“Nature is a Haunted House”: beautiful and somewhat unsettling tricks of microbes and moths.

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Bacteria, the great improviser

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.

The Great Plastic Feast

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Image of  I. Sakaienesis

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.

Dark Moth Rising

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?

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Moths and Microbes

plastic eating bacteria PET enzyme
peppered moth selection
evolution
dark moth
plastic eating bacteria

 

Tangled in the Sheets of Sleep and Science Part TWO

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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?

 

“The last refuge of the insomniac is a sense of superiority to the sleeping world.”

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Image via Flickr

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

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Image Google Image Search

“One does not see with the eyes; one sees with the brain”

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.

“A hallucination is a fact, not an error; what is erroneous is a judgment based upon it.”

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.

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Image Via Nevessart

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.

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“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

Charles Bonnet Syndrome

Hallucinations Oliver Sacks

Demons and Nighmares

Fatal Familial Insomnia

Tangled in the Sheets of Sleep and Science: Part One

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“Sleep that knits up the raveled sleave of care”

 

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.

 

“The death of each day’s life”

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Image Via Medical Press

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.

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image via TIME

 “I love sleep. My life has the tendency to fall apart when I’m awake, you know?”

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

Who The Hell Are You?

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You are Your Brain. Image via Google

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:

  • You were never drinking again (in the case of scenario number one)
  • You knew who You were
  • You may be able to piece together a few flashes here or there and tie together the last hours or days of your existence.

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).

The Tale of The Disappearing Firefighter

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Case of the Missing Firefighter. Image Via Google

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.

Electricity and Clean Slates

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.

Eternal Sunshine of The Spotless Mind

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Electricity Image via Google

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.

Not all those who wander are lost

 

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?

Temporal Lobe Hotel

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Hippocampus.  Image via Google

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.

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Biopsychology. J Pinel. 2017
Sex Amnesia
Excuse me, Who am I?
Multiple personality and related dissociative phenomena in patients with temporal lobe epilepsy. Schenk, L.
Dissociative Fugue
Dissasociative Drugs
Dissocative disorder after TBI. Cantagallo. 1999
Focal Lesions of Human Hippocampal CA1 Neurons in Transient Global Amnesia Impair Place Memory. Bartsch. 2010
Memory Storage Fidelity in the Hippocampal Circuit: The Role of Subregions and Input Statistics. 

 

The Science of Sex

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The MRI Machine of Love (via Google)

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.

Sorry.

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 Four Fs and Dirty Dopamine

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Brain Structures of Importance (Image via Google)

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.

Love in the Shape of an Almond

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Amygdala, our lovely “Almond” (Image via Google)

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?

Microbes and Immunocomplexes – Oh My.

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”

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Lana Del Rey prefers the company of older men (Via Google)

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.

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Our Mate Compatibility Complex? (Via google)

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.

Birds Do it, Bees do it, Even Blind, Bisexual, Polyamorous Geese Do it

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 your brain on porn
Dopamine
Ventral Striatum Activity
Where does Sex live in the Brain
Neurobiology of Desire. K. NeuroQuantology | June 2013 | Volume 11 | Issue 2 |
Sex differences in the Amygdala
Fruit flies
Gut Bacteria changes sexual preference in fruit flies
Influence of HLA on human sexual satisfaction
How Microbes Influence Your Love Life
Evolution of Orgasm

Portrait of Science: What do Cows, LSD and The Salem Witch Trials have in Common? Ergot!

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Vanessa and Her Research Bulls. Image: Erin Matthews

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.

Shop Local

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.

 Science in the time of Nazis

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Rita Levi-Montalcini  (Google)

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.

Incredible.

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.

Portrait of 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.

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Image: Vanessa Cowan

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.

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Image: Vanessa Cowan

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

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Image: Vanessa Cowan

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.

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Image: Vanessa Cowan

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.

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Image: Vanessa Cowan – taking silver and her first BJJ match

 

Meaning Message and Misinformation

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In the beginning there was a post on the importance of science communication and thus this blog was thrust into creation. ( HERE, if you haven’t read it and want to jump back). The area of science communication is currently exploding, much like the gaseous expanse of our universe during it’s infancy.

I am going to spare you any pseudo-philosophical musings on cosmology or astrophysics. I do find the beauty of a galaxy awe-inspiring and the cold, vast, apathy of space a reflection of the way we should view the world (The universe doesn’t care about your beliefs, a person once uttered) but I can’t pretend to know much about it.

It’s a cold, cruel mistress born from explosions, implosions and volatility.

Sorry, I got a little carried away.

I am going to spare you from an extended pseudo-philosophical musing because, frankly, I know nothing about space, astrophysics or cosmology.  My understanding is so minimal that I would butcher it until it was hardly recognizable. In the end it would be a mutation riddled with so many inaccuracies that it would come out looking much like Jeff Goldblum at the end of The Fly.

I want to maintain accuracy and in order to do that, I won’t attempt to write about a topic I have a hard time wrapping my own squishy brain around.

My focus is much more micro – a introspective viewpoint of the tiny universe that you contain inside every cubic centimeter of your body. Your blood, your bones, your neurons, your cells, the colony of creatures living on and inside of you, and the way all those things miraculously work in perfect synchronization to make you the person you were, the person you are and the person you will eventually become.

Sci Comm is not Science Fiction

In terms of science communication all science is important. All scientific discovery should be talked about and not just in laboratories and conferences and symposiums by the scientific elite. The intellectuals with tightly guarded scientific prowess who woo each other in their rapid dialogue of jargon; an attempt to one up the next in a gladiator battle of the frontal cortex and sheer strength of their action potentials.

Science should be talked about anywhere.

It should be talked about in bars, at dinner, to wide eyed curious children or while you are on the couch with your feet in your partner’s lap winding down from the long day. The discussion of scientific ideas should be an activity that people engage in every day.

It should be a continuous dialogue.

Science Communication, or Sci Comm, is a relatively new animal. Before an explosion of blogs and books and Instagram and Twitter it was a relatively lonely universe occupied by the very outspoken Carl Sagan and his lovely turtleneck collection.

