The Domesticated Brain: A Pelican Introduction (Pelican Books)

There was a time when it was acceptable to stare at individuals who, through the misfortune of the lottery of life, had been dealt a bum hand of cards when it came to their genes. Regarded as ‘freaks of Nature’, they came in all sorts of shapes and sizes – the victims of genetic abnormalities. These included dwarves and giants, people without limbs, bearded women, albinos and, most famously of all, the severely deformed Joseph Merrick, also known as The Elephant Man because of the massive tumours that disfigured his face and body.¹ Although Merrick went on to lead a celebrity life, most of these people ended up in travelling circuses or freak shows where the public would pay to simply gawk at them.

In an attempt to understand such unfortunates, a widely held view at the time was that the birth defect was caused by some frightful event that traumatized the mother when she was pregnant. This idea, known as maternal impression, is thousands of years old and reflected a common belief that there was a correspondence between the nature of the birth defect and the supposed shock. A mother being accidentally burned during pregnancy may cause a patch of discoloured skin on the baby. Cleft palates or harelips occurred because a leaping hare had surprised the mother. Or, more commonly, the pregnant woman was so frightened by the sight of some deformity on another person that her unborn baby would be afflicted by the same defect. In the case of Joseph Merrick, it was claimed that a rogue fairground elephant startled his pregnant mother.² These ludicrous ideas are consistent with magical thinking – the idea that there is a causal link between two events that are similar in appearance rather than an unrelated coincidence.

Although magical thinking has been largely abandoned in the West since the nineteenth century, maternal impression is still widely believed in many parts of the world today.³ Some countries have rituals, talismans and customs to ward off harm to protect the unborn child. In India, pregnant women avoid certain individuals such as barren women who may affect their foetus by casting the ‘evil eye’.⁴ While it may seem absurd that frightening a pregnant woman would have a permanent effect on her offspring, recent findings suggest that we may have been a little too hasty to dismiss maternal impression, or at least the susceptibility of unborn children to traumatic external events.

In this chapter we examine the possibility that early domestic environments not only shape what we learn, but also how we respond emotionally in terms of temperament. Temperament refers to the individual differences people have in their emotional responses. Some of us are more anxious whereas others are more outgoing. Some are more aggressive and others are more fearful. From the very beginning, babies differ in temperamental styles in that some cry more easily or startle suddenly whereas others are more laid-back and placid. Individually, we tend to be more like our parents when it comes to our emotional dispositions, which indicates this dimension of personality has a genetic contribution. However, early environments can also shape the development of temperament in ways that shape who we become as adults, and how well we adapt to domestication.

The day the world stood still

I can still vividly recall it as if it were yesterday. Those of a certain age will remember exactly where they were on that fateful day in 2001. It was a September afternoon in the UK but a bright, sunny morning in New York with crisp blue skies. Colleagues knew that I had a television in my office and had come in to watch the terrifying news unfolding. Two planes had been flown into the World Trade Center and now there was dense smoke billowing out of both. People were jumping to their deaths. If you saw the footage, then you, like me, will probably still have those events emblazoned on your memory as the world changed for ever.

For some, these recollections have become flashbulb memories, as if the scene were lit up in harsh lighting to capture everything – even trivial details of little relevance. Our memories can be supercharged with detail when we experience something terrifying. This is because we become more alert and attentive, on the lookout for danger as our hippocampus, the seahorse-shaped repository for long-term memories in each of the temporal lobes, receives input from the amygdala – a structure the size of an almond, also in each temporal lobe, that is active when you laugh, cry and scream in terror.⁵ They also don’t let you forget.

Experiences that eventually become memories start out as patterns of neural firing or traces that come flooding into the brain. Raw sensory input is interpreted into representations and given meaning. This in turn updates and changes the knowledge we have about the world by forming memories. Whether details become consolidated into the memory stores of the hippocampus depends on filtering mechanisms that are regulated by the action of neurotransmitters released by the amygdala during surprising, arousing or rewarding events. The neurotransmitters are the molecules that trigger activity in the connecting gaps between neurons. Flashbulb memories stimulate the amygdala to invigorate the activity of the hippocampus, thereby enhancing the memory trace for those events that move us the most.⁶ As the world watched in helpless shock, a generation would never forget what they saw. But even some from the next generation of unborn babies were left with the legacy of that terrible day.

