* Like all good science, this needs some testing…

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When news hit that Disney bought the rights to Star Wars, and that J.J. Abrams would be manning the first movie of a new trilogy, my inner geek went into giddy overdrive. This was because it gave me a chance to revisited my bucket list, which had previously scratched off “be an extra in a Star Wars movie” as something that was unattainable having presumed the prequels were my last chance. But now, there is (literally), A NEW HOPE. Even better, is the fact that my kids are old enough to also want this.

And so, being a science-y sort and all, I figured the first step would be to actually try and come up with a way to calculate the odds of such a thing happening, and hence you see the above – or what I have termed the Abrams’ Stormtrooper Axiom. In effect, this is an equation that aims to calculates the odds of you (or anyone) being cast as a stormtrooper in one of these new movies¹.

Here’s how it works. We’ll first look at (1) which expresses the equation in its most obvious form.

When you look at this equation, there are three main components: two in the numerator: W_kS_blaster and bmi_opth_opt

And one in the denominator: 5.4^(1+b^o_p+b^o_w).

The denominator is an expression designed to address the likelihood of being cast, as having a dependence on the individual’s chance of contact with J.J. Abrams. Specifically, b^o_p refers to the degrees of personal separation the individual is from the Director, whereas b^o_w refers to the degrees of internet separation the individual is from the Director. The base of the exponential relationship is, of course, the standard May The Force Be With You Constant (or 5.4).

All told, if you have very little connection to the director, your odds can dwindle significantly, about 5.4^(1+6+6) times, or roughly one in 3.3 billion! It also infers that even if you know JJ Abrams personally, it does not guarantee being cast – mathematically, the closest association would still work out to 5.4^(1+1+1), or roughly a chance of one in 158. This is because there are other factors that need to come into play when determining whether an individual is right for a stormtrooper part.

Which is where the numerator expressions exert their influence. We can first begin with the bmi_opth_opt element, which essentially considers the physicality of the individual vying for a stormtrooper part. The bmi portion considers body shape, whereas the h portion considers height.

Each element can be further derived as:

Where (2) calculates divergence from an average body type (as expressed by an individual’s body mass index with m equals to the individual’s weight in kilograms, and h is equal to the individual’s height in metres). You’ll note that the more you veer away from an “average” body type, the greater the modification of the bmi_opt number to a number less than one (and therefore further lowering your odds).

In the same manner, (3) calculates divergence from an optimal height (deemed 1.8 metres as determined from casual examination of Star Wars’ trivia – i.e. calculating Mark Hamill‘s height and noting the “Aren’t you a little short to be a Stormtrooper?” comment). Like the BMI calculation, the more you deviate from the optimal height, the greater the modification of the h_opt number to a number less than one (and therefore further lowering your odds).

Note that both (2) and (3) are included in the overall equation for pragmatic prop design reasons (not every extra can have a custom made set of armour, so it makes sense if casting aimed for similar body types). Then, of course, there is the whole clone army narrative which might also presume the troops having similar physical features. (Also note that in case you weren’t familiar with the symbol, the straight up and down lines enclose a value where you only use the absolute number – i.e. remove the plus or minus sign).

Anyway, when you put it all together you get the expression (4).

Which only leaves W_k and S_blaster to be defined. Here, these two variables relate to two specific personality traits that are deemed important for the stormtrooper casting decision.

For instance, I don’t think I’m the only Star Wars fan who notices the incredibly poor marksmanship exhibited by the stormtroopers. There are many instances in the movies where there are many of them (with their weapons – presumably high tech in nature), in close proximity to the target, and yet, they still always fail to hit their target.

Given this observation, I’m left to assume that Stormtroopers, as a whole, have a deep distrust of guns, and with that discomfort tend to misfire (perhaps subconsciously). This also leads me to hypothesize that not only are they not very skilled, but that they are probably the sort that are not at all familiar with gun culture in their private lives.

Consequently, S_blaster is a number assigned to measure the individual’s relative experience wth guns, whereby a value of 1.0 represents full disconnect from the use of guns in their personal lives, and a number closer to zero represents an individual who is very familiar with gun culture.

Of course, perhaps the most important tangible characteristic (that could translate to a positive casting decision) is relative fandom itself. In other words, casting may be partly governed by how “into Star Wars” an individual is. Here, and in honor of Chewbacca’s reference of “pulling arms out of their sockets when they lose,” I’ve decided to use Wookie knowledge, or W_k as an indicator that can further increase casting chances. Essentially, this is a scale that ranges from 1 to 10, whereby 10 represents fanatical knowledge on all things Wookie, and 1 represents no knowledge at all. In effect, if you’re nuts about Star Wars (and wookies specifically), you can increase your chances of being cast by 10 fold.

In conclusion, I want to stress that this is the Abrams’ Stormtrooper Axiom, and by its very definition, an axiom is just a starting point. This means the equation will need more work, and it would be great suggestions to make it better. As it stands, it works as a general guideline using a number of test values². As well, there is also the very real caveat of whether J.J. Abrams will even have stormtroopers in the new movies – never mind the fact that if he does, they may come in a different size, or be better at shooting, etc. In some respects, this reminds me a little of Schrödinger’s cat (we can call our version Abrams’ Stormtrooper): we won’t really know what he has in mind until he lets us open the box.

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Footnotes

1. In general, I’ve used information from the original trilogy for points of reference.

2. For instance, an individual with no connection at all will result in a number that works against the backdrop of the total human population numbers. For J.J. Abrams, himself, where b^o_p and b^o_w are equal to zero, and his W_k is likely quite high, the equation would further calculate that he has practically perfect odds of being cast as a stormtrooper (which makes sense given his role in the movie). For the sake of comparison, I’ve calculated my own odds to be approximately: 0.00000519 or about one in 19,000.

Think about what you ate for breakfast this morning. You might have had some fruit or protein, but you most likely ingested wheat. This is a probable assumption because wheat is the most widely consumed food group in the North American diet [1]. Common wheat-based breakfast foods such as pastries, bagels, granola bars, pancakes, cereal, muffins, and oats all contain flours or starches prepared with wheat, rye and barley grains [1]. When flours are mixed with water, the wheat proteins create a 3D network giving dough elastic and viscous properties that food-processing companies have chemically manipulated to formulate better quality foods [2]. Due to ease of industrial production of wheat flour and high availability, these companies have taken advantage of the main structural protein of wheat and utilized it as an ingredient for many other food items that do not have a dough base. Thus, even if you consciously did not eat wheat for breakfast you might have ingested wheat in other non-dough foods, such as dry roasted nuts, baked beans, processed meats and poultry, icings and frostings, chocolate, or seasonings and sauces1. So what is this highly valued wheat protein by the food industry and why should we care about it?

Gluten is the main structural protein in wheat and other grains. It is composed of two types of similar proteins called gliadins and glutenins [2]. Glutenins are simple proteins that can be easily broken down with secretions from the stomach, pancreas and small intestine. However, gliadins are bulkier and resistant to acidic secretions in the stomach. Enzymes further down in the digestive tract cannot chew them up, so they remain insoluble and stick to the small intestinal tube. Gliadins are formed from crossbreeding wheat plants and genetically modifying them for high production at harvest (i.e. altering wheat DNA to select genes that are resistant to harsh weather, fertilizer absorption and pesticide damage) [2]. With farmers creating these new hybrid wheat plants, they also created variant gluten proteins that some individuals’ bodies can have reactions to. For most of the population these proteins aren’t harmful and they eventually are scraped out of your body with mucus and other digested food, but for about 1% of the population these proteins are toxic [3]. For these people, gluten ingestion can present harmful effects in different organs with varying degrees of severity. For example, one individual may develop a painful skin rash and complain of intestinal discomfort, whereas another may suffer an anaphylactic attack and have troubles breathing after eating gluten. Due to the wide variability of symptoms wheat proteins can cause, gluten disorders are difficult to diagnose until the patient adjusts to a gluten-free diet and symptoms subside or disappear completely [2]. For this individual, they must abstain from ingesting food, beverages or medication that contain wheat, barley, rye and or oats for the rest of their life [1].

With high global consumption of gluten-laced food products more individuals are identifying illnesses that were originally diagnosed by a neurologist, psychologist, dermatologist or nutritionist to be symptoms caused by an underlying gluten disorder. Gastroenterologists are urging more patients to switch to a stringent gluten-free diet, and with this lifestyle change more health complications of gliadin toxicity are being uncovered. From statistics generated by clinician reports and confirmation obtained with the aid of laboratory research, there are 3 main forms of gluten-related disorders. This spectrum of gluten reactions entails celiac disease, wheat allergy and gluten sensitivity, and each evoke differential adverse reactions in the body’s immune system. In order to properly diagnose patients, clinicians need to be educated in what symptoms to recognize and how the existing forms of gluten-disorders are classified. Similarly, for clinicians to treat their patients and give adequate advice on managing the illness they must understand how gluten affects the body at a molecular biology level.