Carl Sagan Cosmos

Carl Sagan Cosmos

 

And while Sagan wrote books, ruminated on a cliff about the vast expanse of our beautiful universe and made the 1980s talk show circuit –he was also a scientist loathed by the scientific community for his attempts at communicating science ideas to the public. They thought him to be a narcissistic showman. That his “altruistic education” of the public was a charade for his celebrity advancement. Perhaps a plausible theory. Even so, few people have been both a passionate contributing scientist and such a captivating communicator of ideas. It’s a rare gift.

Now, Sagan was a more contemporary example of the human experience of science. He wasn’t a cold, white male in a lab coat with a questionable beard and round glasses viewing the public skeptically over a clip board. He was a philosophical, mildly poetic thinker with questionable taste in clothing and hair cuts. He was also a ladies’ man – married three times. (His second and third wives an artist and writer, respectively.) He pondered the existence of an omnipresent deity. He asked questions to the public and encouraged a discussion. He was a human who engaged in science and in thought and in emotion.

(Aside: I found this lovely quote from his wife, the writer Ann Druyan, who was married to him at the time of his death. If you are also a person that finds strange things beautiful read along, if not, skip over.)

” When my husband died, because he was so famous and known for not being a believer, many people would come up to me—it still sometimes happens—and ask me if Carl changed at the end and converted to a belief in an afterlife. They also frequently ask me if I think I will see him again. Carl faced his death with unflagging courage and never sought refuge in illusions. The tragedy was that we knew we would never see each other again. I don’t ever expect to be reunited with Carl”

Strange Science

The strange thing about science is that it is an entirely human activity. Humans, in all of our fallibility and emotional tendencies, are embarking on these curious discoveries of how the world around us works. We have evolved a detached, objective methodology in order to try to avoid contamination of this wondrous world.

Sometimes we are successful. Other times we let too much of our humanness seep into that which we are looking at, clouding it over until all we can see is our own reflection.

The world is wonderful and mysterious and sometimes a little bizarre. Science has evolved as a way to explain the strange and unusual– giving names to things, describing the function and importance of things that would otherwise appear mystical in nature. It’s quite wonderful. Yet, the process of such discovery is often not well explained by scientists.

In decades prior, science has been prescribed as an authority. Often described as an ivory tower,  the process is locked away and the secrets of thought are only available to those elite shadow scientists.

Traditionally, science dishes out it’s explanations, guidelines, facts and findings while keeping much of the process in the darkness. This has bred suspicion and distrust in the public, especially in individuals who haven’t had much experience with the scientific method (which is a stunningly high percentage of the population).

This distrust and suspicion has been around for hundreds of years and, with the dawn of the internet, has seemed to explode into a chaotic fever.  The Second Law of Thermodynamics states that entropy always increases over time.

Now scientists and non-scientists alike are attempting to destroy that ivory tower of authoritative and prescriptive science.

You have PhD students like Toronto’s Samantha Yammine  instagramming her own research and laboratory adventures (along with fun facts about current science). There is Daniel Toker out of Berkeley doing some absolutely incredible neuroscience research in consciousness (and waxing philosophical while staring out at the Mediterranean sea). You have science journalists like Ed Yong who is quite prolific over at The Atlantic. Before that he was a humble blogger. He is also a New York times best selling author.

Science Communication and the importance of accessible science has grown in recent years. It has it’s own hashtag. It has people, all over the world — whether students of science and writers (like myself) or legitimate laboratory scientists — talking to the public about the wonders of science and what she has to offer.

But, with this celebration of science and attempt at unmasking the mystery comes misinformation, melodrama and a loss of meaning.

Zombie Deer Disease

A couple weeks ago I ran into some pretty bizarre news stories about Chronic Wasting Disease, a prion disease that afflicts Deer, Elk and Moose. Prion diseases are terrifying in their own right, and really don’t need any hypeman to up the horror of their progression and pathology.

Prion disease involves progressive neurodegeneration caused by misfolding proteins. These misfolded proteins have a Midas touch – their causal glancing into others causes their sister proteins to misfold. This causes a cascade that eventually leads to neuronal death and destruction of the organism whose poor brain happens to be afflicted. Another terrifying component is that Prion diseases have an excruciatingly long incubation period. Meaning an animal (humans too) may be infected with the disease and not show any symptoms of deterioration for a very long time.

Mad Cow Disease (Bovine Spongiform Encephalopathy or BSE) is probably the most well known prion disease, sparking panic at BBQs and picnics all over the UK decades ago. There is evidence that it is transmissible from cows to humans via consumption of BSE contaminated meat.

There is also an aptly named prion disease, Scrapie, that affects sheep. One of the hallmark behaviours is the mindlessly scraping of their wooly bodies against objects until they are a ratty, bloody mess.

Kuru – a prion disease that afflicted the Fore people of  New Guinea — was transmitted via cannibalism of the dead. It appeared to die out after the funeral practices were stopped. It has the terrifying nickname of “The Laughing Disease”

And, there is my personal favourite nightmare, Fatal Familia Insomnia. This appears to be a genetic prion disease that a poor Italian family has suffered from for quite a few generations (the book, The Family Who Couldn’t Sleep, explains it all).

In short, prion diseases are a death sentence and the reality of them are more terrifying than any misinformation propagated by media outlets.

Enter stage left, Zombie Deer disease.

Yes, Fear The Walking (Deer) Dead.

This unfortunate headline was everywhere, spreading misinformation on Chronic Wasting Disease and attempting to get the paranoid public riled up.

 

My personal favourite article was this gem HERE

Especially the headline:

“Black Death: Scientists fear health DISASTER as deadly ‘ZOMBIE deer virus’ may soon infect humans. A HORRIFIC virus that has killed thousands of deer may soon infect humans, sparking fears of a Mad Cow Disease-like epidemic.”

First of all, prions are misfolded proteins. They are not viruses. Viruses are completely different creatures.  Prions do not replicate the way viruses do. They are their own terrifying abomination.

Secondly, the unfortunate thing about misinformation in the media is that it is about as detrimental as misfolded proteins. It creates a cascade of fear and mass delivery of misinformation.

It is a plague far beyond what the so- called zombie deer disease could manifest.

Prions have a special place in my strange and morbid heart. They are the perfect illustration of how bizarre and terrifying science can be. They are something so incredible they altered the dogma of biology and biochemistry.

They illustrate perfectly how fluid science is. It is not set in stone. It must change with the unearthing of new evidence; everything needs to be altered in the light of discovery.

