The Journal of Life Sciences, by Julie Chao — “The first thing they teach you in engineering school is that the engineer’s role is to take what scientists have learned and transform it into what people want to use and enjoy.”

“Hello there. My DNA likes your DNA. Wanna mate?”

That’s the premise of a new dating website, With a mere trace of genetic material, you can find a partner with whom you’ll have, among other benefits, better sex, a higher chance of a monogamous relationship, and healthier children, the site says. Could romantic bliss really be just a cheek swab away?

ScientificMatch founder and President Eric Holzle has bet $50,000 of his own money on the answer being “yes.” The science is based on research suggesting that people prefer mates whose immune systems are dissimilar from their own—and that the preference can literally be sniffed out. The most oft-cited study, and the one that initially inspired Holzle to start his service, was conducted by Swiss researcher Claus Wedekind in 1995. In the study, some 49 female students smelled T-shirts worn by male students for two consecutive nights. The ones they judged to be most pleasant and sexy were the ones worn by men whose immune systems—or whose major histocompatibility complex (MHC), a collection of genes that play an important role in immune system functions—were most different from their own. Another study, conducted in 2006 at the University of New Mexico involving 48 couples, concluded that dissimilar MHC profiles led to benefits touted by ScientificMatch, including a more satisfying sex life and less chance of cheating by women.

From an evolutionary standpoint, it would make sense that a woman would want to find a man with whom she can produce healthy offspring, and a varied MHC likely means a baby with a more robust immune system. A $995 fee (already slashed from the original $1,995 the site was charging when it launched in December 2007) buys a lifetime membership. For that, ScientificMatch will examine your DNA, then give you possible love matches based on your MHC.

“We have over 40 peer-reviewed studies that support the method we use,” says Holzle, 43, a lifelong bachelor who is still looking for a mate. “This is the only scientifically proven method for matching people together.”

Since the self-funded company launched, Holzle, a mechanical engineer by training, says business has been “great” but offers no specifics, except that lovelorn customers have been pretty evenly split between men and women. So far, ScientificMatch is available only to residents of the greater Boston area, parts of New Hampshire, and Rhode Island. Holzle intends to expand nationally, but has no concrete plans for doing so. Instead of advertising, he has relied on press accounts to get his story out.

“The first thing they teach you in engineering school is that the engineer’s role is to take what scientists have learned and transform it into what people want to use and enjoy,” he says. Yet Holzle might be a bit ahead of the science, cautions evolutionary biologist Craig Roberts, a lecturer at the University of Liverpool who has been researching mating preferences since 2000. For starters, research has not definitively established that humans prefer mates with dissimilar MHC, he says. In both the lab and in population studies that measure the levels of genetic similarity of actual couples, evidence of disassortative mating in terms of MHC is mixed at best, Roberts says. Further, the website, although an intriguing idea, Roberts says, ignores other factors that have been found to influence mate choice, such as height, body shape, symmetrical features, and, perhaps most importantly, facial preferences. “My own work shows that people prefer faces of people who share similar MHC, not dissimilar MHC,” he says.

Even assuming the science supports ScientificMatch’s premise, its main selling point—finding a person with whom you’ll share incredible “chemistry”—is questionable given that MHC is highly polymorphic. In other words, the site will show you matches for individuals whose immune systems are dissimilar from yours, but most people in the population have dissimilar immune systems anyway. “Think how difficult it is to obtain organ donors and recipients,” Roberts says. “The genes physicians use to achieve this aim are exactly the same genes that this company is using. People using this site are therefore paying thousands of dollars to exclude a very small proportion of the people on the company’s book. I don’t think it’s worth the money.”

Holzle counters that, on average, a person would be deemed romantically compatible with about 20 percent of the population (meaning their MHC is similar with 80 percent), but adds that the percentage can vary wildly for individuals.

The site is not a bad idea, but is missing a crucial component, says Dr. Rachel Herz, author of The Scent of Desire and a visiting professor at Brown University Medical School who has conducted extensive research on smell and emotion. What ScientificMatch fails to take into account is the behavioral or psychological response to the scent, or in other words, the act of smelling the sweaty T-shirt. “The behavior part is more important than the genetic part,” she says. “My research shows that women’s response of, ‘I like this guy’s smell,’ is the most important feature of physical attraction.”

