“Most of the great coral reefs on the planet will likely be gone by 2020‚” says U of T’s Dr. Rowan Sage‚ a botanist and climate change ecologist.

While many Canadians have accepted that global warming is real‚ it is commonly believed that we have yet to see any major consequences. Most of us are aware of some of the more dire predictions—that the ice caps will melt‚ that polar bears will disappear and that some oceanic islands may be submerged—but we tend to think that while the effects may one day be dramatic‚ most of us will not live to see them.

“[But] biological systems throughout the world have already responded to the relatively small amount of warming that has taken place‚” said professor Dr. Chris Thomas‚ a conservation biologist based in England.

“Probably the greatest [effect seen so far] is the coral reef die–off‚ which pretty clearly results from episodic heat events‚” said Sage.

Corals often die when stressed by heat‚ turning white in a process called bleaching. It is estimated that most species of coral will bleach if the average summer temperature rises by only one degree Celsius‚ and as corals live in shallow waters‚ their habitat can warm extremely easily. Since 1979 scientists have observed six mass bleaching events. The largest occurred in 1998‚ when 16 per cent of all corals on Earth died.

The global temperature rose by an average of 0.6 degrees Celsius in the 20th century‚ and is expected to rise by two or even three degrees in the next 100 years. This may sound like a small increase‚ “but it is not the average that is critical‚ it is the timing and distribution [of the changes]‚” said Sage. “Warming tends to be non–uniform‚ with greater warming at night‚ at high latitudes‚ and in the winter. So a global one degree Celsius increase has a much greater effect in the high arctic‚ especially during the winter. The ice pack may thin‚ with consequences for sea levels‚ and the arctic ecosystems may be wiped out.

“[With abnormally high temperatures] drastic changes can come into play quickly‚” continued Sage. His research shows that vegetation worldwide is going to be dramatically affected by global warming‚ primarily due to increased heat‚ drought‚ and fires. “Large areas of ecosystems will burn up‚ and they will be replaced by [fire–tolerant] grasses and shrubs. This has already happened with the great Indonesian fires of the late 1990s. It is happening as we speak. You can watch it by logging into NASA’s website and seeing recent satellite photos of widespread landscape burning.”

Canada is also experiencing more forest fires. “Our recent increase in fire activity is a result of human–caused climate change‚” says Canadian Forest Service ecologist Dr. Mike Flannigan.

Scientists the world over have documented hundreds of biological anomalies that they have linked to global warming. “Changes in the geographic distributions of species‚ their abundances‚ and the times of year at which they breed seem to be ubiquitous‚” says Thomas.

Many migrating animals are moving north and south‚ away from the equator‚ as regions closer to the poles become warmer. Storms are becoming more frequent and more intense. Many species of plants and animals are declining in numbers‚ and even disappearing.

Since the 1960s‚ higher temperatures have caused spring to come early in many places throughout the world‚ by a full week in some areas. The onset of spring can be seen for example in butterflies appearing earlier‚ frogs spawning sooner‚ and plants flowering prematurely.

Dr. Donald W. Thomas of the Université de Sherbrooke in Quebec reported in the journal Science in 2001 that early springs have been linked to the decline of a population of blue tits in southern France. The birds are genetically programmed to breed at the precise time of the year when caterpillar populations explode‚ giving them an abundant supply of food for themselves and their fledglings. But early springs have caused the caterpillars to hatch out of syn with the leafing of oak trees‚ leaving insufficient numbers of insects to sustain the blue tit population.

Other species of birds have also suffered as a direct consequence of warming. In 1997 short–tailed shearwaters died in huge numbers in the Bering Sea. Dr. Sharon Smith at the University of Miami says the warmer water caused plankton to bloom‚ turning the water opaque and preventing the birds from being able to see and catch prey.

The disappearance of the golden toad is also being blamed on global warming. Prior to its disappearance in the late 1980s‚ tourists flocked to see this animal during its mating season‚ when thousands of the small‚ brilliantly coloured toads gathered in the mountainous cloud forests of Costa Rica. Dr. J. Alan Pounds and Dr. Robert Puschendorf‚ conservationists working in Costa Rica‚ reported in Nature in 2004 that increased cloud cover and drier seasons‚ both a direct result of global warming‚ allowed a frog skin disease to proliferate and wipe out the toads.

Dr. Chris Thomas says that the loss of the golden toad is not an isolated incident—he says that global warming is going to lead to mass extinctions. “My greatest concern is that climate warming could‚ in the end‚ drive a quarter or more of all of the land animals and plants to extinction‚” he said. “In some cases‚ they may experience new extreme conditions that they are unable to survive. In other cases‚ some species are expected to be out competed by other species that thrive in hotter conditions.”

In a study he published in the journal Nature in 2004‚ Thomas estimated what percentage of all species will be able to adapt to the Earth’s changing climate. He calculated that anywhere from 18 to 37 per cent of all species on this planet will be “committed to extinction” by 2050 due to global warming—meaning that even if some individuals remain‚ the species will never recover.

Of greatest significance to us‚ however‚ is the impact global warming is having on our own species.

“The heat wave of 2003 in Europe caused several tens of thousands of excess heat–related deaths in [older people]. These conditions are expected to be close to the norm in 25 to 50 years‚” says Thomas.

“And when it is hot you are more likely to lose the power grid [as in North America in 2003]‚” says Sage. “Without air conditioning‚ people will not be able to escape the heat. With North Americans being heavier than in the past‚ and hence more prone to heat stress‚ it seems likely that heat–related deaths could soar into the hundreds of thousands.”

Global warming will also have dramatic consequences for our food supplies. In 2004‚ the International Rice Research Institute (IRRI)‚ located in the Philippines‚ reported in the Proceedings of the National Academy of Sciences (PNAS) that an average daily temperature rise of one degree Celsius resulted in a 10 per cent drop in rice yields‚ one of the world’s most important crops. Rice‚ like coral‚ grows in shallow waters‚ and is particularly vulnerable to warming.

While some contend that the evidence for warming is weak‚ it is important to note that the majority of the studies mentioned here were reported in the journals Science and Nature‚ considered the two most prestigious scientific publications in the world.

“The scary thing is‚ many‚ if not most‚ don’t think [global warming] is real but instead is a left–wing plot‚” said Sage.

Such a “plot” is in fact the topic of Michael Crichton’s new book‚ State of Fear‚ which contends that global warming is merely a hoax devised by environmentalists trying to get research funding. The book‚ generally reviled by ecologists‚ was praised by Capitalist Magazine for illuminating the “the flawed science behind the global warming and other imagined environmental crises.”

“How is a member of the public to know where the truth lies?” asked biologist Chris Thomas. “It is not a topic like education or health‚ where everyone can judge pronouncements against their personal experience.”

“One thing to keep in mind‚” said Sage‚ is that “humans are impacting the global environment in a number of major ways‚ for example by deforestation‚ by using excessive amounts of fertilizer‚ by spreading new species into virgin ecosystems. These combine with global warming to produce dramatic effects. [But] these environmental insults are more tractable‚ so we could be making real progress.

“Climate change is a human–caused problem that requires a human–based solution‚” Sage said.

Possibly the smartest thing I have done wasn’t dropping twenty grand on an Honours B.Sc. – it was bartending at a nightclub to pay for it. I’m a self-respecting, independent woman, but I’m not above smearing on thick eyeliner and hiking on a push-up bra three nights a week if it gets me the funds to educate myself without having to rely on daddy or hubby. If slack-jawed alcoholics want to entertain the notion that tipping me a toonie might get them a screw in the bathroom at the end of the night, that’s fine by me.

But even more valuable than the cash I earn that prevents me from falling into a Kraft Dinner-ridden, debt-filled existence, are the stories I have to tell. Having spent the vast majority of my weekends for the past few years behind the bar instead of in front of it (or under it), I’ve seen some pretty fucked up things.

It wasn’t me, it was the one-armed raver. I left the club at two in the morning after a rave. A Happy Hardcore rave, to be exact, which are only populated by obese candy kids from upstate New York wrapped in spandex. Sitting on the sidewalk outside was a very high, very young, very fragile-looking girl. She was from Scarborough (of course), and couldn’t get home until the subway opened, but was too scared to go back inside and face the flashing lights. I decided to do my good deed for the day: I bought her a coffee, which kept her from falling asleep (Ecstasy breaks down your spinal fluid if you sleep, apparently). After a while she wanted to find her boyfriend. I asked what he looked like. “Well, he’s wearing a red shirt and a red hat,” she said. “Oh, and he has one arm. And one leg.” I thought she was just high, but there in the middle of the dance pit was a one-armed, one-legged raver. Turns out he was an E-tard when he was sixteen and decided to climb a Hydroelectric pole. Moral of the story: if you raise your kids in Scarborough they might end up so bored they’ll electrocute themselves.

A punk spat a tooth on my bar. I can’t remember which punk band was playing – we put on so many hardcore acts, they’re all interchangeable to me. As a zoology student, I’ve come to appreciate these shows for the unique opportunity they afford to observe human biology. Legions of D-cupped, 12-year-old skanks in early puberty, poster children for the bovine growth hormone. Drunk teenage boys competing for their attentions like baboons in rutting season. And best of all, watching natural selection in action as 200 intellectually-depleted teenagers kick the shit out of each other in a circle pit. I’ll always remember the tooth a bloody-nosed kid spat on my bar. Watching these putzes nail each other in the balls with steel-toed boots always leaves me content in the knowledge that some of the lesser members of my species will not be able to contribute their genes to the next generation.

That’s right, Mr. Slave! About once every two months, 900 gay guys in assless chaps descend on our club for a Leather Ball. Sounds intimidating, but I feel more comfortable working these shows than any other. Where else can a girl wear a leather mini-skirt and hooker boots and instead of being asked “How much?” be greeted with “Oh my gawd I love your hair! And look at those boots!” Like punk shows, leather balls are educational. I would never have learned that the human sphincter is capable of stretching to the diameter of a honeydew melon, or that with a little lube a man can get his arm up past the elbow inside another man’s rectum.

This guy set his afro on fire. New Year’s Eve, 2002. Before I served even one drink, a guy with a giant ‘fro stumbled over the bar, obviously having pre-drank. “Kinigeddadrink?” he slurred, the Jew-Fro wavering far too close to the candelabra. “Christ no,” I told him, moving the candles away. “Come back when you’re sober.” Somebody else asked for a beer in coherent English, so I turned around to grab it. “C’mon, pleezIjus’wannadrink!” I heard behind me, followed by a loud gasp. I turned around to see the smiling dimwit, his ‘fro aflame, gigantic tongues of fire shooting up into the air. I screamed and tried, ineffectively, to spray him with the soda gun. The rest of the crowd poured their beers over him. He loudly protested, having not realized that his head was on fire. I didn’t see him for the rest of the night, though he left half his hair in soggy clumps on my bar.

Who’s your daddy? Probably the most horrifying experience I’ve had was the Maxim Coors Light Girl Toronto contest. Thirty scantily-clad, borderline retarded women, and hundreds of hooting, drunk, certifiably retarded men drooling. There was even a spelling bee. “Jessica,” asked the host, “Can you spell ‘spaghetti?’” She paused, obviously in a panic. Fortunately, she knew how to think on her feet. “S…E…X!” she replied, to a deafening chorus of “Aww YEAH!” from the audience. However, the most memorable moment came at the end, when they announced the winner. As soon as the host proclaimed “Starla” the Maxim Toronto Girl, a middle-aged man with grey hair, glasses, and khakis jumped on to my bar, beer in hand, and started dancing and cheering. As I called security to get him the fuck down, I wondered who he could be. Her sugar daddy? Oops, no, my mistake – he was her actual father. He ran to the stage and embraced his daughter, who was only wearing a transparent bra and thong, revealing her hairless, razor-scarred crotch (which no doubt reminded him of the blessed day she was born).

Tory Party. Every year we host a party for the provincial Conservatives. Man, you ain’t neva seen people gettin’ down ’til you seen 900 Tories do the White Man Shuffle. Oh yeah, mmm. Let’s get fiscally responsible, baby. Thankfully it wasn’t open bar, or else as a taxpayer I’d have been really pissed off. I’d like to tell you about what happened after Mike n’ Ernie parked themselves at the shot bar, but libel concerns keep my lips sealed. Let’s just say it was memorable.

Working the VIP room. During Canadian Music Week, top executives for a worldwide record label descended on the VIP room. I dressed up, put on my best smile, and got ready to kiss executive ass. I dreamed of making enough money to buy my books the next term with one night’s earnings. I smiled, I chirped, I chatted with the Euro-American trash, serving drink after drink. And what did the coked-up suits bestow on me? Fif. Teen. Dollars. Trickle-down economics, my ass.

Tobacco company twats and film industry twats can also be just as cheap. The other night a television executive blatantly stared at my breasts, said “You’re a stoke fox, you know that? Heh heh, all riiiiiiight,” paid for six drinks without leaving me a dime, and then sat down with his wife and six-year-old son.