The most well-known and severe reaction to gluten exposure is celiac disease. It is a condition that results in damage to the lining of the small intestine and prevents nutrients from being absorbed into the blood stream. This damage is caused by accumulated gliadins that attach permanently to cells and disrupt their shape, which impairs their function of absorbing nutrients. The unhealthy intestinal cells eventually die and an inflammatory response is signaled from the gut to recruit a type of white blood cells, called lymphocytes, to destroy the gliadin protein and help stimulate growth of healthy intestinal cells. However, celiac disease is an autoimmune disease, which means the white blood cells are misdirected and attack healthy tissue that is mistakenly marked for destruction. These ‘search and destroy’ signals are specific to attack gliadin proteins and circulate in the blood to their final destination at the intestine, but sometimes they adhere to healthy tissues on the ride there. These signals, which take anywhere from weeks up to years to develop, can be concentrated at the intestinal tissue or migrate to other organs, such as the skin, joints, brain and heart [4]. This is problematic because these organs become infiltrated with lymphocytes when they aren’t supposed to and health complications result. Thus, not all celiac patients have the same symptoms (depending on where the signals migrate) and gluten affects each individual differently.

Classically, susceptible individuals suffer from gastrointestinal symptoms such as extreme abdominal pain, bloating, chronic diarrhea, weight loss, nausea, vomiting, and lactose intolerance [4]. Though from the immune system responding to inflammatory signals in organs away from the intestinal source, extra-intestinal symptoms can result from gluten exposure. These can include depression, fatigue, headaches, blistering skin rashes (called dermatitis herpetiformis), poor coordination (muscle spasms), seizures, joint pain, stunted growth and iron deficient anemia4. Due to damaged intestinal lining and malabsorption of vitamins, celiac individuals can become highly deficient in folic acid, vitamin B₁₂, iron, calcium and vitamin D, which can attribute to the severity of the disease [5]. Celiac disease cannot be cured, but with compliance of a diet excluding gluten-containing food items recommended by a dietician, these symptoms can improve dramatically.

Celiac disease is most common in people of European origin and can be triggered by either environmental factors or genetics [6]. With genetic testing, doctors have found that individuals with the genes HLA-DQ2 and HLA-DQ8 are predisposed to develop an autoimmune reaction to gluten7. These genes produce DQ2 and DQ8, which are the ‘search and destroy’ signals that bind to gluten. However, presence of DQ2 and DQ3 isn’t the only factor for celiac disease and doctors are able to test patients’ blood for an increase in an antibody that recognizes an enzyme normally found in the intestinal cells, called transglutaminase [6]. Regardless of the detection method, celiac disease is becoming more prevalent and if its symptoms are not identified early in life then it can progress to severe gastrointestinal damage and, in rare cases, lymphoma (blood cancer) and infertility [6].

Another condition that stimulates an immune response in the body to gluten exposure, yet does not present with intestinal damage is classified as wheat allergy. It is less harmful than celiac disease because it involves your body responding to gluten as an allergic reaction, rather than an attack of healthy tissue by an autoimmune reaction. Allergic reactions are a buildup of a subpopulation of white blood cells to the skin or mucus area when a foreign allergen, or in this case gluten, comes in contact with it. These white blood cells are called basophils and they secrete chemical messengers called histamines, which signal your body to produce defense mechanisms such as mucus, tears, pain and inflammation. These ‘protection strategies’ are carried out because your body suspects that gluten is attacking it. Depending on the route of exposure to gluten, an allergic reaction to wheat can affect the skin, gastrointestinal tract or respiratory tract. Also, the intensity of the allergic reaction can vary with the type of gluten food product, for example eating cereal could produce a small rash, but eating toast results in hives.

The most common wheat allergies include baker’s asthma through inhalation, contact urticaria through skin contact and wheat-dependent, exercise-induced anaphylaxis through ingestion [6]. Baker’s asthma is usually developed in work environments that contain cereal flour and dusts that are inhaled and result in difficulty breathing, irritation and inflammation of the nose (rhinitis), chest tightness, coughing and wheezing [8]. Contact urticaria is an immediate skin rash with swelling, redness, itchiness or pain with direct contact of gluten food products to skin. These two allergies present with minimal health complications, however wheat-dependent, exercise-induced anaphylaxis can be deadly without diagnosis and EpiPen (emergency injectable epinephrine) administration upon attack. Individuals with this condition can experience an anaphylactic attack upon physical activity within hours after ingesting food without consciously being aware of a gluten ingredient. This attack includes symptoms of nausea, vomiting, respiratory distress, choking and hives [8].

Despite various routes of exposure and symptoms, wheat allergic reactions are all stimulated minutes to hours after gluten exposure and can be prevented through avoidance of gluten [6]. Its prevalence is found to be approximately 0.4% in the United States and about 0.5% in two population-based studies from the UK and one from Germany conducted over the last decade (2000-2010) [6]. Although wheat allergies are not strongly associated with certain genes, they are found to be heritable, which means other family members experience similar symptoms after gluten exposure. Family members can be diagnosed for gluten allergy by skin prick tests, where an area on the body is scratched and drops of purified wheat protein are tested, or by blood tests for antibodies that bind to the gliadin protein. Subsequently, these tests are followed by a dermatological or oral food challenge for symptom recurrence and final diagnosis of wheat allergy. Though having a wheat allergy is usually not life threatening, it is important to diagnose those individuals early in life who are afflicted by anaphylactic attacks upon ingestion of gluten.

On the other side of the gluten disorder spectrum is a condition that is gaining popularity through fad diets with scientific research proof to support its existence, called “nonceliac gluten sensitivity”. These individuals are gluten-reactive and experience adverse symptoms and distress within hours to days after gluten ingestion [6]. Symptoms can include intestinal irritation and abdominal pain, but they are mostly extraintestinal involving leg or arm numbness, depression, iron deficiency anemia, ‘foggy mind’, joint or muscle pain, headache, eczema, fatigue, and painful or itchy skin rashes [3]. Gluten sensitive patients report having similar, yet less severe, symptoms of celiac disease though the reaction is found by doctors to be neither autoimmune nor allergic. Diagnostic tests reveal that their small intestines are normal and healthy on endoscopic pictures (a long, flexible camera that looks at intestinal tissue) and they have no classical antibodies that recognize gluten proteins in their blood [6]. The diagnosis is usually made through elimination of other allergic and autoimmune mechanisms, since there are no detectable markers in the blood specific for gluten sensitivity. However, research has shown that gluten sensitivity elicits a slight immune reaction in the body with mild increase in white blood cells at the small intestinal lining and with gluten withdrawal the symptoms diminish or disappear [2]. From this information, doctors and patients should be wary that gluten can cause behavioural and psychological effects and that diagnosis of gluten sensitivity cannot be confirmed with classical immune markers for other well-studied gluten disorders.

Though the gluten-free diet has been shown to benefit individuals with gluten-related disorders, there is no evidence-based research to support that following a gluten-free diet in the general population is healthier or promotes weight loss [9]. In fact, more scientific research is available that demonstrates the positive health benefits of ingesting gluten and on the potential drawbacks in unnecessarily adopting a gluten-free diet. Not only do gluten-free baked goods contain higher fat content and total energy than their gluten-containing counterparts [10], but gluten-free items are deficient in whole grains and fiber, which have both been shown to be associated with improved body mass index (BMI) status [11]. In other words, a person is more likely better off eating a whole-grain wheat breakfast cereal than snacking on a bag of gluten-free pretzels, since the latter is actually helping you put on weight. Furthermore, in one study that monitored ten individuals (who had no medical need to avoid eating gluten) eating certified gluten-free foods in place of all grain products for one month, it was shown that their healthy, beneficial gut bacteria was significantly depleted [12]. This appeared to be due to wheat products having natural starches called fructans. These starches stimulate the growth of healthy bacteria in your gut and help your body stay healthy – a high composition of good bacteria in your colon is important to protect the gut from inflammatory diseases and cancer, and the body from heart disease.

This fad and lack of gluten in a healthy individual’s diets has received criticism from the scientific community, given that there are currently no statistics to support that gluten is the direct cause in weight gain and that it is unhealthy for the body. Indeed, the only justification the general public has for going gluten-free is that in doing so, they may reap the benefits of a general lifestyle change. In other words, the effect of reducing gluten items is most likely due to an improvement in people’s awareness in food choices and adopting a more well-balanced diet with more legumes, vegetables and protein in replacement of meals loaded with starches and including little to no vegetables. All in all, this speaks to the importance of proper diagnosis and education, so that gluten sensitive individuals can be properly treated, whilst the rest of the general public can be made aware of the facts pertaining to adopting a gluten-free diet.

With the U.S. market for gluten-free food products soaring to $4.2 billion in retail sales in 2012 and the increased number of patients describing symptoms related to gluten exposure, it is imperative that doctors and patients become knowledgeable of all conditions that exist under the gluten-disorder umbrella and how each illness affects the body’s immune system [13,6]. Since symptoms of gluten disorders can be misdiagnosed for other illnesses years before a gastroenterologist is referred, North Americans should become informed about the complications that can result with prolonged exposure to gluten and inquire if they have a family history of gluten-disorders. Conversely, people with gluten sensitivity that are planning to adjust or are already compliant with eating a gluten-free diet should contact a dietician to ensure their body is obtaining the nutritional quality it needs to stay healthy. Research towards furthering the understanding of gluten-disorders and how the human body’s immune system reacts to specific wheat proteins is ongoing. Scientists are developing medication that helps break down gliadin for celiac patients, characterizing the biochemical pathway in wheat-dependent, exercise-induced anaphylaxis, and determining an immune system profile to identify earlier diagnosis of gluten sensitivity. These scientific advances will help doctors increase awareness, provide effective treatment and ameliorate the quality of life of those affected by a gluten disorder.