Holzle admits the science is in its infancy, but says the methodology will be adapted as the science advances. Until then, ScientificMatch is covering its bases by also using the old-fashioned matchmaking methods: It encourages its users to post pictures, take a personality test, and fill out a personal preference survey. Fond of long walks on the beach, anyone?


Sick of clichés? — Take heart, scientists have discovered that people can have a love that lasts a lifetime.

Using brain scans, researchers at Stony Brook University in New York have discovered a small number of couples respond with as much passion after 20 years together as most people only do during the early throes of romance, Britain’s Sunday Times newspaper reported.

The researchers scanned the brains of couples together for 20 years and compared them with results from new lovers, the Sunday Times said.

About 10 percent of the mature couples had the same chemical reactions when shown photographs of their loved ones as those just starting out.

Previous research has suggested that the first stages of romantic love fade within 15 months and after 10 years it has gone completely, the newspaper said.

“The findings go against the traditional view of romance — that it drops off sharply in the first decade — but we are sure it’s real,” said Arthur Aron, a psychologist at Stony Brook, told the Sunday Times.


“I don’t care if she is a tape dispenser. I love her.”
by Sam Gross, The New Yorker Magazine

Lauren Fleischman for The New York Times

Is your relationship still filled with sparks?

The New York Times — For some couples, passion and romance eventually fade over time, and a more calm, contented love takes over as the years go by.

Take the following quiz to find out how you score on the passion meter. This passionate love scale was developed by Elaine Hatfield, psychology professor at the University of Hawaii, and Susan Sprecher, psychology and sociology professor at Illinois State University. It was designed to assess the cognitive, emotional and behavioral aspects of passionate love and has been widely used by relationship researchers for the past two decades.

Dr. Hatfield notes that the scale is useful for researchers, but that couples should only take the test for fun and not make major decisions based on how they score on the 15-item scale. “Love and life are very complex, and a person’s emotions are always nuanced,” she said.

Answer the following questions to test your level of passionate love. Think of the person you love most passionately now, and respond by circling the appropriate response. Answers range from (1) not at all true to (9) definitely true. Then, add up your scores and check the scale below to see how hot your love fires burn.

I would feel deep despair if my partner left me.
1 2 3 4 5 6 7 8 9

Sometimes I feel I can’t control my thoughts; they are obsessively
on my partner.
1 2 3 4 5 6 7 8 9

I feel happy when I’m doing something to make my partner happy.
1 2 3 4 5 6 7 8 9

I would rather be with my partner than anyone else.
1 2 3 4 5 6 7 8 9

I’d get jealous if I thought my partner were falling
in love with someone else.
1 2 3 4 5 6 7 8 9

I yearn to know all about my partner.
1 2 3 4 5 6 7 8 9

I want my partner physically, emotionally and mentally.
1 2 3 4 5 6 7 8 9

I have an endless appetite for affection from my partner.
1 2 3 4 5 6 7 8 9

For me, my partner is the perfect romantic partner.
1 2 3 4 5 6 7 8 9

I sense my body responding when my partner touches me.
1 2 3 4 5 6 7 8 9

My partner always seems to be on my mind.
1 2 3 4 5 6 7 8 9

I want my partner to know me — my thoughts, my fears, and my hopes.
1 2 3 4 5 6 7 8 9

I eagerly look for signs indicating my partner’s desire for me.
1 2 3 4 5 6 7 8 9

I possess a powerful attraction for my partner.
1 2 3 4 5 6 7 8 9

I get extremely depressed when things don’t go
right in my relationship with my partner.

Passionate Love Scale Scores
106-135 points — Extremely passionate. Your love is wild and reckless.
86-105 points — Passionate. The fires of passion still burn, but not as intense.
66-85 points — Average. Contentment, with occasional sparks.
45-65 points — Cool. Tepid, infrequent passion.
15-44 points — Extremely cool. The fire is out.