Post-traumatic stress disorder (PTSD) is an anxiety condition that appears weeks after traumatic events such as rape, battle and other acts of violence. It is characterized by recurrent dreams, flashbacks and flashbulb memories, as if the victim is haunted by the past. After witnessing 9/11, one in five New York residents who lived closest to the World Trade Center suffered from PTSD. Rachel Yehuda, a New York psychiatrist, followed up a sample of pregnant women from this group. She found that these women had abnormal levels of cortisol in their saliva – a hormone that is released as a natural response to stress but depleted in individuals with PTSD.⁷ Different hormones and neurotransmitters form part of an elaborate signalling system that the brain uses to activate different functions. Some have general effects whereas others seem to be more specific in the roles they play.

The depleted levels of cortisol in the chronically stressed mothers were to be expected. But what was unexpected was the plight of their unborn children. One year after the attack, infants born to the mothers who had developed PTSD also had abnormal levels of cortisol compared to babies of other mothers who did not develop the disorder after witnessing 9/11. Vulnerable mothers had passed something on to their children. As Yehuda put it, children of PTSD victims bore ‘the scar without the wound’.⁸

It is well known from various disease models that events early in development can have consequences later in life. There is a whole category of substances known as teratogens (literally, ‘monster makers’) that, if the pregnant mother is exposed to them, can result in birth defects. Various drugs, both legal and illegal, as well as environmental toxins such as radiation or mercury can damage the unborn child. However, some diseases resulting from harmful substances take decades to manifest. My own father-in-law died from mesothelioma, a rare form of lung cancer that was probably caused by exposure to asbestos when he was growing up as a child in South Africa. Toxins that enter our bodies can alter the functions of our cells but lie dormant for years. Over a lifespan we may replenish our cells many times, but each reproduction of the cells can carry genetic time bombs that lie in wait for the right circumstances to kill us. Physical substances like asbestos from the environment are obvious candidates as being poisonous to our systems, but what about exposure to psychological toxins? How can our mind’s reaction to non-physical events, such as watching something horrific, produce long-term consequences? How could a mother’s stress in response to 9/11 cross over to the next generation? What could she possibly pass on to her unborn child?

Jerry Kagan, a Harvard developmental psychologist, reckons that around one in eight babies are born with temperaments that make them highly irritable, which is due to their over-reactive limbic systems. They startle easily and respond excessively to sudden noises.⁹ The limbic system mobilizes the body for action and its circuitry includes the amygdala. It triggers a cascade of hormones and neurotransmitters that prepare the body to respond to threat. Reactivity of the limbic system is a heritable trait meaning that it can be passed on to the child in the genes they inherit.¹⁰ These are the highly-strung children who find uncertainty and strange situations upsetting. Depending on how they react to sudden sounds as a four-month-old baby, you can even predict personality many years later.¹¹ Reactivity is like a disposition, which makes some of us twitchy, but others are born more laid-back and chilled. Maybe mothers who developed PTSD after 9/11 gave birth to babies with a nervous nature because of their genes.

Yehuda thinks not. She found that the lowered cortisol effect was only present for those mothers who were in the third trimester of their pregnancy, so it could not just be the genes working alone. There seems to be a critical period when exposure to stress alters the child’s development. To begin to understand how such a maternal impression restricted to a window of vulnerability could possibly happen, we need to look at the history of difficult childhoods and the way that they affect how we respond to stress as adults.

War child

World War II disrupted normal life for thousands of families. In Europe, many children were separated from parents by the turmoil and ended up in institutions. Even though they were generally cared for, many of them grew up into socially impaired and delinquent teenagers. To explain this, John Bowlby, a British psychiatrist, proposed that these children had missed out on a critical phase in development that he called attachment.¹² Bowlby believed that attachment was an evolutionary adaptive strategy to form a secure, nurturing bond between the mother and her infant. This early experience not only protects the vulnerable child, but also provides the necessary foundation for coping mechanisms to deal with problems later in life. Without this early secure attachment, the child would grow up psychologically impaired.