References

1. Case S. The gluten-free diet: how to provide effective education and resources. Am Gastroenterol Assoc. 2005; 128(suppl): S128-S134.

2. Volta U & De Giorgio R. New understanding of gluten sensitivity. Nat Rev Gastroenterol Hepatol. 2012; Advance Online Publication: doi:10.1038/nrgastro.2012.15.

3. Sanders DS, Patel D, Stephenson TJ, et al. A primary care cross-sectional study of undiagnosed adult celiac disease. Eur J Gastroenterol Hepatol 2003; 15: 407-413.

4. Ryan M & Grossman S. Celiac disease: Implications for patient management. Gastroenterol Nursing. 2011; 34: 225-228.

5. Hadjivassilou M, Sanders DS, Grünewald RA, et al. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010; 9: 318-330.

6. Sapone A, Bai JC, Ciacci C, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Medicine. 2012; 10: 13.

7. Drago S, El Asmar R, Di Pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scandinavian J of Gastroenterol. 2006; 41: 408-419.

8. Tatham AS & Shewry PR. Allergens in wheat and related cereals. Clin Exp Allergy. 2008; 38: 1712-1726.

9. Gaesser GA & Siddhartha SA. Gluten-free diet: Imprudent dietary advice for the general population? J Acad Nutr Diet. 2012; 112: 1330-1333.

10.  Niewinski MM. Advances in celiac disease and gluten-free diet. J Am Diet Assoc. 2008; 108: 661-672.

11.  Gaesser GA. Carbohydrate quantity and quality in relation to body mass index. J Am Diet Assoc. 2007; 107: 1768-1780.

12.  De Palma G, Nadal I, Collado MC & Sanz Y. Effects of a gluten-free diet on gut microbiota and immune function in healthy adult human subjects. Br J Nutr. 2009; 102: 1154-1160.

13.  Packaged Facts. Gluten-free Foods and Beverages in the U.S., 4^th ed. Rockville, MD: Packaged Facts. October 2012. MarketResearch.com Academic (accessed March 7, 2013).

I have to admit, it was difficult at first. You think otherwise? Try balancing on a particle that has a surface area less than a mote of dust! With a few steps, though, I found the best photons—deep sumptuously violet-colored—in which to support my weight. My legs, having long been atrophied from only walking on the rather pedestrian terra firma, needed a little stretch, and a short jaunt to the upper atmosphere only a handful of kilometers away seemed apropos.

Simultaneously, Earth’s curvature manifested as the shadow of night marched across its surface. I dipped my hand into a stream of orbiting junk and snatched out a wayward screw: small and pristine, with slowly meandering threads. There is no rust in space.

This time of year so near periapsis is perfect for walking on light. I prayed to Michelson and Morley to conjure me a cane from the aether, a nice sturdy knotted one with a worn handle speaking silently of past adventures. Of course the old codgers refused. Still bitter about your failed experiment, gentlemen? As the Earth occulted the sun leaving only the fiery corona to pave my way, I struggled to keep my footing. But, some how, some way, I kept upright by some philanthropic object. Who could it be? I scanned the heavens. What—? Is that…? Orion’s Nebula! Thy haziness doth suporteth my path! Capital! To think: for hundreds of thousands of years, humans have looked at this dot and thought it to be just another star. The arrogance. Serendipitously, the first Übermensch raised His fancy polished glass and—what do you know!—it’s a big splotch of fiery gas, dust, and infant stars.

I passed by Beteigeuze and doffed my proverbial cap. Now this is a star, my friends! Bloated and boiling! Our star is but an ant, an aphid! Orion’s Nebula eventually expanded so large as to fill my field of vision. Plenty of paintings have been inspired by this tepid dust cloud, and I can safely say they got the colors all wrong; too heavy on the fuchsia, or magenta. I recognized the Horsehead by the breed, and maneuvered myself such that if any learn’d astronomer were to point their engorged tubes this way they would see a man straddling a horsey, hand raised in mid-gallop, face contorted in a yokel grin.

Having had my fill of this particularly average universe formation, I set out on a random walk, strolling across gamma rays towards whatever piqued my fancy. I passed through super-heated clouds of electrons and giggled as the nanoest of amps tickled my feet. I crawled inside the core of a neutron star and played marbles with free quarks, keeping in mind to collect three for Muster [sic] Mark. I stumbled across two merging galaxies, frozen in a chaotic dance which had torn apart their bodies but left their cells intact. A wayward chunk of Dark Matter lent itself as an ideal chair as I waited for the galaxies to make a pretty picture. They never did, not even a bunny rabbit, even after a hundred thousand years of melancholic observation.

There was little left to see in this universe. Dark Energy turned out to be a simple misunderstanding. Really, just a mistaken sign somewhere. I’ll explain later. For a bit, the jet of a blazar propelled me towards The Great Void, but eventually the friction from lonely hydrogen slowed me to a stop. There I rotated, watching as the Great Black “Nothing” orbited me. Sure, fine, I’ll walk towards it and try to find this fabled Supermassive Black Hole with its postmodernist properties.

On exactly my thirty-third step, a photon beneath my left foot gave way and I tumbled downward. Despite my lightning-fast reflexes, the radio photon I nabbed—a regrettably redshifted A note from some ancient and forgotten civilization—was not enough to support my weight. I fell. My flailing arms and legs eventually quit from exhaustion, and my voice had no medium in which to send out vibrations. As the lights of even the closest galaxies blinked out, I resigned myself to an eternity of meditation towards the single-minded task of converting mass to energy. Only then would I be rid of this cursed existence.

I struck something and heard my back snap. Several decades passed as I rolled like a terrapin trying to right myself. During my frequent breaks of frustration I ran my hand over the surface below me: smooth, not chaotic like the other photons. I tried to push through the surface but found it rigid. When I righted myself and popped two vertebrae back into position, I explored a shell of colored light, stretching off to the horizon of four dimensional space.

Only when placing my eye yoctometers away from the shell did I notice a variance in the color: mostly blue and green, with a few scant islands of yellow and red. My silly Earth-centered culture resurged when I found a huge patch of blue in the shape of South America.

The sight, feel—and, why not be literary, smell!—of the shell pleased this universe-wise and weary traveler. Its gentle caress and cool temperature soothed the knowledge that I would never breach it. None of my species would. The aggregate of the joy and suffering felt beyond the wall, the thousands of confident religions, ideologies, and—oh—of course I would forget the rest of the damned quote now!

It was then I decided to take a nap. I lay back against the shell and caressed it lightly with my fingertips, trying to differentiate between the colors as I lulled to sleep.

Authors: Jean-Pierre Marielle III & Justin Case | pdf version

In this study we present the preliminary finding of what could be the first record in history of hybridization between mammalian Orders (Perissodactyla and Cetacea). Phylogenetic analyses from the unicorn (Equus unicornus) mitochondrial genes (protein-coding Cytochrome b, Cytb) show a matriline belonging to the Narwhal (Monodon monceros) while nuclear (V-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog, Kit) clearly show a sister relationship of the unicorn-pegasus (Equus alatus) clade with the rest of the Perissodactyl family Equidae. Our preliminary study strongly suggests the need for further investigation because this finding could completely revolutionise our understanding of the processes of hybridization in mammals.

Introduction

The unicorn (Equus unicornus J.P. Marielle I) is a charismatic and iconic species of the Equidae (Peryssodactyla, Mammalia), forming with its sister species pegasus (Equus alatus S. Barrett) a clade sister to the wild horse and the donkey (Yule et al. 2001). This mysterious Equid is notoriously hard to study, and has been recorded sporadically appearing on all continents. The only known stable populations are recorded in the Arctic circle, Antarctica and the remote island of Tristan da Cunha (Klaus et al.  1993). Unicorns are one of the highest ranking endangered species alongside the Giant Panda (Ailuropoda melanoleuca David) and the Albino Alligator of the NYC sewers (Crocodilus newyorkensis H.G. Rogers), therefore recent studies have concentrated on its habitat, and how it might be affected by global climate warming (IUCN 2012). Future conservation strategies would greatly benefit from a deeper understanding of the evolutionary history of this species.

Today, as far as it is known, this species is threatened mostly by illegal poaching, historically the populations were decimated in Victorian times by the trend of collection of the natural world because of the alleged magical properties of its blood, and the ivory of the horn. This beast has been reduced to sparse populations, hardly spotted in the wild anymore and shrinking (Gold et al. 1991).

This species has been listed as a species of concern by the IUCN because of their low population numbers. The changing of global climate weather patterns is also considered a threat to unicorns because of their well studied and long documented association with rainbows, the occurrence of which will be compromised with shifting precipitation patterns (Ackbar et al. 2006).