A meeting of lips can spark a chain of chemical changes that really turn your head, February 13, 2009, by Jonathan Leake — If you always thought you had a special chemistry with your loved one, you may finally have been proved right.

Researchers have found that a passionate kiss unleashes a complex chemical surge into the brain which makes a lover feel excited, happy or relaxed.

There is also speculation that this hormone release may be triggered directly by an exchange of sexually stimulating pheromones in the saliva.

“This study shows kissing is much more complex and causes hormonal changes and things we never thought occurred,” said Wendy Hill, professor of psychology at Lafayette College, Pennsylvania, in an interview.

“We tend to think more about who we are kissing and how it feels, yet there are a lot of other things happening.”

Scientists may have taken a while to catch up on kissing but others have been clear about its impact for centuries.

William Shakespeare described the effect in Romeo and Juliet where, after the couple kiss for the first time, Romeo says: “Sin from thy lips? O trespass sweetly urged! Give me my sin again.”

Hill wanted to find out just what happens to evoke such a powerful emotional response from simply rubbing lips. Her research looked at the impact of kissing on levels of two hormones, oxytocin and cortisol, in 15 male-female couples before and after holding hands and before and after kissing.

Oxytocin is known to be involved in social bonding so the researchers predicted that its levels would rise, while cortisol, a stress hormone, would fall. The results showed cortisol levels fell in both sexes, although oxytocin levels rose in men but fell in women.

This was an unexpected result but Hill and her co-researchers believe the fact that the tests were carried out in an unromantic campus health centre also played a part. Over the past year they have run the tests again in a softer setting complete with romantic background music.

Detailed results will be published at the American Association for the Advancement of Science’s annual conference in Chicago this week but are understood to confirm a close association between kissing and hormone levels.

Other scientists have been looking at the importance of the first kiss, an act long known to have the power to make or break a relationship.

In the 2005 film Hitch, Will Smith plays a New York matchmaker who helps men get dates. He says: “One look, one kiss, that’s all we get . . . to make the difference between happily ever after and, ‘Oh, he’s just some guy I went to some thing with once’.”

Such views are underlined by Professor Susan Hughes, a psychologist at Albright College, Pennsylvania, and co-author of Sex Differences in Romantic Kissing among College Students: An Evolutionary Perspective, whose research suggests that women use kissing as a way of screening potential lovers.

She said: “Females place a lot more importance on the breath and teeth of the person. This shows how well you care for yourself and your hygiene and women are a lot more picky when it comes to that.”

One puzzle is just how kissing might induce hormonal changes of the kind found by Hill. There are clearly psychological factors involved but some researchers suspect saliva contains pheromones, chemical messengers known to be important in other mammals.

In humans the role of pheromones is controversial because we lack organs to detect them. However, Sarah Woodley, an assistant professor at Duquesne University, Pittsburgh, who will speak at the same meeting, believes that people can still detect them via the nose.

Helen Fisher, professor of anthropology at Rutgers University, New Jersey, and author of Why We Love, believes that kissing produces not just a chemical, sexual thrill but can even improve overall health: “If you’re sharing your germs with somebody, you’re boosting your internal defense system.”


Science Develops Bionic Sex Chip, by John Harlow — Forget Viagra: scientists are working on an electronic “sex chip” that will be able to stimulate pleasure centres in the brain.

The prospect of the chip, which could be a decade away, is emerging from progress in deep brain stimulation, in which tiny shocks from implanted electrodes are given to the brain. The technology has been used in America to treat Parkinson’s disease.

In recent months scientists have been focusing on an area of the brain just behind the eyes known as the orbitofrontal cortex. This is associated with feelings of pleasure derived from eating and sex.

A research survey conducted by Morten Kringelbach, senior fellow at Oxford University’s department of psychiatry, and reported in the Nature Reviews Neuroscience journal, found that the orbitofrontal cortex could be a “new stimulation target” to help people suffering from anhedonia, an inability to experience pleasure from such activities. Stimulating this area can produce pleasure as intense as “devouring a delicious pastry”, he said.

His colleague Tipu Aziz, a professor of neurosurgery at the John Radcliffe hospital in Oxford, predicted a significant breakthrough in the science behind a “sex chip” within 10 years.