I tell you, suits will order two dozen difficult-to-make cocktails without leaving me a tip, while the average Joe who works in a factory will always, always leave a dollar for every beer I uncap. The only time a suit will tip you is when they think they might get something in return. Only once was I impressed by an exec’s generosity, when a cigarette representative left me a 50 after seeing that none of his co-workers had tipped all night. I must say though, I don’t doubt that the next morning he woke up and thought, “I gave that chick a 50 and I didn’t even get a blow job?”

Definitely smells fruity. Orange? But there’s something else there‚ something almost bitter‚ I can’t tell what. Everyone knows that feeling‚ when you recognize a smell‚ you know you’ve smelled it before‚ but you just can’t quite put your finger on it.

Everyone‚ that is‚ except perhaps Turin‚ who has spent the better part of his life thinking‚ writing‚ and philosophizing about smell. “How about carrot?” he asks. And that’s exactly what it smells like—orangey carrot. But the scent does not come from orange and carrot extracts—it comes from a synthetic chemical that Turin created in his basement‚ using simple machinery and a radical idea.

Since childhood Turin has been fascinated by smell. “I’ve always loved perfume with a passion‚” said Turin‚ born to Argentinean–Italian parents and raised in France. In 1992 he authored France’s bestselling perfume guide‚ Parfum: Le Guide‚ a gigantic tome listing and critiquing almost every perfume ever created—the Guerlains‚ the Yves Saint Laurents‚ Chanel no. 5‚ White Linen ‚ and all manner of obscure‚ nineteenth–century antiques he dug up in the dusty perfume stores of Nice.

This book brought Turin into contact with the perfume giants‚ and permanently changed the course of his academic career.

Only six companies‚ who collectively generate about $20 billion a year in economic activity‚ make virtually all the synthetic scents you can buy‚ from the smell of Tide detergent to Cool Water. And after reading his perfume guide‚ they wanted to know what Turin thought of their new scents.

It was while exploring the labs of the perfume giants that Turin realized one extremely important thing about smell: we do not understand how it works.

The perfume giants employ thousands of chemists (each at a sizable salary) to create new molecules that they can patent. A successful molecule will net tens of millions of dollars in profit. But‚ in order to produce even 20 good molecules‚ chemists have to produce anywhere between 500 and 2‚000 molecules. They take the appropriate chemical building blocks‚ rearrange them into hundreds of new molecules‚ and then sift through them one by one to find the precious few that smell good.

Why go through such a wasteful‚ time–consuming process? “Because they don’t have a clue [about how smell works‚]” said Turin. “They readily admit they don’t have a theory—otherwise they wouldn’t be making thousands of molecules.”

Scientists figured out decades ago how vision and hearing work. They know which wavelengths of light look like which colours; they know which frequencies generate vibrations in which parts of the ear and what that sounds like; any standard physiology text will have detailed descriptions of the eye and the ear‚ but will contain little information on the nose.

Why have scientists taken so long to crack the sense of smell?

“One reason is that ‘real men’ don’t smell things‚” says Turin. “And‚ science being chiefly male‚ it’s always been considered a field where you could not rely on your sensation. I’m always struck by this—even professionals in the field do not understand that when perfumists say something smells musky‚ or woody‚ or ambery‚ it means something very precise. They think these are just words that wine experts might say‚ like ‘I’m getting strawberry‚’ or some such bullshit. They just don’t think that the sensation of smell has the same legitimacy as vision‚ or hearing.”

Classical biological thinking assumed that smell must work the same way that most other biological systems work: by recognizing molecular shape. Enzymes in your stomach‚ for example‚ will recognize specific molecules‚ like lactose‚ by their shape. The lactose molecule fits into the enzyme like a key in a lock‚ and the enzyme breaks it down. If you don’t have the enzyme for lactose‚ you can’t digest it.

The human body can only digest about a hundred different molecules‚ so we have only about a hundred different enzymes. Most biological systems‚ like the neurotransmitters and hormones‚ work by shape. It was assumed smell worked the same way. But there’s a problem. You can smell anything—any molecule that fits the appropriate chemical criteria you can smell. You can even smell perfumes that were invented last year‚ that our ancestors were never exposed to. You can digest glucose because your ancestors evolved the appropriate enzymes. But if ancient humans never smelled Tommy Girl‚ why can you?

To date‚ scientists have identified at least 10‚000 molecules that we can smell. If smell works by shape recognition‚ should we not then have at least 10‚000 different kinds of odour receptors in our noses?

In 1991 Linda Buck and Richard Axel made history when they identified the genes for olfactory receptors in rats‚ a feat for which they were jointly awarded the Nobel Prize this year. It turns out humans have about 1‚000 different kinds of olfactory receptors. An impressive number for sure‚ but not enough to suggest that shape is the only thing determining a molecule’s smell.

There are other problems with the shape theory. Some molecules that are shaped very similarly have different smells. Vanillin smells like a rich vanilla‚ and isovanillin smells richer and spicier‚ “somewhat phenolic‚” says Turin.

And some molecules that have completely different shapes smell exactly the same; Osyrol and betasantalol‚ for instance‚ both smell like sandalwood.

Turin came to believe that smell works not by shape‚ like digestion‚ but by vibration‚ like hearing. We can only hear sounds within a given range (we can’t hear the high pitches of echolocating bats‚ for example)‚ but we can hear every sound in our range.

So if you think of molecules in musical terms‚ the theory is easier to understand. A molecule is made up of a collection of atoms‚ and each bond between those atoms has a particular energy. If you think of one bond as being like a note on a keyboard‚ you can think of every molecule as being like a “miniature musical instrument‚” having its own particular chord‚ or combination of notes‚ says Turin.

A laboratory spectroscope works by this principle—it shoots light at a sample‚ “plays” the notes‚ and figures out what a molecule is made of. Turin argued that the nose works like a spectroscope‚ and that these notes correspond to smell.

This‚ he said‚ explains how two molecules‚ ferrocene and nickelocene‚ both shaped like “burgers‚” smell different‚ because buried in their interiors they contain different metal atoms‚ iron and nickel‚ with different bond energies. And he said this also explained how hydrogen cyanide‚ made of three atoms‚ and benzaldehyde‚ a ring–shaped molecule‚ both smell like bitter almonds‚ because although they are made of different atoms‚ their bonds have the same energies‚ the same notes.

This idea is not new. An English scientist‚ Malcolm Dyson‚ first proposed a vibrational theory of olfaction in 1938‚ and a Canadian‚ R.H. Wright‚ revived the idea in 1977. But neither scientist could explain how the human nose could accomplish what a piece of laboratory equipment made of metal and glass and lights can do.

Turin‚ however‚ did have an idea about how a nose made of flesh could perform spectroscopy: electron tunneling. It is possible to read the bond energies in a molecule not by shooting photons of light at it‚ but by shooting electricity at it.

In 1989 Turin became the first person to show that proteins can conduct electricity. He created a diode that used albumin (egg white protein) to conduct electricity.

So he thought it was possible that a protein could channel electrons like a battery‚ and probe odorous molecules for their chords. Using the code for the receptors that Axel and Buck had found‚ Turin came up with a model of how the nose receptors could channel electrons into a molecule.

He took his model‚ his same–shape different–smell molecules and same–bond energy same–smell molecules‚ and submitted a paper to the prestigious journal Nature.

The editors deliberated for a year on the paper‚ and eventually rejected it. “It seemed to them an unnecessary gamble‚” said Turin. So Turin had to settle for publication in 1996 in a less notable journal‚ Chemical Senses.

Turin’s vibration theory was not well received by other smell scientists; he says that not only did most smell scientists reject his theory outright‚ they did so without even reading his paper.

“I don’t think any scientist has any business dismissing an interesting paper as crap unless they’ve read it. No scientist worth a damn should ever do such a thing‚” he said.

But while other olfactory scientists were not interested in his idea‚ the popular press was; the BBC produced a documentary on him‚ and American journalist Chandler Burr wrote a book about him—which did not go over well with the scientific community. As one recent anonymous editorial in Nature Neuroscience complains‚ Turin’s theory‚ “while provocative‚ has almost no credence in scientific circles…[but has received an] extraordinary—and inappropriate—degree of publicity from uncritical journalists.”

Indeed‚ many smell scientists are not fond of Turin’s idea. Columbia’s Dr. Stuart Firestein‚ “who thinks I’m less than shit‚” commented Turin‚ responded to initial emails from The Varsity‚ but ceased replying after he was asked for his opinion of Luca Turin.

But not every scientist thinks the vibrational theory should be cast aside. U of T’s Dr. David Lovejoy‚ who has spent a large part of his career studying the same kinds of proteins that comprise the nose receptors‚ had not heard of the idea in November‚ 2004. But when asked about it two months later he replied‚ “Every time I think about it‚ the idea makes more sense.”

Dr. Zach Mainen‚ who works at the Cold Spring Harbor Laboratory‚ New York‚ had enough interest in Turin’s idea to test it. He and his team tried to see if rats could smell the difference between isotopes‚ molecules that differ not in shape but in weight (and hence bond energies).

“And indeed they can discriminate them‚” he said. “But we also found that they could discriminate different batches of the same isotope‚” said Mainen‚ which meant that maybe the rats were simply smelling the impurities in the mixtures.

“One of the problems with the theory is that it’s based on sort of hearsay‚” commented Mainen. Turin’s descriptions about what things smelled like were largely based on what he alone thought‚ “so all these claims about what smells similar to what are actually not so clear‚” said Mainen.

“Turin’s theory is sort of weird‚ but it’s conceivable. I wouldn’t say this idea is dead in the water‚ but there isn’t much evidence for it yet‚” said Mainen. “[But] can you absolutely rule his theory out? Not yet. Ultimately we still don’t really know how these receptors work.”

While most of academia continues to ignore the vibrational theory‚ Turin has left academia. He is now the CTO for a startup company‚ Flexitral‚ which creates scent molecules based on his theory.

But unlike all the other major scent producers‚ Flexitral employs only one fragrance chemist: Turin. After all‚ if you have a theory that allows you to make molecules that smell like whatever you wish‚ what do you need hundreds of chemists for? And‚ if Turin is right‚ his theory will make him a very‚ very rich man—he won’t have to split the profits with hundreds of other chemists.

And so far‚ it seems that his idea is working. “I thought an orange–carrot smell would go nice with an orange–coloured soap‚” said Turin‚ so he made it.

Although Turin hopes that his idea will‚ within his lifetime‚ be accepted‚ he concedes that understanding how the receptors work is just one tiny part of the smell puzzle. Not all the nerves in the nose are activated by the same odorants‚ and it seems like the patterns of which nerves are activated at which times are important in determining what you perceive something to smell like.

“The real miracle is the work done by the brain‚” says Turin.

A quick search in a database of scientific journals will tell you that yes‚ it does‚ as evidenced by the substantial amounts of time‚ energy‚ and money researchers have spent answering this question. Despite Scottish comedian Billy Connolly’s assertion that “One size fits all‚ m’dear‚ I haven’t got a fucking telescope‚” scores of psychologists‚ surgeons‚ and evolutionary biologists have scrutinized the size of the male organ and tried to discern its importance.

Kinsey pioneered the systematic study of penis length‚ being the first to ask patients to report their penis size using paper strips. A 1991 study however found “considerable discrepancies” between the lengths of the strips that men handed in and how long their penis actually was (naturally meriting a “duh” response from any layman). Modern penis researchers have solved this problem by devising new high–tech ways to measure penis size‚ like “volumetric plethysmography” (essentially sticking your member in a tank of water and measuring the volume of liquid that spills out).

With new techniques in hand‚ scientists have carried out an abundance of rigorous‚ serious studies on the nuances of the penis. Research has found‚ for example‚ that shoe length has nothing to do with penis size. Gay men will no doubt be pleased to hear that they have larger penises on average‚ according to some research. One study even looked at correlations between penis size and political preferences.

Numerous studies have asserted that ethnicity‚ in accordance with certain popular beliefs‚ is correlated with penis size. Researchers claim that people of African descent have‚ on average‚ the largest penises‚ Caucasians come next‚ and Asians have the smallest ones.

One researcher‚ University of Western Ontario’s Dr. J. Philippe Rushton‚ who has been termed a racist by many‚ has taken this trend a step further. He says having a small penis might not be so bad‚ because his research says that intelligence is inversely correlated with penis size; in other words‚ the smarter you are‚ the smaller your penis (which‚ of course‚ merits suspicion as to his intellectual motives). Rushton says this relates to the fact that Asians are statistically “more intelligent” than whites‚ and blacks “less intelligent” than whites—more penis‚ less brain. Rushton also asserts that blacks are statistically more promiscuous‚ have higher crime rates‚ and do not spend as much time caring for their children.

When asked by The Varsity in a phone interview if he could further comment on the significance of penis size‚ Rushton replied‚ in his faded English accent: “I think you’re focusing on this trait too much. You see there are 60 different traits that [consistently rank Asians‚ whites‚ and blacks sequentially]…these factors are based in biology‚ and we have to begin to accept that there are different varieties‚ or subspecies‚ of humans.” It is curious to note that missing from Rushton’s list are verbal dexterity‚ a sense of rhythm‚ musical ability‚ and athletic prowess (sound familiar?).