The physiology of E. unicornus has always been an enigma mostly due to its chimeric appearance, as it is a mystery in its sister species E. alatus. Evolutionary theory always struggled with the apparent physical adaptations of this clade in the Equidae, so far that for some time the clade was called Chimerae (Mashruk 1972). In the middle of the 20^th century there were some speculative studies suggesting the hybrid nature of these animals, however the evidence was never taken seriously and the data were weak. In the 1990s some study suggested the possibility of horizontal gene transfer through virus, however, these data were dismissed as far-fetched fantasies, recurring to a “near-religious illusion on systems science does not yet understand”, the harsh critique of the theory led to a fierce battle over the subject which continued for about a decade (Bond & Penny 2000).

Hybridization is widely known from the plant kingdom (Rieseberg & Carney 1998) and horizontal gene transfer has been repeatedly reported in prokaryotes (Jain et al. 1999). However, these forms of genetic exchange have never been prevalent (or even recorded in the case of horizontal gene transfer) in the Mammalia and never been recorded at such an evolutionary distance between organisms (Equidae and Cetacea).

Here are presented the incongruent results from two phylogenies built with mitochondrial and nuclear genes of E. unicornus showing relatedness to two different orders of the Mammalia.

Materials and Methods

Sampling

We examined a total of 7 E. unicornus from different populations: 3 from the Arctic, 3 from Antarctica and 2 samples from Tristan da Cunha. The rest of the sequence material used was downloaded from the GenBank website (samples are summarised in Table 1).

DNA extraction, sequencing, and mitochondrial and nuclear markers

We amplified sequences of two genes from exonic and intronic regions, one mitochondrial gene [Cytochrome b, Cytb (1140 bp)] and one nuclear gene [V-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog, Kit (273 bp; 1215 bp)] (Steiner & Ryder 2011). New sequences were submitted to GenBank (accession numbers in S1). PCRs were performed in a 20µL volume using Eppendorf Mastercycler Gradient thermal cyclers. Each reaction included 30ng of template DNA, 10µL of Taq buffer with 1.5 mM MgCl₂ (Applied Biosystems), 0.3 µL of 10 mM deoxynucleoside triphosphates, 0.6 µL 1M of each primer, and 0.15 units AmpliTaq DNA polymerase (Applied Biosystems). PCR forward and reverse primers were designed in conserved exonic regions by using alignments of samples of Scrotifera mammalian sequences.

Sequences were assembled and edited using Sequencher 3.1.1 (Gene Codes, Ann Arbor, MI) software and then compared with GenBank using BLAST. Alignment was achieved using MAFFT (Katoh et al. 2002) and manual editing. Phylogenetic analyses were carried out using PAUP (Swofford 2003) and RaxML (Stamatakis 2006).

Phylogenetic analysis

Likelihood analysis: ModelTest 3.7 (Posada and Crandall 1998) selected a TIM + I + G model using Akaike weights, which we approximated in RAxML 7.0.4 (Stamatakis et al. 2005) with the GTRGAMMAI model of evolution. We ran the RAxML 7.0.4 likelihood analysis with 200 search replicates and 460 bootstrap replicates.

Results

While the alignment of the nuclear genes did not show any problem, the alignment of the mitochondrial sequences proved to be difficult, if not impossible. A blast search of the sequences showed the samples of E. unicornus to belong to Monodon monoceros. The sample was thought to be contaminated, however unlikely, by narwhal DNA, and therefore the extraction was performed several times, producing each time the same sequence as result. This was beyond unexpected.

Two trees were produced with Maximum likelihood and sampling across the Scrotifera was carried out. The comparison between the alignments and phylogenetic analyses show a clear incoherence. Without the shadow of a doubt, the conflicting phylogenies between nuclear (Fig. 1) and mitochondrial (Fig. 2) genes suggest the acquisition of the mitochondrial gene possibly through the process of hybridization.

Discussion

Hybridisation

Hybridisation of closely related species has happened in several mammalian lineages; the black bear and the polar bear have shown hybridisaiton (Edwards et al. 2011; Miller et al. 2012), the Equidae themselves show several instances of hybridisation histories (Steiner & Ryder 2011). This is the first time that a hybridisation between species so far apart evolutionarily has been recorded. This finding needs to be confirmed by further research involving other genes and regions and including samples, that were unavailable for this study, for mitochondrial gene sequences from E. alatus.

Unfortunately the lack of a fossil record prevents us from investigating the evolutionary age of these hybridisation episodes any further than speculation. The application of a molecular clock could be a very rough estimate. The lack of fossil record and the limited access to samples and populations also limit the possibility of investigating if this is a single episode or hybridisation has occurred more than once.

Physiological considerations

When Marielle first described E. unicornus he was fascinated by the appearance of the horn and immediately made the connection with M. monoceratus. He was able to investigate the nature of the horn, from the carcass he was basing the his description on: the first record of a unicorn (aside from visual representations). When describing the attachment of the horn he stressed his uncertainty on where the horn was developing from, in fact, he could see a ridge of hardened bone along the nose. Now we know from observing the extant colonies that the horn is a tooth, which grows along the nose and at the height of the eyes changes orientation in development and at puberty will protrude from the animal’s forehead (Rudolf & Noel 2002). What seems to be puzzling at first is that only male narwhals will develop the horn, in the case of unicorns this will not occur; furthermore, considering the hypothesis of the matriline belonging to the narwhal, the sex chromosome Y would not be passed to the unicorn in this hybridisation event. One possible explanation would be that in the narwhal it is the chromosome X carrying the gene to code for the horn phenotype and it activated by the Y chromosome, while in the unicorn it is activated in both sexes.

It seems that if the E. alatus rose as a species in the same way as E. unicornus, then the nature of the wings would resemble that of the species that hybridised with the ancestor. In the 1970s Zev Mashruk, a prominent and active mammalian physiologist, published on the resemblance between the wings of the pegasus and the pelican (Mashruk 1973). This account was however dismissed due to his notorious and vastly self-advertised, extensive use of psychoactive drugs. Mashruk’s theory, so ridiculed, could be re-evaluated in the light of these new findings.

Conclusion

Further work is strongly suggested because of the highly significant implications of the finding: never it has been recorded such exchange of genetic material between such evolutionarily distant taxa.

Further research should include work on E. alatus as well as E. unicornus, addressing the question regarding the nature of this clade, specifically if this particular lineage is especially prone to this new type of hybridisation.

Acknowledgements

We would like to thank the Rainbow Foundation, Santa’s Workshop, Foxy Luddite Co-op for financial support. Thanks also to the Buddha, Old Ben Kenobi and our anonymous editor for helpful feedback on the manuscript. If you haven’t figured it out already, this paper is not real.  Courtesy of Anna Bazzicalupo

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In order to better understand the sophisticated reproduction of orchids, let us begin with a quick run-down of the basic mechanisms. Flowers are the reproductive parts of angiosperms (a.k.a flowering plants). Their reproduction cycle begins when a pollen grain produced by the anther (male organ) comes into contact with the stigma (female organ) of the same flower species. This transfer of pollen from male to female parts is called pollination. Fertilization occurs when sperm formed in pollen grains unite with the female ovule, developing into the seed and fruit. Most angiosperms have both male and female reproductive organs, meaning that they can self-pollinate and self-fertilize (a.k.a selfing). The main benefit of “selfers” is that they are guaranteed to find a mate (themselves!). On the downside, offspring inherit their parent’s exact genome, including any mutations that are present. This lack of genetic diversity and the potential accumulation of damaging mutations over time, reduce a plant’s “genetic arsenal” for adapting to changes in its environment – orchids resort to this strategy only in pollinator-poor communities (Roberts & Dixon 2008). It is thus not surprising that many angiosperms have evolved intricate mechanisms to avoid selfing and instead promote cross-pollination with other individuals of their kind. Vectors for pollen transfer include wind and water (abiotic), as well as animals and insects (biotic).

Angiosperms are attached to a substrate and unable to move freely, but many of the species that rely on biotic vectors have effectively gained mobility by manipulating the behavior of their pollinator – they “borrow” their wings, legs, or abdomens to transfer pollen. Pollination is not a deliberate event, but rather occurs by chance as insects reap the rewards offered by the flower, which may include nectar, pollen, fragrant compounds, and shelter. Orchids in particular, have developed exquisite pollination syndromes through their coevolution with their pollinators. By coevolution I mean that each party has helped shaped the other over time, resulting in both becoming increasingly specialized. Flowers can evolve features to attract, guide, and orient pollinators for efficient pollen transfer (pollen is energetically expensive to make!) Pollinator behavior and appearance can evolve to “fit” into the flowers they visit, as is beautifully shown by the Malagasy orchid Angraecum sesquipedale. The petals of Angraecum flowers are fused at the base, forming a slightly curved floral tube that can be over 40 cm long and is filled with nectar at the very bottom. Having seen only the flowers, Darwin predicted that giant moths with long tongues pollinated this plant; moths fitting Darwin’s description were in fact discovered four decades later (Rodriguez-Girones & Santamaria 2007; Nillson et al. 1985).

