Why do we have allergies?

This story first appeared on Mosaic and is republished here under a Creative Commons license.

Photo by William Brawley | CC BY-SA 2.0

By Carl Zimmer

Allergies such as peanut allergy and hay fever make millions of us miserable, but scientists aren’t even sure why they exist. Carl Zimmer talks to a master immunologist with a controversial answer.

For me, it was hornets.

One summer afternoon when I was 12, I ran into an overgrown field near a friend’s house and kicked a hornet nest the size of a football. An angry squadron of insects clamped onto my leg; their stings felt like scorching needles. I swatted the hornets away and ran for help, but within minutes I realised something else was happening. A constellation of pink stars had appeared around the stings. The hives swelled, and new ones began appearing farther up my legs. I was having an allergic reaction.

My friend’s mother gave me antihistamines and loaded me into her van. We set out for the county hospital, my dread growing as we drove. I was vaguely aware of the horrible things that can happen when allergies run amok. I imagined the hives reaching my throat and sealing it shut.

I lived to tell the tale: my hives subsided at the hospital, leaving behind a lingering fear of hornets. But an allergy test confirmed that I was sensitive to the insects. Not to honey bees or wasps or yellow jackets. Just the particular type of hornet that had stung me. The emergency room doctor said I might not be so fortunate the next time I encountered a nest of them. She handed me an EpiPen and told me to ram the syringe into my thigh if I was stung again. The epinephrine would raise my blood pressure, open my airway – and perhaps save my life. I’ve been lucky: that afternoon was 35 years ago, and I haven’t encountered a hornet’s nest since. I lost track of that EpiPen years ago.

Anyone with an allergy has their origin story, a tale of how they discovered that their immune system goes haywire when some arbitrarily particular molecule gets into their body. There are hundreds of millions of these stories. In the USA alone, an estimated 18 million people suffer from hay fever, and food allergies affect millions of American children. The prevalence of allergies in many other countries is rising. The list of allergens includes – but is not limited to – latex, gold, pollen (ragweed, cockleweed and pigweed are especially bad), penicillin, insect venom, peanuts, papayas, jellyfish stings, perfume, eggs, the faeces of house mites, pecans, salmon, beef and nickel.

Once these substances trigger an allergy, the symptoms can run the gamut from annoying to deadly. Hives appear, lips swell. Hay fever brings sniffles and stinging eyes; allergies to food can cause vomiting and diarrhoea. For an unlucky minority, allergies can trigger a potentially fatal whole-body reaction known as anaphylactic shock.

The collective burden of these woes is tremendous, yet the treatment options are limited. EpiPens save lives, but the available long-term treatments offer mixed results to those exhausted by an allergy to mould or the annual release of pollen. Antihistamines can often reduce sufferers’ symptoms, but these drugs also cause drowsiness, as do some other treatments.

We might have more effective treatments if scientists understood allergies, but a maddening web of causes underlies allergic reactions. Cells are aroused, chemicals released, signals relayed. Scientists have only partially mapped the process. And there’s an even bigger mystery underlying this biochemical web: why do we even get allergies at all?

“That is exactly the problem I love,” Ruslan Medzhitov told me recently. “It’s very big, it’s very fundamental, and completely unknown.”

Medzhitov and I were wandering through his laboratory, which is located on the top floor of the Anlyan Center for Medical Research and Education at the Yale School of Medicine. His team of postdocs and graduate students were wedged tight among man-sized tanks of oxygen and incubators full of immune cells. “It’s a mess, but a productive mess,” he said with a shrug. Medzhitov has a boxer’s face – massive, circular, with a broad, flat nose – but he spoke with a soft elegance.

Medzhitov’s mess has been exceptionally productive. Over the past 20 years, he has made fundamental discoveries about the immune system, for which he has been awarded a string of major prizes. Last year he was the first recipient of the €4 million Else Kröner Fresenius Award. And though Medzhitov hasn’t won a Nobel, many of his peers think he should have: in 2011, 26 leading immunologists wrote to Nature protesting that Medzhitov’s research had been overlooked for the prize.

Now Medzhitov is turning his attention to a question that could change immunology yet again: why do we get allergies? No one has a firm answer, but what is arguably the leading theory suggests that allergies are a misfiring of a defence against parasitic worms. In the industrialised world, where such infections are rare, this system reacts in an exaggerated fashion to harmless targets, making us miserable in the process.

Medzhitov thinks that’s wrong. Allergies are not simply a biological blunder. Instead, they’re an essential defence against noxious chemicals – a defence that has served our ancestors for tens of millions of years and continues to do so today. It’s a controversial theory, Medzhitov acknowledges. But he’s also confident that history will prove him right. “I think the field will go around in that stage where there’s a lot of resistance to the idea,” he told me. “Until everybody says, ‘Oh yeah, it’s obvious. Of course it works that way.’”

The physicians of the ancient world knew about allergies. Three thousand years ago, Chinese doctors described a “plant fever” that caused runny noses in autumn. There is evidence that the Egyptian pharaoh Menes died from the sting of a wasp in 2641 BCE. Two and a half millennia later, the Roman philosopher Lucretius wrote, “What is food to one is to others bitter poison.”

But it was a little more than a century ago when scientists realised that these diverse symptoms are different heads on the same hydra. By then researchers had discovered that many diseases are caused by bacteria and other pathogens, and that we fight these invaders with an immune system – an army of cells that can unleash deadly chemicals and precisely targeted antibodies. They soon realised that the immune system can also cause harm. In the early 1900s, the French scientists Charles Richet and Paul Portier were studying how toxins affect the body. They injected small doses of poison from sea anemones into dogs, then waited a week or so before delivering an even smaller dose. Within minutes, the dogs went into shock and died. Instead of protecting the animals from harm, the immune system appeared to make them more susceptible.

Other researchers observed that some medical drugs caused hives and other symptoms. And this sensitivity increased with exposure – the opposite of the protection that antibodies provided against infectious diseases. The Austrian doctor Clemens von Pirquet wondered how it was that substances entering the body could change the way the body reacted. To describe this response, he coined the word ‘allergy’, from the Greek words allos (‘other’) and ergon (‘work’).

In the decades that followed, scientists discovered that the molecular stages of these reactions were remarkably similar. The process begins when an allergen lands on one of the body’s surfaces – skin, eye, nasal passage, mouth, airway or gut. These surfaces are loaded with immune cells that act as border sentries. When a sentry encounters an allergen, it first engulfs and demolishes the invader, then decorates its outer surface with fragments of the substance. Next the cell locates some lymph tissue. There it passes on the fragments to other immune cells, which produce a distinctive fork-shaped antibody, known as immunoglobulin E, or IgE.

These antibodies will trigger a response if they encounter the allergen again. The reaction begins when an antibody activates a component of the immune system known as a mast cell, which then blasts out a barrage of chemicals. Some of these chemicals latch onto nerves, triggering itchiness and coughing. Sometimes mucus is produced. Airway muscles can contract, making it hard to breathe.

This picture, built up in labs over the past century, answered the ‘how?’ part of the allergies mystery. Left unanswered, however, was ‘why?’ And that’s surprising, because the question had a pretty clear answer for most parts of the immune system. Our ancestors faced a constant assault of pathogens. Natural selection favoured mutations that helped them fend off these attacks, and those mutations accumulated to produce the sophisticated defences we have today.

It was harder to see how natural selection could have produced allergies. Reacting to harmless things with a huge immune response probably wouldn’t have aided the survival of our ancestors. Allergies are also strangely selective. Only some people have allergies, and only some substances are allergens. Sometimes people develop allergies relatively late in life; sometimes childhood allergies disappear. And for decades, nobody could even figure out what IgE was for. It showed no ability to stop any virus or bacteria. It was as if we evolved one special kind of antibody just to make us miserable.

One early clue came in 1964. A parasitologist named Bridget Ogilvie was investigating how the immune system repelled parasitic worms, and she noticed that rats infected with worms produced large amounts of what would later be called IgE. Subsequent studies revealed that the antibodies signalled the immune system to unleash a damaging assault on the worms.

Parasitic worms represent a serious threat – not just to rats, but to humans too. Hookworms can drain off blood from the gut. Liver flukes can damage liver tissue and cause cancer. Tapeworms can cause cysts in the brain. More than 20 per cent of all people on Earth carry such an infection, most of them in low-income countries. Before modern public health and food safety systems, our ancestors faced a lifelong struggle against these worms, as well as ticks and other parasitic animals.

During the 1980s, several scientists argued forcefully for a link between these parasites and allergies. Perhaps our ancestors evolved an ability to recognise the proteins on the surface of worms and to respond with IgE antibodies. The antibodies primed immune system cells in the skin and gut to quickly repel any parasite trying to push its way in. “You’ve got about an hour to react very dramatically in order to reduce the chance of these parasites surviving,” said David Dunne, a parasitologist at the University of Cambridge.

According to the worm theory, the proteins of parasitic worms are similar in shape to other molecules we regularly encounter in our lives. If we encounter those molecules, we mount a pointless defence. “Allergy is just an unfortunate side-effect of defence against parasitic worms,” says Dunne.

When he was an immunologist in training, Medzhitov was taught the worm theory of allergies. But ten years ago he started to develop doubts. “I was seeing that it doesn’t make sense,” he said. So Medzhitov began thinking about a theory of his own.

Thinking is a big part of Medzhitov’s science. It’s a legacy of his training in the Soviet Union in the 1980s and 1990s, when universities had little equipment and even less interest in producing good scientists. For his undergraduate degree, Medzhitov went to Tashkent State University in Uzbekistan. Every autumn the professors sent the students out into the cotton fields to help take in the harvest. They worked daily from dawn to dusk. “It was terrible,” said Medzhitov. “If you don’t do that, you get expelled from college.” He recalls sneaking biochemistry textbooks into the fields – and being reprimanded by a department chair for doing so.

Graduate school wasn’t much better. Medzhitov arrived at Moscow State University just as the Soviet regime collapsed. The university was broke, and Medzhitov didn’t have the equipment he needed to run experiments. “I was basically spending all of my time reading and thinking,” Medzhitov told me.