While Rushton’s work is generally considered illegitimate and offensive‚ most research that looks at penis size is usually accepted‚ even if it may denigrate some ethnic groups.
Studies suggest that‚ despite the assertion of Kyle’s parents on the series South Park that circumcision makes the penis “look a little bigger‚” circumcised penises actually tend to be a bit smaller. In fact‚ it is not unknown for “over–exuberant” circumcisions‚ as one MD calls them‚ to cause a condition known as “trapped penis‚” where a normal–sized phallus appears small because it has been trapped in the fat of the groin and must be surgically liberated.

Medical science must come to the rescue for thousands of misfortunate baby boys born with physical abnormalities that fall under the umbrella term “inconspicuous penis.” This includes “concealed penis‚” (also known as “buried penis” or “hidden penis”)‚ “webbed penis‚” “micropenis‚” and no doubt most unfortunate‚ “absent penis‚”" in which the penis does not form at all but the testicles do (this happens to about one in 20 million boys).

As methods for correcting debilitating birth defects have advanced‚ so have methods for enlarging the penises of adult men. Between 1990 and 1997‚ 10‚000 American adult men underwent surgical penis enlargement‚ or “phalloplasty.” Surgeons will typically increase the girth or length of a penis with the patient’s own tissue‚ much like using a woman’s own fat to enlarge her breasts. Veins and fat are normally used‚ but one study from Yugoslavia reports‚ in a pseudo–Biblical spirit‚ how to use a piece of a man’s own rib to enlarge his penis (giving new meaning to the term‚ “ribbed for her pleasure”).

But do most men seeking surgery really need it? Studies show again and again that a man with a normal–sized penis will commonly underestimate his size. This psychological condition even has a name: penile dysmorphophobia. One study of Korean military men found that fully 70 per cent of them believed their penises were “small‚” while only five per cent thought theirs was “normal” in size. Moreover‚ those men who underestimated the size of their penis were found to have higher rates of hypochondria‚ depression‚ phobias‚ obsessions‚ compulsions‚ and anxiety. These‚ results‚ however may have more to say about the effects of being in the Korean military than about penis size.

So science has established that men think size matters. They will underestimate how large theirs is‚ exaggerate when reporting lengths for scientific studies‚ and will readily undergo experimental surgery for lengthening (which‚ on a number of occasions‚ has resulted in unforeseen side effects and costly law suits).

But what do women think? Surely the real value of penis length should be measured by what those who don’t have one think?

Out of some 450–odd studies found in scientific databases‚ The Varsity was able to find only one study that looked at the feminine perspective. It found that 55 per cent of women surveyed said the length of the penis was not important‚ and 22 per cent of all women said length was “totally unimportant”; more than three–quarters of all women don’t think length matters. Twenty per cent said it is important‚ and only one per cent said it is “very important.” In fact‚ more women‚ 32 per cent‚ said that girth was important‚ although they were still in the minority.

So‚ if you ask women‚ it is usually the motion‚ not the meat. In fact‚ studies show that many women may in fact find their partner’s penis too big—pain during sex is one of the most commonly reported problems.

Three years ago Lovejoy and his colleagues discovered a family of hormones that‚ based on studies in rodents‚ seem to reduce fear. To discover a new hormone is an extremely rare feat. To discover an entirely new family of hormones is even less common.

A year ago Lovejoy created a startup company to do further research into these new hormones‚ and he has recently acquired funding for his company. He is still in the process of finalizing the contracts‚ so at the moment all he can say is that “the funding is coming from a group of private American investors‚ a lot of whom have invested because they have an interest in depression and bipolar disorder.” The identities of the investors should become known to the general public within the next few weeks.

Lovejoy is hoping to use his group of hormones‚ called “teneurin C terminal associated peptides‚” or TCAPs for short‚ to treat human emotional problems like manic depression. But he realizes that his hormones could be used for less altruistic purposes‚ perhaps even by military forces.

“No matter what you discover‚ an evil mind can turn it to something bad‚” he said. “This is the problem with discovery.”

But this concern will not deter him from investigating further TCAPs‚ he says. “Say I build a car to get from point A to point B; somebody could put armour and guns on it and make a tank out of it. If I create a hammer to build a house‚ somebody could use it to kill somebody. So when you come up with something like this‚ do you focus on the bad things‚ or do you focus on the good things?”

The general effect of Lovejoy’s hormones seems to be to “reduce anxiety.” In a world where “anxiety disorders” are attracting more and more attention from health professionals‚ Lovejoy’s discovery may be very significant indeed.

His colleague Dr. Denise Belsham‚ also of U of T‚ is also hoping that TCAPs will help people who suffer from anxiety problems. But she does not think we should worry about the hormones being hijacked by the military. “I’m not too concerned because there are other bioterrorist things out there that could be used long before therapeutics for anxiety could be used‚” she said. “I think it really will result in only good things.”

Lovejoy and his colleagues‚ however‚ have a long way to go before they will be able to create any sort of anxiety–reducing drug. They have only just scratched the surface of these hormones‚ and they still have a lot to figure out.

For example‚ the way TCAPs work is not yet fully understood. Inject these hormones into the brains of rats and you can dramatically reduce what lab techs would call their “fear response.” They won’t jump anywhere near as much if you try and startle them with a loud noise—they literally become less jumpy. If you put them on a suspended plank of wood‚ they are much more comfortable exploring around the edge.

“If you inject TCAPs into a high–emotionality rat‚ it will reduce its emotional levels‚” said Lovejoy. He also found that if you give TCAPs to hamsters‚ which normally run up to eight kilometres a night in search of food‚ they stop running altogether. In the lab “they get on the wheel‚ kind of look at it‚ and decide they don’t feel like running.”

“But here is the really interesting thing‚” Lovejoy continued. “If you inject TCAPs into the brains of low–emotionality rats‚ it will make them more active. It basically normalizes behaviour.”

Almost every hormone that we know of has a number of different‚ complicated effects on how you feel and act‚ and so it is very difficult to accurately summarize how any chemical will affect you. At its simplest level‚ TCAP reduces anxiety.

But despite the novelty of Lovejoy’s discovery and the potential he feels these hormones hold for treating human emotional problems‚ he has had a great deal of difficulty getting his work recognized by mainstream science.

“[Our work] was rejected [by journals] time and time again; we spent three years trying to publish our work. It was a novel family of hormones—well‚ most scientists think that families aren’t discovered‚ and they certainly aren’t discovered by little labs at U of T—they’re discovered by big Nobel Prize–winning labs.”

Lovejoy had the same problem trying to get funding for his company after creating it a year ago. “We got rejected three times from grant agencies‚ including the Canadian Institutes of Health Research. They usually said ‘wow‚ this is great science‚ come back to us when you’re ready to do clinical trials.’”

But it takes a long time to go from lab rat studies to actually experimenting on humans‚ and they needed funding to do the preliminary research. Finally they received it‚ from US sources. Lovejoy is ecstatic. “It turns out that we are the first company in the history of the U of T to get American funding‚” said Lovejoy.

Lovejoy’s work on TCAPs was first published in June 2004 in the journal General and Comparative Endocrinology.

Researchers from U of T‚ Switzerland‚ and the U.S. transplanted stem cells from adult human eyes into young mouse embryos that had had some of their eye tissue removed. Stem cells are like “blank cells”; they have‚ to a degree‚ the ability to grow into almost any kind of tissue. Contrary to popular belief‚ stem cells are found in both embryos and in adult animals.

When put in the eyes of mice embryos‚ the human stem cells proliferated and developed properly‚ forming the different kinds of cells that line the back of the eye and allow us to see: photoreceptor cells‚ that catch light‚ and retinal pigment epithelial (RPE) cells‚ which supply nutrients to the photoreceptors and ensure their proper functioning. The stem cells formed the right kinds of cells in the right places‚ resulting in healthy eyes indistinguishable from normal mouse eyes.

“The stem cells are making the cell types that we’d desperately like to make for clinical applications‚” said Brenda Coles‚ lead author of the study. Researchers are hoping eventually to use stem cells to treat eye diseases that involve the death or degeneration of photoreceptor cells and RPE cells.

Degenerative eye diseases usually occur later in life‚ and involve the slow gradual loss of vision‚ often resulting in total blindness. An estimated 1.5 million people worldwide suffer from degenerative eye diseases.

“Right now there’s very little out there that can truly help people that are progressively going blind‚” said Coles.

Coles notes that while it may be ten years before we see any clinical applications from this study‚ the prospects of growing new eye tissue in humans appear good. “[Eye] stem cells behave the same in mice and in humans‚ which is great because it means anything we can do in mice for the most part is going to be directly transferable to humans‚” said Coles. Stem cells found in the brain‚ on the other hand‚ don’t act the same in mice and humans. This might slow the progress of research because any discoveries researchers make in lab animals might not work in humans.

Coles and her colleagues‚ however‚ still have more work to do on regenerating eye tissue in mice before they can be confident in the usefulness of their work. This study was performed on healthy mice that would otherwise have still grown normal eyes. The goal now is to treat unhealthy eyes. The stem cells might grow properly if they are put into a diseased eye.

Researchers are also hoping to find a way to use stem cells that come from patients themselves. Not only would this extinguish a lot of ethical concerns‚ but it would also be a great deal easier on the patients if stem cells from their own eyes could be enticed to grow properly. “We’re trying to go at this from a couple of different angles‚” said Coles.

When asked if this treatment could be used to help people who were born blind‚ her reply was not optimistic: “Probably not.” In addition to having normal eyes‚ humans also need to have properly formed nerve connections between the eyes and brain. People who were born blind never had these connections form properly as a fetus‚ so as of now there is not much hope of restoring their sight.

“[Developing as an early embryo] is one of the hardest things you will ever have to do‚” says developmental biology grad student Mary Kubesh. “Considering its complexity‚ it’s amazing how often it actually succeeds.”

Biologists at U of T have uncovered a piece of the incredibly intricate puzzle of embryological development. Dr. Rudolf Winklbauer and his postdoctoral fellow Hiromasa Ninomiya found that the lengthening of the embryo‚ and the subsequent development of the spine‚ is intrinsically linked to the designation of the head and the tail at opposite ends. This discovery may aid in the treatment of diseases like cancer and spina bifida‚ a birth defect where part of the spine is formed outside of the body.

All animals start off as a single cell‚ the fusion of an egg and a sperm. This single cell divides‚ creating a sphere of cells shaped a bit like a basketball. Through a number of complicated shape changes‚ this sphere folds in on itself‚ expands and grows‚ and eventually turns into something resembling the adult animal. As the sphere folds in on itself groups of cells that are destined to grow into particular organs‚ muscles‚ and other structures are placed in their appropriate locations‚ and the stage is set for the embryo to grow into a full animal.

“You have thousands of cells‚ and they all have to know where to go and when to go there; all of these cell movements have to be coordinated‚” says Kubesh‚ giving an idea of just how complex the growth of an embryo is.

One of the most important changes that takes place as the sphere folds and grows is a process called convergent extension. The cells of the future spine and back muscles converge at the midline and interlink‚ creating a narrow band of tissue in the middle of the embryo’s back and extending the animal from a ball into an elongated shape.

Ninomiya and Winklbauer showed that the extension of the back is intrinsically tied to the establishment of which end of the animal will become the head and which end the tail.

When they took the soon–to–be back cells of a frog and mixed them up in a petri dish‚ the cells moved back to their original positions. “These cells know where they come from‚” said Dr. Winklbauer. Only once the cells were back in their original places‚ and the head to tail axis had been re–established‚ did the back stretch out.

Ninomiya and Winklbauer found that the expression of two genes determines the direction of the head to tail axis. One gene‚ called Xenopus Brachyury is expressed the most at the future tail‚ fading off towards the head. The other gene‚ called chordin‚ is expressed in the opposite manner: the most at the head‚ and the least at the tail.

This pattern of gene expression‚ which determines the “head or tail” identity of the back cells‚ also tells the cells to converge at the midline and extend the embryo (although this mechanism has yet to be determined). “So this is an elegant way to ensure that you always get the axis elongated in the right way‚ not perpendicular or at an angle; you always push the head away from the tail‚” said Winklbauer.

The intellectual credit‚ he noted‚ should be attributed to Ninomiya‚ the lead author of the study. Ninomiya was fascinated by the process of convergent extension even in his undergraduate days and has dedicated himself to studying it for the past several years.

Why do we find certain things sexually attractive? Why might you be drawn to tall men‚ large breasts‚ strong chins‚ or big eyes? A graduate student at U of T may have found a piece of the complex puzzle that is human sexuality.

Ph.D. student Mark Fitzpatrick has shown that genes that underlie our sexual traits‚ both physical and behavioural‚ have effects that stretch beyond the sexual. Genes that affect body shape‚ fertility‚ libido‚ and a huge number of other sex characteristics‚ are also involved in totally unrelated processes‚ such as how well you fight disease. A woman’s large breasts‚ for example‚ may be partially caused by the same genes that give her a heightened immune system. Like many of our sexual traits‚ we still do not know why human breasts evolved—no animal has mammary glands like ours‚ and large breasts do not produce more milk than smaller ones. So why did large breasts evolve‚ and why do some men seem to prefer them?