“There is evidence that this chip will work,” Aziz said last week. “A few years ago a scientist implanted such a device into the brain of a woman with a low sex drive and turned her into a very sexually active woman. She didn’t like the sudden change, so the wiring in her head was removed.”

The wiring remains a hurdle: Aziz says current technology, which requires surgery to connect a wire from a heart pacemaker into the brain, causes bleeding in some patients and is “intrusive and crude”.

By 2015, he predicts, micro-computers in the brain with a range of applications could be self-powered and controlled by hand-held transmitters.

“When the technology is improved, we can use deep brain stimulation in many new areas. It will be more subtle, with more control over the power so you may be able to turn the chip on and off when needed.

“In 10 years’ time the range of therapies available will be amazing – we don’t know half the possibilities yet,” he said.

An electronic machine that generates sexual sensations is already under development by a North Carolina doctor, Stuart Meloy, who is modifying a spinal cord stimulator to produce pleasure in women. He calls it the Orgasmatron, a name taken from an orgasm-producing device in the 1973 Woody Allen film Sleeper. A similar device, the Excessive Machine, featured in Jane Fonda’s 1968 film, Barbarella.

Some critics regard the techniques as only a step away from brain washing.

“We are being led to big philosophical questions by rapid technological advances,” said Mahlon DeLong of Emory University in Atlanta, who has pioneered breakthroughs in brain stimulation to help Parkinson’s sufferers. “If we don’t discuss them now, they may be taking place before we can resolve the issues.”

Don’t forget Valentine’s Day, send this rose

This human heart destined for transplant, lies in a TransMedics Organ Care System. The device can keep a heart warm and beating – and viable for many hours longer, than the conventional method for handling donor hearts: immersion in a saline solution and packing in ice.

Mending Broken Hearts
National Geographic Magazine, February 2009 — Cheeseburgers, smoking, stress, the rise of the couch potato: These are the usual suspects on the list of risk factors for heart disease, a malady reaching global epidemic proportions. Now discoveries about genetic triggers may help us spot trouble before it starts.

By Jennifer Kahn
Photograph by Robert Clark

Gloria Stevens is lying on her back, sedated but alert, staring at an image of her own beating heart. Metaphorically, Gloria’s heart is the very core of her emotional self—not to be worn on the sleeve, much less displayed on an overhead monitor. More literally, it is a blood-filled pump about the size of a clenched fist whose rhythmic contractions have kept Gloria alive for 62 years, and with a little tinkering will keep her going for an indeterminate number more.

At this moment, her doctor is threading a thin catheter up through her femoral artery from an incision in her groin, on into the aorta, and from there into one of the arteries encircling Gloria’s heart. At the tip of the catheter is a small balloon. The doctor gently navigates the tip to a spot where plaque has narrowed the artery’s channel by 90 percent. With a quick, practiced movement he inflates the balloon to push back the artery wall, deflates the balloon, then inserts an expandable stent—it looks like a tiny tube of chicken wire—that will keep the passage open. As Gloria watches on the monitor, the crimp in her artery disappears, and a wide laminar flow gushes through the vessel, like a river in flood.

The procedure is over. It has lasted only half an hour. In all likelihood, Gloria will be able to go home the next day. So will a few thousand other patients in the United States undergoing such routine angioplasty—more than a million of them a year. Pipe fixed, patient cured, right?


Because of her treatment, Gloria’s quality of life will likely improve. She’ll breathe easier and maybe live longer. But she is hardly cured. Her coronary atherosclerosis—a hardening and narrowing of the arteries that supply the heart with oxygen-rich blood—still leaves her vulnerable to future blockages and coronary heart disease.

Although hearts suffer many maladies—valves leak, membranes become inflamed—coronary heart disease, which can lead to heart attack and ultimately to heart failure, is the number one killer of both men and women in the United States, where 500,000 die annually. Worldwide, it kills 7.2 million people every year. Exacerbated by the export of Western lifestyle—motorized transport, abundant meat and cheese, workdays conducted from the comfort of a well-padded chair—incidence of the disease is soaring.