Bowlby was inspired by the ornithological work of Konrad Lorenz, who had shown that many bird species form a close-knit bond between mother and chicks.¹³ This attachment begins with imprinting, where the young chicks will pay special attention to and follow the first moving thing they see. Famously, Lorenz demonstrated that he could make baby goslings imprint on him by incubating the eggs and hand-rearing the chicks when they hatched. In the wild, imprinting was critical for survival by maintaining the proximity of the chicks to the hen, which is why the chicks would imprint to the first moving thing, usually the mother. Investigation of the chick brain revealed that it is innately wired to follow some shapes more than others and that chicks quickly learn the distinct features of their own mother, to tell her apart from others.

Human infants also pay special attention to face patterns at birth and very quickly learn their mother’s face.¹⁴ However, primate, and in particular human, early social attachment is unlikely to be as rigid as bird imprinting. Whereas the need to imprint in birds has to be satisfied fairly quickly, primates can take a bit longer to learn to know each other. Another important difference between birds and babies is that humans are not up and running about for at least a year. Whenever the human infant needs their mother, they simply have to cry, which will soon send most mothers scurrying to their infant’s side. A distressed infant’s cry is one of the most painful things to hear (which explains why crying babies on aeroplanes can be so upsetting for everyone around them). This ‘biological siren’ ensures that babies and mothers are never that far apart.¹⁵ Infants from around six months of age show separation anxiety when physically separated from their mother, a state characterized by tears and stress as signalled by the rise in cortisol levels in both the infant and mother. These levels eventually return to normal when baby and mother are reunited.¹⁶

With time, both mother and baby learn to tolerate further episodes of separation, but the mother remains a secure base from which the toddler can explore their surroundings safely. Imagine Bowlby’s securely attached toddlers as baseball or cricket players: they feel secure when they are touching the bases or while behind their creases, but become increasingly anxious and insecure as they step farther and farther away from them. Without secure early attachment, Bowlby argued that children would never learn to explore novel situations and develop appropriate coping strategies. They would also fail to become properly domesticated, which was why he believed that children separated from their nurturing parents during the war grew up to become delinquent teenagers.

The lost children

Inspired by Bowlby’s work on social attachment and later psychological abnormality, Harry Harlow in the US set out to test an alternative explanation for the long-term effects of deprived childhoods.¹⁷ Maybe children were simply not looked after or given adequate nutrition if they were raised in institutions. If you gave them food and warmth, they should be fine. To test this, he conducted an infamous series of studies where he raised baby rhesus monkeys in isolation for differing amounts of time. Although these infant monkeys were well fed and kept in warm, safe environments, they were left alone. This social isolation had profound effects on their development. Monkeys with no social contact as infants developed a variety of abnormal behaviours as adults. They compulsively rocked back and forth while biting themselves, and when they were finally introduced to other monkeys, they avoided them entirely. When the females from this group reached maturity, they were artificially inseminated to become mothers, but they ignored, rejected and sometimes even killed their own offspring.

Harlow discovered that it was not just the amount of time that animals spent in isolation that was critical, but also when they were separated. Those born into isolation were at risk if they spent longer than the first six months without the company of their mother. In comparison, monkeys who were isolated only after the first six months of normal maternal rearing did not develop abnormal behaviour, indicating that the first six months was a particularly sensitive period. Bowlby had originally thought that the primary reason for attachment was to ensure that biological needs for food, safety and warmth were satisfied, but Harlow proved that he was only partly correct – monkeys also needed social interaction from the very beginning.

It turns out that human social development, like that of the monkey, is also shaped by a similar sensitive period of socialization. Back in 1990, following the collapse of Nicolae Ceauşescu’s dictatorship, the world discovered thousands of Romanian children abandoned in orphanages. Ceauşescu had outlawed family planning in an attempt to force women to have more children to increase Romania’s dwindling population. The trouble was that families were unable to support these children and so they were abandoned in the orphanages.

On average, there was only one caregiver for every thirty babies, so there was little social interaction and none of the cuddling or intimacy that you would find in a normal, caring environment. The babies were left to lie in their own faeces, fed from bottles strapped to their cots and hosed down with cold water when the smell became unbearable. When these children were rescued, many of them were fostered out to good homes in the West. Sir Michael Rutter, a British psychiatrist, studied just over one hundred of these orphans who were less than two years of age to see how their early experiences would shape their development.¹⁸

On arrival, the orphans were all malnourished and scored low on psychological tests of mental well-being and social interaction. That was to be expected. As time passed, they recovered much of this lost ground in comparison to other adopted children of the same age who had not been raised in the Romanian orphanages. By four years of age, most of this impairment had gone. Their IQs were still below average in comparison to other four-year-olds, but within the normal range that could be expected. However, it soon became apparent that not all was back on track.