Fitzpatrick seems to have found part of the answer: something that makes you sexually appealing may have evolved for totally different reasons‚ as a side effect of another function. Moreover‚ your sexual preferences may also have been shaped for reasons unrelated to sex.

This finding may help us enormously towards understanding our seemingly irrational desires. If the gene that gives a man a strong chin (something women are known to like) also makes him‚ say‚ longer–lived‚ then a woman’s desire may not be so irrational after all. Evolution may simply have shaped her to have desires that result in her having the healthiest children possible‚ because women in history who chose strong–chinned men had more children that lived to adulthood.

Evolution‚ through the mechanism of natural selection‚ is usually understood as “the survival of the fittest.” But “fittest” really just means whoever leaves behind the most offspring. An animal may be unusually fast or strong‚ but if it never gets to mate then its athletic genes will never spread.

So Darwin denoted another type of selection‚ which he called “sexual selection.” He thought that any trait that increased your chances of reproducing‚ say a bright bushy tail that females find attractive‚ will spread into the rest of the population. He said this would explain the tails of peacocks: although the weight of the tails prevents male peacocks from flying‚ and the bright feathers make them more vulnerable to predators‚ peacocks have evolved to look that way simply because females like it.

In almost every species with sexual preferences‚ it is the males who do the courting and the females who do the choosing. A female will only produce a small number of eggs in her lifetime‚ maybe even just a few hundred (human women make about 400). A female has to make an enormous investment when she chooses whom to mate with. She doesn’t have many eggs to spare‚ and pregnancy can be incredibly taxing.

Males on the other hand can produce an almost infinite number of sperm in their lives‚ and in most species their responsibility ends after coitus. So a male’s goal is to mate with as many females as he can‚ while a female’s aim is to mate only with the best males.

Modern biologists have found that Darwin was in fact right on the button—sexual preferences have a lot to do with how life on earth evolved. “It accounts for so much of the diversity we see” in living things‚ says U of T’s Dr. Locke Rowe.

Sexual selection is one of the most intensively studied topics in evolution. Scientists have catalogued an immense number of traits whose evolution was affected by sex‚ such as songs‚ colours‚ smells‚ shapes‚ sizes‚ and behaviours.

Moreover‚ biologists have shown that there is a genetic basis for many of these traits. Males have bushier tails because their genes create bushy tails. Some females are choosier than others because they have genes that make them so.

Scientists have assumed therefore that if you have a trait that the opposite sex is known to like‚ then you have it because the opposite sex likes it.

But geneticists have found that almost all genes have multiple functions. A gene that affects the colour of your hair will also affect another‚ totally unrelated aspect of your body‚ such as your heart rate. “Every geneticist will tell you that they believe every gene is [multi–functional]‚” says Fitzpatrick. “But none of the sex scientists were considering this.”

Fitzpatrick investigated this problem using the genetic information now available with the genome projects. A genome is simply all the genes in a particular species. The genomes of the fly‚ mouse‚ rat‚ and human have all been completed.

But just because you know how many genes are in an animal doesn’t mean that you know what each gene does—finding that out is much more difficult. Biologists know a fair bit about what the genes in flies do‚ but comparatively little about human genes.

So Fitzpatrick looked at fruit flies‚ an animal that has been intensively studied by both sex scientists and geneticists. He found that roughly 75 per cent of all fruit fly genes are multifunctional‚ and that the same percentage of the genes involved in sexual selection are multifunctional.

“These genes are multi–tasking‚” he said‚ “which is a really neat idea because when we were first trying to figure out how many genes humans should have‚ we expected them to have well over 100‚000 and fruit flies to have about 30‚000. But it turns out that flies have about 13‚000 and humans 30‚000. One way you can get an animal as complex as a human with fewer genes is if you multi–task those genes.

“It’s really amazing‚” he added.

So due to this multi–tasking Fitzpatrick argues that the genes that underlie our sexual traits may have evolved for reasons other than sex. A gene that gives a bird a bushy tail may have evolved because that gene also gives that bird a more efficient digestion system. Conversely‚ females may have evolved to like bushy tails because their preference would result in them having healthier young.

Fitzpatrick’s study has huge implications: we may like what we like for reasons we are completely oblivious to.

There are many examples of this in the animal kingdom. Male uakari monkeys have red faces‚ and the females are known to like redder faces. But it is now known that the same gene that makes their faces red also makes them resistant to malaria. So the red faces‚ and the female preference in turn‚ may have evolved primarily because of disease.

It is difficult to expand Fitzpatrick’s study to us because sexual selection is not as well studied in humans. Scientists have been able to find a few traits that people subconsciously prefer‚ such as symmetry‚ or pronounced chins on men. But the real way to prove something scientifically is with experiments‚ and it is ethically problematic to experiment on human sexual tastes.

“Say you take a really short guy who has been striking out every night at the bar. Now you put him on a couple of stilts and [see how women’s reaction changes]. Well‚ people don’t really go for this type of thing‚” said Fitzpatrick.

“It’s also very difficult to think about these problems in a clear way‚” adds Rowe.

But the underlying principle of Fitzpatrick’s study no doubt applies to humans as well—genetically speaking‚ we are extremely similar to other animals. We share 98.8 percent of our DNA with chimpanzees‚ and we even share 60 percent of our genes with flies. So his findings may have a huge impact on our understanding of sex.

And all he had to do was examine the information in an online database. “If you’ve got an idea it’s all there‚” he said. “You don’t have to be a scientist to get a hold of this [information]‚ you don’t need special passwords. The only limitations now are your ideas.”

“I think it’s really cool that an early graduate student‚ by surveying a public database was able to answer a pretty fundamental question‚” added Rowe.

Proteins‚ the molecular machines that all life depends on‚ are first created as long‚ thin strands of material‚ which are then folded into complex structures‚ like a piece of string being tied into a complicated knot. Scientists know a great deal about proteins‚ but they still don’t understand how this folding works. This missing information is very important‚ not just for understanding how biology works‚ but for understanding human illness. Many diseases result from proteins not folding properly‚ including Alzheimer’s‚ cystic fibrosis‚ and plaque formation.

“If you understood what the misfolded proteins looked like‚ you could add a drug that would stabilize the folded form‚” says Kay. At some point along the pathway of folding‚ an error occurs‚ sending the protein along the wrong fork in a road. “If you can reroute things by adding a roadblock‚ your drug‚ you can force the correct structure.”

Every action in your body—the movement of a muscle‚ creation of sperm‚ conversion of sugar into energy‚ intake of oxygen—relies on proteins. When your body needs to create a certain protein‚ say keratin‚ contained in your hair and nails‚ or hemoglobin‚ the substance in your red blood cells that sticks to oxygen‚ it reads your DNA for instructions on how to make that protein. Your DNA is like a cookbook‚ a set of instructions for how to make a living thing‚ and a gene is simply a small stretch of DNA‚ the specific recipe for a certain protein.

Proteins are made up of about 20 simple building blocks‚ called amino acids. After reading the gene for instructions‚ the cell creates a long strand of amino acids linked together. Each protein has a different sequence of these building blocks‚ which can run anywhere from hundreds to tens of thousands of amino acids. This long strand then folds through a complicated process into a 3D structure‚ the finished protein. Some proteins are shaped like spirals‚ others like flat sheets‚ others like globular blobs‚ it depends on what the protein is used for.

But scientists have never been able to understand exactly how proteins go from these simple strands into complex shapes. Some sections of the strand fold before others‚ some parts fold into each other‚ some parts don’t fold at all; it’s extremely complicated. Even if scientists know what the series of amino acids in a protein is‚ which is easier now that the human genome has been sequenced‚ they still don’t know what the actual finished protein looks like.

Understanding the folding process is extremely difficult however‚ because proteins fold so quickly that the intermediate states‚ the semi–folded proteins‚ are very hard to find in a cell. Kay and his team used a method called NMR spectroscopy to try and uncover the secrets of these elusive molecules. By subjecting a sample of a specific protein to an incredibly powerful magnetic force‚ they were able to look at what happens when the rare‚ partially folded proteins change into folded ones‚ and through mathematical calculations get a rough picture of what the partially finished protein looks like.

Although he now works in the science of life‚ Kay received his Ph.D. in physical chemistry. “Working on biological molecules is fun‚ you almost always learn something‚ and there’s always questions in biology that nobody has the foggiest idea about‚” he said. “Physicists and chemists deal with smaller systems‚ say four atoms [at a time]. But at the end of the day‚ we live in a world with people‚ and big molecules…so you’d like to do something a little more relevant.”

Imagine spending 95 per cent of your day talking about having feces sucked out of your intestine with a hose.

“Warm water is gently introduced into the bowel through a metal speculum‚ until sufficient pressure builds up that waste matter is dislodged; the direction of flow is then reversed so that the waste water is then sucked out. This pattern is repeated for up to fifty minutes to give the intestine a thorough cleansing.”

Why would one subject oneself to such an ordeal? In a perfect world‚ nobody should ever have to flush water up her ass just to stay healthy. But the lifestyles of the opulent and the poor alike leave much to be desired‚ and alas a diet of steak wrapped in bacon with a side of cheesecake can leave you with an overloaded system that gets so backed up you might not shit for days. The record so far at the clinic was a woman who came in without having unloaded herself for three weeks.

Twenty–one days worth of decaying food was sitting in her gut‚ and it was the pleasure of our therapist to get it all out of her.

I have to say the job was not without its perils. One day I came in to discover that the holding tank had exploded‚ and the entire lower floor of our building was flooded with old‚ murky shit–water. I had to cancel every single appointment that day‚ so no patient coming in would be assaulted by the vile smells emanating from below. This event was not enough to convince my employer to get the system thoroughly fixed‚ however‚ which had dire consequences.

One afternoon‚ a woman about to have her colonic went to use the toilet located next to the treatment room‚ which was hooked up to the same plumbing system. The pipes unexpectedly burst—while she was on the john. Feces began to spew upwards‚ covering the walls‚ ceiling‚ and‚ last but not least‚ her. She was remarkably placid about the accident‚ however‚ and even rescheduled an appointment for a week later.

I asked the “hydrotherapist‚” as they preferred to be called‚ why she would choose to do this for a living. The registered nurse said‚ “Well‚ I went for one myself‚ and after having one treatment I knew that this is what I was going to do with my life.” Chacun a son gout‚ I guess.

It does sound gross and silly‚ but the treatment I have to admit is pretty effective. Aside from relieving bottled up bowels of unbearable pressure‚ washing your insides with water is a really powerful detox.

The lining of your intestines isn’t smooth; it’s full of ridges and small pockets. Over the years small bits of food can get stuck in these indentations and build up. These bits don’t get fully broken down or flushed out; they just stay there and decay‚ turning into fecal toxic waste.

This built up waste makes it more difficult for other crap coming through to pass on‚ which can make you constipated‚ and the more it builds up the more constipated you can get‚ onwards in a vicious cycle. Your bowel should measure two and a half inches in diameter‚ but it is quite common for people to distend their bowels to five inches‚ which stretches out the muscles and makes it even more difficult to go.

That toxic waste is also bad because‚ well‚ it’s toxic. And it blocks one of the body’s major routes to void itself of other foul debris that may be floating around your body. Normally this debris would drift through your circulatory system and get expelled into the bowel and on into the world‚ but with a lining of ultra–rotten crap around your intestinal wall it can’t escape so easily. A lot of people even feel a bit high after the treatment‚ because things start flowing again and old toxins that have been stuck can now run through your veins and get flushed away.

And if you think I’m exaggerating how serious bowel problems can be‚ just remember how Elvis died: on the toilet. The star was‚ among other things‚ so constipated with Texas steaks and pints of ice cream‚ that his overwhelmed system couldn’t handle it. He died at 42 from “cardiac arrhythmia”—he had a heart attack‚ we presume‚ under the strain of trying to force out cemented waste. It is reputed that the autopsy found that his colon weighed 62 pounds.

It has been said that the British are the most constipated people in the world‚ and from my experience this is in fact true‚ as the clinic I worked at was on the outskirts of London. It was actually a full alternative health clinic‚ stocked with osteopaths‚ acupuncturists‚ homeopaths‚ massage therapists‚ hypnotherapists‚ psychotherapists‚ and nutritional therapists.

But while bookings for most treatments were scant‚ we were delivering 85 colonics a week. The massage therapist offered 90 minute‚ full–body aromatherapy massages for £35 (about $80)‚ but people were instead lining up to have a hose shoved up their butts for £65 ($140). We were always booked two weeks in advance‚ and we kept a four–page waiting list for people who just couldn’t hold on for that long. You can’t imagine what it’s like being told “Oh‚ that’s marvellous!” after you’ve just informed someone that there’s a spare colonic appointment at nine a.m. on Saturday morning.

People would book colonics for their friends as presents. People would book in groups of three or four‚ taking a communal day off of work so they wouldn’t have to be alone. Women would book for themselves and their reluctant husbands to spend a day together doing it‚ and couples would frequently book the week before their wedding. People even booked colonics as presents for their lovers on Valentine’s Day.

Of course‚ we couldn’t treat everybody‚ and denying people an appointment over the phone was usually met with stubborn resistance.