Mostly, he thought about how our bodies perceive the outside world. We can recognise patterns of photons with our eyes and patterns of air vibrations with our ears. To Medzhitov, the immune system was another pattern recognition system – one that detected molecular signatures instead of light or sound.

As Medzhitov searched for papers on this subject, he came across references to a 1989 essay written by Charles Janeway, an immunologist at Yale, titled ‘Approaching the Asymptote? Evolution and revolution in immunology’. Medzhitov was intrigued and used several months’ of his stipend to buy a reprint of the paper. It was worth the wait, because the paper exposed him to Janeway’s theories, and those theories would change his life.

At the time, Janeway was arguing that antibodies have a big drawback: it takes days for the immune system to develop an effective antibody against a new invader. He speculated that the immune system might have another line of defence that could offer faster protection. Perhaps the immune system could use a pattern-recognition system to detect bacteria and viruses quickly, allowing it to immediately launch a response.

Medzhitov had been thinking about the same thing, and he immediately emailed Janeway. Janeway responded, and they began an exchange that would ultimately bring Medzhitov to New Haven, Connecticut, in 1994, to become a postdoctoral researcher in Janeway’s lab. (Janeway died in 2003.)

“He turned out to speak very little English, and had almost no experience in a wet laboratory,” says Derek Sant’Angelo, who worked in the lab at the time. Sant’Angelo, now at the Robert Wood Johnson Medical School in New Jersey, recalls coming across Medzhitov at the bench one night. In one hand, Medzhitov held a mechanical pipette. In the other hand, he held a tube of bacteria. Medzhitov needed to use the pipette to remove a few drops of bacteria from the tube and place them on a plate on the lab bench in front of him. “He was slowly looking back and forth from the pipette down to the plate to the bacteria,” says Sant’Angelo. “He knew in theory that the pipette was used to put the bacteria on the plate. But he simply had absolutely no idea how to do it.”

Medzhitov still marvels that Janeway agreed to work with him. “I think that the only reason that he took me in his lab is that nobody else wanted to touch this idea,” he recalled.

With help from Sant’Angelo and other members of the lab, Medzhitov learned very quickly. Soon he and Janeway discovered a new class of sensor on the surface of a certain kind of immune cell. Confronted with an invader, the sensors would clasp onto the intruder and trigger a chemical alarm that promoted other immune cells to search the area for pathogens to kill. It was a fast, accurate way to sense and remove bacterial invaders.

Medzhitov and Janeway’s discovery of the sensors, now known as toll-like receptors, revealed a new dimension to our immune defences, and has been hailed as a fundamental principle of immunology. It also helped solve a medical mystery.

Infections sometimes produce a catastrophic body-wide inflammation known as sepsis. It is thought to strike around a million people a year in the USA alone, up to half of whom die. For years, scientists thought that a bacterial toxin might cause the immune system to malfunction in this way – but sepsis is actually just an exaggeration of one of the usual immune defences against bacteria and other invaders. Instead of acting locally, the immune system accidentally responds throughout the body. “What happens in septic shock is that these mechanisms become activated much more strongly than necessary,” said Medzhitov. “And that’s what kills.”

Medzhitov isn’t driven to do science to cure people; he’s more interested in basic questions about the immune system. But he argues that cures won’t be found if researchers have the wrong answers for basic questions. Only now that scientists have a clear understanding of the biology underlying sepsis can they develop treatments that target the real cause of the condition – the over-reaction of the toll-like receptors. (Tests are ongoing, and the results so far are promising). “Thirty years ago, it was, ‘Whatever causes septic shock is bad.’ Well, now we know it’s not,” said Medzhitov.

Medzhitov kept thinking after he and Janeway discovered toll-like receptors. If the immune system has special sensors for bacteria and other invaders, perhaps it had undiscovered sensors for other enemies. That’s when he started thinking about parasitic worms, IgE and allergies. And when he thought about them, things didn’t add up.

It’s true that the immune system makes IgE when it detects parasitic worms. But some studies suggest that IgE isn’t actually essential to fight these invaders. Scientists have engineered mice that can’t make IgE, for instance, and have found that the animals can still mount a defence against parasitic worms. And Medzhitov was sceptical of the idea that allergens mimic parasite proteins. A lot of allergens, such as nickel or penicillin, have no possible counterpart in the molecular biology of a parasite.

The more Medzhitov thought about allergens, the less important their structure seemed. Maybe what ties allergens together was not their shape, but what they do.

We know that allergens often cause physical damage. They rip open cells, irritate membranes, slice proteins into tatters. Maybe, Medzhitov thought, allergens do so much damage that we need a defence against them. “If you think of all the major symptoms of allergic reactions – runny noses, tears, sneezing, coughing, itching, vomiting and diarrhoea – all of these things have one thing in common,” said Medzhitov. “They all have to do with expulsion.” Suddenly the misery of allergies took on a new look. Allergies weren’t the body going haywire; they were the body’s strategy for getting rid of the allergens.

As Medzhitov explored this possibility, he found that the idea had surfaced from time to time over the years, only to be buried again. In 1991, for example, the evolutionary biologist Margie Profet argued that allergies fought toxins. Immunologists dismissed the idea, perhaps because Profet was an outsider. Medzhitov found it hugely helpful. “It was liberating,” he said.

Together with two of his students, Noah Palm and Rachel Rosenstein, Medzhitov published his theory in Nature in 2012. Then he began testing it. First he checked for a link between damage and allergies. He and colleagues injected mice with PLA2, an allergen that’s found in honey-bee venom and tears apart cell membranes. As Medzhitov had predicted, the animals’ immune systems didn’t respond to PLA2 itself. Only when PLA2 ripped open cells did the immune system produce IgE antibodies.

Another prediction of Medzhitov’s theory was that these antibodies would protect the mice, rather than just make them ill. To test this, Medzhitov and his colleagues followed their initial injection of PLA2 with a second, much bigger dose. If the animals had not previously been exposed to PLA2, the dose sent their body temperature plunging, sometimes fatally. But the mice that had been exposed marshalled an allergic reaction that, for reasons that aren’t yet clear, lessened the impact of the PLA2.

Medzhitov didn’t know it, but on the other side of the country another scientist was running an experiment that would provide even stronger support for his theory. Stephen Galli, chair of the Pathology Department at Stanford University School of Medicine, had spent years studying mast cells, the enigmatic immune cells that can kill people during allergic reactions. He suspected mast cells may actually help the body. In 2006, for example, Galli and colleagues found that mast cells destroy a toxin found in viper venom. That discovery led Galli to wonder, like Medzhitov, whether allergies might be protective.

To find out, Galli and colleagues injected one to two stings’ worth of honey-bee venom into mice, prompting an allergic reaction. Then they injected the same animals with a potentially lethal dose, to see if the reaction improved the animal’s chance of survival. It did. What’s more, when Galli’s team injected the IgE antibodies into mice that had never been exposed to the venom, those animals were also protected against a potentially lethal dose.

Medzhitov was delighted to discover Galli’s paper in the same issue of Immunity that carried his own. “It was good to see that somebody got the same results using a very different model. That’s always reassuring,” Medzhitov told me.

Still, the experiments left a lot unanswered. How precisely did the damage caused by the bee venom lead to an IgE response? And how did IgE protect the mice? These are the kinds of questions that Medzhitov’s team is now investigating. He showed me some of the experiments when I visited again last month. We sidled past a hulking new freezer blocking a corridor to slip into a room where Jaime Cullen, a researcher associate in the lab, spends much of her time. She put a flask of pink syrup under a microscope and invited me to look. I could see a flotilla of melon-shaped objects.

“These are the cells that cause all the problems,” said Medzhitov. I was looking at mast cells, the key agents of allergic reactions. Cullen is studying how IgE antibodies latch onto mast cells and prime them to become sensitive – or, in some cases, oversensitive – to allergens.

Medzhitov predicts that these experiments will show that allergen detection is like a home-alarm system. “You can detect a burglar, not by recognising his face, but by a broken window,” he said. The damage caused by an allergen rouses the immune system, which gathers up molecules in the vicinity and makes antibodies to them. Now the criminal has been identified and can be more easily apprehended next time he tries to break in.

Allergies make a lot more sense in terms of evolution when seen as a home-alarm system, argues Medzhitov. Toxic chemicals, whether from venomous animals or plants, have long threatened human health. Allergies would have protected our ancestors by flushing out these chemicals. And the discomfort our ancestors felt when exposed to these allergens might have led them to move to safer parts of their environment.

Like many adaptations, allergies weren’t perfect. They lowered the odds of dying from toxins but didn’t eliminate the risk. Sometimes the immune system overreacts dangerously, as Richet and Protier discovered when the second dose of anemone allergen killed the dogs they were experimenting on. And the immune system might sometimes round up a harmless molecular bystander when it responded to an allergy alarm. But overall, Medzhitov argues, the benefits of allergies outstripped their drawbacks.

That balance shifted with the rise of modern Western life, he adds. As we created more synthetic chemicals, we exposed ourselves to a wider range of compounds, each of which could potentially cause damage and trigger an allergic reaction. Our ancestors could avoid allergens by moving to the other side of the forest, but we can’t escape so easily. “In this particular case, the environment we’d have to avoid is living indoors,” said Medzhitov.

Scientists are taking this theory very seriously. “Ruslan is one of the most distinguished immunologists in the world,” said Galli. “If he thinks there’s validity to this idea, I think it gets a lot of traction.”

Dunne, on the other hand, is sceptical about the idea that Medzhitov’s theory explains all allergies. Medzhitov is underestimating the huge diversity of proteins that Dunne and others are finding on the surface of worms – proteins that could be mimicked by a huge range of allergens in the modern world. “My money’s more on the worm one,” he said.

Over the next few years, Medzhitov hopes to persuade sceptics with another experiment. It’s unlikely to end the debate, but positive results would bring many more people over to his way of thinking. And that might eventually lead to a revolution in the way we treat allergies.

