a drug.
This is the part where I usually start with a snarky quip – a little heavy-handed witticism and an awful joke or two about some microbe or your brain (or about some microbe inside your brain). Then I would jump into some educational spiel about some topic in science that I either stumbled across during the week or one that is close my heart.
I am going to do something a little different this week.
It too is close to my heart but is not a long-winded diatribe on science communication (that was last week’s unfortunate post). We are going to take a view through the microscope’s eye piece at a local woman slaying the science game one bucket of grain at a time.
Since this blog came into existence, a few short months ago, I have had the desire to cover some local science content. We have some incredible, world-renowned science happening right in Saskatoon. That is pretty amazing considering we are a tiny little city that is split in half by a tiny little river in a province that most people have a hard time pronouncing.
There is the Synchrotron (the only in the country) where scientists point high intensity beams of light at things so they can gather information… about said thing. (Please, read about it HERE. I promise it explains it more accurately than I can).
We also have VIDO InterVac, an infectious disease and vaccine research organization that works on both human and animal vaccine development.
Both of these high-level research centers can be found tucked away on the humble University of Saskatchewan campus. That’s pretty incredible.
The best thing about science is that you can do it anywhere if you have the smarts and the determination to answer those curious questions.
Take a look at another incredible woman in science, Rita Levi-Montalcini. She won the Nobel prize in Physiology or Medicine in 1986 for her discovery of something called nerve growth factor – which she isolated in the early 1950s. Rita was born into an Italian Jewish family in 1909 and, if you know anything about history, you are aware of what is to come. Rita was an promising rising scientist at the University of Turin in 1936, working in the lab of her mentor Giuseppe Levi. (Fun fact: Levi, was a pioneer of in vitro studies of cultured cells!) Just a few years later, with the Nazi’s rise to power in Europe, Jews were barred from careers and education.
Rita Levi-Montalcini went into hiding to survive the Holocaust but she didn’t let a little genocide get in the way of her love for science. She set up a secret lab in her room – working with chicken embryos and using make-shift equipment she MacGyvered from household items.
When the war ended she went on to continue her research in actual labs. Working with biochemist Stanley Cohen, they managed to isolate nerve growth factor and lay down some pretty amazing foundations in Cell Biology and Neuroscience.
As my friend Vanessa Cowan would say, “YAS QUEEN”.
Vanessa is the local woman in science I had allude to earlier. After some gentle poking for her to answer some interview questions, she came through this week with an amazing look at her research and what it means to be a woman in science.
When did you first get interested or involved in science?
I first was interested in science in my grade 11 and 12 years of high school. I realized that I had a knack for science based on my attention to detail and fastidious studying habits. In my first year of university, although the science classes were more difficult, the material I learned in these classes (as opposed to ancient history and English) was more applicable and tangible. Once I decided that I wanted to major in a scientific field, I chose Toxicology because of its applied aspect. Not to mention that poisons and poisonings are super interesting! My first ‘real’ exposure to science was between my 3rd and 4th years of my undergrad (I did 5 years altogether). I applied for an NSERC undergraduate student research assistant (USRA) scholarship, which was essentially my salary for the summer and an opportunity to have my own research project. I enjoyed the hands-on aspects of sample collection and lab work. The most satisfying part of all, arguably, was compiling all the data and seeing your results. From that point, I was awarded another NSERC USRA scholarship for the summer between my 4th and 5th year of undergrad. I also started working for one Canada’s preeminent veterinary toxicologists, Dr. Barry Blakley, in the toxicology sector of Prairie Diagnostic Services.
What is so appealing to you about Veterinarian toxicology?
Although I had exposure to topics in veterinary toxicology as an undergraduate student, my interest in veterinary toxicology really blossomed when I started working with Dr. Blakley. Part of my work was to do an exhaustive database search on all of the various veterinary toxicoses that Prairie Diagnostic Services received samples for over a 16-year period. I was able to see which poisonings were most common for which animal species, how poisoning patterns changed over time and season, and also insight into why these poisonings were or were not prevalent. Searching through thousands of case records took me nearly 8 months. This work was very rewarding, however, as Dr. Blakley and I were able to characterize and describe poisonings in western Canada over a substantial period of time. This information is practical for veterinarians, regulatory agencies, the agriculture industry, and to farmers/producers.