Influenza and the Plague of Misinformation

Zombie Deer Disease wasn’t the only unfortunate news story I stumbled across lately.

There is a virus of misinformation being disseminated on Facebook in recent weeks.

It has been well documented that this year’s influenza vaccine has, unfortunately, been quite ineffective. I was told by my virology professor that this year it carries a 10% efficacy rate — which is pretty dismal.

Influenza is a tricky virus to create vaccines for because it likes to mutate rapidly.

Some of our most effective vaccines, like that which helped to eradicate Smallpox, was designed for a virus that had one serotype (essentially one type of species of the pathogen). Influenza has dozens of different subtypes. The mutation and drifts that occur every year creates a pathogen that is hard to predict. This unpredictability may lead to a vaccine that is less effective than desired. That being said, any protection is better than no protection.  Influenza kills many people every year and this year has been exceptionally bad.

The influenza misinformation came in the form of a Facebook post being circulated by many individuals. It states that not only was this year’s influenza vaccine ineffective, it was catastrophically dangerous.

The fake news story claims that CDC scientists warn of the vaccine CAUSING super influenza outbreaks that will lead to certain death. It is complete fiction, in the sense that it was written by someone with the intent to spread misinformation. The scientist that is  quoted in the article does not exist, he is a character created by the author of this “news story”.  People are sharing it, without fact checking, as one does on Facebook.

So let’s do some digging to see if any part of this carries a granule of truth or if it’s all an exercise in creative writing.

First, lets start with the flu vaccine itself. The needle that pierces your skin contains a mixture of inactivated, purified surface proteins (HA and NA) of roughly four different strains of Influenza. These surface proteins are recognized by your immune system and your immune cells go to work. The end result? If the real influenza virus bypasses your body’s outer defense system and ends up inside, your immune system recognizes it and neutralizes it (hopefully). This vaccine doesn’t contain a live version of the virus. The purified surface proteins are unlikely to wreck havoc inside your body — meaning they are unlikely to organize into a fully formed infectious influenza virus. Viruses need DNA or RNA – some sort of genetic material -to successful replicate after hijacking our cells. The vaccine that is delivered via a needled syringe does not contain that.

The FluMist – or nasal influenza vaccine – does contain live attenuated virus. Attenuated viruses are still “living” but their ability to cause illness ( their virulence) has been significant altered (the smallpox vaccine I mentioned early was an attenuated vaccine). The mist is used to create a local immune response (the influenza virus likes the respiratory tract) which, in theory, should lead to an greater immunity to the virus. The FluMist is not recommend for use for 2017-2018 session, not because of it’s great danger to mankind, but because it appears to be ineffective.

So, the chance of the flu vaccine giving you a mutant super flu leading to your untimely death is just not likely. It is propaganda being propagated by people who are easily scared and unlikely to fact check the things that scare them.

There is usually a shadow of some reality in these things. It’s just that it’s mutated beyond recognition. It’s jaw has fallen off and it is now dissolving your arm with it’s digestive juices (The Fly again, sorry for ruining it). If we look back into history, we can see where the author of the influenza vaccine hoax piece got his inspiration from.

The Cutter Incident. In 1955, an outbreak of polio was traced back to the very thing that was trying to prevent it – the polio vaccine manufactured by Cutter Laboratories. The vaccine contained a whole virus that was inactivated by formaldehyde. The Cutter vaccines were defective– the virus, in some preparations was resistant to inactivation — and had horrible outcomes.

Some good news — this is unlikely to happen with the flu vaccine. It is merely made from subunits of proteins, not  the whole virus.

Awful, unexpected things can happen but you have to keep your eyes open and make sure that reports are founded in evidence not in historically inspired creative writing exercises.

Ask Questions, Do your Research

This is exactly why we need science communication. Misinformation can kill. It leads to health decisions based on non-information.

I have been the first person to shit talk my nursing education, but it keeps proving itself valuable in some form or another. One of the things nursing teaches is the idea of informed decisions. That is, the idea of people making decisions on their health or treatments based on evidence.

Misinformation is destroying that. You can not make informed decisions if you are no longer informed.

You are shooting in the dark. And unless your name is Clarice Starling, chances are you aren’t hitting Buffalo Bill in the gut and saving the day. (I apologize that all of my movie references are from 1986-1991– please Netflix at your leisure)

Again, as I have mentioned before, be skeptical. If what your reading doesn’t seem plausible– or appears out right ludicrous– do you research. Hell, even if it seems plausible it’s best to triple check.  Follow it back to the source and make sure that source is credible. When it comes to research, make sure you are looking at articles that are based in science and follow protocols (peer reviewed are best).  Always ask questions – Does this make sense? Where is this coming from? Can I find evidence that is reliable and replicable?

Lastly, a general rule for Facebook, chances are it is not what it appears to be.

 

* This has been edited. My first version of this post was, thankfully, called out by someone much more knowledgeable than myself who pointed out the error of my ways and gave me suggestions on how to improve on this piece and avoid my own misinformation missteps. Forever Grateful. The irony is not lost on me. *

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Prion Information
Viral Fake News
The Family Who Couldn’t Sleep
2017-2018 Flu
Zombie Deer Disease
Unscientific America
Tale of the Dueling Neurosurgeons
The Cutter Incident: Poliomyelitis following formaldehyde inactivated poliovirus vaccination in the United States during the spring of 1955
Medical Microbiology. Murray. 2017

 

You Smell Like Death

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Most people use their sense of smell to navigate the world.

Smells enrich the world arounds us, help form memories, warn us about danger or elicit pleasure responses. A few poor individuals have lost all ability to use their nose to sense their surroundings; and, of course, there is a fancy word to describe such a condition — Anosmia. Anosmia can be caused by a multitude of things– from a well placed fist shattering the nasal bone to nasty microbes causing serious sinus infections – one can easily loose the ability to smell. There is even a hypothesis that, for a very small percentage of individuals, an impaired ability to smell may be an early indicator of neurodegenerative diseases. Now, don’t panic because your ability to pick up on the warm scent of baked bread or bacon sizzling away in a pan has diminished – there is probably a much less insidious reason for your lack of olfactory precision.

A Nose By Any Other Name Will Smell As Sweet

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Image: Neuroscience: Exploring the Brain. 2007.