Sitting on Cullen’s lab bench is a plastic box that houses a pair of mice. There are dozens more of these boxes in the basement of their building. Some of the mice are ordinary, but others are not: using genetic engineering techniques, Medzhitov’s team has removed the animals’ ability to make IgE. They can’t get allergies.

Medzhitov and Cullen will be observing these allergy-free mice for the next couple of years. The animals may be spared the misery of hay fever caused by the ragweed pollen that will inevitably drift into their box on currents of air. But Medzhitov predicts they will be worse off for it. Unable to fight the pollen and other allergens, they will let these toxic molecules pass into their bodies, where they will damage organs and tissues.

“It’s never been done before, so we don’t know what the consequences will be,” says Medzhitov. But if his theory is right, the experiment will reveal the invisible shield that allergies provide us.

Even if the experiment works out just as he predicts, Medzhitov doesn’t think his ideas about allergies will win out as quickly as his ideas about toll-like receptors. The idea that allergic reactions are bad is ingrained in the minds of physicians. “There’s going to be more inertia,” he said.

But understanding the purpose of allergies could lead to dramatic changes in how they’re treated. “One implication of our view is that any attempt to completely block allergic defences would be a bad idea,” he said. Instead, allergists should be learning why a minority of people turn a protective response into a hypersensitive one. “It’s the same as with pain,” said Medzhitov. “No pain at all is deadly; normal pain is good; too much pain is bad.”

For now, however, Medzhitov would just be happy to get people to stop seeing allergies as a disease, despite the misery they cause. “You’re sneezing to protect yourself. The fact that you don’t like the sneezing, that’s tough luck,” he said, with a slight shrug. “Evolution doesn’t care how you feel.”

Family Life

Do you need to go to parent school?

This story first appeared on Mosaic and is republished here under a Creative Commons license.

Mom and Baby
Photo by Travis Swan | CC BY-SA 2.0

Is there a ‘right’ way to bring up your child? Linda Geddes asks whether parent school is the answer.

How do you entertain a grumpy three-year-old? My strategy is generally: (a) panic; (b) rustle about in my bag for some breadsticks or – if she’s lucky – a colouring book; (c) hand over my iPhone and let her watch some cartoons – all the while worrying I’m stunting her brain development.

My friend, however, has a different strategy. One morning we were enjoying a coffee when, to distract her three-year-old daughter, she serenely reached into her bag and handed her a sheet of paper with six or seven three-letter words on it and a red pen. She then proceeded to read the words out at random, while her daughter correctly circled each one. It was impressive. I was horrified.

I’d never considered doing similar activities with my own daughter, just four months younger. Although we read to her before bed each night, I’d always assumed formal reading and writing was just something she’d pick up when she went to school. Perhaps I’d got it terribly wrong.

About a week later, when dropping my daughter off at nursery, I was handed a leaflet about parenting classes. Like many mums, no one taught me how to raise my children – I’ve simply muddled by on instinct and the odd book. But perhaps there’s a more evidence-based way to raise happy and successful kids. Maybe I needed to enrol at Parent School.

Trends in parenting have waxed and waned over the years. Although once upon a time, new parents simply fell back on the wisdom and experience of their extended families, doctors started getting involved from the late 19th century onwards. Today there’s no shortage of Supernannys, paediatricians and psychiatrists serving up often conflicting parenting advice. New parents can choose any number of approaches: attachment parenting, minimalist parenting, Tiger Mom parenting.

Even politicians are getting in on the act. In 2012, UK Prime Minister David Cameron launched CANparent, a heavily subsidised network of parenting classes that aspire to teach us all how to become better parents. Parenting has become a public issue, which means it’s now eating up public funding.

All of this begs the question: which approach is best? Whereas many parenting trends reflect the opinions of a single psychoanalyst, paediatrician or nanny, CANparent’s providers claim to draw upon the latest scientific research about how children develop and say their strategies are “proven” to make a real, positive difference to families. Others, meanwhile, claim that such evidence-based parenting policies are based on distorted science and undermine parents’ confidence in their ability to raise their children.

“It transforms the meaning of family life,” says Jan Macvarish, who studies the impact of neuroscience on family policy at the University of Kent. “It says ‘we will be able to measure the quality of your family life by the intelligence or emotional intelligence of your child’.”

Cameron’s intervention in this most personal area of family life came in response to a report published in 2011, entitled Early Intervention: The next steps. On its first page sits an image of a healthy three-year-old’s brain and, next to it, a brain approximately half the size labelled ‘extreme neglect’. The report’s message is simple: “Many of the costly and damaging social problems in society are created because we are not giving children the right type of support in their earliest years, when they should achieve their most rapid development.”

The report goes on to cite several scientific findings, such as the fact that a child’s development score at just 22 months can serve as an accurate predictor of educational outcomes at 26 years. And that while babies are born with 25 per cent of their brains developed, their brains are 80 per cent developed by the age of three. “In that period, neglect, the wrong type of parenting and other adverse experiences can have a profound effect on how children are emotionally ‘wired’,” the report says. “This will deeply influence their future responses to events, and their ability to empathise with other people.”

It makes scary reading for parents like me who have largely muddled through their children’s early years. My kids, now four and two, have probably passed this key window of intervention. If I’ve been doing things wrong, it may already be too late.

Yet many neuroscientists query the significance of this ‘critical’ window of development – or whether it even exists at all. “It may be important to intervene early because the early years come first and may influence later experiences, but later experiences can be very influential in affecting both behaviour and brain structure,” says Sir Michael Rutter, professor of developmental psychopathology at King’s College London.

That said, why not start early – particularly if you can train parents to be more effective over their entire parenting career? There’s no denying the gulf that exists between the achievements of children from rich and poor areas by the time they start school. For instance, according to the UK’s Department for Education, in 2013, 52 per cent of all children reached a ‘good level of development’ at age five, compared to 36 per cent of children from poorer backgrounds who were eligible for free school meals. It’s a similar story in the USA.

“If you look at overall measures of numeracy and literacy, what you see is a huge gap between kids from families in the top and bottom fifth of the income distribution,” says Greg Duncan of the University of California, Irvine, who studies the links between poverty and child development. What’s more, this gap widens as children age.

It may seem logical, then, to look to the quality of a child’s parenting to explain it. Maybe these infant ‘underachievers’ simply need better stimulation or more rigid boundaries.

One solution proposed by the current UK administration is parenting classes from birth – not just for poor families, but for everyone. “We know that the single most important factor in a child’s development is the quality of parenting, yet babies don’t come with instructions included,” says Vera Azuike of CANparent. “Everybody could use a little extra advice or support, but it has to be the right advice.”

Predominant among the classes offered by CANParent are those provided by an Australian company called Triple P (the Ps stand for ‘Positive Parenting Program’). Founded by clinical psychologist Matt Sanders, its original focus was helping children with aggression problems through a series of home visits and interventions drawn from social learning theory – the idea that children develop their model of values and behaviour from what they see and experience around them.

Triple P claims to be one of the few parenting programmes that’s scientifically proven to work, having helped hundreds of thousands of families in 25 different countries to deal with issues ranging from temper tantrums and disobedience to bedtime dramas and teenage rebellion in the 30 years since it was conceived. Today it’s a private company, managed by the University of Queensland’s technology transfer arm, although Sanders – who directs the University’s parenting and family support centre – remains actively involved.

“There are some key principles that we think are very important to children’s development,” he says. “The first is that kids grow up in an interesting and engaging environment with age-appropriate things to keep them busy. The second is that children will do better in a world of encouragement and positivity rather than criticism and putdowns. The third principle is really about boundaries and limits setting; parents should have clear ideas about what they expect of their children, and there should be consistent and predictable consequences if they break those boundaries.”

Triple P doesn’t offer any classes on teaching your three-year-old to read. It does, however, offer a smorgasbord of other parenting interventions, from one-to-one sessions designed to help families experiencing serious difficulties to group courses and one-off discussion groups, covering issues such as developing good bedtime routines and managing fighting and aggression.

I enroll on a two-hour discussion session entitled ‘Dealing with Disobedience’ at a Children’s Centre in Redditch, Worcestershire. Before going, I ask Sanders what he thinks I’d get out of attending a Triple P class. “More than anything else, I think it would give you time to pause and reflect upon how you are dealing with issues with your kids,” he tells me. “It would enable you to think about the kind of skills, behaviours and values that you want to promote to your children and provide you with a toolkit for accomplishing that.”

I arrive, eager to learn the secrets of good parenting. The session is being held in a government-funded Children’s Centre in the middle of a large council estate. My first surprise is that many of the 12 parents in attendance already have multiple children – some of them teenagers. One of them is Rachael Kelly, 35, a mother of five from Redditch whose children range in age from nine months to 14 years. Surely if anyone knows how to parent, it’s her. But she tells me she’s hoping to get some new ideas: “Every parent hits a brick wall at some time or another,” she says. “Children are unique, and they all respond to things differently.”

After introducing ourselves, one of the first exercises we are asked to do is list the problems we have faced as parents over the past month. I tick ‘complaining or whining’, ‘demanding things’, ‘answering back’ and ‘tantrums’. We then talk about reasons why children might be disobedient. I underline the section in my handout about tiredness or hunger being common reasons for disobedience – it strikes me that most sulkiness occurs when my kids have just come home from nursery or after they’ve woken up. Next, we are asked to look at a list of common ‘parent traps’ and tick those that might apply to us. I tick six of the boxes, including ‘giving attention for bad behaviour by arguing or negotiating’ and ‘ignoring good behaviour’.

Our instructor explains the importance of praising children for doing the right thing, as well as pointing out when they’ve done something wrong. “Often you get what you praise for,” she adds. I’m encouraged to think of behaviours that I could look out for and celebrate, such as kindness, tidying up or simply playing quietly together. We’re also taught about setting limits for our children and backing those instructions up with consequences. Triple P advocates the use of ‘time out’ – taking your child away from a troublesome situation, possibly to their bedroom or another room, and having them sit quietly for a short time.

