IT’S a classic philosophical conundrum: how does my perception of the world differ from yours? Take a red rose, for example. We can probably agree it’s red rather than blue, but what exactly is “red”, and do I see the same red as you? And what about the distinctive smell – is my sense of what constitutes a rose’s scent the same as yours?
Philosophers have been wrestling with this question for centuries. Sensory scientists, too, have long been interested in why people report such different experiences of the same odours or flavours. Is it purely subjective, or based on some objective difference in their sensory experiences?
The obvious answer is that there is no way of knowing because sensory experiences are inherently private. But biologists have recently taken a fresh look at the question and concluded that we can know. Sensory experiences are highly individualised. “No two people live in the same sensory world,” says Paul Breslin, a neuroscientist at the Monell Chemical Senses Center in Philadelphia. “The world you see, the foods you taste, the odours you smell – all are perceived in a way unique to you.”
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It’s all down to our DNA. In the past few years geneticists have unearthed huge numbers of genes involved in the perception of taste, smell, touch and vision. Olfactory receptor genes, for example, account for around 3 per cent of the total – only the immune system takes up more houseroom. And not only are sensory genes vastly abundant, they are highly variable too. This means that individuals rarely have exactly the same set of sensory genes. And, crucially, individual genetic repertoires are now being linked to differences in the way people report their experiences of the world. Some scientists even think that the set of sensors you inherit has a profound effect on your life and personality.
If all this is too much to cope with, sit down and have a drink. It’s as good an example as any.
“I love gin and tonic,” announces geneticist Dennis Drayna – he uses his favourite tipple to explain his research. He works at the National Institute on Deafness and Other Communication Disorders in Rockville, Maryland, and his speciality is bitter-tasting substances. “I could even drink the tonic without the gin,” he says. “I really like the bitter taste.”
But not everyone shares his predilections. Give a single concentration of any bitter chemical, such as the quinine in tonic, to a selection of people and they will have remarkably different responses. “Most will tell you it’s moderately bitter, some will say it’s not bitter at all and a few will yell at you for trying to poison them,” Breslin says.
That much has been known for a long time. But Drayna, Breslin and others have now started linking these subjective differences in taste perception to the genes that code for taste receptor proteins in taste buds.
They work with perhaps the most famous bitter flavour, phenylthiocarbamide or PTC. This chemical was discovered in the 1930s by Arthur Fox, an industrial chemist at DuPont who was researching artificial sweeteners. Fox discovered that some of his colleagues found the chemical incredibly bitter while others, including himself, could not taste it at all.
The ability to taste PTC was long thought to be a case of simple Mendelian inheritance. People with two copies of the recessive “non-taster” version were unable to taste PTC; others could. But this distinction has turned out to be too simplistic. Even though the trait is broadly “bimodal” with reasonably distinct taster and non-taster groups, there is a lot of variation within the groups. “If the concentration is high enough [about 360 parts per million] everyone can taste it,” Drayna says. Some tasters can detect PTC at the vanishingly small concentration of 18 parts per billion.
Drayna set out to find the genetic source of this variation. He asked 267 people whose genomes had already been sequenced to take a taste test in which they had to sort six cups of water, three containing a known concentration of PTC and three without. He repeated the test at different dilutions to find each person’s taste threshold. Then he compared the results with the sequence of a region on chromosome 7 previously identified as the location of the genes that code for bitterness receptors. As a result the team identified the PTC receptor gene and also found it came in five different “flavours” that differed from each other by a single base pair. These alterations were sufficient to explain the difference between the volunteers’ taste thresholds.
The PTC gene codes for only one of 23 different bitterness receptors, which gives an idea of the possible diversity. Initial analysis of other taste receptors hints at equally wide variance. So it looks as though your tastes in food really are your own.
Olfaction, too, is proving to be hugely variable, though in a subtly different way. Humans can distinguish around 10,000 different smells via 400 receptor proteins lining the nasal cavity (see Diagram). But it has long been known that not everyone smells the same smells – and now geneticists have shown that this could be because everyone has a different set of receptors.
Olfactory receptor genes are distinctive and easy to spot from their DNA sequence. So it came as a surprise when the human genome turned out to contain about 1000 such genes. How did this tally with the 400 known receptor proteins? It turned out that around 600 are “pseudogenes” – sequences that look like genes and are inherited like genes but have lost their function. For sensory scientists this was an intriguing discovery, as pseudogenes are known to have lost their function very recently. So a team at the Weizmann Institute in Rehovot, Israel, wondered whether some olfactory pseudogenes were still functional in some people, and whether this tallied with differences in what they were able to smell.
In a study published in Nature Genetics (vol 34, p 143), the team identified 51 pseudogenes that are functional in some people. Then they took 189 ethnically diverse volunteers and examined their olfactory receptor genes. They found that each person had a unique combination of functioning pseudogenes, giving them an individualised repertoire of smell receptors.
However, team member Yoav Gilad is not yet prepared to associate this genetic variability with the results of smell tests. “Although studies have shown big differences between smelling abilities, unlike with PTC, there’s no proof that this is genetically based,” he says. Although he concedes that genetics almost certainly plays a role, “there are a lot of other environmental and psychological factors as well”. For example, when people are given coloured water and clear water that smelt identical when sniffed blindly, a majority say the coloured water smells stronger.