Your ability to smell is a pretty neat little trick and is, in fact, a fairly complicated neurophysiological process. Some wormy looking neurons hang out in a bony plate at the top of your nasal cavity. They possess projections called cilia (these guys are found in an astounding number of cells) and these cilia have a little receptor on the tip that odour molecules like to attach themselves too.

A nice cellular hug.

It snaps, crackles and pops some information up the neuronal cell, buzzes through the boney plate and sends the signal along to specific regions – all on a magic carpet of sorts called an olfactory bulb. This bulb sends on this information to higher brain centers to be interpreted.

Receptors that have similar molecular make up all cluster together in zones on the olfactory blub– this clustering forms a spatial map of highly ordered information.

It’s pretty crazy how these tiny cells organize smells into bits of electricity that form organized information like the colour pegs of a light bright. (Are those still a thing? Does anyone born after 1989 have any idea what I am talking about? A quick google search has informed me you can buy one (here) on Amazon.ca for the low price of 70 dollars. Yikes, the price of nostalgia is high.)

So, now that you have been primed from this butchered crash course style explanation of the olfactory system – lets continue on this fantastic journey.

Touchy Tingley Feelings and Things

I would imagine a lot of people are familiar with the fact that smells induce some pretty strong emotional responses from us humans. It has a lot to do with the fact that a little brain structure called the amygdala has its gummy little fingers digging around in our odor evoked memories. The amygdala, adorably named for it’s little almond shape, is located snuggly in your medial temporal lobe and is notorious for emotional perception and processing.  There appears to be a direct line of communication from the olfactory blub and its tracts (fancy word for “nerve fibers”) to the limbic system, where the amygdala hangs out. The amygdala receives a lot of information from our noses and tends to put emotional significance to them.

Smells like our favourite food or the smell of our lover can elicit emotional and, generally, pleasurable, responses. Smells like sulfur, methane or the unmistakable smell of something burning warn us of danger. We are conscious of how theses things smell (you probably thought about it as soon as you read the words) and we have a learned response that makes it possible for us to interpret and react to the stimuli.

This all makes sense to us. We can describe them. We can personally confirm that we experience it.

We perceive it, therefore it’s our reality. And it appears to be a pretty universal experience among other humans, which helps us solidify that reality.

But there is a deeper journey for us in the sinus cavity.

What’s that Smell?

As I mentioned earlier – the loss of smell is thought to be a possible warning sign for neurodegenerative diseases like Parkinson’s disease (PD). But, does PD have a smell?

That is to say, does neurodegeneration, or any disease state, have its own odour?

Well, apparently Parkinson’s has an oily musky scent to it.

Eye brow raising, no?  How, the hell?

The question is then: Is that even possible?

As in any good story, let’s suspend our disbelief for a moment and take a look at the tale of the woman who can smell Parkinson’s disease.

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Joy and her Husband, Les.  Credit:  Dailymail

Joy, a nurse from England noticed her husband’s scent changed. Over the course of a few years, his familiar smell began to slowly morph into an unsettling foreign odor. She scolded her husband, a physician, that he was falling behind on his hygiene. He became annoyed and assured her nothing in his routine had changed. She describes the change in his smell as a gradual one, over the course of a few years it would creep up again and again. Six years after the onset of this shifting scent profile, her husband was diagnosed with Parkinson’s disease. Upon returning from a Parkinson’s support group, she told her husband about a startling realization she had – all of the individuals from the meeting had the same smell.

Joy eventually shared her smell-related hypothesis to a researcher at a Parkinson’s meeting in Scotland. Scientist, Dr. Tilo Kunath, is head of a research initiative in neurodegenerative medicine at the University of Edinburgh. (Interestingly, he has a Canadian connection — obtaining his PhD from the University of Toronto, investigating novel stem cell systems.)

Dr. Kunath took some interest in the idea and decided to test Joy’s alleged ability to sniff out Parkinson’s. Given T-shirts from 6 controls and 6 PD suffers she was tasked to accurately identify which clothing belonged to which group, based only on the information her olfactory system gave her. In the end Joy identified all correctly, save for one subject. She insisted a control participant belonged in the Parkinson’s group.

Are you waiting for the plot twist here? I know you can smell it coming.

Less than a year later, the “incorrectly” identify control participant was diagnosed with Parkinson’s disease.

Currently, Dr. Kunath and his team are using her nose to identify the unique molecules that make up Parkinson’s signature scent. This identification could lead to a diagnostic test that can use fancy science instruments, like mass spectrometry (mass spec to his friends) to interpret a patient’s scent profile. A way to come back with a diagnosis sooner in hopes to better manage the disease progression.

Now, according to the comments on the news stories I have read while researching for this post, Joy is not alone in her abilities. My personal favourite description is one man’s confirmation of the musky signature, adding that it is much more gamey – like when one cooks moose or bear meat.

Delicious.

Now, using our senses to identify disease is not an unfamiliar concept. For example, as a nursing student, I was taught that breath that has a fruity odor is indicative of Diabetic Ketoacidosis, a life-threatening condition when insulin levels are insufficient and blood sugar levels become dangerously high. It’s the smell of ketone bodies escaping the body – a sign that your cells aren’t taking in the glucose they need so they resort to burning other fuels..like your muscles or fat.

Using good old Diabetes as an example again, the name itself, Diabetes Mellitus, comes from the senses once again being utilized as a diagnostic tool. Mellitus means “honey sweet” and came into being after a nice sip of a patient’s urine. The urine carried a sweet taste (from excess glucose spilling into it) and was a way to recognize the condition.

Pour me a pint of that Honey Sweet.

For some reason, one woman’s ability to pick up on a scent that no one else can is going to breed a healthy sense of skepticism. And holy shit it should. The day it doesn’t is a sad day for humanity and I don’t want to be alive to see it.

Until her mapping of scent profiles can be categorized, accurately tested, accurately identified by the mass spectrometry or any other diagnostic tool and, more importantly, be consistently reproducible, the story should leave you feeling a little skeptical.

It’s a great story, but is there any science caught in its nose hairs?

Send in the Hounds

Dogs are notorious for their ability to sniff out all kinds of things and we have been using them for centuries. From finding foxes cowering in their dens to bombs, drugs and thugs — we have harnessed the power of the canine nose.