To help stem this lethal tide, cardiologists can prescribe such cholesterol-lowering drugs as statins to help keep arteries clear. They can advise patients to change their habits, or they can operate to fix an immediate problem. Angioplasty is one procedure, and surgery to bypass the diseased arteries is another—each year more than 400,000 bypasses are performed in the U.S. Transplants can replace severely damaged hearts, and artificial ones can keep people alive while they wait for a donor heart. But in the face of an impending global epidemic, none of these stopgap measures addresses the essential question: Who gets heart attacks and why?

The human heart beats 100,000 times a day, propelling six quarts of blood through 60,000 miles (97,000 kilometers) of vessels—20 times the distance across the U.S. from coast to coast. The blood flows briskly, surging out of a ten-ounce (0.3 kilograms) heart so forcefully that large arteries, when severed, can send a jet of blood several feet into the air. Normally the relentless current helps keep blood vessels clean. But where an artery bends, tiny eddies form, as in a bend in a river. This is where bits of sticky, waxy cholesterol and fat can seep into the artery wall and oxidize, like butter going rancid. Other matter piles up too. Eventually, the whole mass calcifies into a kind of arterial stucco, or plaque.

Until recently, cardiologists approached heart disease as a plumbing problem. Just as mineral deposits restrict the flow of water through a pipe, an accretion of plaque impedes the flow of blood through an arterial channel. The more crud in the system, the greater likelihood that a dammed artery will trigger a heart attack. Doctors now dismiss this
Most heart attacks are caused by plaque embedded within the artery wall that ruptures, cracking the wall and triggering the formation of a blood clot. The clot blocks the flow of blood to the heart muscle, which can die from lack of oxygen and nutrients. Suddenly, the pump stops pumping.

Contrary to the clogged pipes model, heart attacks generally occur in arteries that have minimal or moderate blockage, and their occurrence depends more on the kind of plaque than on the quantity. Scientists have been struggling to figure out what type is most responsible. Paradoxically, findings suggest that immature, softer plaques rich in cholesterol are more unstable and likely to rupture than the hard, calcified, dense plaques that extensively narrow the artery channel. But understanding the root cause of the disease will require much more research. For one thing, human hearts, unlike plumbing fixtures, are not stamped from a mold. Like the rest of our body parts, they are products of our genes.

Don Steffensen was putting duck-hunting decoys out on a small lake one fall afternoon in southwestern Iowa when his heart attack hit. The infarction was massive and unexpected. It’s likely that Steffensen survived only because a buddy was carrying nitroglycerin tablets and quickly slipped one under his friend’s tongue. Nitroglycerin is used to make dynamite; in the body, a heavily diluted form releases nitric oxide, which signals the smooth muscle cells in veins and arteries to relax, dilating the vessels.

The Steffensen clan is enormous: more than 200 relatives spread over three generations, many of the youngest are now dispersed from Iowa to New York and beyond. Although heart trouble is common in the family, it had never struck anyone as unusual. “I attributed it to diet,” shrugs Tina, a slim 38-year-old and the family’s only vegetarian.

It was a reasonable conclusion. The Steffensens were raised on the kind of farm food that the state is famous for—ham balls, meatloaf, pie, macaroni and cheese—and still popular even as careers have moved indoors. Driving north through cornfields to meet some of the family in Buffalo Center, I dined at a restaurant offering deep-fried sandwiches. A single ham and cheese hoagie—dunked in hot fat and served sizzling—seemed capable of stopping a heart all on its own.

But could the high incidence of heart trouble among the Steffensens be related to something else besides high-fat diets? Eleven years after Don’s attack, his wife, Barbara, happened to overhear a doctor describing a study about the genetics of heart attacks.

Curious, Don and 20 of his relatives each sent a vial of blood to the Cleveland Clinic, where the research was being conducted. Eric Topol, a cardiologist and genetics researcher at the clinic, spent a year studying their DNA. Each person’s genome comes with millions of individual variations, but Topol was looking for something distinctive—and shared only by the members of the clan with heart trouble. The mutation he and his team finally spotted, in a gene called MEF2A, produced a faulty protein. “We knew we had something,” Topol says. “But the question was: How does this sick protein, present at birth, lead to heart attacks 50 years later in life?”