Of course, an innate revulsion to tonic water or heightened ability to smell a rose is unlikely to have a major impact on your life. However, differences in other senses could prove more significant.
In humans there is one sense we rely on more than others – sight. But light perception and colour vision can differ markedly between individuals, and again it’s down to genes. Stephen Tsang of Columbia University in New York City studies the genetics of responses to light intensity. He has discovered that many of the genes involved in light perception come in several different forms, and this can lead to huge individual variation in light sensitivity. “Our response to light varies from those who can detect a single photon to others who have a disease known as congenital stationary night blindness, which severely impairs their ability to see in dim light,” Tsang says. “Most of us living in the constant glow of cities don’t realise we might have some degree of impairment.”
Colour perception, too, is hugely variable, and not just for the 8 per cent of people (mostly men) with some degree of colour blindness. “Even among individuals with normal vision, tests of colour perception show a wide variation in how colours are seen,” says geneticist Samir Deeb of the University of Washington in Seattle, who studies colour vision. Again, most of these differences appear to have a genetic basis.
Colour is detected by millions of cone cells in the retina and in a normal person there are three types, responding to red, green and blue light. This makes humans trichromatic and in theory allows us to distinguish between more than 2 million different colours. Blue cones are very uniform but there are at least four versions of the gene that encodes the red visual pigment and four versions of the green. Because these genes are carried on the X chromosome, and men have only one X chromosome, the variant genes are readily expressed in men and often lead to subtle impairments in colour vision.
But these variants don’t just cause defects – they may give some women enhanced colour vision. Because women have two X chromosomes, it is possible for one X to carry the normal genes and the other to carry one or other of the variants. This means some women have an extra type of cone, making them potentially tetrachromatic. Deeb has now begun research on these super-sighted women and says the phenomenon may not be unusual. “Around 15 per cent of women are carriers of colour vision deficiency,” he says. “Looking at 43 of these, two showed evidence of tetrachromacy.”
So what does a tetrachromatic woman see that the rest of us don’t? “I wish I could tell you,” laughs Deeb, although he says it is likely that they are able to distinguish colours that mere trichromatics cannot. They could, for example, be able to tell the difference between two seemingly identical shades of green. Unfortunately, the rest of us will never know what we’re missing.
Meanwhile at McGill University in Montreal, Canada, mice are having their tails dipped in hot water to study their reaction to pain. Jeffrey Mogil’s team has tested 12 strains of mice and found that while some strains flick their tails out of hot water in 2 seconds, other strains take anything up to 6. A series of experiments led him to conclude that this variation in pain perception must be genetic, and he has now set out to find its source.
Recent evidence suggests that humans too have varying perceptions of pain, and that those differences have a biological origin. Bob Coghill of Wake Forest University School of Medicine in Winston-Salem, North Carolina, took 17 volunteers and applied a heat source to the backs of their calves. Then he raised the temperature in steps until it was 49 °C – about the most human skin can take without burning – and asked the volunteers to rate the amount of pain on a scale of 1 (no pain) to 10 (excruciating). The variability in their responses was striking: some found a small temperature rise unbearable while one subject did not feel any discomfort.
By repeating the experiment with the volunteers in an MRI brain scanner, Coghill found a clear correlation between the amount of pain people reported and the amount of brain activity that accompanies it in the cerebral cortex. Those most susceptible showed much more activity. “The perception of pain varies by a strikingly large amount,” Mogil says, “and these experiments show that those differences are real and objective.”
Across at least four of the senses, then, there is enormous scope for individual variation. Your combination of visual, olfactory, taste and pain receptors is almost certainly different from mine. For Paul Breslin this implies something profound. “If you consider that almost everything we learn from birth is dependent on our sensory systems, then our individual sensory differences are all the more interesting,” he says. In other words, we are partly a product of our senses. Breslin suggests that these differences could even affect many of the choices we make in our lives. “There is a significant visual and olfactory component in the kinds of foods we like, the activities we take part in, the music we enjoy and even who we mate with,” he says. If that component is decided by our genes, the logical conclusion is that, to some extent, we are genetically predetermined to prefer certain things or people. Our freedom to choose is limited.
There are also implications for consciousness research. How the physical world becomes our private sensory experiences – what philosophers call “qualia” – is often seen as the key to understanding consciousness. So if qualia are produced by the output of our senses, and people sense the world in ways we can pin down objectively, does that help us understand individual conscious experiences?
Possibly, says philosopher David Chalmers of the University of Arizona. “We might one day be able to say that a person with a particular set of genes has a particular type of consciousness,” he says. But if this is so, you have new problems to solve, “particularly when it comes to trying to find out what someone else’s consciousness is like”. This question, known as the “problem of other minds”, also lies at the heart of consciousness research.
The sensory world we live in is also complicated by the brain’s interpretation of what the senses are telling it. Rather than simply report the output of our senses to the mind, the brain puts its own spin on the world. In a dramatic demonstration of this, Daniel Simons of Harvard University showed volunteers a video of a ball game and asked them to watch one team intently. After about 45 seconds a woman dressed in a gorilla suit walked in front of the camera. Around half the viewers completely missed the gorilla. The rods and cones in their eyes obviously detected it, but their brains chose to ignore it.
And so perhaps the age-old problem remains intractable. The red I see might be different to the red you see, but perhaps our minds still interpret the sensory input to give us a common red experience. You could say that “red” will always be a pigment of the imagination.