“No‚ I’m sorry Ms. Walker‚ we cannot perform the treatment three times in one week; it’s against our policy. In fact the therapist has advised me to put you on our black list.” Clinics often find themselves frequented by people with eating disorders‚ and clinics will not treat them because it only fuels their problem. We usually had one enraged anorexic a week storm out after being told by the nurse that they couldn’t be irrigated.

“No‚ I’m sorry‚ I cannot book for your daughter‚ eleven is just too young to have the treatment…Yes‚ I understand she hasn’t gone in six days…Yes‚ smelling it on her breath really must be terrible.”

You must be wondering then‚ did I take the plunge? I have to admit that I did‚ after feebly telling people on the phone for months that I didn’t know if it hurt or not. I took a spare appointment one day just to see for myself what all the fuss was about.

It didn’t “hurt‚” but it certainly wasn’t all that comfortable—with a speculum lodged up your backside‚ it just felt like taking a dump for a full forty minutes. But afterwards‚ I actually did feel the benefits. My skin was clearer‚ my stomach less bloated‚ and my system was flowing faster than Niagara Falls.

I won’t do it again in the near future‚ however. Not until I become old and clogged‚ or until I become another middle–class mommy with too much time on my hands. Whichever comes first.

Stoichet and Luo are working towards repairing severed nerves‚ both in the spinal cord and in the rest of the body. By getting two severed ends to grow and reconnect‚ nerves could once again flow with information‚ and somebody paralysed by a stabbing wound to the spine may not have to face a lifetime in a wheelchair.

Theirs is not the first method of regrowing damaged nervous tissue‚ but it is far more elegant than older methods. The “goldstandard” for dealing with an injury to the nervous system has always been an autograph—the removal of tissue from another‚ less crucial part of the body and placing it in the injured site‚ as is commonly done for burn victims with undamaged skin from‚ say‚ the buttocks. “This whole field of tissue engineering‚ or regenerative medicine‚ part of the excitement is‚ ‘well‚ what if you didn’t have to do that?’ because when you autograph you create a secondary injury‚ so the idea is to come up with a synthetic replacement‚” says Stoichet.

But not to create synthetic tissue that would remain in the body permanently‚ but to create a kind of temporary scaffolding for somebody’s own tissue to use to grow properly.

Several kinds of temporary synthetics are already available—dissolvable stitches have been used in dental surgery for several years now‚ and there are similar materials used to repair skin and cartilage. Stoichet herself has developed a synthetic scaffolding for bone tissue to grow in‚ Osteofoam‚ which dissolves after new bone has grown through the porous material. Although not on the market yet‚ there is good reason to believe that Osteofoam will find practical use in the very near future.

Tissue regeneration is a huge area of research‚ and a large number of scientists are now trying to come up with ways to repair severed spinal cords and peripheral nerves. But regrowing nervous tissue is considerably more difficult than growing other types of tissue. “The bar is much higher‚” says Stoichet. Nerve cells not only need to grow‚ they need to grow in precisely the right way in order for signals from the brain to reach their proper targets‚ and likewise for sensations from the body to reach the right part of the brain. The highways of the nervous system need to be connected in a particular pattern‚ otherwise a signal intended to move the foot might simply cause a twitch in the knee.

So how do you get a nerve cell to grow in the direction you want it to?

“The idea was‚ ‘let’s start with something nonadhesive‚ agarose [a gel–like substance]‚ and let’s try and create volumes that are adhesive‚’ so we would have adhesive molecules separated by nonadhesive molecules to guide the growth of the nerves.” Nerve cells would be attracted to the adhesive areas at the same time as repelled by the nonadhesive areas‚ and hopefully would grow in just the right direction.

So Stoichet and her former Ph.D. student Ying Luo used a modified agarose gel that‚ if light were shined on it‚ would change chemically.

When photons of light strike the agarose‚ some chemicals are released from the agarose molecules‚ creating new molecules that adhere to growing nerve cells. By striking the agarose gel with lasers they were then able to create channels in the gel—not true physical channels‚ just adhesive areas in the gel.

“So we’re not zapping holes‚” says Stoichet‚ “we’re just changing the chemistry between here and here‚” she says‚ pointing on at the origin and destination of the nerve cell on a diagram.

One further reason that Stoichet’s research is of particular interest is that it does not require the use of new cells. It is the body’s own severed nerves that could be reconnected. There is no need to use stem cells‚ bringing in all the controversy along with them. Stoichet’s method‚ although with no clear practical applications in the foreseeable future‚ could lead to a method of “guided regeneration‚” helping the body’s own nerve cells to reconnect.

“I think it’s really exciting research‚” she said.

A recent study by scientists at U of T‚ McGill‚ and research institutions worldwide has forever changed our understanding of how our genes make who we are—and they did it all by looking at yeast‚ the humble fungus we have used for thousands of years to make beer‚ bread and wine.

How can studying such a simple organism tell us anything about the genetics of humans? Yeast actually share 33 per cent of their genes with us‚ and most of the genes we share are “essential genes‚” genes that we cannot function normally without. Dysfunction in any of these genes leads to death in yeast‚ and in humans leads to a whole host of diseases. So understanding how these genes work in yeast can help us understand the basis for many genetic human diseases‚ like schizophrenia and mental retardation.

Biologists have known for a long time that genes interact in complex ways to determine our traits‚ but “this study shows for the first time just how complex it is‚” says Dr. Charles Boone‚ who co–authored the study along with U of T professor Dr. Brenda Andrews and grad student Amy Tong.

Geneticists used to focus on trying to show how a single gene leads to a single trait—trying to find “the gene” for eye colour‚ or “the gene” for cystic fibrosis. Scientists chalked up differences between individuals to the different versions of each gene that people carry. For example‚ “blue” and “brown” are two different versions of the gene for eye colour. We each have two versions of every gene‚ one from our mother and one from our father‚ for every gene in our body. Some genes have only one form‚ so that all members of a species have two identical copies of each gene. But some genes have two‚ three‚ or even hundreds of versions. The different versions that individuals carry were thought to be responsible for the huge diversity we see in the human race.

But increasingly biologists have come to realize that the way a certain gene expresses itself varies depending on what other genes are present in the same animal. Two people who carry the exact same version of a gene for a certain trait might develop very different versions of that trait‚ depending on the rest of the genes that they carry.

In order to further investigate the problem in humans biologists would require a database of hundreds of thousands of people’s genetic make–ups and their corresponding physical characteristics. But this is currently impossible‚ so scientists are stuck researching much simpler organisms.

Dr. Boone and his colleagues studied the puzzle in yeast. Amy Tong‚ lead author of the study‚ said: “It’s really exciting—we’ve been working for over two years just on this project.”

Yeast have about 6‚000 genes. It is possible to create strains of yeast that are defective in a single gene; scientists therefore have created 6‚000 strains of yeast‚ each defective in only one gene. 1‚000 of these strains die instantly‚ so we know that 1‚000 of the genes in a yeast cell are absolutely essential for the fungus to live. The other 5‚000 strains could still live despite their one single defective gene. But the researchers then asked what would happen if you bred two yeast cells together‚ each defective in one gene‚ to create a yeast strain defective in two genes.

In order to fully investigate this question‚ Andrew‚ Boone‚ Tong and their colleagues had to cross 5‚000 strains of yeast against each other‚ creating 12.5 million doubly defective strains. “It was a lot of fun‚ but it was definitely a lot of hard work‚” said Tong.

“The cool thing about this‚” says Dr. Boone‚ “is that Tong and I got together with a local biotech company and we built some robots that allowed us to cross all the genes together systematically.” So modern automation spared the scientists the arduous task of cross breeding 12.5 million strains of fungus by hand. The result was a “genetic network‚” a kind of abstract representation of all the genes in a species and how they interact with each other. If an individual carrying two defective genes dies‚ those genes are said to interact with each other—they are probably both involved in a similar biological process‚ and when both are defective the system collapses.

They found that there were 100‚000 pairs of defective genes that caused the yeast cells to die‚ or at the very least grow very slowly. For any one gene‚ they found on average that there were 30 other genes that if present in a defective form in the same yeast cell‚ caused the fungus to die.

“This means that genetic interaction networks are very complex and very common. So we think that the genetic basis of probably most of our inherited traits are associated with pairs of [defective genes] rather than [defections] in a single gene‚” said Dr. Boone. “This has huge implications for human disease.”

“We think the importance goes beyond just a bunch of yeast people being interested in how yeast behave‚” said Dr. Andrews‚ “this also tells us how these same genes must be networked and interacting with each other in human cells. So the implications extend beyond the coolness factor in yeast.”

In order for a defective gene to seriously affect you‚ you usually must carry two copies of the defective gene; albinos for example must carry two albino copies of the gene for skin colour‚ one from the mother and one from the father. So if a defective version of any gene doesn’t show up in an individual who has a normal copy of the gene as well as the defect‚ that means that the defective version can spread throughout the population before any people are born that carry two copies of the defective version. In this way diseases can pervade a population unnoticed.

Humans possess somewhere between 30‚000 and 50‚000 genes. To cross 30‚000 individuals‚ each defective in a single gene‚ would result in 450 million people defective in two genes.

If you apply the findings of this study to humans‚ “this means something like one per cent of all humans formed will be screwed up in a particular biological system [due to the presence of two defective genes]‚ which is about the level we see of inherited diseases in the human population‚” said Dr. Boone.

“The importance of this work cannot be overstated‚” says U of T geneticist Dr. Peter Roy‚ who works on a tiny species of worm. He will be using a similar technique on his worms to uncover the genetic interaction network in that species. The ultimate goal for all these researchers is to create a genetic interaction network in humans‚ but in the meantime they must settle for studies on simpler species. Worms are far more closely related to humans than yeast‚ so what Roy finds out will bring us even closer to understanding the genetic basis for hundreds of human disease.

“So yeah‚ like‚ I was just trying to copy down the notes from the last screen on methanosilicate…something or other‚ when like‚ this shot of Anabelle Chong comes up‚ and we’re all like ‘whoa‚ dude!’” said third year chemistry major Jeff Canstellana. “But like‚ nobody said anything‚ we just let him keep going on about the valence electrons and all that shit‚ ’cause like‚ nobody was about to tell him and let him get rid of it. I mean‚ fuck‚ it was like 4:30 that day‚ and nobody was up for learning more chemistry.”

Dr. Lithoovenstein continued his lecture‚ unaware that his presentation had gone awry. The pornographic video of Ms. Chong’s “The World’s Greatest Gang Bang” continued to play onscreen for a further two and a half minutes‚ report students‚ until second year student Jane Stanton quietly approached the professor and informed him of the mix up. Dr. Lithoovenstein‚ after seeing the screen‚ tried to fix the situation with no success.

“So at this point we fucking lost it‚” said third year student Chad Bewicks. “I mean‚ there’s the prof you nailed you with a fucking C minus on your last lab report for not indicating which solvents you used‚ and there he is up on stage frantically trying to hide the fact that he’s a big perv. Fucking genius.”

After being unable to close the program‚ Dr. Lithoovenstein cut the power to his lap top computer. He reportedly left the auditorium immediately afterwards and did not stay to answer students questions as he normally does.

“Yeah‚ that was totally lame of him. I was all ready to ask him if what we had observed was an endothermic or exothermic reaction‚ and which of the three agents was the primary force generating her reaction‚ but buddy totally bailed on us‚” said Canstellana. “That was so not cool.”

Dr. Lithoovenstein was unavailable for comment.

In the classic and often replayed episode‚ Homer whisks the entire family away from Springfield so he can escape a duel with a southern gent. They decide to try and live off the land at Homer’s childhood farm. After no success growing crops in the conventional way‚ Homer laces the barren fields with plutonium to “give Mother Nature a little boost.” The result is a field of tomatoes cross–bred with tobacco plants. Upon biting into the fruit‚ they discover that the tomatoes are filled with tobacco. The townspeople‚ farm animals and Bart become addicted to the “tomaccos.”

Rob Baur‚ a 53 year– old operations analyst for an Oregon wastewater treatment plant‚ was inspired by the episode and decided to try and create the world’s first tomacco plant. He first cut the tops off of a tobacco and a tomato plant and switched them onto the opposite stems—the plants simply died. He then tried hollowing a portion of each plant out and grafting them together. This time it worked.

He now has a plant growing on his kitchen table with the roots of a tobacco plant and one tomato branch. The plant has sprouted one solitary fruit. The roots are pumping tobacco juices‚ so to speak‚ into the tomato branch.

Tests have shown that the leaves do indeed contain nicotine. Now the fruit is being tested for the addictive chemical.

Baur‚ despite being pleased by his sudden notoriety‚ is now feeling anxious about the plant. If the fruit contains nicotine as well‚ the levels might be high enough to kill a human. Orally ingesting a mere 150 milligrams of nicotine can be fatal. He was thinking of selling the plant on E–bay (Homer was offered 150 million for his plant by a tobacco company)‚ but Baur is afraid that the buyer might leave the plant on an office desk or around their house where some unsuspecting person might eat the fruit. His wife allegedly yelled at him for leaving the plant on their kitchen counter‚ as it looks just like any other tomato plant.