To understand how this all came to be, we have to think about Darwin’s theory of natural selection. Individuals that make up a population vary in the traits they possess. Some of these traits, such as size and shape, are heritable and affect an individual’s ability to survive and reproduce. Individuals with traits that are particularly well suited to an environment are more likely to survive and reproduce; natural selection occurs when individuals with certain traits produce more offspring than individuals without these traits. The frequency of “selected” traits thus increases from one generation to the next and leads to evolution – a change in the heritable characteristics of a population over time. In the case of Angraecum, deep floral tubes select for moths with the longest tongues as only they can access nectar situated deep in the floral tube, leaving individuals with shorter tongues at the disadvantage of having to look for an alternative food source or perish. At the same time, long tongues select for the deepest floral tubes because these flowers can achieve higher fertilization rates, making them more prevalent in the population than flowers with shorter tubes. Long floral tubes force moths to insert the entire length of their tongues in order to reach the nectar; the moth’s thrusting increases friction and its withdrawal after consuming all the nectar triggers a mechanism that attaches two sticky pollen clumps to the base of its tongue. Selfing is prevented as moths carrying pollen (attached only after tongue withdrawal) continue their search for nectar by moving on to a different flower in which they inadvertently deposit the pollen. (Nillson et al. 1985). As you can see, an evolutionary “arms race” between the floral tube and the moth’s tongue has resulted in the lengthening of the two organs over time as well as reducing the likelihood of self-pollination (Roberts & Dixon 2008).

One third of all orchids have evolved features that are perceived as rewards by pollinators, but do not end up materializing (Roberts & Dixon 2008). Species from the Mediterranean group Ophrys use sexual deceit to achieve pollination by tricking the males of a specific type of bee (Schiestl et al. 1999). To the surprise and awe of countless naturalists, Ophrys flowers remarkably mimic the appearance of receptive female bees. In the species O. speculum, the flower’s top petal (called labellum) is enlarged and appears swollen; it is dark purple and has red bristles along its edges. During development, the stalk of the flower twists 180º so that the labellum ends up at the bottom, giving it the appearance of a female bee’s abdomen with its wings at rest. As if impersonation was not enough, Ophrys flowers emit an odour that is almost identical to that of the sex pheromone of mature female bees. These visual and olfactory floral cues prove irresistible to male bees and trigger “pseudocopulation”, whereby the bee mounts the flower in a very specific position, causing it to rub up against the anther which attaches two sticky clumps of pollen to the bee’s bum. Pseudocopulation elicits sexual behaviors in males but does not cause them to ejaculate. The quick habituation of males moderates their response to previously visited flowers, whereas flowers on other plants remain highly attractive to them due to subtle differences in appearance and odour. Once a male realizes that a flower is not good enough for him, it is already carrying the pollen that it will unknowingly deposit in the next flower it visits as his search for love continues (Nilsson 1992). Thus, this finely-tuned mechanism does an excellent job of promoting cross-pollination between different flowers of the same species.

The chemical compounds used for odour mimicry in Ophrys orchids initially had the sole purpose of contributing to the formation of a waxy leaf layer that prevents water loss. Genetic mutations causing changes to the relative proportions of these compounds occasionally resulted in the production of an odour blend that resembled that of the sex pheromone of a pollinator species. This would have led to an excited male bee pollinating the mutant plant. Over time, the process of natural selection favoured plants with the mutant odour trait as they likely attracted more pollinators –albeit by chance– than non-mutants (Schiestl et al. 1999). The same argument could be extended to explain how inadvertently, pollinators fueled the natural selection of mutant orchids displaying traits for visual and odour mimicry. Yet another factor driving the evolution of sexual deception in Orphys is that mutants could reduce the production of energetically costly attractants and rewards for pollinators. This gave them a reproductive advantage over non-mutants by allowing them to reallocate valuable resources to improve their vigor as well as that of their offspring (Schiestl et al. 1999).

Orchids in the Coryanthes group (a.k.a. bucket orchids) also rely on a suite of traits to obtain pollination from a specific group of male bees. Coryanthes species are epiphytic (they grow on top of other plants) and their fragrant flowers are some of the most complex among the orchids (Gerlach & Schill 1989). I will use the species C. speciosa to illustrate this. Male bees are attracted to the floral fragrance emitted by floral glands. The bee pokes around in search of the source of the smell, which causes fluid secreted by glands right above the bee’s head to dislodge. The drop of fluid washes the bee down to a petal that is shaped like a bucket and filled with gooey liquid. The only way out of this trap is a tube-like petal which forces the bee to rub against the anther. By the time the pollinator emerges with pollen stuck to its back, the flower is no longer emitting a fragrance and the bee flies away, effectively preventing the same bee from returning and self-pollinating the plant. Fragrance production is resumed the following day, in an attempt to attract a pollen-carrying male that will fall into the trap but this time when it escapes it will deposit pollen on the stigma, fertilizing the plant (Baker 1963; Gerlack & Schill 1989).

The population density of epiphytic orchids is usually quite low, so highly specialized pollination systems are essential for effective cross-pollination between individuals (Gravendeel et al. 2004). Research comparing the reproduction of orchids offering nectar rewards with orchids offering fragrance rewards shows that the former are more successful. Without the genetic capacity to produce nectar, Coryanthes rely solely on their flowers and fragrance. The Coryanthes flowers that happen to inherit the most attractive fragrances and complex flowers will have the highest pollinator visitation frequency and fertilization rates, which over time will increase the number of individuals in the population displaying these traits. Through natural selection, Coryanthes have evolved to become the nectar-less tropical orchids with the highest reproductive success (Neiland & Wilcock 1998).

It would be impossible to discuss all modes of orchid pollination in this short paper (entire books have been devoted to this topic!), so may aim was merely to illustrate just how diverse, intricate, and flat-out beautiful these mechanisms can be. The effect of natural selection on orchids is so powerful that sometimes I cannot help but think of them as organisms with personalities and the intelligence to manipulate those around them. Their intimate and specialized relationships with their pollinators are a remarkable example for the study of coevolution, but also raise issues about their conservation.      Just like Darwin asserted that the extinction of Angraecum orchids would be imminent should their long-tongued moth pollinators disappear, the same argument could be made for most orchids species as they rely on only one or very few types of pollinators (Micheneau et al. 2009). Mounting evidence showing a worldwide decline in pollinators, including those of orchids, shows how vulnerable to extinction these plants are (Zayed et al. 2004; Swarts & Dixon 2009; Vereecken et al. 2010). The economic importance of orchids in the horticultural trade poses yet another challenge for their conservation as collectors pay big bucks to acquire the rarest of specimens, creating incentives for illegal poaching even though many species are now protected under the Convention on International Trade in Endangered Species. Hopefully I have shown in this paper that the study of orchids can provide many insights into our understanding of how life on Earth was shaped by natural selection and evolution. For this reason, if not only for their intrinsic value, biologists should be thinking very seriously about the design and implementation of strategies for the conservation of this fascinating group of plants.

Cited Literature

An update of the Angiosperm Phylogeny Group classification for the orders and families of flowering plants: APG III. 2009. Bot. J. Linn. Soc. 161: 105-121.

Baker, H. G. 1963. Evolutionary Mechanisms in Pollination Biology. Science.  139:877-883

Darwin, C. 1892. The various contrivances by which orchids are fertilized by insects. 2^nd ed. rev. (1^st ed. 1862). New York: Appleton.

Freeman, S., M. Harrington, J. Sharp. 2011. Biological Science.

Gerlach, G. and R. Schill. 1989. Fragrance analyses, an aid to taxonomic relationships of the genus Coryanthes (Orchidaceae). Pl. Syst. Evol. 168: 159-165.

Gravendeel, B., A. Smithson, F. J. W. Slik, A. Schuiteman. 2004. Epiphytism and pollinator specialization: drivers for orchid diversity? Phil. Trans. R. Soc. Lond. B. 329: 1523-1535.

Micheneau, C., S. D. Johnson, M. F. Fay. 2009. Orchid pollination: from Darwin to present day. Bot. J. Linn. Soc. 161(1):1-19.

Neiland, M. R. M. and C. C. Wilcock. 1998. Fruit set, nectar reward, and parity in the Orchidaceae. Am. J. Bot. 85(12): 1657-1671.

Nillson, L. A., L. Jonsson, L. Rason, E. Randrianjohany. 1985. Monophily and pollination mechanisms in Angraecum arachnites Schltr. (Orchidaceae) in a guild of long-tongued hawk-moths (Sphingidae) in Madagascar. Biol. J. Linn. Soc. 26:1-19.

Nillson, L. A. 1992. Orchid pollination biology. Trends in ecology & evolution. 7(8):255-259

Roberts, D.L. and K.W. Dixon. 2008. Orchids. Current Biology 18(8): R325-R329.

Swarts, N. D. and K. W. Dixon. 2009. Terrestrial orchid conservation in the age of extinction. Ann. Bot. 104: 543-556.

Vereecken, N. J., A. Dafni, S. Cozzolino. 2010. Pollination syndromes in Mediterranean orchids – implications for speciation, taxonomy, and conservation. Bot. Rev. 76: 220-240.