None of this, frankly, is rocket science. The threat of time out already looms large in our household, although I hadn’t come across its gentler cousin, ‘quiet time’, where your reaction to disobedience is to make your child sit quietly near the activity they were doing for a couple of minutes while they reflect on what went wrong. Even so, I leave the session feeling uplifted. Talking to other parents reminds me that these issues are common, and makes me think I’m probably not doing such a bad job. Also, as Sanders suggested, taking two hours out of my usual routine to reflect on the values I want to instil in my children, and on how to achieve this, feels as though it was a valuable investment.

Several days after my course, I put my new parenting skills to the test. I take my two children to a local toddler group and my daughter hits the ball pit, showering multicoloured balls around the room. It looks like great fun, but as she meanders off to play with a large plastic kitchen I remind her that she needs to tidy up afterwards. I am ignored, so I try backing up my instruction with some quiet time: I ask my daughter to sit with me, and I describe how tired it makes me feel always having to do the tidying up. I beseech her to help me; I even suggest that we turn it into a competition, and it works. Soon all the balls are tidied away, and I thank her for working so hard. Although I feel like Supermum, it also feels a little bit contrived. Still, my daughter seems happy, and she responds to the additional praise with a big smile and a “thank you” in return.

I call up Rachael and ask how she’s got on. She recounts a similar experience of using quiet time to emphasise the need to share a garden swing. She’s also taken a tip from a session on promoting good bedtime routines, constructing a chart to remind her son of what he needs to do before bed and in what order. “It is working brilliantly,” she says.

Both of us feel a renewed sense of confidence in our ability to parent, and it seems we’re not alone. A pilot trial of CANParent in the London borough of Camden, Middlesbrough and High Peak in Derbyshire reported that 91 per cent of those who attended classes said they had learned new parenting skills, and 84 per cent said they felt more confident as a result. Seventy-five per cent thought their relationship with their children had improved.

All the same, I wonder if parenting classes are really the solution to social inequality that some – including the UK government – would have us believe, especially considering that just 4 per cent of eligible parents took up the offer of subsidized classes during the CANParent trial. Presumably anyone signing up for parenting classes is already motivated to try to improve their parenting.

A week later, I attend a conference in Bristol where a number of parent class providers are setting out their stalls to the local authorities that commission (and pay for) their services. Although each of the providers is trying to hype up their unique selling point, as I work my way around the room I hear the same strategies repeated again and again: firm boundaries, loving and responsive care, positive praise.

Like Triple P, most of these programmes draw on social learning theory as their base, with a smattering of attachment theory – the idea that a strong emotional bond to at least one caregiver is critical to personal development – on the side. Their founders tend to be child psychologists, keen to put their theories about how to get the best out of children into practice. But there’s also a financial incentive: an eight-week Triple P course costs a local authority approximately £250 per parent, while the Solihull Approach’s online course, which is marketed directly to parents, costs £39.

Most claim empirical evidence that their interventions work, but some are more evidence-based than others. Sanders cites a recent study that measured outcomes from 16,099 families who had participated in a Triple P programme: “We found significant positive effects on child social, emotional and behavioural problems, plus significant effects on parenting practices and satisfaction,” he says. “These are persistent effects that don’t disappear once the parent has completed the programme.”

It sounds impressive, and Triple P can indeed cite hundreds of other scientific studies, including randomised controlled trials, the gold standard for evaluating how effective a drug or intervention is. Often, though, these studies have relied on parental reports of child behaviour, rather than independent assessment – and if parents are feeling better, they may rate their children’s behaviour as less troublesome. The evidence for Triple P providing lasting benefits is also stronger for children with more serious behavioural problems, whose parents receive more intensive parenting support, than for the everyday child on the street whose parent attends group-based classes like I did.

Other scientists have raised concerns about a high risk of bias and potential conflicts of interest in many studies that have investigated Triple P. “We found no convincing evidence that Triple P interventions work across the whole population or that any benefits are long-term,” wrote the authors of a recent analysis that compares previous studies of the programme.

But Triple P isn’t the only parenting programme with such methodological issues, adds the report’s lead author, Philip Wilson at the University of Aberdeen: “In general, studies of the effectiveness of parenting programmes have been small, underpowered and have had methodological problems.”

That’s not to say they don’t work. But if parenting classes are supposed to be a prescription for a better society, perhaps we should be demanding the same standard of evidence as we do for new drugs. “There is a real need for head-to-head comparisons of different parenting programmes which are adequately powered to see if there is any real benefit,” Wilson adds.

I think back to my own Triple P experience. I certainly feel like I’m putting more effort into how I interact with my children. Even if it makes no difference to their long-term academic or social development, it’s difficult to see how this could be harmful. But it’s also true that I might have reaped similar benefits by going to a coffee morning and swapping tips with other parents.

And the very fact that I had to seek expert advice to confirm that I’m good enough at parenting troubles some sociologists. It worries me how many of the things that we all do naturally – reading, relaxing, cuddling, singing, talking to our children – have been repackaged in a commercialised and expert-led way,” says Macvarish. Although what we’re doing is probably no different to what our own parents and grandparents did when we were infants, we’re no longer just doing it to provide comfort or entertainment; we’re also doing it to stimulate their brains.

For some of us, that added sense of purpose can bring anxiety. I’ve certainly had moments where I’ve wondered if I’m doing enough cuddling, singing or reading with my children, or whether I’m somehow stunting their brain development by letting them watch more than an hour of television.

However, most of the experts I speak to reassure me that what comes naturally is probably more than enough for most children. As Claire Hughes, professor of developmental psychology at the University of Cambridge, told me: “The difference between being an adequate parent and Supermum – well, it’s diminishing returns, frankly.”

According to Hughes, the children we really need to be thinking about are those “facing toxic levels of stress, and whose parents are unable to provide support because they are facing their own health problems or other concerns”. By placing such a strong emphasis on parenting, are we leaching resources away from other social issues that need to be tackled to really close the gap between rich and poor kids?

“Partly what parents get from attending a parenting class is a sense of reassurance and the support and companionship of other parents, and that’s so important,” says Val Gillies at London South Bank University. “The problem comes if you present parenting classes as the key to social mobility.”

So if inadequate parenting isn’t to blame for the poorer academic performance of children from low-income families, what is? Gillies points out that family income and parental education have a far greater impact on children’s educational attainment and well-being than any particular parenting style. Money doesn’t just buy your children toys, books and a house in a good school catchment area; it can also buy museum trips and foreign holidays, which enhance children’s knowledge about the wider world.

“One of the roadblocks to literacy and more general achievement once kids get to school is the background knowledge that will enable them to understand what they are reading about,” says Duncan. “That kind of background knowledge is conveyed effortlessly in a lot of households with higher socioeconomic status.”

Education is another factor that often goes hand in hand with affluence. Studies have found that highly educated parents are more likely to read to their children, and use a wider vocabulary and more descriptive sentences when speaking to them. They are also more inclined to use mathematical language – terms like ‘more’ and ‘less’ or ‘half’ and ‘quarter’.

“Vocabulary development is critical for your ability to communicate, your understanding of the world and your ability to decode the meaning of novel words as you’re reading them,” says Fred Morrison, a psychologist at the University of Michigan. “A child’s understanding of mathematical language may also influence their rate of mathematical development and achievement in late preschool and the early school period.”

Obviously, it’s easier to send mums and dads to parenting classes than it is to tackle inequalities in wealth or persuade parents to go back to college and boost their own education. Yet at least one study has suggested that when poorly educated young mothers return to school, their children’s academic performance – particularly their reading skills – also increases.

In recent years, some American kindergartens have introduced a teaching method known as ‘Tools of the Mind’, which is specifically designed to foster a set of skills called ‘executive function’ in preschool children. “A good analogy is to an air traffic controller,” says Duncan. “It’s about being able to keep a lot of things up in the air at the same time, so it involves working memory, impulse control and being able to shift from thinking about one thing to another.”

Until recently, executive function wasn’t thought to kick in until adolescence; it certainly wasn’t something people thought you could train. Yet some recent studies have suggested that executive function is a good indicator of later literacy, numeracy and general personal adjustment.

In 2007, a study published in Science found that preschool children who completed a Tools of the Mind programme had higher levels of self-control than children who received a standard preschool education. One strategy that Tools of the Mind teachers use is engaging children in extended sessions of make-believe, where they are encouraged to plan scenarios that change as their play progresses and to swap roles.

High-quality childcare has been shown to balance out some of the effects of social deprivation. Nursery teachers are often trained in how to teach basic numeracy and literacy to young children, as well as helping them to solve problems for themselves using a technique known as scaffolding. “You might have a child who is completely unable to do a jigsaw, but when supported by an adult they can complete it,” says Hughes. One potential alternative to parent classes is to skip the parents and target the children directly, using methods such as Tools of the Mind.

Yet more recent studies have cast doubt on how much of a difference Tools of the Mind truly makes to children’s development. “If you really want to know what skills or behaviours best equip children to be successful at school, it’s not executive function; it is about getting along with others, and it’s concrete academic numeracy and literacy skills,” says Duncan. “It’s not a case of bringing three- and four-year-olds into a classroom and lecturing to them, but building structured learning experiences into their play activities.”

Of course, middle-class, well-educated parents like me seize upon statements like this, wanting to know: how do I do that? And yet many of the things proven to be associated with better early school grades – immersing children in language, talking about mathematical concepts, scaffolding – are things we’re doing already. “Kids from middle-class families are generally supported to fulfil their potential, whatever their genetic tendencies,” says Adam Perkins, a personality researcher at King’s College London.

Even so, middle-class parents aren’t perfect. If parenting classes have taught me anything, it’s the value of paying attention to your child – even when they’re being good. All too often I’ve caught myself using this kind of quiet time to check for emails or read Twitter, rather than taking an interest in what my children are doing. It’s a bad habit I’m trying to change.

I decide against writing out three-letter words for my daughter to recognise, at least until she shows a genuine interest in reading for herself. Instead, I carry on much as before: asking my children to describe leaf shapes when we go for walks, singing songs about numbers and reading them a book or two at bedtime.