No tobacco companies have contacted Baur yet. Many have suggested that he now try creating a tomannibis‚ or maritomato plant and see if that turns a profit‚ but he says he does not plan on it. He may however try creating another Simpson’s delight—the flaming Moe.

He doesn’t do it by himself—a team of engineers‚ armed with electrical stimulators‚ a treadmill and a harness‚ force his legs to move and get him to walk. But the hope is that someday‚ after enough treatment‚ practice and repetition‚ he will be able to get up out of his wheelchair by himself.

Daniel is a subject in a study being conducted by a team of biomedical engineers from U of T and Toronto Rehab. They help people regain the ability to move muscles that became paralyzed‚ either from a stroke or a spinal cord injury. This might involve taking a stroke victim and helping them to move an immobile arm again‚ or getting a car crash victim to move their legs again.

The study is still in its early stages “but so far the results are surprising‚” says Dr. Milos Popovic‚ head of the two labs where the research is being done. One is located in the Rosebrugh Building at U of T‚ and one is at Toronto Rehab’s Lyndhurst Centre near Sunnybrook Hospital.

“If you define ’success rate’ by the number of people that have improved function after going through our study‚ we have a 100 per cent success rate.”

What Dr. Popovic and his colleagues perform is called “functional electrical stimulation.” They apply small electric shocks to the surface of a patient’s skin‚ causing their muscles to contract‚ mimicking what normally happens when a person with an intact nervous system moves.

When you decide to lift your arm or kick your foot‚ your brain sends a signal down through your spinal cord‚ which acts like a highway‚ to activate the nerves that run to the muscle you’re trying to move. A small electrical impulse goes running down your nerve. When it reaches the muscle‚ the muscle contracts‚ in the wave of a hand or the swing of a bat.

But in people with spinal cord injuries the spinal cord‚ the message route‚ has been cut. The muscles and accompanying nerves are all still intact‚ but no signals can reach them. By applying electric shocks to the surface of a patient’s skin‚ you can hopefully get that impulse to reach the nerve you’re targeting. This then triggers an impulse to go down the nerve fibre and replicate what happens in a normal contraction. If you sequence a group of muscles to contract in a specific order‚ you can create a useful movement‚ like the clenching of a fist or the gait of a leg.

This technology isn’t new—people have been using functional electrical stimulation for about 40 years. Many researchers in fact have implanted wires into the muscles of paralyzed people to create movement in their otherwise motionless limbs. Often however‚ after 20 years patients wanted the wires removed because they migrated around their body or even broke‚ and were no longer of any use in replicating motion.

But for about the past five years‚ many scientists all over the world have made the same startling discovery: without surgery‚ with only surface stimulation‚ some patients can actually regain voluntary control of those muscles‚ after just a few months of treatment.

Ten years ago‚ nobody thought this was possible. If you had a spinal cord injury or you had a stroke‚ there was nothing modern science could do for you. Even worse‚ 50 years ago‚ if you had a paralyzing injury you weren’t expected to live even a year. This was mainly due to a lack of bowel and bladder control that led to severe infections‚ because handicapped patients then simply did not receive adequate care and attention.

Yet today labs all over the world‚ including several others in Canada‚ are reporting the same thing: paralyzed muscles can in fact be reawakened.

There are other labs that perform this same basic procedure‚ but Dr. Popovic and his associates add another layer to the treatment: they ask their study subjects to do a certain task‚ for example‚ picking up a pen‚ when they apply treatment. The subject has to imagine what it would feel like to make the motion‚ and they have to strain themselves. The electric shock is then applied‚ and the muscles contract. The idea is that if the brain is giving output to the hand to move‚ and the muscles actually contract‚ the brain will get feedback about what has happened in the system and will in a sense “relearn” how to move those muscles. “The brain has a certain amount of plasticity‚ so you can retrain it‚” says Dr. Popovic.

One of the most remarkable things about this study however is that nobody knows how or why it works. It may be that damaged nerves get re–grown‚ or that pre–existing nerves get rewired to perform different tasks. Nobody knows for sure. But one thing is certain: the treatment works.

It hasn’t worked for all patients‚ thus far‚ but it has for many. Christopher Reeves used a similar method to regain the use of one of his fingers after four months of treatment. “But for us that’s very little improvement‚” says Dr. Popovic. “You spend too much time and energy just to move one finger‚ it’s a waste of time.”

The electrical shocks are certainly not pleasant‚ says Dr. Popovic. “But it doesn’t damage the tissue‚ it doesn’t cause any side effects‚ you just have to get used to it. It’s like a bad–tasting medicine that is good for you.”

The attitude around the lab does feel a bit like “tough love”—Dr. Popovic can be quite firm with squeamish subjects. He often resorts to stimulating his own arm to demonstrate that it is safe.

Dr. Popovic mainly conducts studies on grasping—trying to help people regain the ability to pick up and manipulate objects. Dr. Adam Thrasher‚ a Canadian Paraplegic Association of Ontario post–doctoral fellow‚ is in charge of something even more ambitious: the locomotion study. He is helping people in wheelchairs walk again.

Until recently‚ Dr. Thrasher has only been able to help about 10 to 15 per cent of the population of people with spinal cord injuries. Every spinal cord injury is different‚ and there are varying degrees of paralysis‚ from total body‚ to just below the waist‚ to just one side of the body. Some people are unable to move their legs at all and are completely confined to their wheelchairs. Others however are able to get up out of their chair and stand‚ hobble around a bit‚ or even walk very short distances. They usually do so with help or with assisting devices‚ like rollers‚ leg braces‚ and canes. It is only these people‚ called “partial ambulators‚” that Dr. Thrasher has been able to treat‚ because they are able to stand up and try out various walking exercises. After three or four months of repeated stimulation‚ Dr. Thrasher has been able to get some patients to walk faster‚ and with fewer assisting devices. “I firmly believe from our pilot studies so far that we can make them walk better‚” says Dr. Thrasher.

The most dramatic example he cited was a man that came in walking at only 0.2 meters per second‚ who after the study could walk at 0.6 meters per second (normal walking speed is about 1.0 meters per second). This may not sound like a huge difference‚ but it means that now this man can cross the street before the light changes to red. “I mean‚ that just opened up a whole new world for him‚” he says.

But now‚ with a shiny new piece of equipment called a body weight support treadmill‚ Dr. Thrasher can expand his treatment to a possible 50 per cent of the spinal cord injury population. “A lot of my subjects are calling it the ‘50 Cent machine‚’ after the rapper’s music video‚ so I’ve started calling it that because it means a lot more to them than ‘body weight support treadmill.’”

With harnesses and counterweights to take the load off a patient’s feet‚ a running treadmill‚ the right sequence of electric shocks‚ and sometimes even a pair of hands to help move their feet‚ Dr. Thrasher can take people who cannot walk at all and get them to cruise along the treadmill‚ their chair sitting unused in the corner. “They’re walking with a lot of assistance‚ but you know‚ it’s walking‚” said Dr. Thrasher.

Daniel is one such patient. He is paralyzed from the waist down‚ but because he still has some sensation in his legs and relatively strong muscles compared to many other handicapped individuals‚ Dr. Thrasher thinks he may be able to help him regain the ability to stand and move about a bit on his own. “If we can help them restore some of their walking functions so they can do more than they could‚ it’s a huge jump in independence and it’s a huge increase in their quality of life as well‚ and that’s the bottom line for us. We just want to make their lives better.”

Daniel’s treatment is particularly exciting‚ because textbook knowledge states that the only way to help people with a spinal cord injury or a stroke is immediately after their accident—wait a few years and the window of opportunity is lost. But Dr. Popovic and Dr. Thrasher have already cast doubt on this‚ having helped several people years after their injury.

Dr. Thrasher is modest about what he hopes to achieve with his subjects. The science is still very new. But his patients seem more optimistic about his ability to help them. “He’s the man‚” says Daniel.

Dr. Popovic’s patients show similar enthusiasm. “I was thrilled to death right off the bat to be one of the lucky ones to be included in the electric chair program‚” jokes Ivaan Kotulsky‚ who lost the use of his right arm after his second stroke in December of 2002. He began treatment with Dr. Popovic in January of 2003‚ stopped in February‚ and then started again in August. He can now freely move his arm about the shoulder joint‚ and can pick up objects easily. “I can open a can‚ I can cut a bagel now‚” says Kotulsky. He isn’t however ready to quit the treatment. Kotulsky‚ a jeweller‚ used to own a store on Queen St. West called The Lord of the Rings where he sold his own handcrafted jewellery. “That’s why I want my hand back. I don’t care if I hobble‚ but I want to impress the hell out of everybody by showing them the bracelets and rings I can still make‚” he says.

Dr. Mark Tonack is an anthropologist with Toronto Rehab‚ who is conducting an independent survey of Dr. Popovic’s patients to assess how much the treatment has really helped them‚ to see if the lab is all it’s cracked up to be. “Even I’m quite surprised that everybody that I have talked to has very positive feedback on the treatment‚” he says. “There were clients that came in that couldn’t even open or close their fingers‚ or grasp objects‚ and after participating in the treatment regime they were able to open their hand‚ move their fingers and grasp objects. It may not sound remarkable if you’re not familiar with people with spinal cord injuries‚ but for a quadriplegic it means the difference between being able to hold a pen‚ being able to drive their wheelchair themselves‚ being able to shave themselves.”

Subjects in the study do not have to pay for the treatment‚ nor does OHIP pick up the bill. Research money pays for treatment given to study subjects‚ but both Thrasher and Popovic provide treatment free of cost to other people as well. Neither feel the clinic is adequately funded—the waiting list is quite long with people desiring treatment for whom there just isn’t the time or money for yet. Their intention is to establish a stable funding source that would allow them to treat any patient desiring it. They also stress that more student volunteers would help them considerably.

Nevertheless‚ improvements in treatment for paralyzed people are not likely to stop here. A great deal of research is investigating the potential to re–grow damaged nervous tissue‚ one of the goals of stem cell research. “If stem cell research can truly start re–growing central nervous system cells [the cells of the brain and spinal cord]‚ that’s great‚ because that’s something that we didn’t use to think was possible a long time ago‚” says Dr. Thrasher.

But‚ stress both Dr. Thrasher and Dr. Popovic‚ even if you successfully re–grow such tissue‚ that doesn’t mean that a patient with a new set of nerves will be able to walk—the nerves and the spinal cord will still have to be “taught” how to work in the right way to create an action as complex as walking‚ and functional electrical stimulation is clearly one way to accomplish this. “A very simple example is that of the Russian astronauts sitting on MIR for 300 days straight—you bring them back‚ they have complete nervous systems‚ but they can’t walk‚” says Dr. Popovic. “You have to train them for months‚ literally‚ to teach them again how to walk.”

They might only be truly walking around a controlled lab environment now‚ but considering that 10 years ago they had no hope at all‚ the future is clearly bright for people who never thought they would get out of their wheelchairs again.

Amid the clutter of textbooks‚ journals‚ papers and reams of notes in the office of Dr. Mohini Sain sit a car door‚ a bus seat‚ an instrument panel‚ a deck plank‚ and a car bumper—all of them made from hemp.

Dr. Sain is a professor in U of T’s Faculty of Forestry and the Department of Chemical Engineering and Applied Chemistry‚ and has conceived of more things to do with hemp than you can think of to do with the strongest (mechanically speaking) of hemp plants‚ cannabis. “We look at the potential for hemp in automotive parts‚ sports apparel‚ the furniture industry‚ aeronautics‚ and the medical industry‚” Dr. Sain said. You can make skis‚ dashboards‚ bumpers‚ I beams‚ cross ties for railroad tracks‚ canoes‚ tennis rackets‚ basketball stands‚ car door panels‚ roof shingles and a myriad of other things from the materials that he and his collaborators have developed. And hopefully‚ in the very near future‚ we will be able to make biomedical supplies‚ like bloodbags‚ and even airplane parts from hemp.

“Our direction is to move away from fossil fuel based synthetics to more natural alternatives‚” said Dr. Sain.

How does he manage to turn fluffy green cannabis plants into car siding capable of withstanding a full–on impact? A long chemical process allows Dr. Sain to extract long‚ thin strands of pure starch‚ or cellulose (a long chain of sugars) from hemp. In the plant‚ many of these strands put together make a hemp fiber. By first isolating individual strands and then reassembling them back into fibers‚ chemists make fibers with as few defects as possible‚ making them much stronger. They can also control the length and diameter of the strands—the longer and thinner the strand‚ the stronger it is.

By enmeshing hemp fibers into a matrix of glue‚ Dr. Sain has been able to create plastics almost identical to conventional plastics (save for their brown colour). The glue could be synthetic‚ or it could be natural—there are already many bioplastics made from soy or corn being used. Dr. Sain is particularly interested in producing construction materials from a glue of wood resin interwoven with hemp fibers. The wood resin could easily come from leaf litter and forest floor debris‚ he said. Fewer trees would have to be cut down than are needed to support our current construction business.