Zayed, A., D. W. Roubik, L. Parker. 2004. Use of diploid male frequency data as an indicator of pollinator decline. Proceedings: Biological Sciences 271(3): S9-S12.

]]> http://www.scq.ubc.ca/tis-the-season-so-why-not-a-sciencegeek-advent-calendar-extravaganza/feed/ 0 http://www.scq.ubc.ca/a-moment-of-your-time-about-bill-c-398-and-how-canadians-can-contribute-to-global-health/ http://www.scq.ubc.ca/a-moment-of-your-time-about-bill-c-398-and-how-canadians-can-contribute-to-global-health/#comments Mon, 26 Nov 2012 19:22:35 +0000 David Ng http://www.scq.ubc.ca/?p=2871 Dear Canadians:

On wednesday, a very important piece of policy will be discussed in parliament.   It’s called Bill C-398 and it deserves our attention.  It seems that it has been challenging for some to see its merits, and so, I’d like to take moment to clarify what it’s all about.  It turns out that it’s not just important – the narrative is intriguing as well: it has a rich history of political intrigue; it is a story where viruses factor in prominently; it has a plot that involves armies of angry grandmothers; and above it all, learning about Bill C-398 can literally save lives.

Note, that the below piece is a re-edit of sorts, an update of a piece I wrote for Boing Boing that was an attempt to discuss that political intrigue.  And also note that there is some bias in my commentary – but I think this is natural.  There are obviously a variety of viewpoints involved and my own happens to disagree with those who choose to listen to corporate and political interests – more so when those interests rely on reasoning that is often spun a certain way to misrepresent useful facts. My bias happens to fall on the side of human dignity: something I think we should all spend a moment to contemplate, and something I think all Canadians would feel is a cause worth fighting for.

- – -

“Access to life-saving medicines is not a luxury, but a human right.”

~Canadian HIV/AIDS Legal Network

To me, the above statement is one of those things that sound like a no-brainer. Put another way, if I were to ask you whether you thought a person’s income should determine whether they live or die from something like HIV/AIDS, then I think you would see that the answer is nothing but obvious. But here I am, in Canada, writing this post, because there is a very real danger that members of my government think that this isn’t such an easy decision after all – that maybe wealth and business interests do matter when dealing with such ethical choices, and that there is a hierarchy where certain lives are worth more than others.

Let me backtrack a bit, and provide a little context. I’d rather not write a rant, emotional and heart wrenching as this discussion can be – I’d prefer to rely on reason, and not on rhetoric. Yes, rhetoric helps, but reason and validity are much more powerful.  I want everybody to understand why this is an important issue, one that deserves coverage, and one that deserves our involvement. More importantly, I want everybody to understand why the right thing to do is obvious.

To start, let me mention the letters and numbers that make up the label, “Bill C-398.” Keep them in your head – at least for a moment. If you’re the sort that prefers hearing at least a quick definition, then this one might work:

“Bill C-398 aims to reform CAMR and make it easier for Canada to export affordable, life-saving, generic medicines to developing countries.”

~Canadian HIV/AIDS Legal Network

If you’re thinking that this is a Canadian thing, then think again. Other rich countries are watching how Canada will behave. There’s always a few in Europe, and apparently even China is curious. In the U.S., the topic appears to be quenched, but the behaviour of the Canadian government could catalyze dialogue. And if you’re not from a rich country? Well, you might actually have lives that will be affected by it, millions of lives even.

Here’s the problem in a nutshell: the developing world is heavily burdened with a variety of diseases, many of which are causing massive numbers of suffering and deaths.

This is understandably big. It’s a huge global challenge, and there are many reasons for why it exists and why it is difficult to both comprehend and fix. However, the presence of effective medicines is not one of the reasons. There is medicine out there that can help, and there is also a flow (sometimes slow) of discoveries that make these medicines better and more effective. In the case of HIV/AIDS, there are drugs that essentially turn the disease from a death sentence to something that is chronic and manageable. I can’t overstate how significant that piece of information is: it tells us that people do not have to die from HIV/AIDS.

So what’s the issue?

The issue is control without regard for doing the right thing: This is essentially about patents. It’s not that patents are bad, but rather that patents can be bad. As you probably already know, patents are a service provided by government to protect an inventor, such that the inventor has an element of control over how their innovation/product gets used. This is generally a good thing, because ultimately it provides order to a process that would get very chaotic very quickly should the patent not exist. However, sometimes the inventor isn’t the best person to make decisions about control. Sometimes, the inventor doesn’t have the best information to take stock of a situation, or sometimes there might be a moral argument where monetary performance should not take precedent. In other words, sometimes, there are special circumstances where you could say it is reasonable that this control is tweaked.

To illustrate this, here are some hypothetical (and not so hypothetical examples):

1. Your country has experienced a massive storm, perhaps one named after a character in Grease, and it has hit the East coast very very hard.  Many folks are still without power and water, but there is technology that would be incredibly useful to mitigate this. However, your resources are already stretched and this technology is too expensive at the scale that is required in such an emergency.

2. Someone has declared war on your country. To defend yourself, you would like to utilize a particular product. Unfortunately, it is under a cost prohibitive patent and therefore out of reach.

3. There are markets where your life saving drug is not being sold because no-one can afford them anyway. However, the drug (which could be a matter of life and death for millions) could be made at a cost (i.e. a generic) that makes it accessible in these markets, but if and only if, the patent over them is adjusted.

Here is my point. In all of the above cases, you would like to live in a civil society where the government can step in and forcibly change the patent, because in every case, there is an element of morality involved. And guess what – governments can do this and they do! It’s called a “compulsory license,” and they exist for this very purpose.

In fact, even the WTO is on board with this idea. They recognize that in some circumstances, such as those pertaining to global health, there needs to be an understanding that using such compulsory licenses is both necessary and an obligation. In fact, if you have a hankering for the legalese that outlines this for patents over essential medicines, you need only look up info on the Doha Declaration.

Canada actually took this to heart with a bill that came into force in 2005. Often referred to as “Canada’s Access to Medicine Regime” (or CAMR), it was an effort to put into action, the principles and details provided by the Doha Declaration. It was a way to try and enact compulsory licenses for the home production of generic drugs so that more accessible drugs could be produced. It was a good gesture.

Unfortunately, this initial attempt was flawed. The process was simply way too complicated, contingent on an army of legal expertise to navigate, which was all the more problematic because many of the actors involved did not have the means or access to do this. Indeed, the bill seems to contain a paradox in it, in that it can be interpreted as logically impossible to use. If you look closely, there’s a “you can’t do B until you do A” and a “you can’t do A until you do B” error in the details (see question 9 in this document for more details).

It was also very inefficient in that when a compulsory license was negotiated, it was always a one time affair, a one order affair, with specific amounts that could not be changed despite possible reassessment of needs, only good for one country, etc, etc, etc. Indeed, in the years that the law has been available, it has pretty much sat idle (I believe there has still only been one successful case where drugs were actually made and delivered, which provided ample evidence to demonstrate that this process was difficult at best). In fact, if someone were to asked me how difficult things are, the best description I could come up with, is that is it “catastrophically high maintenance.”

Which (finally) brings us to “Bill C-398.” This bill is basically “the edit.” Its sole purpose is to address the things that made the previous bill so ineffective, and at its heart it allows a more streamline and efficient way to issue these compulsory licenses so that production of these generics is more feasible.

No brainer right?

“Oh, but it’s not that simple,” they say. “There are many counter arguments,” they say. Only these counter arguments tend to sound like this:

Q: Shouldn’t we focus on other aspects of the problem. Like health infrastructure, or public education for HIV?

A: Hmmm… Let me get this straight. A government can only do one thing at a time? Nevermind the fact that passing this bill doesn’t actually cost the taxpayers anything. If anything, research has suggested that the foreign aid that we do provide will likely have greater bang for its buck.

Or maybe something like this:

Q: Wouldn’t these changes effect the pharmaceutical company’s bottom line, which in turn will effect R&D funding, and drive the home costs of medicine up?

A: The language is pretty clear in that these are generics that can only be sold in certain markets. These markets happen to constitute a very small percentage of pharmaceutical revenues (we’re talking single digits here). Oh yeah, plus you get royalties from doing this anyway. Also, there’s nothing stopping you from making your own generic version, so that you can enter the market yourself. Indeed, all research and current evidence would suggest a possible gain in bottom line. Plus, the R&D argument is totally a red herring. If that were so crucial, it might help if you spent less on PR and the like. Sneaky.

But what kills me, is that even if there is a reasonable and say unforeseen cause for concern, the Bill has a freaking “sunset clause” which is basically something that gives all parties a “we’ll see how it goes, in case it’s not working” escape route.

All to say, that because of this kind of political and big pharma semantics, there is a very real likelihood that the Bill will die (perhaps in the next few days when it is up for a second reading).  This would be an interesting commentary on the values of our government, although there is already a rich backdrop to this political story.

You should know that this is a Bill that had a previous incarnation two years ago.  It once lived in the country calling itself Bill C393, and it was one of those few Bills passed by the House of Commons where party lines were clearly broken.  Unfortunately,  during that time, the Conservative Senate stalled their vote to make it law, and they did this because they knew that there was an opportunity to “save face” with their industry interests by avoiding the issue altogether.