Although most of us worry from time to time that we’re not being the best parents we could be, I’m inclined to believe that we don’t need experts to tell us how to raise our children if we’re honest about our anxieties and prepared to swap notes with other parents. In 1946, paediatrician Dr Benjamin Spock wrote the Common Sense Book of Baby and Child Care, which remains one of the bestselling books of all time. Its opening line: “Trust yourself. You know more than you think you do.”

This story first appeared on Mosaic and is republished here under a Creative Commons license.


Hyatt Offers Free Wi-Fi to Guests Worldwide

Hyatt Hotels Wi-Fi
Photo: Hyatt

The internet has become a ubiquitous, with hotels, airports, cafes and even fast food restaurants offering their guests free Wi-Fi. This week marks the announcement of Hyatt hotels and resorts’ roll-out of global free Wi-Fi to all of their guests. That’s right, Hyatt will be offering free internet connectivity to all of their guests, regardless of their booking method or loyalty program participation. Guests can connect an unlimited number of mobile devices or laptops in private rooms or public spaces throughout the hotel.

“We continue to evolve our offerings by listening to our guests, and for Hyatt, it didn’t feel natural to put barriers around something travelers view as an essential part of their hotel stay,” said Kristine Rose, vice president of brands, Hyatt. “More than 500 Hyatt-branded hotels and resorts worldwide are excited to now provide Wi-Fi free of charge in guest rooms and social spaces, no strings attached.”

“With free Wi-Fi for all guests at all Hyatt hotels and resorts, guests can worry less about their Internet connections and focus on the things that matter most.”

Platinum and Diamond Hyatt Gold Passport members will receive a free upgrade to premium Wi-Fi service in those spaces wherever available. The premium service will likely offer fast speeds for streaming content and teleconferencing. The basic service does not extend to conference rooms or business meetings.

For more information, please visit

Art Featured Life Social Issues Stage

How Not to Make Love to a Fat Girl

Holding Hands
Photo: Leonardo Rizzi

People — and in this context, women — are more than just their body parts: their fat, their bellies, their thighs, their skin.

When you are attracted to a person of size (or any one who has a marginalized body or identity), and they invite you to share sexual intimacy with them, don’t objectify or fetishize them. As this poet says, “Make love to the whole of them.”

If you are intimidated by the stigma, or unsure of yourself, be vulnerable and open-hearted and ask questions. Ask your partner what they desire and don’t desire. Allow them to teach you how they want to be treated.

Learn their boundaries and get consent. Not only is consent required, but it allows for the sort of physical and emotional safety necessary for intimate connection to truly be fulfilling for all parties involved.

“Trust me, you’ll get luckier this way.”

This article was originally published at Everyday Feminism. It is republished here with permission.

Featured Travel

World’s Safest Airlines for 2015

Photo: Angelo DeSantis | CC BY-SA 2.0

Have recent reports in the news made you question if you should fly internationally? All airlines are not created equally, but how much do they really differ? A new report showcases the world’s safest airlines.

In 2014 the world´s death toll in commercial air transport has risen nearly four times over the 2013 numbers. About half of the fatalities came from the Asia-Pacific region.

Although flying remains the safest way of travelling, 2014 marks an untypically year compared to a series of years with falling numbers of victims.

JACDEC’s (Jet Airliner Crash Data Evaluation Centre) annual report compiles data more than 3,500 airlines and over 30,000 different accidents or incident data points. Below is the 2015 safety ranking, compiled from 2014 data.


  1. Cathay Pacific Airways (China, Hong Kong)
  2. Emirates (UAE)
  3. EVA (Taiwan)
  4. Air Canada (Canada)
  5. KLM (Neterlands)
  6. Air New Zealand (New Zealand)
  7. Qantas (Australia)
  8. Hainan Airlines (China)
  9. JetBlue Airlines (USA)
  10. Etihad Airways (UAE)
  11. All Nippon Airways (Japan)
  12. Lufthansa (German)

For an in-depth look at the report, including safety index data and regional safety, read the full report

Featured Life

How the zebra got its stripes, with Alan Turing

This story first appeared on Mosaic and is republished here under a Creative Commons licence.

Photo by Benh Lieu Song | CC SA 2.0
Photo by Benh Lieu Song | CC SA 2.0

Where do a zebra’s stripes, a leopard’s spots and our fingers come from? The key was found years ago – by the man who cracked the Enigma code, writes Kat Arney.

In 1952 a mathematician published a set of equations that tried to explain the patterns we see in nature, from the dappled stripes adorning the back of a zebra to the whorled leaves on a plant stem, or even the complex tucking and folding that turns a ball of cells into an organism. His name was Alan Turing.

More famous for cracking the wartime Enigma code and his contributions to mathematics, computer science and artificial intelligence, it may come as a surprise that Turing harboured such an interest. In fact, it was an extension of his fascination with the workings of the mind and the underlying nature of life.

The secret glory of Turing’s wartime success had faded by the 1950s, and he was holed up in the grimly industrial confines of the University of Manchester. In theory he was there to develop programs for one of the world’s first electronic computers – a motley collection of valves, wires and tubes – but he found himself increasingly side-lined by greasy-fingered engineers who were more focused on nuts and bolts than numbers. This disconnection was probably intentional on Turing’s part, rather than deliberate exclusion on theirs, as his attention was drifting away from computing towards bigger questions about life.

It was a good time to be excited about biology. Researchers around the world were busy getting to grips with the nature of genes, and James Watson and Francis Crick would soon reveal the structure of DNA in 1953. There was also a growing interest in cybernetics – the idea of living beings as biological computers that could be deconstructed, hacked and rebuilt. Turing was quickly adopted into a gang of pioneering scientists and mathematicians known as the Ratio Club, where his ideas about artificial intelligence and machine learning were welcomed and encouraged.

Against this backdrop Turing took up a subject that had fascinated him since before the war. Embryology – the science of building a baby from a single fertilised egg cell – had been a hot topic in the early part of the 20th century, but progress sputtered to a halt as scientists realised they lacked the technical tools and scientific framework to figure it out. Perhaps, some thinkers concluded, the inner workings of life were fundamentally unknowable.

Turing viewed this as a cop-out. If a computer could be programmed to calculate, then a biological organism must also have some kind of underlying logic too.

He set to work collecting flowers in the Cheshire countryside, scrutinising the patterns in nature. Then came the equations – complex, unruly beasts that couldn’t be solved by human hands and brains. Luckily the very latest computer, a Ferranti Mark I, had just arrived in Manchester, and Turing soon put it to work crunching the numbers. Gradually, his “mathematical theory of embryology”, as he referred to it, began to take shape.

Like all the best scientific ideas, Turing’s theory was elegant and simple: any repeating natural pattern could be created by the interaction of two things – molecules, cells, whatever – with particular characteristics. Through a mathematical principle he called ‘reaction–diffusion’, these two components would spontaneously self-organise into spots, stripes, rings, swirls or dappled blobs.

In particular his attention focused on morphogens – the then-unknown molecules in developing organisms that control their growing shape and structure. The identities and interactions of these chemicals were, at the time, as enigmatic as the eponymous wartime code. Based on pioneering experiments on frog, fly and sea urchin embryos from the turn of the 20th century – involving painstakingly cutting and pasting tiny bits of tissue onto other tiny bits of tissue – biologists knew they had to be there. But they had no idea how they worked.

Although the nature of morphogens was a mystery, Turing believed he might have cracked their code. His paper ‘The chemical basis of morphogenesis’ appeared in the Philosophical Transactions of the Royal Society in August 1952.

Sadly, Turing didn’t live long enough to find out whether he was right. He took his own life in 1954, following a conviction for ‘gross indecency’ and subsequent chemical castration – the penalty for being openly gay in an intolerant time. In those two short years there was little to signpost the twists and turns that his patterns would take over the next 60 years, as biologists and mathematicians battled it out between the parallel worlds of embryology and computing.

In a cramped office in London, tucked away somewhere on the 27th floor of Guy’s Hospital, Professor Jeremy Green of King’s College London is pointing at a screen.

A program that simulates Turing patterns is running in a small window. At the top left is a square box, filled with writhing zebra-like monochrome stripes. Next to it is a brain-bending panel of equations. “It’s astonishing that Turing came up with this out of nowhere, as it’s not intuitive at all,” says Green, as he pokes a finger at the symbols. “But the equations are much less fearsome than you think.”

The essence of a Turing system is that you have two components, both of which can spread through space (or at least behave as if they do). These could be anything from the ripples of sand on a dune to two chemicals moving through the sticky goop holding cells together in a developing embryo. The key thing is that whatever they are, the two things spread at different speeds, one faster than the other.

One component is to be auto-activating, meaning that it can turn on the machinery that makes more of itself. But this activator also produces the second component – an inhibitor that switches off the activator. Crucially, the inhibitor has to move at a faster pace than the activator through space.

The beauty of it is that Turing systems are completely self-contained, self-starting and self-organising. According to Green, all that one needs to get going is just a little bit of activator. The first thing it does is make more of itself. And what prevents it from ramping up forever? As soon as it gets to a certain level it switches on the inhibitor, which builds up to stop it.

“The way to think about it is that as the activator builds up it has a head start,” says Green. “So you end up with, say, a black stripe, but the inhibitor then builds up and spreads more quickly. At a certain point it catches up with the activator in space and stops it in its tracks. And that makes one stripe.”

From these simple components you can create a world of patterns. The fearsome equations are just a way of describing those two things. All you need to do is adjust the conditions, or ‘parameters’. Tweaking the rates of spreading and decay, or changing how good the activator is at turning itself on and how quickly the inhibitor shuts it down, subtly alters the pattern to create spots or stripes, swirls or splodges.

Despite its elegance and simplicity, Turing’s reaction–diffusion idea gained little ground with the majority of developmental biologists at the time. And without the author around to champion his ideas, they remained in the domain of a small bunch of mathematicians. In the absence of solid evidence that Turing mechanisms were playing a part in any living system, they seemed destined to be a neat but irrelevant distraction.