The technology is not entirely new—for years Dr. Sain and many other scientists have been making biomaterials‚ or industrial materials made from natural products. You may even have already ridden in a car made with hemp parts. Dr. Sain’s fiberglass–like hemp material has been used in car door siding for two years now. Transit seats made from 100 per cent hemp with a polyester glue are already in widespread use. “The first generation of biomaterials has already been in use for several years. For example‚ in the construction industry‚ if you go to places like Home Hardware‚ you can find decking materials made from synthetic plastics combined with wood fibers or rice husks‚” said Dr. Sain.

Dr. Sain is working towards improving the strength and durability of these materials‚ and devising even more ways of using hemp commercially. He hopes that he will be able to create steel interfused with hemp. Weaving hemp fibers into steel makes the metal stronger‚ which would allow auto manufacturers to lower the thickness of the steel they use. Not only would this mean using less steel‚ but it would also mean making a much lighter car that would use far less fuel‚ costing less for everyone and creating less pollution. Win–win.

With such a development you could literally build a car from the inside out with hemp–the steel frame and body‚ hubcaps‚ bumpers‚ instrument panel‚ seats‚ and seat coverings all could be made with hemp.

Dr. Sain is also optimistic that within a few years we will have blood bags and other biomedical supplies made from hemp. Syringes and gloves and other medical gear‚ by and large‚ cannot be reused‚ but ones made from hemp would be 100% biodegradable. He and his associates will first have to ensure however that these biodegradable materials will be safe for human use. No matter how fond you are of environmentally friendly alternatives‚ an IV bag that slowly disintegrates into your drip and your veins is not a pleasant thought.

Hemp alternatives not only make environmental sense‚ says Dr. Sain‚ they make economic sense. “We look to make environmentally and economically sustainable materials.” By creating industrial products with hemp‚ “you can bring some of this value back to the farmers who grow the plants‚ and then you can develop some small industries and employ some people to make these materials. You not only give added value to the farmers‚ you also get additional employment.

“This is a public issue. That’s why we are scientists—we are interested in accepting the challenges and finding solutions. We meet the concerns of the public.”

“It was all–consuming. Everything stopped. My whole life was put on hold‚ it was completely focused on SARS. Some nights lying in bed after I’d finally got home I’d think ’Is this ever going to end?’”

Dr. Donald Low‚ Chief Microbiologist at Mount Sinai Hospital and Professor of Microbiology and Medicine for U of T‚ was Toronto’s man of the hour during the SARS outbreak last spring. He dealt with patients himself on the front lines. He reviewed treatment and containment procedures‚ and helped develop policies with the city. He reviewed reams of suspected and probable SARS cases. He became an ad hoc spokesperson for the city’s health care system‚ appearing on the evening news almost daily.

“He fulfilled a need that we had—Don is very much an expert in infectious diseases and his help and assistance to Toronto Public Health was just invaluable in helping us to learn about this disease and how to control it‚” says Bonnie Henry‚ Toronto’s assistant medical officer of health. “Don speaks his mind‚ he’s very honest and open‚ and I think that made him a perfect spokesperson for these complex issues. He was able to put them in a framework that people understood.”

“He did a fantastic and exemplary job—he had quite an intense amount of responsibility‚ and he certainly met the challenge extremely well…the pressure was on‚ and he rose to the challenge‚” says Dr. Hanif Kassim‚ associate medical officer of health for York region. “He is different in the sense that he took a lot of time out of his busy schedule to assist us and to provide information to the public.”

“None of what I did for this city was in my job description‚” says Dr. Low. He stretched himself so far that his weight dropped from 170 lbs. to 145 lbs. during the outbreak.

“In the early days of SARS‚ it was incredibly stressful…we really didn’t know what we were dealing with‚” he says. “When we saw the disease spread to [nurses and hospital workers]‚ we thought ‘Oh god‚ are we going to be remembered as the entry point for this disease for the rest of North America?’”

Dr. Low was put into quarantine himself after coming into contact with a colleague who had developed SARS. “There was a real concern that he may have gone on to get sick‚ and we were very grateful that he didn’t because we needed his help‚” says Dr. Henry‚ who ordered Dr. Low into isolation.

Dr. Low didn’t really think he really had the disease‚ but being in an age group with a mortality rate of 40 per cent made his safety a real concern. By going into isolation‚ he became the quarantine poster child‚ setting an example for all those who disregarded orders to remain in isolation. The quarantine however was not an opportunity for rest—Dr. Low found himself just as swamped with work at home. Sitting through two–hour–long conference calls and fielding phone calls and faxes from the media every day barely left him time to eat.

Despite the toil‚ Dr. Low doesn’t regret offering his help to the city. “I wouldn’t have missed it for the world. It was probably one of the most significant things that’s happened in my life…it was just so surreal‚ medically nothing compares to what happened in those four months.”

Not being connected to Toronto Public Health or the Ministry of Health placed Dr. Low in a unique position‚ one that many people in this city found reassuring. “I think people appreciated having somebody as spokesperson that was more involved at the grassroots level‚ instead of [Ontario’s Chief Medical Officer of Health] Colin D’Cunha or [Commissioner of Safety] James Young‚ who were involved at a much higher level and hadn’t even seen a patient‚” he says.

Dr. Low became particularly well known for saying that the WHO travel advisory was “a bunch of bullshit‚” a gut reaction that came moments after hearing about the advisory from a CBC journalist. “I was absolutely livid‚” says Dr. Low. The advisory was issued after the first phase of the outbreak was over and it was clear that the spread was not going to get worse.

“It was actually quite funny—that day‚ we were so busy‚ I had two cell phones and a pager. These people came in from the Center for Disease Control [in Atlanta] to help us. They were sitting across a table from me at a hotel‚ and I was on both cell phones for fifteen minutes…they were just shaking their heads…they must have been wondering what the hell they’d gotten themselves into.”

Dr. Low himself held a phone meeting with the WHO to discuss the advisory. “There was no good explanation. They didn’t present any data to convince any of us that this was an appropriate thing to do‚ it was not based on any science‚” he says. As scary as the SARS outbreak may have been‚ the disease spread was almost entirely confined to the hospital environment. Many assume that the advisory was issued for political reasons‚ as China was outraged at being given travel advisories themselves. The WHO had no criteria for a travel advisory at the time. They came up with criteria later‚ which Toronto did not in fact fulfill during the peak of the outbreak.

Dr. Low became notorious during the SARS outbreak for refusing to mince his words or gloss over the truth. He received more than 1500 requests for interviews through Mount Sinai. “The media attention was unbelievable.

“You have to give the government credit‚ nobody ever once told me to shut up. They used to shudder when I spoke. I wasn’t trying to be sensationalist or anything‚ I mean if somebody asks me a question I give an honest answer.”

Dr. Low wasn’t even reprimanded after he criticized Health Canada’s definition of what constitutes a “probable” SARS case. The definition categorized a “probable” case as being “severely progressive‚” but to define an individual as such would require monitoring them over a period of time. So an individual walking into emergency with a cough‚ a fever‚ a suspicious chest X–ray‚ and who had been working at a hospital could only be defined as “suspect‚” lowering the total number of defined cases and masking the severity of the outbreak. After Dr. Low told CBC radio‚ “I can tell you that there’s a lot more patients out there that have SARS than we’re letting the rest of the world believe‚” Health Canada changed its definition within 24 hours.

Toronto’s response to the crisis was at best makeshift‚ and many mistakes were made. Dr. Low surmises that somebody should have been put in charge of the entire affair from the beginning‚ a “SARS Czar‚” to effectively coordinate the city’s efforts. Dr. Low doesn’t however think that he himself should have been Toronto’s SARS Czar. “I wanted that to be David Naylor [Dean of the Faculty of Medicine at U of T]‚ somebody with that kind of organizational ability.” Dr. Naylor’s report on the SARS outbreak‚ yet to be released‚ is expected to be highly critical of the way the outbreak was handled.

Dr. Low doesn’t think that SARS will come back to Toronto. Should any new disease threaten the city in the future‚ it is likely that the infrastructure will be in place so that somebody like him won’t be loaded with so much responsibility.

Since the outbreak Dr. Low’s schedule has in fact gotten busier. A SARS expert‚ he is constantly traveling to conferences throughout North America to discuss the outbreak. “It’s another layer of responsibility. But‚ you know‚ its fun.”

Dr. Low is the author of over 170 published articles. His laboratory at Mount Sinai conducts research on antibiotic resistance in bacteria and on necrotizing fasciitis (the “flesh–eating” disease). He also has part–time teaching responsibilities‚ mostly through the Faculty of Medicine.

When asked if he would rather be a full–time professor at U of T‚ Dr Low replied‚ “Oh‚ god‚ no—this is the best job in the world.”

The scientists‚ led by Dr. Mircea Sanduloviciu of Cuza University in Romania‚ created a low temperature plasma of argon gas—a mixture in which some of the argon atoms have split into positively charged ions and negatively charged electrons. They then inserted electrodes into the gas and sparked the chamber with electricity. Spheres of gas formed spontaneously‚ with a layer of positively charged ions on the inside and negatively charged electrons on the outside. The spheres were filled with normal argon gas atoms. The researchers were able to create bubbles as small as only a few micrometers in diameter‚ to as large as a few centimeters in diameter.

These spheres are capable of more than just floating around their chamber‚ however. The scientists say that they can split in two‚ like a bacterium divides into two daughter cells. They apparently are also capable of growing—under the right conditions they can turn normal argon atoms into plasma‚ which is then used to expand the boundary of the sphere. Even more remarkable‚ the spheres are purportedly able to communicate. By emitting electromagnetic energy‚ the spheres could make the atoms inside of other spheres vibrate at a specific frequency. The results of this experiment appear in the 2003 issue of Chaos‚ Solitons‚ and Fractals (volume 18).

For something to be considered alive it has to meet five requirements: it must have a clearly marked boundary separating itself from its environment‚ it has to be able to reproduce‚ grow‚ communicate information‚ and it has to have some kind of inherited genetic information‚ like DNA‚ that it can pass on to offspring.

These spheres meet only the first four criteria‚ so they aren’t alive in the traditional sense. This doesn’t mean however that they don’t constitute some form of life‚ in an expanded sense. Viruses for example aren’t technically alive‚ as they can only reproduce when they have a host cell to use‚ but they meet all the other criteria for life‚ including having their own genetic material.

More importantly however‚ these spheres may help to expand our understanding of the origins of life.

It is thought that life began about 3.7 billion years ago‚ when the Earth’s atmosphere was rife with the gases methane‚ ammonia‚ and carbon dioxide. Electrical storms were frequent at this time‚ and electrical energy may have sparked the formation of the first biological molecules in pools of water (i.e. complex molecules that are created and used by living organisms‚ like sugars‚ or nucleotides‚ the building blocks of DNA). In a now famous experiment conduced in the 1950s‚ Stanley Miller shot an electric current through a mixture of water‚ ammonia and methane. He was able to create several different kinds of complex organic molecules‚ including amino acids‚ which are the building blocks of proteins.

Biomolecules aren’t only found on Earth however. Sugar and alcohol have been found in deep space. An amino acid was also detected in a cloud of gas and dust in deep space last year by scientists at the National Taiwan Normal University. German scientists found earlier last year that amino acids can be generated in deep space simulators‚ by irradiating a mixture of gases and ice with UV light. NASA scientists were also able to create bits of material similar to cell membranes using deep space simulators.

Scientists have been finding amino acids in meteorites for decades. They have found over 70 different amino acids on meteorites. Only about 20 amino acids are used by living organisms on earth.

Europa‚ one of Jupiter’s moons‚ is covered with ice‚ underneath which is believed to lie an ocean of liquid water. The Galileo space probe (which ended it’s 14–year career this Sunday‚ see brief) has detected yellow–brown stains on the surface of Europa‚ possibly implicating the presence of organic substances. Moreover‚ scientists at NASA found that simulating meteor impacts on Europa by shooting aluminum bullets into blocks of ice could generate electrical sparks.

So the potential for life to have evolved elsewhere in the universe as it has on Earth is quite high. Some even surmise that life on Earth was spawned by asteroids carrying biomolecules or even bacteria.

While the synthesis of biomolecules can occur rather quickly‚ the evolution of a living cell is thought to have taken millions of years through an incredibly complex process.

But these new argon spheres take only a few microseconds to form. Dr. Sanduloviciu and his colleagues believe that they have not simply created some new form of pseudo–life—they think they might have found the origin of life on earth. The early atmosphere on Earth was full of ionized gases like the argon gas used in this experiment‚ due to the prevalence of electrical storms. The Romanian scientists postulate that these spheres could have in fact been the starting point for the evolution of life on earth.

Most scientists won’t be swayed to this theory any time soon—the gas bubbles can only be created at temperatures too high for other biomolecules to be synthesized. But these gas bubbles‚ should they stand up to scientific peer review‚ certainly challenge the definition of exactly what constitutes a living thing‚ and raise the number of possibilities for how life could have emerged elsewhere in the universe.

“Fluoridation is the greatest fraud that has ever been perpetrated‚ and it has been perpetrated on more people than any other fraud.” Dr. Albert Shatz.

We all take for granted that adding fluoride to our drinking water is a safe and effective way to prevent cavities‚ but just how much do we know about the side effects of water fluoridation?