Recently that went next level. Dogs have now been used as furry blood sugar monitors, warning their owners when their blood sugars start to rollercoaster. A feat that seems a little supernatural in itself.

Recently, there have been studies conducted to see if dogs can be used as diagnostic tools in cancer identification. This was tested through the sniffing of breath, urine and other bodily fluids.

Overall, the dogs performed pretty well. When tested to see if they can discriminate lung cancer from COPD (chronic obstructive pulmonary disorder) in breath samples the dogs had a sensitivity rate of 71% and a specificity rate of 93% — the dogs were able to pick up the scent more times than chance would account for and were then able to discriminate between different smell profiles 9 times out of 10.

Another study used urine as the vehicle for cancer’s smell. This time it was a test to identify the presence of prostate cancer. The dogs in this study had a very high sensitivity rate (98.6%) and specificity rate of 96.4%. A promising find, as PSA (prostate specific antigen) serum (blood) testing  doesn’t have a great track record for its ability to accurately assess a man’s prostate cancer risk. A high serum PSA does not equate a malignant condition and often men go through painful, risky prostate biopsies to rule out cancer. The outcome of said biopsies may be a benign result and some less than desired complications that lead to loss of function. Sorry guys.

Now, the future is not a German Shephard in a lab coat hanging out in an medical laboratory waiting patiently for urine and breath samples to analyze.

But the future of scent diagnostics might be in the development of electronic noses.

E- noses may, eventually, become a diagnostic tool to accurately identify various types of cancers. There are dozens of studies testing the efficacy of a robot nose to detect cancer at the earliest stage possible in order to maximize survival rates. However, these E-noses have been tested for several years and are still in their infancy. It will be a long while before the Electro nose is hanging out in your standard diagnostic lab.

Volatility and Psychic Cats that Sense Death

So what does a nurse from England, a German Shepard and a electronic nose have in common?

They all may able to pick up on something called volatile organic compounds or VOCs.  We all apparently have an odour fingerprint and according to one study (THIS ONE) infections and certain disorders can produce new VOCs or change which molecules in our repertoire are the most pungent – essentially changing how we smell.

Something that is not likely to be picked up consciously, if at all, by the rudimentary human olfactory system.  Dogs and machines, perhaps.

What about cats?

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Oscar. Image:  Nejm.org

For centuries, these adorable furry felines have been associated with death. The Ancient Egyptians worshiped them and regarded them as guardians of the underworld.

When Christianity came around, cats were thought to be consorts of Satan; demons in fur suits that whisper in the ears of witches.

I have a point I am getting to I swear.

There is another great story, this time it’s about the cat that can “accurately” predict when someone is about to die. His name is Oscar and he lives in a nursing facility. When Oscar pays you a visit and curls up at your feet, chances are you are not going to live to see another day. You can read about Oscar (HERE).

So, is Oscar using VOCs to accurately foretell the deaths of the poor souls he visits or is he a consort of Satan?

All questions of the natural world have answers; sometimes we just don’t have access to them yet.

My money is on the smells. Sorry Satan.

Skeptical Sighing

From nurses who smell Parkinson’s to Cats who can sense death, there are a couple things to package up and take home with you

Let’s finish off where we began — your olfactory system. This little guy is so wonderfully complex and beautifully orchestrated. It helps you interpret your world, form memories and evoke emotions. From the aromas that help you get the most out of your wine or whiskey to the putrid smell of a natural gas leak – your nose and its neurons are there for you

Next, never underestimate the power of a good story. They can be seductive. They can overwhelm our senses and our reason. Beware the beguiling narratives.

Third, stay skeptical in everything you do. Never stop questioning. That’s the only way you are going to get any answers. I hope you asked yourself, how the hell can someone smell the decay of the nervous system? Because, yeah that’s weird. How can we test it and how can we disprove it? Also a good question.

We will see if Joy can accurately identify PD’s scent profile. Then we will let biochemists and finely tuned equipment see if they can accurately detect it in those afflicted. Until then, we can enjoy the story but err on the side of caution.

Lastly, the next time you see a dog, imagine them in whimsical lab coat. You’re welcome.

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Neuroscience: Exploring the Brain
Olfactory System of Highly Trained Dogs Detects Prostate Cancer in Urine Samples. 2014
Canine scent detection in the diagnosis of lung cancer: revisiting a puzzling phenomenon. 2011
Sniffing out cancer using JPL electronic nose: A pilot study of a novel approach to detection and differentiation of brain cancer. 2009
The scent of disease: Volatile organic compounds of the human body related to disease and disorder. 2011
Woman who can smell Parkinson’s disease helps scientists develop early detection test. CBC. 2017
A Day in the Life of Oscar the Cat. 2007

 

 

 

The Monstrous Microbiome: Good Bowel Buddies

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cellls

DIY Fecal Transplants – putting the “Y” in DIY

A few weeks ago, I received an email from a friend with a link to one person’s journey through the valley of the shadow of poor gut health to the eventual crest over into the promised land of microbial-intestinal paradise. All achieved with a Do -It-Yourself fecal transplant.

If you just read that and went – wait … DIY fecal transplant? — that is the same, dumbfounded, slow blink realization that I had when I clicked on that link. Reading through the testimony and step-by-step guide I was reduced to tears as I laughed at the glorious one liners and anecdotes. Despite my amusement, the author of the website is entirely serious in their step-by-step instructions, key tips and tricks and, especially, in their belief in the power of good microbes in the all the right places. But, honestly, despite the misguided nature of their website, they are right about one thing – the power of bacteria and their influence on our health.

Now it’s not all shits and giggles (I am so sorry, I couldn’t help myself), fecal transplants are a real deal, medical procedure. I was first introduced to the idea of fecal transplants a few years back, sitting in a microbiology class during my short, misguided stint in nursing school. It was presented as a new approach at curing resistant Clostridium Difficile infections – or C. Diff for short.

Bad Bowel Buddies

C. Diff infections are nasty, dangerous events that generally kick those who are already down right in the gut. C. Diff is a type of bacteria that exists in very small amounts within the normal flora (your body’s resident bacteria) of your intestinal track. They are kept in check by the other “good” bacteria that populate the cozy folds of your intestinal wall. These are opportunistic pathogens, meaning they will seize the perfect moment to gain control over your guts and wreak havoc on your insides. Carpe Diem and the like.