Topol himself is as lean as a greyhound and weathered in a cowboyish way. He talks slowly and eats minimally: salads for dinner and high-fiber cereal for breakfast. He doesn’t eat lunch at all. Like almost every cardiologist I’ve talked to, he takes statins preventively, and his cholesterol count is a low 135. His children, 22 and 25, also eat uncommonly well for their ages. “People have looked at the cadavers of men in their 20s who died in car accidents or as casualties of war, and nearly all had arterial cholesterol deposits,” Topol said as we walked to his lab. “This disease starts much earlier than people realize.”
Using endothelial cells (which line the inside of the artery wall) grown in culture, Topol set about figuring out what the MEF2A mutation does. He and his coworkers created some cells carrying the Steffensen variant, and others with the normal form of the protein. Both cell proteins were tagged fluorescent green so their locations could be visualized on a computer screen. The resulting images revealed a striking difference.

In a normal cell, all the MEF2A protein was inside the nucleus; on the screen, the cell resembled a fried egg with a fluorescent green yolk. But in the cells carrying the mutated version, the nucleus did not glow; instead the cell membrane was edged by a thin, luminous green line: a layer of MEF2A protein, trapped where it cannot serve its usual purpose. Topol believes that this defect affects the integrity of the coronary artery walls, rendering them more vulnerable to cracking when the plaque embedded in them ruptures. And each crack brings an increased chance of a heart attack.

Since this discovery, the Steffensens have become famous, appearing on shows like 60 Minutes II. Their mutant gene turns up in a Robin Cook novel titled Marker, about a health insurance company in New York that secretly screens patients for the MEF2A mutation and then kills them to preempt future medical-care payouts. Lively reading, but the Steffensen gene is an unlikely target for an insurance company, in part because it is an uncommon genetic defect.

Topol’s study did find that although dysfunctional MEF2A is very rare, the chance of heart disease in those carrying it may approach 100 percent. Most other genetic variations identified thus far increase the risk by much less. As it turns out, Topol himself carries a bum gene: apoE4, which affects inflammation in the arteries. Unlike MEF2A, it is common; every fourth person has it.

“Heart disease is not a one- or two-gene problem,” says Steven Ellis, a Cleveland Clinic cardiologist who oversees a 10,000-person genetic study known as GeneBank that collects DNA samples from patients who enter hospitals with atherosclerosis. Ellis, like most cardiac researchers, suspects that dozens of genes end up contributing to a predisposition: Some affect arterial integrity, others inflammation (which both causes and exacerbates arterial cracks), and still others the processing of lipids (the fats and cholesterol that turn into plaques). Of the several dozen genes, each may contribute just one percent to a person’s total risk—an amount that may be compounded, or offset, by outside factors like diet. As one doctor told me, any person’s heart attack risk is “50 percent genetic and 50 percent cheeseburger.”

The point of tracking down all these small mutations, Ellis explains, is to create a comprehensive blood test—one that could calculate a person’s genetic susceptibility by adding up the number of risky (and, eventually, beneficial) variables. Combined with other important factors, such as smoking, weight, blood pressure, and cholesterol levels, doctors could decide which patients need aggressive treatment, such as high-dose statins, and which ones are likely to benefit from exercise or other lifestyle changes. Some genes already can predict whose cholesterol level will respond strongly to dietary changes and whose won’t. Assessing risk is crucial, Ellis says, because heart disease is often invisible. In fact, 50 percent of men and 64 percent of women who die of heart disease die suddenly, without experiencing any previous symptoms.

Although standard tests can detect atherosclerosis, they aren’t foolproof. They may reveal plaques, but give no indication whether or not they are life-threatening. Tests like angiography, for example, where doctors inject a dye into the bloodstream and track it with x-rays, can show how much blood is flowing through an artery, but not discern the plaques embedded inside the artery wall—often the culprit in a heart attack.

Researchers have been working to solve this problem with scanners that provide pictures of the arterial wall itself, but it’s a tricky task. Normal cardiac artery walls are about a millimeter thick. Coronary arteries move with every beat of the heart, 70 times a minute. It’s tough to get a clear image of something so small in constant motion.