Children who had spent longer than six months in the orphanages were failing to catch up with their matched group. Only the children who were rescued before they were six months old went on to a full recovery. The children were followed up again at six, eleven and fifteen years of age. Again as a group they fared much better than expected, given such a horrific start in life, but problems started to appear. Those who had spent the longest time in the orphanage were beginning to show disturbed hyperactive behaviour and difficulties in forming relationships. Just like Harlow’s monkeys, social interaction during that first year was crucial for normal development. To understand what is so important about having someone around to look after you and not just to give you food and warmth, we have to consider what upsets babies.

Why not knowing is stressful

Have you ever waited for someone to call you with important news? Maybe it was an exam result, the outcome of a job interview or, worse, a call from the hospital. The reason that waiting for important news produces anxiety is that brains are pattern detectors that have evolved to seek out regularities in life; not being able to predict what will happen next is therefore upsetting. We can brace ourselves for important events, but it is stressful to maintain that level of preparedness for a long time. The stress comes from high levels of arousal – a state of readiness and expectation. Just like the US Army, when we face a threat, we enter a defence-readiness condition (DEFCON). When that threat is at a peak, it’s like being at DEFCON 1. This is why we jump at the slightest sound, because we are in a state of heightened alertness. It is not until we can stand down our defences that we can relax.

Even though we may not be actively dealing with a threat, nevertheless the uncertainty of threat still makes the situation stressful. In fact, our brains are not very good at dealing with random events, which is why we tend to see structure and order everywhere. That is why when you are in the woods late at night or an old spooky house, every noise sounds like a threat. Adults start to see patterns in random noise when you remove their ability to control outcomes or remind them of times when they were helpless.¹⁹

This lack of control is not only psychologically distressing, but it also affects how our bodies respond. Even our tolerance to pain is reduced. Adults can withstand much more painful electric shocks if they think they can stop the punishment at any point in comparison to those who do not think they have this option.²⁰ Believing you can stop the pain whenever you want means that you can tolerate more. However, when faced with unpredictable and uncontrollable shock, both animals and humans develop both psychological and physiological illness.

This need for control and predictability is present from the very start. Babies prefer regularity and predictability, which is why they startle to sudden unpredictable noises, lights or movement. In fact, there is a reflex controlled by the brain stem – the most primitive part of the brain that controls vital functions – known as the startle reflex, that jolts the child to attention. If a newborn does not startle, there is a chance that they have some form of damage to their nervous system. This need for predictability forms the basis for contingent behaviour where the baby starts to learn how they are synchronized with others. Such a sensitivity to external events means that a nurturing domestic environment is one that is going to be predictable and less threatening – attributes that can be controlled by caregivers.

Infants thrive on predictable contingent behaviour, but the flipside is that they find unpredictable or non-contingent events upsetting, especially when they involve their mother. When mothers are depressed, they often have flattened emotions and so the quality of their interaction with their infants is impoverished.²¹ Other depressed mothers, rather than being sad and dull, over-compensate in an animated, exaggerated form of communication, which can be equally distressing to the infant because it is not contingent with their own efforts at communication. Early experiences like this, where the baby’s needs for contingent responses are not met, can lead to social and cognitive difficulties many years later.

Other people provide reassurance in an uncertain world. The stress of uncertainty is reduced if there is an adult around, so our brain benefits not only from the wisdom of others but their presence as well. As the saying goes, a problem shared is a problem halved because there is strength in numbers. If you think about it, the world is full of surprises for the young infant and development must include discovering what is going to happen next. With knowledge and experience, the world becomes more predictable. That understanding takes time to acquire, but until then, adults provide protection and reassurance, which is why babies cry if there is uncertainty because it is how they signal to the adult to resolve the situation.

Taken together, these studies indicate that extreme early environments can have long-term effects on developing monkeys and humans. It would seem that primates need some form of contact from the very start, especially in environments that are particularly threatening or socially vacant. However, it is not just the deprivation of not having others around, but not having others around who are reliable. How do such stressful environments shape who we become and what role do others play in our reaction to stress?