“Well, the stripes are easy. But what about the horse part?”
– Alan Turing on the zebra, quoted by Francis Crick (1972)

Biologists were busy grappling with a bigger mystery: how a tiny blob of cells organises itself to create a head, tail, arms, legs and everything in between to build a new organism.

In the late 1960s a new explanation appeared, championed by the eminent and persuasive embryologist Lewis Wolpert and carried aloft by the legion of developmental biologists that followed in his footsteps. The concept of ‘positional information’ suggests that cells in a developing embryo sense where they are in relation to an underlying map of molecular signals (the mysterious morphogens). By way of explanation, Wolpert waved the French flag.

Imagine a rectangular block of cells in the shape of a flag. A strip of cells along the left-hand edge are pumping out a morphogen – let’s call it Striper – that gradually spreads out to create a smooth gradient of signal, high to low from left to right. Sensing the levels of Striper around them, the cells begin to act accordingly. Those on the left turn blue if the level of Striper is above a certain specific threshold, those in the middle turn white in response to the middling levels of Striper they detect, while those on the far right, bathing in the very lowest amounts of Striper, go red. Et voila – the French flag.

Wolpert’s flag model was simple to grasp, and developmental biologists loved it. All you had to do to build an organism was to set up a landscape of morphogen gradients, and cells would know exactly what to become – a bit like painting by numbers. More importantly, it was clear to researchers that it worked in real life, thanks to chickens.

Even today, chicken embryos are an attractive way to study animal development. Scientists can cut a window in the shell of a fertilised hen’s egg to watch the chick inside, and even fiddle about with tweezers to manipulate the growing embryo. What’s more, chicken wings have three long bony structures buried inside the tip, analogous to our fingers. Each one is different – like the three stripes of a French flag – making them the perfect system for testing out Wolpert’s idea.

In a series of landmark experiments in the 1960s, John Saunders and Mary Gasseling of Wisconsin’s Marquette University carefully cut a piece from the lower side of a developing chick’s wing bud – imagine taking a chunk from the edge of your hand by the little finger – and stuck it to the upper ‘thumb’ side.

Instead of the usual three digits (thumb, middle and little ‘fingers’), the resulting chicken had a mirror wing – little finger, middle, thumb, thumb, middle, little finger. The obvious conclusion was that the region from the base of the wing was producing a morphogen gradient. High levels of the gradient told the wing cells to make a little finger, middling ones instructed the middle digit, and low levels made a thumb.

It was hard to argue with such a definitive result. But the ghost of Turing’s idea still haunted the fringes of biology.

In 1979 a physicist-turned-biologist and a physical chemist caused a bit of a stir. Stuart Newman and Harry Frisch published a paper in the high-profile journalScience showing how a Turing-type mechanism could explain the patterning in a chicken’s fingers.

They simplified the developing three-dimensional limb into a flat rectangle and figured out reaction–diffusion equations that would generate waves of an imaginary digit-making morphogen within it as it grew. The patterns generated by Newman and Frisch’s model are clunky and square, but they look unmistakeably like the bones of a robot hand.

They argued that an underlying Turing pattern makes the fingers, which are then given their individual characteristics by some kind of overlying gradient – of the sort proposed by the French flag model – as opposed to the gradient itself directing the creation of the digits.

“People were still in an exploratory mode in the 1970s, and Turing’s own paper was only 25 years old at that point. Scientists were hearing about it for the first time and it was interesting,” says Newman, now at New York Medical College in the USA. “I was lucky to get physics-oriented biologists to review my paper – there wasn’t an ideology on the limb that had set in, and people were still wondering how it all worked.”

It was a credible alternative to Wolpert’s gradient idea, prominently published in a leading journal. According to Newman, the reception was initially warm. “Straight after it was published, one of Wolpert’s associates, Dennis Summerbell, wrote me a letter saying that they needed to consider the Turing idea, that it was very important. Then there was silence.”

A year later, Summerbell’s view had changed. He published a joint paper with biologist Jonathan Cooke, which made clear that he no longer considered it a valid idea. Newman was shocked. “From that point on nobody in that group ever mentioned it, with one exception – Lewis Wolpert himself once cited our paper in a symposium report in 1989 and dismissed it.”

The majority of the developmental biology community did not consider Turing patterns important at all. Fans of the positional information model closed ranks against Newman. The invitations to speak at scientific meetings dried up. It became difficult for him to publish papers and get funding to pursue Turing models. Paper after paper came out from scientists who supported the French flag model.

Newman explains: “A lot of them got to be editors at journals – I knew some colleagues who felt that pressure was put on them to keep our ideas out of some of the good journals. In other areas people were as open to new ideas as you might expect, but because Wolpert and his scientific descendants were so committed to his idea it became part of the culture of the limb world. All the meetings and special editions of journals were all centred around it, so it was very difficult to displace.”

Further blows came from the fruit fly Drosophila melanogaster – another organism beloved of developmental biologists. For a while the regimented stripes that form in the fly’s developing embryo were thought to develop through a Turing mechanism. But eventually they turned out to be created through the complex interplay of morphogen gradients activating specific patterns of gene activity in the right place at the right time, rather than a self-striping system.

Newman was disappointed by the failure of the research community to take his idea seriously, despite countless hours of further work on both the mathematical and molecular sides. For decades, his and Frisch’s paper languished in obscurity, haunting the same scientific territory as Turing’s original paper.

I’ll take spots, then,” said the Leopard, “but don’t make ’em too vulgar-big. I wouldn’t look like Giraffe – not for ever so.”
‘How The Leopard Got His Spots’, from Rudyard Kipling’sJust So Stories (1902)

High up in the Centre for Genomic Regulation in Barcelona is an office papered with brightly coloured pictures of embryonic mouse paws. Each one shows neat stripes of developing bones fanning out inside blob-like budding limbs – something the room’s decorator, systems biologist James Sharpe, is convinced can be explained by Turing’s model.

Turing’s idea is simple, so one can easily imagine how it could explain the patterns we see in nature. And that’s part of the problem, because a simple likeness isn’t proof that a system is at work – it’s like seeing the face of Jesus in a piece of toast. Telling biological Just So Stories about how things have come to be is a dangerous game, yet this kind of thinking was used to justify the French flag model too.

In Sharpe’s view it was the chicken’s fault. “If studies of limb development had started with a mouse,” he says, “the whole history would have been very different.”

In his opinion there was a built-in bias right from the start that digits were fundamentally different from each other, requiring specific individual instructions for each one (provided by precise morphogen ‘coordinates’, according to the French flag model). This was one of the primary arguments made against a role for Turing patterns being involved in limb development – they can only ever generate the same thing, such as a stripe or a spot, again and again.

So how could a Turing system create the three distinctive digits of a chick’s limb? Surely each one must be told to grow in a certain way by an underlying gradient ‘map’? But a chick only has three fingers. “If they had 20, you would see that wasn’t the case,” says Sharpe, wiggling his fingers towards me by way of demonstration. “They’d all look much more similar to each other.”

I look down at my own hand and see his point. I have four fingers and a thumb, and each finger doesn’t seem to have particularly unique identity of its own. Sure, there are subtle differences in size, yet they’re basically the same. According to Sharpe, the best evidence that they aren’t that different comes from one of the most obvious but incorrect assumptions about the body: that people always have five fingers.

In reality the number of fingers and toes is one of the least robust things about the way we’re made. “We don’t always have five,” he says, “and it’s surprisingly common to have more.” In fact, it’s thought that up to one in 500 children is born with extra digits on their hands or feet. And while the French flag model can’t account for this, Turing patterns can.

By definition Turing systems are self-organising, creating consistent patterns with specific properties depending on the parameters. In the case of a stripy pattern, this means that the same set-up will always create stripes with the same distance (or wavelength, as mathematicians call it) between them. If you disrupt the pattern, for example by removing a chunk, the system will attempt to fill in the missing bits in a highly characteristic way. And while Turing systems are good at generating repeating patterns with a consistent wavelength, such as regular-sized fingers, they’re less good at counting how many they’ve made, hence the bonus digits.

Importantly, a particular Turing system can only make the same thing over and over again. But look closely at the body and there are many examples of repeating structures. In many animals, including ourselves, the fingers and toes are more or less all the same. But, according to the flag model, structures created in response to different levels of morphogen would all have to be different. How to explain the fact that the same thing can be ‘read’ out from a higher and lower morphogen level?

Sharpe maintains that the concept of an underlying molecular ‘road map’ just doesn’t hold up. “I don’t think it’s an exaggeration to say that for a long time a lot of the developmental biology community has thought that you have these seas of gradients washing over a whole organ. And because they’re going in different directions, every part of the organ has a different coordinate.”

In 2012 – the centenary of Turing’s birth and 60 years since his ‘chemical morphogenesis’ paper – Sharpe showed that this idea (at least in the limb) was wrong.

The proof was neatly demonstrated in a paper by Sharpe and Maria Ros at the University of Cantabria in Spain, published in Science. Ros used genetic engineering techniques to systematically remove members of a particular family of genes from mice. Their targets were the Hox genes, which play a fundamental role in organising the body plan of a developing embryo, including patterning mouse paws and human hands.

Getting rid of any of these crucial regulators might be expected to have some fairly major effects, but what the researchers saw was positively freakish. As they knocked out more and more of the 39 Hox genes found in mice, the resulting animals had more and more fingers on their paws, going up to 15 in the animals missing the most genes.

Importantly, as more Hox genes were cut and more fingers appeared, the spacing between them got smaller. So the increased number of fingers wasn’t due to larger paws, but to smaller and smaller stripes fitting into the same space – a classic hallmark of a Turing system, which had never been observed before in mouse limbs. When Sharpe crunched the numbers, Turing’s equations could account for the extra fingers Ros and her team were seeing.