This was the frustrating part, and I have to admit, my trust in Canadian politics really took a hit.  Here, certain members of Senate, a place that traditionally falls in line with the vote of the House of Commons (because that is, after all, the democratic element of decision making), stalled discussion on this Bill 4 times over 4 days, and in doing so, Bill C-393 got killed by association when a new election was called.

To put this in perspective (and to use internet vernacular), let me just say that this horrific series of events represented a political facepalm of the highest possible order. In fact, we invented a term for it: we called it a #megafacepalm.

And so here we are with another attempt. This is the essence of why you should care about BILL C-398. But what can you do?

Well, for starters, you can lend a hand by speaking out. Retweet this blog post, write about it yourself. You should definitely send an email to Prime Minister Harper and a few of his key Members of Parliament by using this ridiculously easy petition. If you’ve got something meatier to say, how about copy pasting this entire list of emails, and let the Canadian government know how you feel. If you’re not Canadian, do these things anyway, and then make this issue pertinent in your own country. This is an urgent matter, and for Canadians, there is only so much time to advocate. It’s really an amazing chance for Canada to lead the way.

You can also immerse yourself in this cause and get as much information as possible. You can check out organizations such as the Canadian HIV/AIDS Legal Network, which has all sorts of great documents including this informative myth versus fact sheet.

If you’re a university student, you can check out your local UAEM chapter. If you’re a Grandmother, you can hear what Grandmothers Advocacy Network have to say. Better yet, check them all out, or join these groups and volunteer your time.

There is also a twitter campaign in progress.  Flood the feed with hashtags like #C398, #fixCAMR, #medicinesforall, #cdnpoli and tweet out your support with phrases like:

“Please vote YES to Bill #C398 on Wed! We need to #fixCAMR and improve #accesstomedicines! #cdnpoli”

“Have you signed the petition in support of #accesstomedicines yet? Go to www.medicinesforall.ca! Let’s #fixCAMR & pass #C398!”

If you think the idea of Bil C-398 above seems reasonable and just, please do whatever you can. Because through it all, you should never ever forget: “Access to life-saving medicines is not a luxury, it is a human right.”

Illicit drug use is a problem that drains public health and medical resources around the world. There are many ways in which we, as a society, can deal with this problem. We may adopt: drug treatment programs in order to get drug users permanently off their drugs; harm reduction programs that have the aim of limiting the damages from drug use; or find the root causes of drug use in an effort to prevent the problem before it even begins.

One aspect of this latter approach is to identify these substance(s) that leads to more severe drug use. This approach is often referred to as the gateway hypothesis. Simply stated, when an individual uses a particular substance that individual is more likely to move on to a more severe substance. For example, it is often hypothesized that marijuana is a gateway to cocaine and other illicit drugs. In fact, this hypothesis has international evidence.

In an analysis of Australian high school students, Swift et al. (2012) found that increased frequency of marijuana use leads to increased rates of illicit and licit (tobacco) drug uptakes; moreover, Swift et al. (2012) found that cessation of marijuana use leads to lower rates of licit and illicit drug uptake. Using survey data from the United States, O’Brien et al. (2012) found that marijuana is a trigger for cocaine uptake. In the analysis of data from a cohort study of teenagers in France, Mayet et al. (2012) found that marijuana use greatly increased the risk of illicit and licit (tobacco and alcohol) uptake.

This literature fundamentally works backward from the most severe drugs to the least severe drugs. However, because of data limitations, previous research has not identified the gateway drug. In this paper, I add to this literature through the identification of the ultimate gateway drug. This identification has clear implications for theory, practice, public policy, and potential drug users around the world.

Data and Methodology

Data for this study were gathered from an ethnographic analysis of historical and foundational surveys of interviews for focus groups with participant observers. In an effort to be a part of the phenomenon of mixed methods, I wanted to have as much statistical power as possible. Because I did not want to invoke Type I or Type II error, I employed the largest sample possible to increase sample size and statistical power. According to a survey of certain tables of numbers in the back of statistics textbooks, I found that a sample size greater than 30 is equivalent to infinity. Therefore, I chose to gather a sample size of 31.

All analysis was performed within the extremely complicated regression framework that included the unintelligible maximization algorithm. Through the application of 25 axioms found within various fields of research (each with a 99 percent probability of being correct), it clearly follows that the extremely complicated regression framework using the unintelligible maximization algorithm reduces to a linear equation that can be estimated using ordinary least squares. As such, all analysis is performed in a spreadsheet.

Results

The results of the analysis are summarized in Table 1. Clearly the results show that my results are consistent with previous research: lower level illicit and licit drugs necessarily lead to the use to more severe illicit drugs, namely cocaine. One result that is notable is that cocaine is not much of a gateway drug for cocaine use. As such, drug policy does not need to focus on “hard” drugs such as cocaine.

Table 1. Results of analysis of data, predictors of cocaine use, percent of cocaine users that have used potential gateway substance

Note. All data and results represent a terminological inexactitude.

More specifically, Table 1 shows that 95, 94, and 93 percent of cocaine users previously used marijuana, alcohol, and tobacco, respectively. Obviously, all three of these illicit and licit drugs need to be banned to prevent the onset of cocaine use.

It is important to note at this point that the sampling method employed for data gathering focused on current cocaine users. In order to properly test the gateway hypothesis I would have needed data that would allow me to differentiate between marijuana actually opening the gate for cocaine use or simply a phenomenon of individuals successively moving from soft to hard drugs. However, I prefer to stick my head in the sand on this issue and assume that my data are representative of the former process and not the later.

Continuing with the results from Table 1, it is important to note that toast has been used by 96 percent of current cocaine users in our sample. This shows a strong positive relationship between cocaine use and the eating of toast. Future research is necessary in this regard to identify which form of toast has the greatest predictive power—we did not ask the participants for details regarding their toast. For example, is plain toast, butter, margarine, marmalade, or jam the best predictor? Perhaps most importantly, does it matter which side of the piece of toast has any topping?

The most remarkable result is in regard to infant formula and mother’s milk. Though individually each of these substances have been used by a relatively low percentage of cocaine users, compared to the other substances, one must remember that all infants have likely had one or both of these substances. Combined together, 129.8 percent of cocaine users in our sample have had either infant formula and/or mother’s milk—this number of greater than 100 percent because a subset of our sample received both mother’s milk and infant formula because they were ravenous beasts as infants.

Conclusion

We have clearly identified the ultimate gateway substance(s): mother’s milk and/or infant formula. Though our results are only in the context of cocaine, each and every one of our individuals had at least one or the other substance. A clear direction for future research is to replicate this study in other contexts: other places, other people, and other drugs. Despite the push for providing adequate nutrition for our infants that is supported by the World Health Organisation, we as a society are clearly pushing these infants toward hard-core drug use as a result. Therefore, we must now perform a cost-benefit study to investigate any gains for our society from this adequate nutrition for infants given their greater risk of hard-core drug use and its corresponding social ills.

References

Mayet, A., Legleye, S., Falissard, B., and Chau, N. (2012). Cannabis use stages as predictors of subsequent initiation with other illicit drugs among French adolescents: use of a multi-state model. Addictive Behaviors 37(2): 160 – 166.

O’Brien, M.S., Comment, L.A., Liang, K.Y., and Anthony, J.C. (2012). Does cannabis onset trigger cocaine onset? A case-crossover approach. International Journal of Methods in Psychiatric Research 21(1): 66 – 75.

Swift, W., Coffey, C., Degenhardt, L., Carlin, J.B., Romaniuk, H., and Patton, G.C. (2012). Cannabis and progression to other substance use in young adults: findings from a 13-year prospective population-based study. Journal of Epidemiology and Community Health 66(7): Article Number e26.

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Lately, I’ve been listening to a lot of Radiohead.

This might be because there is an anniversary of sorts – the epic O.K. Computer was released just over 15 years ago, and so is finding a renewed presence in various media outlets. But it’s also because I’m simply a fan: I find their musical compositions, instrumentations, and Thom Yorke’s heart wrenching vocals a compelling mix; although admittedly, I do sometimes miss the days when some of their material was a little less challenging to radio ears.

Truth be told, I’m such an admirer that I sometimes bring up Radiohead in my role as a science educator. Here, I might play a specific song of theirs and then project the below statement on the screen:

“The song you are listening to is the title track of a Billboard number one CD. The song and CD appear to have been specifically written and dedicated to the first putative human clone.”

Then I ask my students, “Is this true or false?”

Inevitably, the students will concentrate on the song coming over the speakers, and they will note that what they are hearing, sounds somewhat unconventional. It’s distorted in many places, and doesn’t adhere to any semblance of common chord progressions. It definitely does not sound like an obvious reflection of a Billboard number one CD.

And then the reveal: yes, the statement is true. The song is the title track of the CD Kid A, and on October 21st, 2000, it did chart at number one. Not on the Alternative Billboard chart, or the Electronic Billboard chart, but on the whole-freaking-thing Billboard chart. Furthermore, it does apparently connect with the topic of cloning. At least, that is what you might surmise when you read what Thom once said on the subject:

POSTED BY Thom ON JULY 30, 2000 AT 23.39:21:
IN REPLY TO: Thom, why Kid A?
dedicated to the first human clone.
i bet it has already happened.