C. Diff is an anaerobic (does not need oxygen), spore forming (can package its DNA into a very tough shell go to sleep and hang around for MONTHS), toxin producing bacteria that cause inflammation and diarrhea. In some cases, this inflammation is so severe it leads to bowel perforation (a hole where you do not want one) and death. If your bowel manages to stay intact, the dehydration that follows severe diarrhea could kill you too.

The infection generally occurs in patients who are on long term or very potent intravenous antibiotics; recently hospitalized; immunocompromised; and/or post surgical patients. In short, C. Diff is a bastard.

Now, if that wasn’t horrible enough – this hardy little microbe can be very difficult to destroy.  This has to do with C. Diff’s ability to bundle itself into a spore. Spore forming bacteria are pretty amazing but also pretty terrifying things, and are responsible for some pretty nasty illnesses. Other spore forming clostridia bacteria include those that cause tetanus and botulism – some horrifying illnesses that involve prolonged muscle spasms and muscle paralysis, respectively.

And then there is anthrax, a deadly, spore-forming, bacillus bacteria that has been harnessed for biochemical warfare and bioterrorism. Oh, behold the wondrous power of microbes.

But wait, it gets even better.

C. Diff has a reputation for developing resistance to the course of antibiotics that are used to treat the infection. Just when you think you’ve gotten rid of the thing, a few resistant rods drifting in your intestines wage a Viking raid on your intestinal epithelium, conquering and pillaging your gut.

This is where the fecal transplants come in.

Fecal Transplants

Please, do not attempt a DIY fecal transplant at home. It would be, pretty much, the most uncomfortable, horrifying experience of your life. According to the DIY website and step-by-step guide, it involves: a kitchen funnel, a big brown towel, a diagram of the colon and some personal lubricant (or coconut oil!).  Oh, and some other person’s fecal matter. Please, save the big brown towel and personal lubricant for more fun activities that don’t involve an enema of another person’s poop. Unless, of course, that’s your idea of a wild night, then you may want to rethink your life choices. Not judging, really.

Fecal transplants are a relatively new therapy, and the process of getting someone else’s feces into your bowel is pretty similar to the horrifying steps outlined in the DIY version – minus the kitchen funnel and coconut oil. There are only two ways to the intestines, meaning there are limited avenues to get the good microbes where they need to be. Unfortunately, it generally involves some very unpleasant placements of tubes. Although, with fecal transplant proving itself to be an effective tool in treating C. Diff infections, capsule forms are being engineered to deliver the microbes to where they need to be — minus the tubes. You can unclench now.

Now, it is not the feces we really want. Unfortunately, that’s just the delivery vehicle — a way to keep the colonies of beneficial bacteria happy, alive and thriving until they reach their new intestinal environment. The treatment relies on the transplanted bacteria to settle down, lay down roots and maybe buy that house with the white picket fence at the corner of the Sigmoid colon. We want something called colonization to happen – lots of health promoting, beneficial bacteria sticking to your intestinal wall, choking out the C. Diff and reclaiming territory lost to the toxic pathogenic microbe.

Fecal transplants may have a future that doesn’t involve the feces. Something called RePoopolate took bacteria from an optimal donor, purified it and cultured three dozen different strains. It’s more like a probiotic– a capsule filled with good microbes and none of the BS (or in this case I guess it would be HS). The trial was given to a very small amount of people, not even a handful (two C. Diff patients), and it appeared to be an effective treatment. Unfortunately, the small population size doesn’t make this trial very statistically relevant — one can not draw any conclusions based on only two patients. Some, not so encouraging news, is that another poop-free transplant, Ser-109, failed in a clinical trial a few years back.  They are pushing through with a new phase of a clinical trial this year, so perhaps we will see a future of poop-free microbe laden transplants. One can only hope.

Now, not surprisingly, there is a dark side to fecal transplants. Like the DIY guides found deep in the bowels of the internet, there is also a prevalent idea that it is a cure all.

A miracle.

A saving grace to those afflicted with a variety of ailments from irritable bowel syndrome to autism. That’s some pretty dangerous thinking.

First of all, not all bacteria are created equal and the transplantation of your friend’s, or spouse’s, or a stranger’s bowel buddies into your intestines can have severe consequences. Let’s jump back to the DIY fecal transplants for a second. If that specimen is not rigorously tested, you could be potentially exposing yourself to a variety of diseases, from hepatitis to HIV. That’s not the only obstacle, if the sample is disease free, the bacterial colonies may not be the ones you want. It’s not a one size fits all — there needs to be some vetting and customization when it comes down to what bacteria we are going to let spend the night in our colons.

Now, secondly, animal studies have shown transplanted microbes can cause a whole host of trouble that include obesity, irritable bowel syndrome and psychiatric aliments. Bear in mind, these are animal models, so we can’t extrapolate this with confidence to the human population; however, it shows that transplanting microbes is not without its risks. In fact, it may create the very problems people are trying to cure.

The Weird, Wonderful Microbiome

Now we have already touched on the microbiome but haven’t really explored what it is. And honestly, within the confines of this one blog post, I won’t be able to do it justice. The “omes” are so complex; and the sheer number and variety of “omes” are astounding.  There is, of course, the microbiome and the genome (which hopefully everyone knows about) but there are also the more obscure ones hanging around. For example, we also have the proteome, the kinome and the connectome – that is the systematic study and organization of proteins, kinases (really cool enzymes that have a hand in a ton of functions) and neural connections, respectfully. Amazing!

So, the microbiome is just the collection and organization in the study of microbes. And it is everywhere. You have your individual, personalized microbes living on your skin and inside you gut. It’s that normal flora I was talking about. Good bacteria that we have developed a cooperative relationship with. They keep things in check and in return they get all they need from living on and in us.

We are all unique.We have a completely different flora then the person next to us — the microbes on my skin are a different combination of species compared to the person sitting next to me in the library. There are various populations taking up residence on all of us. Its is, essentially, its own universe.

One of the most incredible things is that we appear to share the same microbial flora with the people we live with. If we cohabitate long enough, our microbes will eventually synch. It’s almost romantic.