That’s great for the near-identical digits of a mouse, I say, but it doesn’t explain why the chick’s three digits are so different. Sharpe scribbles on a piece of paper, drawing a Venn diagram of two scruffy overlapping circles. One is labelled “PI” for positional information à la Wolpert, the other “SO” for self-organising systems such as Turing patterns. Tapping at them with his pen, he says, “The answer is not that Turing is right and Wolpert was wrong, but that there’s a combination at work.”

Wolpert himself has conceded, to a certain extent, that a Turing system could be capable of patterning fingers. But it can’t, by definition, impart the differences between them. Morphogen gradients must work on top of this established pattern to give the digits their individual characteristics, from thumb to pinky, marrying together Wolpert’s positional information idea with Turing’s self-organising one.


Other real-life examples of Turing systems that have been quietly accumulating over the past two decades are now being noticed. A 1990 paper from a trio of French chemists described the first unambiguous experimental evidence of a Turing structure: they noticed a band of regular spots appear in a strip of gel where a colour-generating reaction was happening – the tell-tale sign of the system at work.

While studying elegantly striped marine angelfish, Japanese researcher Shigeru Kondo noticed that rather than their stripes getting bigger as the fish aged (as happens in mammals like zebras), they kept the same spacing but increased in number, branching to fill the space available. Computer models revealed that a Turing pattern could be the only explanation. Kondo went on to show that the stripes running along the length of a zebrafish can also be explained by Turing’s maths, in this case thanks to two different types of cells interacting with each other, rather than two molecules.

It turns out that the patterned coats of cats, from cheetahs and leopards to domestic tabbies, are the result of Turing mechanisms working to fill in the blank biological canvas of the skin. The distribution of hair follicles on our heads and the feathers on birds are also thanks to Turing-type self-organisation.

Other researchers are focusing on how Turing’s mathematics can explain the way tubes within an embryo’s developing chest split over and over again to create delicate, branched lungs. Even the regular array of teeth in our jaws probably got there by Turing-esque patterning.

Meanwhile in London, Jeremy Green has also found that the rugae on the roof of your mouth – the repeated ridges just above your front teeth that get burnt easily if you eat a too-hot slice of pizza – owe their existence to a Turing pattern.

As well as fish skins, feathers, fur, teeth, rugae and the bones in our hands, James Sharpe thinks there are plenty of other parts of the body that might be created through self-organising Turing patterns, with positional information laid on top. For a start, while our digits are clearly stripes, the clustered bones of the wrist could be viewed as spots. These can easily be made with a few tweaks to a Turing equation’s parameters.

Sharpe has some more controversial ideas for where the mechanism might be at work – perhaps patterning the regular array of ribs and vertebrae running up our spine. He even suspects that the famous stripes in fruit fly embryos have more to do with Turing patterning than the rest of the developmental biology community might have expected.

Given that he works in a building clad in horizontal wooden bars, I ask if he’s started to see Turing patterns everywhere he looks. “I’ve been through that phase,” he laughs. “During the centenary year it really was Turing everywhere. The exciting possibility for me is that we’ve misunderstood a whole lot of systems and how easy it can be to trick ourselves – and the whole community – into making up Just So Stories that seem to fit and being happy with them.”

Stuart Newman agrees, his 1979 theory now back out of the shadows. “When you start tugging at one thread, a lot of things will fall apart if you’re on to something. They don’t want to talk about it, not because it’s wrong – it’s easy to dismiss something that’s wrong – but probably because it’s right. And I think that’s what turned out to be the case.”

Slowly but surely, researchers are piecing together the role of Turing systems in creating biological structures. But until recently there was still one thing needed to prove that there’s a Turing pattern at work in the limb: the identities of the two components that drive it.

That mystery has now been solved by James Sharpe and his team in a paper published in August 2014, again in the journal Science. Five years in the making, it combines delicate embryo work with hardcore number crunching.

Sharpe figured that the components needed to fuel a Turing pattern in the limb must show a stripy pattern that reflects the very early developing fingers – either switched on in the future fingers and off in the cells destined to become the gaps, or vice versa.

To find them, graduate student Jelena Raspopovic collected cells from a developing mouse limb bud, in which only the merest hint of gene activity that leads to digit formation can be seen. After separating the two types of cells, and much painstaking molecular analysis, some interesting molecular suspects popped out. Using computer modelling, Sharpe was able to exactly recapitulate a gradual appearance of digits that mirrored what they saw in actual mouse paws, based on the activity patterns of these components.

Intriguingly, unlike the neat two-part system invoked by Turing, Sharpe thinks that three different molecules work together in the limb to make fingers. One is Sox9, a protein that tells cells to “make bones here” in the developing digits. The others are signals sent by two biological messenger systems: one called BMP (bone morphogenetic protein) signalling, which switches on Sox9 in the fingers, and another messenger molecule known as WNT (pronounced “wint”), which turns it off in the gaps between fingers.

Although classic Turing systems invoke just two components – an activator and an inhibitor – this situation is a little more complicated.  “It doesn’t seem to boil down to literally just two things,” Sharpe explains. “Real biological networks are complex, and in our case we’ve boiled it down to two signalling pathways rather than two specific molecules.”

Further confirmation came when they went the other way – from the model to the embryo. Another of Sharpe’s students, Luciano Marcon, tweaked the program to see what would happen to the patterns if each signalling pathway was turned down. In the simulation, reducing BMP signalling led to a computer-generated paw with no fingers. Conversely, turning down WNT predicted a limb made entirely of digits fused together.

When tested in real life, using tiny clumps of limb bud tissue taken from early mouse embryos and grown in Petri dishes, these predictions came true. Treating the cultures with drugs that dampen down each pathway produced exactly what the program had predicted – no fingers, or all fingers. An alternative simulation with both signals turned down at the same time predicts two or three fat fingers instead of five neat digits. Again, using both drugs at once on real mouse limb buds created exactly the same pattern. Being able to flip from the model to the embryo and back again – making testable predictions that are borne out by experiments – is a key piece of proof that things are working in the way Sharpe thinks.

And if the theory is finally accepted, and we figure out how and where Turing systems are used to create structures in nature, what can we do with this knowledge? Quite a lot, according to Jeremy Green.

“You can live without rugae but the things like your heart valves or your whole palate, they really matter,” he says. “The regenerative medics working on any stem cell technology or cell therapy in the future are going to need to understand how these are made. The growth factor research in the 1980s was the bedrock of the stem cell therapies that are starting to go into clinical trials now, but it inspired the whole world of regenerative medicine. That’s the kind of timescale we’re talking about.”

At Guy’s Hospital he sees close-up what happens when development goes awry. His department specialises in birth defects affecting the face and skull, and Green believes that understanding the underlying molecular nuts and bolts is the key to fixing them. “What we’re doing now is very theoretical, and we can fantasise about how it’s going to be useful, but in 25 years that’s the kind of knowledge we’ll need to have. It’ll probably be taken for granted by then, but we’ll need to know all this Turing stuff to be able to build a better body.”

In the last years of Alan Turing’s life he saw his mathematical dream – a programmable electronic computer – sputter into existence from a temperamental collection of wires and tubes. Back then it was capable of crunching a few numbers at a snail’s pace. Today, the smartphone in your pocket is packed with computing technology that would have blown his mind. It’s taken almost another lifetime to bring his biological vision into scientific reality, but it’s turning out to be more than a neat explanation and some fancy equations.

Featured Life Social Issues

Can medical marijuana curb the heroin epidemic?

This article first appeared at The Conversation. It is republished here with permission.

Photo by Matt Oberski | CC BY-SA 2.0
Photo by Matt Oberski | CC BY-SA 2.0

By Miriam Boeri, Bentley University

In the 1930s, Harry J. Anslinger, the first head of the Federal Bureau of Narcotics, embarked on a fierce anti-marijuana campaign. Highlighted by the 1936 anti-marijuana film Reefer Madness – where marijuana is depicted as a dangerous narcotic that makes good kids become sex-crazed killers – his propaganda efforts also maliciously linked marijuana use to African Americans and ethnic minorities.

By 1970, legislation codified cannabis as one of the nation’s most dangerous drugs: the Controlled Substance Act classified marijuana as a Schedule 1 drug, meaning it possessed high potential for abuse and had no acceptable medical use. Over 40 years later, the classification remains.

But research has shown that marijuana, while still criminalized at the federal level, can be effective as a substitute for treating opioid addicts and preventing overdoses. Massachusetts, which recently legalized medical marijuana – and where heroin overdoses have soared – could be a fertile testing ground for this potentially controversial treatment.

The medical case for marijuana

Before being criminalized, marijuana was used in the US to cure depression and a variety of other mental health ailments. Many studies have supported the therapeutic benefits of cannabinoids, along with the ability of marijuana’s psychoactive ingredients to treat nausea, help with weight loss, alleviate chronic pain, and mitigate symptoms of neurological diseases.

Other research, however, contradicts claims regarding the benefits of cannabidiol treatment. Some say marijuana actually poses a risk for psychosis and schizophrenia. Although the FDA has approved some synthetic cannabinoids for medical treatment, federal agencies do not support marijuana as a legitimate medicine until more clinical studies have been conducted.

The scientific debate over the harms and benefits of marijuana has impeded federal lawmakers from moving forward on marijuana legislation reform. As a result, in 23 states, medical marijuana has become legalized by popular vote.

Marijuana policy dilemma

With each state crafting unique medical marijuana regulations, we find ourselves at a crucial turning point in drug policy. Public health professionals claim the road map used by “big tobacco” will be copied with legal marijuana, and addiction rates for marijuana will increase to those we see for tobacco. Others warn that if medical marijuana is used indiscriminately and without focused education on the uses and forms of medical marijuana, a prescription pain pill-like crisis could occur.

Among drug treatment specialists, marijuana remains controversial. Although some research has shown marijuana to be an alternative treatment for more serious drug addiction, addiction treatment specialists still view marijuana as highly addictive and dangerous. These views handicap policy reform, but despite its status as a Schedule 1 drug, recent research shows marijuana could be part of the solution to the most deadly drug epidemic our country has seen in decades.