In any event, I tend to use this little activity as an excuse to talk about science perceptions, and how topics like genetics can be quite pervasive in popular culture. Not only pervasive, but often with a negative connotation. Think of all the movies where genetics plays an integral part of the conflict in the plot; be it biological warfare in spy franchises, clone armies in science fiction sagas, or even battle scenes between Pokemon characters and their angry identical copies (Yes, there is a central cloning plot to the movie, Mewtwo Strikes Back). In its own way, the song Kid A also presents a certain kind of tone that is both foreign sounding and haunting. Maybe Radiohead did this to add their own criticism of technology to the mix, or maybe it’s more to do with simple representation. Think of how strange an episode of human cloning might be in the here and now, to the clone in particular. Of course, maybe the song just came out that way because the band thought it sounded cool.

Interestingly, the idea of coolness also brings up a strange thought I’ve been considering.

That is: let us assume that Radiohead were right – that they were right about the first putative human clone being produced, or say, conceived roughly in the year 2000. This would mean that their sonic ode would be temporally, fittingly, and perhaps even devastatingly relevant. Furthermore, it would mean that somewhere out there, on our busy little planet, is a child who is technically the song’s point of inspiration, and also a child who is now probably around 11 years old.

What if this child found out? What would it think when it learns that an iconic British band wrote a song for him/her. Would the child write a letter? What would the letter say?

Perhaps, he/she would comment on the science?

“To be honest, I’m not even sure what “human cloning” means, since right now, the science I’m learning at school, is mainly to do with habitats, and food chains and why the sun is super important. Someone did once try to explain the cloning thing to me, but I just got confused.”

Or maybe there would be mention of Radiohead’s popularity

“My parents tell me that you are famous. In fact, they tell me that you are very famous. I have to admit that this is surprising to me, since I have never even heard of you, or even seen you on TV. As well, I tried to listen to the song Kid A, but I think the song was broken since it sounded strange…”

Which, not surprisingly, might culminate in a request to meet, or possibly something more selfish:

“I’m wondering that since you are super famous musicians, that maybe you can introduce me to some of your friends. For instance, have you heard of One Direction? My friends keep playing their CD – it’s really good. It would also be cool to meet Katy Perry or Jay-Z. Even chatting with Justin Bieber might be interesting…”

Which leaves us with an idea that is so deliciously meta. What kind of music would the real Kid A actually listen to? Here, having kids of my own (and despite my best attempts at steering them away from the Disneyfied pop that fills the current musical landscape), I’m pretty sure that this Kid A is not going to be listening to Radiohead. Which is actually very sad – although the glimmer of hope is that maybe it’s sad enough for Radiohead to write a song about.

Approach it calmly – there’s no need to work yourself up into a lather by drinking turpentine and spitting fire. But be careful. Intellectual escapades like this are deceptively difficult and it’s easy to blow a synapse, or worse.

Witness the man of stone. It takes an eternity for his eyes to blink even once. He stares at the sun, the moon, and the stars as they pass by turns overhead. One day he crumbles and only a pile of rubble remains. He wasn’t cut out for the eternal.

To avoid such a fate, you should first distinguish between eternity and time. Note, however, that it’s easy to bogged down in the vagaries of time, which are considerable.

In the fifth century, Augustine of Hippo famously confessed, What then, is time? If no one asks me, I know what it is. If I wish to explain it to him who asks me, I do not know.

Best ask someone else then.

Like a geologist, who will show you that time is stratified into layers like the pages of a book. Or a paleontologist. He or she will hand you a fossil trilobite and describe it as an icon of time past. Astronomers will point to different stars that are billions of years old. Meanwhile, children will tell you their ages to the nearest half year and poets will lament its passing.

Time’s passing is a great enigma for science and you may be interested to know that some physicists will tell you that both past and future are fixed and time is laid out in its entirety in a timescape, akin to a landscape. There, all past and future events are laid out together. No special moment is singled out as the present because there’s no known mechanism to convert future events into present then past events. This is why the universe often fails to wish you a happy birthday.

Here is where a little Plato comes in handy. He described time as an imperfect moving image of eternity which remains forever at one. We don’t know what he means either. Perhaps each moment of your life is a frame of a film strip illuminated by the brilliance of the eternity’s lamp? Try that on your mental trapeze.

Whether time passes or is simply an illusion, an appreciation of its fleeting nature could help in pondering eternity. You can start by thinking about things that are ephemeral. Some examples will help.

Shooting stars are ephemeral, as are summer thunderstorms, rainbows and haloes around the sun. Unfortunately, the full moon is ephemeral too, even though its glistening light seems to hold everything still as a stone. You can’t step in the same river twice, so the river is definitely ephemeral. Blossoms and leaves also come and go.

But don’t get carried away. Some things that appear ephemeral are actually eternal. Listen to Basho:

Old pond:
frog jumps in,
sound of water.

The frog jumped in three centuries ago and today the sound waves of that tiny splash continue to ripple. But look, there is the frog again on the lily pad, waiting to jump. Now it’s on a log. In it goes, head first, legs last, another splash. Now it’s back on a lily pad, spying a bug on the surface of the old pond. Once more it lunges in to the sound of water.

Once you see the frog, you know that it exists in a timeless space, in the old pond of your mind, always waiting, always ready to jump, always jumping and splashing into a vast silence that erupts briefly before resettling into soundlessness. When you can imagine moments like this standing still forever, and repeating forever, you are starting to get the hang of eternity.

Remember the Little Prince, his sheep and his flower? They are eternal.

On the other hand, according to Magritte, eternity is a cylindrical block of butter with a spatula in it, on a pedestal for all to see, between the bronze heads of the suffering Christ and the scowling Dante. If you stare long enough at the painting, the butter will begin to melt before your eyes.

Or look at Giacometti’s walking figures. Corroded as if baked too long in time’s oven, do they stride from the present into the future, gazing blankly ahead, or from one eternity to another?

Or read some Emily Dickinson. She often sailed to eternity and back in a single line of verse.

Why not take a trip to Paris and admire all the pairs of lovers lolling on the bridges or spoon feeding each other crème glacée in the cafés? Rather than smashing their heads together in a fit of jealousy, pose yourself a philosophical question: What are they doing? Aren’t they trying to suspend time and glimpse eternity? Extend your stay and see if you can become one of them. The crème glacée will do you good.

Alternatively, if you want to think about eternity as a duration, you could think about the spacecraft, Voyager 1, launched in 1977 and now leaving the solar system at a speed of sixty thousand kilometers per hour. Forty thousand years from now it will drift past another star, AC +79 3888, seventy-fifth on the list of nearest stars to Earth, though it won’t come within shouting distance of any of that star’s putative planets. In two hundred and ninety six thousand years, its sister ship, Voyager 2, will drift past Sirius, the brightest star in the sky. Go ahead. Think about the sparseness of space, think about two hundred and ninety six thousand years and you’ll get a hint at why Pascal shuddered “The eternal silence of these infinite spaces frightens me.”

Treat it all more circumspectly, then, and mull over this quote by Thomas Browne, “The night of time far surpasseth the day, and who knows when was the equinox?”

Despite that teaser, it may be hard to improve upon the wisdom of the shepherd boy in the tale by the Brothers Grimm. In response to the king’s question, “How many seconds of time are there in eternity?” the boy describes a mountain in Lower Pomerania two and a half miles tall and just as wide and deep, and he says, “Every hundred years a little bird comes and sharpens its beak on it, and when the whole mountain is worn away by this, then the first second of eternity will be over.” Continue in this vein and try to convince yourself that the number of years between here and eternity exceeds the number of grains of sand in all the beaches and deserts of the world, the number of stars in all the galaxies and even the number of particles in the known universe.

But you should be aware that some people, like Dostoyevsky, weren’t impressed with such efforts to create an abyss out of time. We always imagine eternity as something beyond conception, he said, something vast, vast! But why must it be vast? Instead of all that, what if it’s one little room, like a bathhouse in the country, black and grimy and spiders in every corner, and all that? Book one for the summer and see if he was right.

Even the Buddha wasn’t sure that it was possible for such thoughts to get anywhere. “Our theories of the eternal,” he’s reputed to have said, “are as valuable as those of a chick that has not broken its way through its shell might form of the outside world.”

Don’t let that deter you. According to cosmologists, the universe had a beginning, so it is not eternal. One day, long after the man of stone has crumbled, the stars will blink out, and, thanks to dark energy, the mysterious force that’s driving the universe apart, eventually all the other galaxies will be pushed away too far for us to see them. After the bird saws off a couple of seconds of eternity, there won’t be much left in the cosmos except for black holes.

This kind of thinking might depress you, but take heart. In the 1980’s, physicists tried to find out if the proton, the elementary particle that makes up all normal matter, including you, me and crème glacée, might one day decay. Having found no evidence, physicists now think protons are eternal. So, after your mental trapeze artist has dismounted and you have exhausted your experiment with eternity, and your experiment with life, your protons will go on living.