I love the variety of veterinary toxicology. Livestock can become poisoned from grazing poisonous plants or consumption of old car batteries on pasture. Minerals in feed in the wrong proportions can make animals sick. Drinking water with blue-green algae (cyanobacteria) can result in sudden death. Dogs may be poisoned maliciously with strychnine-laced meat. Regular use or misuse of agricultural pesticides can result in non-target species toxicity, which has been seen in bald eagles. From all of these examples, one must rule out other differential diagnoses based on the known mechanism of action of each toxic agent, the symptoms reported in the animals, the animal species poisoned (i.e., dogs may have a different toxic response to an agent compared to cats), and the laboratory results of what is actually in the animal tissues.
Explain your PhD research and the most intriguing part of it
I’m studying the effects of ergot alkaloid mycotoxins on the bovine cardiovascular, endocrine, and reproductive systems. I am also developing a method to detect ergot alkaloids in bovine plasma with the goal of running pharmacokinetics studies. Mycotoxins are a global hot topic issue right now because they are difficult to control, they are diverse in terms of their toxicity and systems affected in people and animals alike, and they occur in mixtures. Mixtures are notoriously difficult to study in toxicology.
Ergot was once considered an old-world disease; ergot contaminated rye bread was the culprit for the gangrenous/burning syndrome St. Anthony’s Fire in the Middle Ages. Ergot had also been implicated in the Salem witch trials.
As a woman in science, have you faced any road blocks?
Certainly. There seems to be an inherent requirement of women to explain themselves, explain their rationale, and to prove themselves as competent and capable of their work. I have personally had to repeat instructions that I had already made clear because the other parties involved were not really listening to what I was saying. It can be very frustrating. With that being said, however, that is not the case with all people that one might interact with in science. I have been very fortunate to get to where I am today because of (male) professors who believed in me. I am glad that the work environment for women in STEM fields is evolving, however more work is still needed on changing ‘out-of-date’ attitudes.
What does your typical research day look like?
It really depends on the day! The variety of day-to-day work is something I really enjoy about research. I’ll describe a farm day, though.
My cohort and I head out to the research farm outside of Saskatoon in my car (which is essentially a ‘farm car’ now, as I feed the bulls out of it and has driven 1000s of km on grid roads. RIP tires). We feed the bulls and set up the barn space while they’re chowing down. Once we are all set up, we round up the bulls. It has only been like a rodeo a few times. I can tell you first hand that 2000 lbs of pure meat and testosterone barreling towards you is horrifying. So, we move the bulls up to the barn and start our sample collection. We can usually collect all we need from each bull in about 8-10 minutes. I measure their scrotal circumference, take blood, and we collect semen through a process called electroejaculation. This is essentially stimulating the bull’s prostate with low electrical current to get him to ‘produce his sample’. Once we have collected samples from all the bulls, we clean up the mess of crap, urine, and semen in the barn (gross) and head back to campus. Any work with semen is time sensitive, as the cells as actively respiring and are sensitive to temperature and osmotic changes. Back in the lab, I assess the motility of the sperm
Your research, on the surface, is not what comes to mind when one thinks about science. What would you say to people who don’t see what you do as a contribution to science?
Certainly, my research may not have the ‘sexy’ aspect of cutting edge work with the synchrotron or vaccine development or molecular markers of cancer. However, I am of the opinion that generating basic scientific information is absolutely crucial in the scientific community. The audience meant to receive your work has different needs/expectations. For example, livestock producers simply do not care/do not benefit from high tech molecular research. They want to know if their animals can eat mycotoxin-contaminated feed, what concentration of the toxins in the feed is acceptable for animals without affecting growth/reproduction, and first indicators of sickness in the animals. Regulatory bodies need basic scientific research to develop relevant safety guidelines for dealing with mycotoxins in food and feed.
What’s your long term goal?
My long term goals are to finish my PhD and my degree in veterinary medicine (I start at the WCVM this fall). After that, I would be interested in a career that combines clinical field work, research, and teaching.
Who is Vanessa when she isn’t stomping in cow shit and counting sperm?
I really do try and have a life outside of grad school. It’s very easy to forgo ‘work-life-balance’ in Academia. I’m a fairly introverted person, so at the end of the day I like to hang out at my apartment with my cat and drink a cup of coffee. On most evenings of the week, you can find me training in Brazilian Jiu Jitsu (white belt, yas). I also enjoy rugby, soccer, and going to the gym as well. Some of my favourite times are spent with friends over a coffee or beer/cider.