Massachusetts: a case study

In 2012 Massachusetts became the 18th state to legalize medical marijuana, though the first 11 dispensaries are not scheduled to open until sometime in the coming year. This situation presents an opportunity to implement sensible, research-based policy.

Massachusetts, like many states across the US, has seen a dramatic rise in opioid addition fueled by the increase in opiate prescription pills. In Boston, heroin overdoses increased by 80% between 2010 and 2012, and four out of five users were addicted to pain pills before turning to heroin.

Meanwhile, the leading cause of death among the Boston’s homeless population has shifted from AIDS complications to drug overdoses, with opiates involved in 81% of overdose deaths. This is an alarming finding given recent expansion in clinical services for the city’s homeless.

Addiction specialists and health care professionals in Boston have been at the forefront of integrating behavioral and medical care. Naloxone and methadone are currently the main solutions to address the growing opiate addiction and overdose problem. But Naloxone is an overdose antidote, not a cure or a form of preventative therapy.

Methadone, like heroin and other opioids, has a very narrow therapeutic index (the ratio between the toxic dose and the therapeutic dose of a drug). This means that a small change in dosage can be lethal to the user. Marijuana, however, has one of the safest (widest) therapeutic ratios of all drugs.

Research shows that marijuana has been used as a form of self-treatment, where users take cannabis in lieu of alcohol, prescription opiates, and illegal drugs. That’s one reason why researchers are calling for marijuana to be tested as a substitute for other drugs. In this capacity, marijuana can be thought of as a form of harm reduction. While researchers don’t seek to discount some of the drug’s potential negative effects, they view it as a less damaging alternative to other, harder drugs. Despite these findings, marijuana is rarely incorporated in formal drug treatment plans.

A recent study might change this policy. Comparing states with and without legalized medical marijuana, it found a substantial decrease in opioid (heroin and prescription pill) overdose death rates in states that had enacted medical marijuana laws. In their conclusions, the researchers suggested that medical marijuana should be part of policy aimed to prevent opioid overdose.

Outside marijuana’s harms and benefits, missing in this discussion is the social environment of drug use. Drug use is social in nature. Where and with whom drugs are used influences why and how they are used. Socially acceptable or moderate use of drugs can be learned through social rituals in socially controlled settings.

Studies in the Netherlands found that using marijuana in Amsterdam coffeehouses encouraged a “stepping-off” hard drug use. These studies also found that when young people used marijuana in a controlled coffeehouse setting instead of a polydrug-using environment, they learned to use marijuana moderately without combining with other drugs. Along with providing access to marijuana, it’s important to instruct users on safe and effective medical marijuana consumption.

Since Massachusetts has not yet opened its medical marijuana dispensaries, it is too early to see if medical marijuana legislation will help reduce opiate addiction in the Commonwealth. Using recent research findings, Massachusetts policymakers have a unique opportunity to implement medical marijuana policies that address its contemporary opiate overdose. Medical marijuana could be part of drug treatment for heroin and opiates.

For homeless people, however, getting a marijuana card is expensive and buying medical marijuana from a dispensary is beyond their economic means. Street drugs are more prevalent in their social setting, easier to obtain, and can be much cheaper. From a policy perspective, addressing the alarming rates of overdose deaths among the homeless in Boston could mean distributing medical marijuana cards to homeless addicts for free and providing reduced cost medical marijuana.

What if medical marijuana cards were offered to homeless addicts? Photo: Wikimedia Commons

Formerly demonized and later legislated as a Schedule 1 substance, marijuana could diminish the damage wrought by harder drugs, like heroin. While opioid use is a nationwide epidemic, Massachusettes – long at the forefront of developing scientifically based public policy – has the opportunity to be at the forefront of cutting-edge, socially-informed drug policy.

This is the second in a series of three articles on alternative strategies to treat addiction. To read the first in the series, click here.

The Conversation

Food Life Restaurants

Will Starbucks delivery ruin coffee culture?

Photo: James Maskell, CC BY-NC-SA 2.0

Delivering a pumpkin spice latte to your doorstep may become as common as ordering a pizza in the near future. Starbucks announced it will begin delivering coffee and food in 2015. CEO Howard Schultz shared the plan during the company’s quarterly earnings conference, stating delivery service will launch first to loyalty program members through a new app. The new app will allow members to order and pay for their food and coffee without going to a Starbucks location.

The move is among a series of plans to bring the coffee chain into the digital age. In July this year, Starbucks announced mobile ordering via their smart phone app, allowing patrons to pre-order their drinks.

The launch date for the delivery service has not been announced, nor has there been any talk to expand the service outside of the United States.

With dwindled human interaction via the ordering app, and no real reason to stay in its stores, is the new profitable and speedy technology the right move?

Starbucks has largely been responsible for the establishing the European-style coffee culture throughout the United States. Patrons can linger in the stores, enjoying free wi-fi and mellow soundtrack, while utilizing its various locations as makeshift offices or meeting spots.

The new mobile initiatives are targeted toward a faster crowd that cares less about atmosphere and more about convenience. In the world of food, honing prep and speed time can drastically increase volume and profits. This is the model most popular fast food restaurants work under. With chains such as Panera Bread also utilizing  mobile app ordering for pick-up, the cafes are becoming less relaxed and more fast-paced.


Can you be a sustainable tourist without giving up flying?

Airport Travel
Photo by Anna & Michal | CC BY-SA 2.0

By Morgan Saletta, University of Melbourne

Australians love to travel. About 9 million Australians travelled overseas last year, 60% of them on holiday. For most tourists, sustainable development and climate change were probably not high on their list of concerns. But increasing numbers of travellers are concerned about these issues.

Is sustainable tourism possible when tourism accounts for about 5% of global greenhouse gas emissions? If the tourism sector were a country, it would be the fifth-largest greenhouse emitter in the world.

By far the largest source of these emissions is transport, particularly air travel. If the current growth trend continues, these emissions could triple within 30 years.

On the other hand, tourism is incredibly important for local development.
Indeed, it offers the only sustainable means of economic development for many developing countries. The UN World Tourism Organization says that tourism will be important in reaching the Millennium Development Goals, which include ensuring environmental sustainability and eliminating extreme poverty.

Exactly how the tourism industry can best help to meet these goals is a matter of debate. However, it seems clear that tourism can make a positive contribution to conservation efforts around the world as well as boosting local economies, although you do have to pump out greenhouse gases to get there.

To travel or not to travel, that is the question

What options does the environmentally concerned tourist have? Is the only responsible action to restrict holidays to places that can be reached by foot, bike, or train? This is certainly not impossible, but it seems unlikely that enough people would be willing to do it to deliver much of an impact. And even if they did, they would deprive many developing countries of the economic and environmental benefits of tourism.

As the UN Environment Programme points out, tourism is one of the main ways to pay for nature conservation and protection. For example, the Orangutan Foundation project in Indonesia’s Tanjung Puting National Park receives US$45,000 (A$51,000) every year from wildlife travel agency Steppes Discovery, a member of the Tour Operators Initiative for Sustainable Tourism Development. This money pays for rangers, the care of orphaned orangutans, and helps fund the park.

So is it possible to enjoy an overseas holiday without contributing to catastrophic climate change? Will our enjoyment of a remote tropical beach literally submerge it under rising sea levels? Is there a balance between the environmental costs of tourism and its benefits? Sustainable tourism arguably means working out what this balance is, and then ensuring we stay on the right side of it.

Carbon offsets: atoning for sins of emission?

Reducing emissions growth projected in a “business as usual” scenario requires changes both in consumer behaviour and in the way the tourism industry is structured.

Carbon-offset schemes are not universally supported, and can be confusingly complex. It is important to understand that there are uncertainties involved in such offset schemes. Because they aim merely to offset emissions rather than reduce them, some people reject these schemes altogether as an option. Some even portray the notion of offsetting as a modern-day indulgence for climate sins.

Some of the criticisms are valid. But purists miss an important point: many activities that are vital to global development goals are unlikely ever to be emissions-free. Tourism is one such activity.

Carbon-offset schemes and the standards by which they are accredited certainly need monitoring and regulation. Ultimately this will need to be done within the framework of a global climate treaty. They are, however, a positive example of business opportunities generated by the demand for low-carbon tourism options.

For the individual tourist, offsetting is increasingly easy and cheap. According to the Qantas calculator, offsetting a round-trip from Melbourne to Los Angeles only costs about A$25 at present. Flights within Australia can be offset for as little as the price of a cup of coffee.

Other tourism activities can be offset too – rental car firm Europcar, for instance, offers offsets purchased though carbon forestry company Greenfleet.

Other companies offering offsets in Australia include Climate Friendly, Carbon Planet, and Carbon Neutral. These firms engage in many types of offset projects including forestry, wind power, and others. Our Planet Travel recommends that consumers look into the types of projects an offset scheme uses, to ensure it is one they support.

Forestry projects, in particular have attracted a lot of attention. It is generally accepted that forest growth can store carbon dioxide, and an analysis of forest carbon sink projects found that this approach can be useful in meeting emissions-reduction targets. However, these projects come with inherent uncertainties: if a forest burns, for example, the stored carbon is re-emitted.

Of course, climate change itself may exacerbate the risk of such fires. On the other hand, timber harvested from forestry projects is safe from bushfires and could still be counted towards the offset total, because it still contains much of the carbon from the tree. All of these different factors will need to be studied carefully, preferably at an international level as part of an agreed climate treaty.

A guilt-free pleasure?

Given that offsets seem to be a way of having one’s cake and eating it too, these schemes should appeal to tourists. By offsetting, they can enjoy their holiday and contribute to global development while at the same time atoning for their sins of emission. Unfortunately, according to Qantas, only 5% of air travellers currently choose to offset.

Sadly, this is an area where consumer choice may not be best and responsible governments as well as corporations need to take the lead. Ecotours, for example, often bundle carbon offsets into their price. It can only be hoped that airlines will follow suit.

Ultimately, however, what’s required is a clear global framework for reducing emissions, in which offsets can play a part. We need, in other words, an international climate agreement. The devil, as always, will be in the details.

The Conversation

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