Difficult, but not impossible. As I walk through the basement of the Cleveland Clinic, I pass a room containing a large, blue, plastic doughnut as tall as I am, with a woman’s legs sticking out of the middle. The doughnut is a computed tomography (CT) scanner, a kind of three-dimensional x-ray machine that’s also used for imaging tumors. The scanner, aided by medications that reduce a patient’s heart rate and an injectable dye that highlights the arteries, can produce startlingly clear pictures.

Scrolling through images on his computer monitor, Mario Garcia, the clinic’s director of cardiac imaging, retrieves one that looks like a black-and-white landscape photographed from a plane, with a single, large river running through it. As Garcia zooms in on the river, a series of white lumps appears on the bank—hard plaques bright with calcium. But there is also a tiny black smudge. “That’s the type we believe causes a heart attack,” he says with satisfaction, pointing to the smudge of soft plaque. “It’s a rare opportunity to see that.”

As compelling as the CT scan is, it’s still an imperfect tool for predicting heart disease. It’s expensive, for one, and the dose of radiation from the x-rays makes it ill suited for use in healthy-patient annual exams. And although it sees arterial plaques, even soft plaques inside arterial walls, it can’t reveal whether those plaques are likely to crack and cause a heart attack.
Until there are tests, genetic or otherwise, that give a clearer measure of risk, everyone would be advised to exercise, watch their diet, and take statins for elevated cholesterol—the same advice doctors gave when the clogged-pipes model of heart disease reigned unchallenged.

At the Cleveland Clinic, cardiologist Stephen Nissen has conducted several studies on statins such as Lipitor, which reduce the amount of LDL (“bad” low-density lipoprotein) cholesterol made by the liver. Nissen is an advocate of lowering cholesterol by any means necessary. Does he take a statin? “You bet!” he says. “I have no intention of dying of the disease I treat.” His LDL level is a paltry 51. Of eight cardiologists I spoke with, all but one were taking the medication. (Some studies now seem to show that lowering even normal cholesterol levels has a protective effect.) HDL (“good” high-density lipoprotein) cholesterol is another story. Nissen calls it the “arterial-wall garbage barge” because of its ability to remove cholesterol from clogged arteries. Not all HDL can do this; some is dysfunctional. But tests have shown that raising the HDL level in genetically engineered lab mice can shrink their arterial plaques.

A drug that could raise functional HDL levels in humans would likely become the next multibillion-dollar blockbuster, and a few are in various stages of testing. However, the trial of a Pfizer drug called torcetrapib ended in failure. Torcetrapib had been shown, in combination with Lipitor, to raise HDL levels 44 to 66 percent with a once-a-day pill. But the increase was not necessarily in functional HDL, and the drug was also associated with elevated blood pressure. In December, when data showed a 60 percent higher death rate in patients taking torcetrapib with Lipitor than in those taking Lipitor alone, Pfizer abruptly ended the trial.

It’s not clear whether the problem lay with one drug or an entire class of drugs. Until further research is completed, the several different statins on the market will remain the most prescribed class of drugs in the world, with 11.6 million prescriptions filled monthly in the U.S. alone. Pfizer’s Lipitor may be the best-selling drug ever made, with 12 billion dollars in annual worldwide sales.

But statins, like any drug, carry the risk of side effects: Muscle aches are a well-known effect, and periodic blood tests to check liver function are recommended. The fact is, many of us just like to eat cheeseburgers, watch television, and get around in cars. And it’s hard, says Leslie Cho, director of the Cleveland Clinic’s Women’s Cardiovascular Center, for a person to worry about a disease that hits ten years down the road—particularly since heart patients, unlike cancer patients, can’t easily observe the progress of their disease. “You’ve done damage over years, and it will take years to undo that damage,” she says. “That’s a very hard thing to sell to Americans. We do what we can, but then people go home.”

The good news is that genetic research continues to thrive. Should we want to, we will soon be able to know the state of our hearts—and our genes—in ever growing detail. That knowledge, and what we do with it, could make the difference between dying at 65 and living until 80. The choice, increasingly, will be ours.