For a way better written, and more in-depth journey into the microbiome, check out Ed Yong’s book I Contain Multitudes. His exploration isn’t limited to the human microbiome, instead the book covers the microbiome of all multicellular organisms – from pangolin to the coral reef – and what it all means.

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Image: http://www.wbur.org/npr/218987212/microbiome -Gut Bacteria Might Guide The Workings Of Our Minds –

Brain Gut Connection

The last word on the human microbiome might sound a little out there, but there is some hard science behind it.

Unbeknownst to most of us, there is a tiny, second brain living in your abdomen and it communicates and influences the big guy in the skull. Seriously. It’s called the gut-brain axis, and it is described in one study (This one here) as a “bidirectional communication network that monitors and integrates gut functions and links them to cognitive and emotional centers in the brain.” Meaning the gut and the brain appear to talk to each other and may even have a strong influence on one another.

When we think of neurons we generally think of the ones in our brain that snap, crackle and pop when we have an sudden idea or when we reach out to touch someone. However, neural tissue is intimately intertwined within our gut with a staggering number of neurons that, according to some sources, outnumber the spinal cord. The Enteric Nervous System, or ENS, is the name for the mesh of neurons that tell your gut what to do. Not only does it tell your entrails how to behave, it appears to be signaling messages to your brain via the tenth cranial nerve, the vagus nerve.

Your gut also uses neurotransmitters. A whopping 90% percent of your body’s serotonin is used and synthesized in your gut. Altered levels of serotonin are thought to play a role in not only digestive diseases, like IBS, but also diseases beyond the gut, like osteoporosis.

So, if you are mulling over the idea that your gut is actually a very long, squirmy, squiggly brain and you feel like it’s more science fiction than science, it actually gets a little weirder. Cue the microbes.

As we explored earlier, the microbiome plays a huge role in a lot of aspects of our health. There is emerging evidence that the gut microbiome may play a large role in CNS and brain function as well. For example, there is an apparent link between the use of antibiotics and altered mental states – psychiatric side effects like depression and even psychosis. On the flip side, in mice, the stress of untreated bacterial infections may also lead to disruptions in memory and cognition. Microbes appear to be capable of influencing the grey matter in many different ways, at least when we are looking at animal models.

In fuzzy little mice models, altering the microbes of the gut with antibiotic like agents caused a change in behaviour and increased the expression of a chemical called brain-derived neurotrophic factor or BDNF. An altered expression of BDNF has been suggested to play a role in a variety of neuropsychatric disorders, including Schizophrenia.

Antibiotics aren’t the only culprits, diet and alcohol use also appear to influence and alter the composition of those good bowel buddies. And, as evidence keeps coming in, this disruption of our gut’s inhabitants may have a crucial role in behaviour, cognition and memory…at least when we look at mice brains.

The End of the Road

Now, if you have survived my awful poop jokes and heavy-handed wit, we have reached the end of the line when it comes to the human microbiome and the gut, at least as far as this post is concerned. It was an long journey from C. Diff and DIY fecal transplants to the unnerving idea that our brains may be under the influence of the microbes bouncing around in our squiggly entrails.

In the end, we’re not only a skin suit of endogenous biomolecules and chemicals, but we are also a comfy home to tiny living things that may have a huge hand in the fate of our health and even the inner workings of our nervous system.  So, be kind to your microbes and they might not engage in a full fledged mutiny on your bowels and brain.

Also, put down the kitchen funnel and leave the fecal transplants to the experts.

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I Contain Multitudes: The microbes within us and a grander view of life. Ed Yong
The Power of Poop (thepowerofpoop.com)
From gut dysbiosis to altered brain function and mental illness: mechanisms and pathways. Rogers. Nature. Molecular Psychiatry
Think Twice: How the Gut’s “Second Brain” Influences Mood and Well-Being. Scientific America
Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders. Autry. 2012
Serotonin in the Gut: What Does It Do? Bornstein. 2012. Frontiers Neuroscience
Stool substitute transplant therapy for the eradication of Clostridium difficile infection: ‘RePOOPulating’ the gut. Petrof. 2013
CDI. Seres Therapeutics
Medical Microbiology. Murray. 2016
First Image: Erin Mattthews
Second Image:http://www.wbur.org/npr/218987212/microbiome

What’s Your Poison?

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(Shameless wine drinking boomerang from New Years. Press play to watch me cheers you over and over again. Or don’t. It’s fine. I’m lame, It’s ok.)

The inspiration for this particular post came in the form of an incredibly nasty hangover. One of those head spinning, stomach curdling, moan-out-loud-and-beg-for-death kind of hangovers. As I rapidly approach the end of my twenties, with my thirties standing in a robe holding a scythe on the horizon, hangovers are no walk in the park. But maybe it’s just me, since this particular hangover occurred after one of my good mates came back from a holiday trip to his family home in the UK. He’s in his forties, a horrible influence with a pint in one hand and a glass of bourbon in the other and was probably able to walk with a spring in his step, whistling some Mary Poppins song the next day.  Meanwhile, I was struggling to pull myself together with crackers and a glass of water.

So, what is the biology behind alcohol?

We all know the effects alcohol has on our fragile little bodies. A nice spreading warmth and delusional bold feeling that comes with the flow of liquid courage.  This followed by some slurring of our speech (Dysarthria) and the tell-tale weeble-wobble (Ataxia), some nausea and maybe vomiting followed by the eventually slip into blissful unconsciousness. Ah, lovely.

But let’s take a look at some of the biological implications of alcohol consumption

The Gastrointestinal Tract

Alcohol is absorbed into your blood stream rapidly through your stomach and intestinal lining. It burns through your mucosal cells with a fiery vengeance. The nausea and vomiting that generally follow a night of making it rain ethanol down your gullet is from inflammation of the stomach lining.

Bad news. Chronic, heavy alcohol consumption can lead to malabsorption and vitamin deficiencies, which may lead to some terrifying effects. Thiamine is the vitamin that takes a substantial hit when alcohol consumption becomes heavy and chronic. Thiamine is a wonderful little molecule called a coenzyme – it is needed for proper cell functions to occur. It plays a big role in carbohydrate metabolism (getting sugar broken down to feed your hungry cells), neurotransmitter synthesis (helps make those happy little brain chemicals) and even in the building blocks of our DNA (nucleic acids).