“The evidence shows that it is effective and safe‚ and has made a wonderful contribution to the health of kids in North America‚” says Dr. James Leake‚ head of Community Dentistry at U of T. “In 1959‚ 89 per cent of 13–year–old children examined in Toronto had had one or more cavities in their life.” Toronto began fluoridating its water in 1963. “By 2000‚ only 39 per cent of 13 year olds had had one or more‚ so 61 per cent of all children had never had a cavity. It’s hard not to appreciate what a difference fluoridation has made.”

Thousands of other such studies that have been done all over the world since water fluoridation began in 1945. Dr. Leake pointed to a study done in 2000 by the University of York in the UK. “They did the best and the most comprehensive review of all the world’s literature and came to the conclusion that it was both effective‚ and the doses being provided are safe.”

But not all dentists and health professionals agree on the benefits of fluoride. A sharp divide is emerging between those for and against water fluoridation.

“I used to teach dental students that fluoridation was the most inexpensive way to deliver fluoride to everyone in the community‚” said Dr. Hardy Limeback‚ head of Preventive Dentistry at U of T. “But‚ after thoroughly reviewing the literature‚ I discovered that there was little‚ if any‚ benefit from swallowing fluoride‚ and that there were significant risks from the long–term ingestion of fluoridated water.”

When ingested‚ as opposed to applied directly to the teeth as in a fluoride treatment or with toothpaste‚ fluoride accumulates in the body‚ and according to Dr. Limeback‚ can cause health problems. “There has been a huge increase in dental fluorosis in Toronto‚” he says. Dental fluorosis is a condition caused by an excess of fluoride exposure‚ which can range from faint white markings to unsightly brown stains. “This condition is the first sign that the body has been over–dosed with fluoride‚” said Dr. Limeback. About 12 per cent of the population of Toronto has dental fluorosis‚ according to both Dr. Leake and Dr. Limeback.

“Symptoms of too much fluoride accumulation over a long time include the early stages of skeletal fluorosis (joint pain)‚ an increased risk for bone fracture‚ and thyroid dysfunction‚” said Dr. Limeback. Other studies suggest links between fluoridated water and cancer‚ genetic damage‚ neurological impairment‚ and early menstruation in girls.

“Many researchers have published that the main effect of fluoride is a topical one‚ and that there is little benefit to ingesting fluoride‚” said Dr. Limeback. “The Centre for Disease Control in Atlanta has acknowledged this in their recent report‚ stating that ‘The laboratory research that has led to the better understanding of how fluoride prevents dental caries indicates that fluoride’s effect is…topical and that the effect depends on fluoride being in the right amount and in the right place at the right time.’”

A Brita filter does not remove fluoride from drinking water—the only way to remove fluoride is through distillation‚ or by the use of ion–exchange columns.

Of particular concern for opponents of fluoridation are the chemicals used to fluoridate tap water. More than 90 per cent of the tap water in North America is fluoridated using hexafluorosilicic acid and its sodium salts. “These are waste products obtained from the pollution scrubbers of the phosphate fertilizer industry‚” said Dr. Limeback. “They contain trace amounts of arsenic‚ lead‚ and other toxic chemicals.”

An official from the City of Toronto Water and Wastewater Services confirmed that hexafluorosilicic acid is used‚ but was uncertain of the precise composition of the mixture—which is not produced in Canada but in the United States. The distributor for Toronto’s water fluoridation chemicals is LCI Ltd.‚ located in Jacksonville‚ Florida. Gustavo Navar‚ senior chemical engineer for LCI Ltd.‚ confirmed that the hexafluorosilicic acid used in water treatment is obtained from phosphate fertilizer companies‚ which produce the compound as a by–product from the production of phosphoric acid.

When asked about the precise composition of the mixture‚ Navar said: “These are not 100 per cent pure chemicals—I’m sure there are traces of arsenic in there.” He added‚ “The material meets Canadian and American standards for products to be used in water treatments.” Further information about the company that produces the mixture was not forthcoming.

“Repeated analysis of this toxic waste product shows it to be contaminated with up to 2 per cent by weight with toxic‚ carcinogenic trace elements such as radium and arsenic‚” Dr. Limeback said. “Even when the liquid is diluted and trickled into the drinking water‚ it adds between 0.5 to 1.4 parts per billion arsenic to the drinking water‚ which‚ according to the National Academies of Sciences in the US‚ increases the cancer risk from between 1 in 10‚000 to 1 in 5‚000. That means that it is possible that up to 1‚000 cancers in the GTA area can be attributed to the drinking water fluoridation chemicals.”

Two published studies have shown that silicofluorides significantly raise blood lead levels in children. One study found higher rates of violent crime‚ hyperactivity‚ heart disease‚ and drug abuse in communities using silicofluorides—all conditions known to be linked to lead and other heavy metals.

“These chemicals were never tested for safe use on humans‚” said Dr. Limeback. Clinical trials were performed on sodium fluoride‚ which was originally used when water fluoridation began in 1945. Those studies found no adverse health effects. However‚ communities began to switch to silicofluorides in 1947‚ “”without any animal or human tests having been done.”

“No one has explained to me why governments would allow toxic waste to be trickled into our drinking water but the conclusion is obvious—large corporations save enormous amounts of money by selling the toxic waste to cities rather than paying large sums of money to clean it up and dispose of it properly‚” said Dr. Limeback. “Conservative governments won’t push corporations to clean the fluoridation chemicals.”

Dr. Limeback is not alone in his public opposition to water fluoridation.

Dr. Charles Gordon Heyd‚ past president of the American Medical Association‚ said in a July 2000 letter concerning the proposal to fluoridate the water in Palo Alto‚ California: “I am appalled at the prospect of using water as a vehicle for drugs. Fluoride is a corrosive poison that will produce serious effects in a long–range basis. Any attempt to use fluoride in this way is deplorable.”

On July 7‚ 1997‚ 1‚500 Environmental Protection Agency (EPA) scientists‚ engineers and lawyers who assess the scientific data for the Safe Drinking Water Act standards and other EPA regulations went on record against the practice of adding fluoride to public drinking water. “It is our hope that our co–sponsorship of the Safe Drinking Water Initiative to prohibit fluoridation will have a beneficial effect on the health and welfare of all…by helping to keep their water free of a chemical substance for which there is substantial evidence of adverse health effects‚ and‚ contrary to public perception‚ virtually no evidence of significant benefits. We conclude that the health and welfare of the public is not served by the addition of this substance to the public water supply.”

Dr. John Colquohoun‚ once Auckland‚ New Zealand’s Principal Dental Officer and former fluoridation advocate‚ initially dismissed studies that showed that dental decay did not significantly decrease in fluoridated communities compared to non–fluoridated communities. He later said in a 1997 report‚ “I now realize that what my colleagues and I were doing was what the history of science shows all professionals do when their pet theory is confronted by disconcerting new evidence: they bend over backwards to explain away the new evidence.”

Despite mounting evidence shedding doubt on the safety of water fluoridation‚ Dr. Limeback has found it difficult to present his case. “It has been hard defending my views. I have been ridiculed and I have suffered character assassination. I have been accused of lying‚ misrepresenting scientific evidence‚ citing literature selectively and quoting only so–called ‘junk’ science to support my views. I have been ridiculed by dentists and politicians at public hearings‚ and I have been formally attacked by other scientists in the field. The most opposition has been from the public health sector. That’s understandable. The public health officials do not want to lose face. They may even fear litigation.
“To be honest‚ my career has suffered so much‚ that I regret ever coming forward at all in the first place—I wish I had just kept my mouth shut.”

Dr. Limeback‚ however‚ is not the only individual who has found himself challenged on water fluoridation.

In 1992 Dr. William L. Marcus‚ the Senior Science Advisor to the EPA’s Office of Drinking Water‚ was fired after calling for a national review of water fluoridation. The EPA stated that he was fired due to professional difficulties; Marcus claimed that he was fired for his views on fluoride. A judge ordered him reinstated to his job‚ concluding that he was fired “because he publicly questioned and opposed the EPA’s policy.”

In 1994‚ Dr. Phyllis Mullenix‚ the head of Toxicology at the Forsyth Dental Center in Boston was fired after her publication of a study that found fluoride to be a central nervous system toxin‚ causing a reduction in IQ in children. Forsyth claimed she was dismissed because her work was not “dentally related.”

“Public health scientists have‚ for over 50 years‚ used selective literature citation to push water fluoridation‚” said Dr. Limeback. “It is the responsibility of the public health authorities to prove that fluoridation is absolutely safe. There are warning labels on toothpaste in the US that recommend you contact a poison control centre or a physician if you ingest more that what’s used for tooth brushing. That means if you ingest the equivalent of about 0.5 L fluoridated drinking water‚ you’ve just been poisoned with fluoride‚ according to the toothpaste warning label.”

When asked why governments would advocate fluoridation‚ Dr. Limeback replied: “To appear to be ‘helping the poor’ and at the same time trying to reduce dental care costs–poor people have a higher rate of dental decay. More children on social services requiring dental care are being turned away by dentists who can no longer afford to provide dental care below cost.”

Dr. Leake‚ in favour of fluoridation‚ echoed Dr. Limeback’s concern for the dental health of the poor. “About a third of children in Toronto live in poverty‚” said Dr. Leake. “Public health is aware of the needs of those kids‚ and need to maintain fluoride levels for children who wouldn’t get the benefits from fluoride in any other way.

“I think it’s an absolute necessity to establish a universal dental health care plan‚” said Dr. Leake‚ but added that the costs of such a program would far exceed the current expenditures on water fluoridation.

“Most of Europe has rejected fluoridation‚” said Dr. Limeback. “So has Japan. It’s time that North America looked really carefully at the practice of fluoridation. The benefits no longer outweigh the risks. I would like to see fluoridation stopped and the money spent providing better preventive care to targeted groups of the population.”

“Pathologists assume when they see a bruise that it was made before death‚ but there has never been any research done that proves that one can tell if a mark was made before death or after death‚” said Avon. This seemingly minor detail could be crucial in court‚ and Avon set out to study the subject.

Her method of investigation: biting pigs.

“Pig skin is the closest animal equivalent to human skin‚ histologically‚ physiologically‚ and immunologically‚” said Avon. So she decided to inflict bite marks on a juvenile Yorkshire pig at four different time intervals—one hour before death‚ five minutes before death‚ five minutes after death‚ and one hour after death‚ to see if any difference could be seen between the bite marks. But what to bite the pig with?

“We had to design an appliance to inflict a bite mark‚ because I certainly didn’t want to bite the pig myself. We also wanted to make sure the bite would be consistent each time‚ so we needed an appliance to control the pressure accurately.” The result: a device flown in from the Bureau of Legal Dentistry in British Columbia known as the Bite–O–Matic. It consists of an upper and a lower set of chrome–cobalt teeth attached to a vice grip‚ with a detector connected to measure the pressure of the bite delivered.

Avon bit her pig at the stated time intervals on both the left and right sides. After killing the animal‚ she laid the pig on its side‚ as a murder victim might lie. “After you die‚ blood sinks to one side of your body under gravitational force‚” she explained. The side that the blood flows towards is known as the dependent side‚ and the side that the blood flows away from is known as the non–dependent side.

Avon found that bite marks could only be seen on the non–dependent side‚ and the clearest marks were those made five minutes before death‚ followed by five minutes after death‚ followed by one hour before death.

While that confirmed Avon’s suspicion that bite marks made before death may not be clearer than marks made after death‚ Avon discovered something else that shocked her: The bite marks weren’t bruises.

For a mark on someone’s skin to be technically considered a bruise‚ blood vessels need to be broken and blood cells released into the surrounding tissue‚ where they form immuglobin and eventually degrade. “”When I looked at the bite marks under the microscope‚ I was surprised to see no red blood cells at all.”" said Avon.

In other words‚ Avon has discovered that red marks on one’s skin may not necessarily be caused by blood‚ and this finding did not shock her alone. “I did a presentation of my results to a committee‚ and the director of the morgue at the coroner’s office‚ a pathologist‚ said flatly ‘That’s impossible.’ I asked him if he wanted to see the slides‚ and he said yes. So I left him with the slides by himself so as not to influence him. I waited in another room for half an hour‚ after which time he came back and simply said ’I don’t understand!’”

What could cause a red mark on one’s skin‚ if not blood? “I have a theory‚” said Avon‚ “but I can’t say. We’re now continuing the project‚ to test my theories.” Avon is optimistic about her continuing research. “I’m onto something!” she said happily.

Avon is also challenging another accepted concept in forensic science: the current practice of matching bite marks to suspects’ dental patterns. “In a court of law‚ it’s generally accepted that the dentist is correct because they are considered to be an expert witness in the field. But there is no conclusive scientific proof to date that a bite mark can be identified for a particular suspect.” So in phase two of her research‚ Avon will be biting three pigs with three different sets of teeth‚ and then sending photos of the bite marks along with moulds of the teeth to more than thirty experts around the world‚ asking them to match the bites to the teeth.

“I can’t wait to see the examiner’s results‚ because if they can’t show themselves to be reliable then that proves our current system of forensic investigation is flawed.” said Avon. She continues her research this fall.