Our brains, in particular, take the hardest hit from alcohol – both in the acute effects of short term use and the long-term effects of thiamine deficiency in the form of Wernicke-Korsakoff syndrome.

So, let’s travel on up from the gut to the brain and see what goes on when we throw back a few.

The Brain

The Brain, swishing around in a cozy little hot tub of cerebral spinal fluid in the iron fortress of the skull, is seemingly protected from the outside world. And it is– to an extent. Like a large blow to the head can cause a nasty effect on the brain, so too can some of the things we ingest. Alcohol has the ability only a few molecules have — it can pass through the blood brain barrier (the BBB). The BBB is a collection of densely packed cells that prevent the passage of many harmful substances into the brain’s circulatory system.  Alcohol happens to be the right size and shape to slip past the guards at the gate and wreak havoc inside the gooey tissue.

The Cerebellum (which adorably translates into “little brain”) is a wrinkly little structure at the back of our brain near our spinal cord. Its main job is to keep a tight regulation of our voluntary movements including posture, balance and coordination. Your slurred speech is also a direct result of alcohol’s unforgiving assault on your adorable “little brain.”

What about that booming headache the next morning? Well, it is a few parts dehydration and a few parts angry pain receptors that dot the meninges – the layers of tissue that cover your brain. Alcohol appears to be toxic to these protective coverings and the next day they are reeling from the effects.

And that is just the acute effects of alcohol consumption. Abusive alcohol use can do some very serious damage to your ooey-gooey center.  Remember the thiamine deficiency that occurs with chronic over use? The lack of thiamine really messes with your neurons and glial cells. A deficiency eventually leads to damage in areas of the brain, triggering apoptosis (a fun word that means programed cell death. Okay, it is actually Greek for “falling off” but it’s really a process that your cells undergo as they die. All cells are destined to do it but sometimes they are bullied into it). All this neuronal damage leads to an interesting pair of disorders.

So, let’s pour a pint and have a chat about Wernicke-Korsakoff syndrome

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Two Guys Walk into a Bar

Wernicke’s encephalopathy (fancy word for “something is wrong with your brain.” Seriously.) and Korsakoff Syndrome are two different disease states but they often go hand-in-hand so neurologists frequently lump the two together.

Wernicke’s encephalopathy is characterized by:

  • Confusion or a change in mental state
  • Some pretty noticeable changes in the eyes, including Nystagmus – involuntary rapid eye movements (Check out a video of it HERE!)
  • Difficulty with walking and balance – otherwise known as Ataxia

The presence of at least one of these symptoms, coupled with being thiamine deficient, usually points to Wernicke’s. With increasing apoptosis and accumulating neurological damage, the encephalopathy often gives way to Korsakoff syndrome.

Korsakoff Syndrome is all about your memories. Or lack there of. The syndrome incudes amnesia (or memory loss) in both the anterograde (memories that come after or “new memories”) and retrograde forms (memories that happened before the onset — sometimes extending years into the past).

An interesting feature of Korsakoff is the ability of the person affected with the syndrome to try and compensate for their deficits. They often engage in something called confabulation – they lie without any intent to deceive. The afflicted will come up with fabricated or imaginary experiences in order to fill in all the memory gaps.

So now that we have explored the gut and the brain let’s zoom into what alcohol does to our DNA.

Yeah, drink up, it gets worse.

Our DNA

There is a recent study that popped up on a popular Facebook page (that has something to do with passionately loving science) that shows alcohol’s damaging effects to haematopoietic stem cells – or the cells that renew our blood. Accumulation of damage can lead to a horrible cascade that eventual leads to mutations and quite possibly, the C word.  The study specifically looked at damage caused by acetaldehyde.

Acetaldehyde is the by product of alcohol metabolism.  There is a multistep process that our body undertakes in order to rid ourselves of the alcohol we have ingested.

First – an enzyme called alcohol dehydrogenase breaks down ethanol (our friend alcohol) into acetaldehyde, which is toxic to our body – as the evidence suggests. Then another little enzyme called aldehyde dehydrogenase 2 (ALDH2) breaks down the nasty metabolite into something that won’t poison us.

The unfortunate news is that some people have a defective ALDH2 enzyme and acetaldehyde builds up rapidly in their body. More unfortunate news, enzymes get saturated. This means that there may be too much acetaldehyde and the enzyme just can’t work fast enough to remove it from our system.

From the mouse model, the evidence suggests that aldehydes can do some nasty things to DNA, including DNA protein cross linking, which can damage chromosomes. This chromosomal damage can cause some funky chromosomal rearrangements when cells undergo division, which would eventually lead to malignancies (fancy word for cancer).

On Prophecies of Doom

Now before we vow to never drink again, much like the ritual that follows a hangover, the study had a fairly narrow scope. First, the focus was on a specific disease called Fanconi anemia, a rare disease caused by unrepaired DNA mutation. They looked specifically at acetaldehyde’s role because many of those afflicted with Fanconi anemia have a defective ALDH2 enzyme, namely Japanese Fanconi patients. The hallmark of Fanconi anemia is the failure of specific DNA repair mechanisms, which leave mutations unchecked, leading to blood disorders and eventually specific cancers.

Acetaldehyde still appears to have the ability to crosslink DNA and really screw it up, but the good news is that most of us have a working mechanism for fixing these DNA mutations.  Specifically, a repair protein called FANCD2, that is directly defective in the case of Fanconi anemia patients. Loosely meaning, we can repair the damage acetaldehyde may do to our haematopoietic stem cells.

The researchers argue that it does illustrate that acetaldehyde can damage our DNA which may explain the epidemiological link between alcohol and cancer risk; however, this study, frankly, is not very relevant to the general consumer of alcohol.

Can alcohol cause cancer? Sure it could, what doesn’t?

Can it damage your brain? You bet your ass it can.

Can it make you dance? No, absolutely not.

So, drink up friends and enjoy that pint of beer or glass of bourbon, but for the love of God put down that tequila shot … even if it is free.

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Cheers!

 

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Images: Erin Matthews

Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells. Garayocechea et al. Nature. 2017
The role of thiamine deficiency in alcohol brain disease. Martin et al. NIH. 2004
Effects of ethanol on the cerebellum: advances and prospects. Luo. 2015
The effects of alcohol consumption upon the gastrointestinal tract. Bujanda. 2000