Learning to fight or flee

To understand how aversive unpredictable environments affect growing brains, we need to understand the normal response mechanisms to stress. When faced with a threat, we can either stand up to it or run away. There is a rapid fight-or-flight response where we get that sudden emotional rush that requires us to mobilize as quickly as possible that is triggered by activity in the limbic system of the brain. This preparedness is achieved by a system called the hypothalamic-pituitary-adrenal (HPA) axis.

Following exposure to stress, the hypothalamus releases two hormones, corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP), that stimulate the nearby pituitary gland to release adrenocorticotrophic hormone (ACTH) into the blood stream. ACTH targets the adrenal glands that sit atop the kidneys way down in the guts to release adrenaline, noradrenaline and cortisol. The balance of adrenaline and noradrenaline regulates the autonomic nervous system (ANS), which in turn increases breathing, heart rate, sweating and pupil dilation, and shuts down digestion. After all, you don’t have time to chew the cud when you are about to do battle. If you have ever felt butterflies in your stomach before going on stage, that was your ANS operating. Cortisol works by increasing the concentration of glucose in the bloodstream, thereby making more fuel available for muscles. All of this activity is fine when there is a real threat that needs to be dealt with immediately. However, the fight-or-flight response has to be wielded appropriately and used in moderation.

Figure 6: The hypothalamic-pituitary-adrenal (HPA) axis

Maintaining high levels of stress over long periods leads to chronic impairment in our ability to cope with life’s ups and downs. It is like keeping your foot on the accelerator pedal, revving the engine, and it will eventually cause damage to the HPA axis mechanisms and subsequent illness and impairment of your immune system. Chronic stress has also been linked to psychiatric disorders such as depression, with most individuals suffering from major depression having increased HPA activity.²² So, to keep body and mind in a healthy state, you need to be able to regulate your stress response. Part of this regulation is provided by the hippocampus. Within the hippocampus, there are glucocorticoid receptors (GR) that monitor levels of glucose and cortisol in the bloodstream. When levels of circulating glucose and cortisol reach a critical level, the hippocampus signals the hypothalamus to shut down the HPA process in the same way that a thermostat on a heater regulates temperature. If a thermostat is faulty, the house freezes or overheats. Likewise, if the HPA is disrupted, either you do not respond adequately to stress or you overreact.

Children raised in abusive households suffer not only from episodes of violence and harm but also from the unpredictability of when the next abuse will happen. Unpredictability is corrosive to coping, as we are not able to relax but must maintain our stress response in a state of high alert. This will produce long-term disruption of the HPA system, which can have consequences many years later. This may be one reason why PTSD sufferers have abnormal patterns of circulating cortisol, because their HPA remains on high alert and is unable to relax.²³ In a study reminiscent of Bowlby’s original work, Finnish scientists followed up 282 children evacuated during World War II to test the effects of separation from parents on their stress responses decades later. Those separated from their parents during the war as young children had higher cortisol reactivity to stress tests sixty years after the early separation, indicating that the physiology of their HPA system had been altered permanently by this experience.²⁴ The older the child was at the time of the evacuation, the more resilient they were and the less disruption to their HPA system as adults.

Even before you are born, stress can alter the functioning of the HPA axis. Female rhesus monkeys in the later stages of pregnancy were taken from their cages and exposed to unpredictable, loud, stress-inducing noise. After giving birth, not only did these young mothers have disrupted HPA responses, but so did their offspring, in comparison to other mothers who had not been stressed during pregnancy or their infants.²⁵ In the same way, experiencing a terrifying, unpredictable event like the attack on the World Trade Center in which no one knew what was going on, some pregnant mothers may have inadvertently passed on a legacy of fear to their unborn children.

Once born, the long-lasting effects of early exposure to stressful households have been shown to alter the way babies respond to aggression even when they are not awake.²⁶ Infants between six and twelve months of age had their brains scanned when they were asleep inside an fMRI scanner. They were played nonsense sentences spoken in very angry, mildly angry, happy and neutral tones of voice by a male adult. Even though they were unconscious, those babies from households where there were high levels of conflict showed greater reactivity to the very angry voice in the ACC, caudate, thalamus and hypothalamus – all brain regions of the HPA system. Already their stress response had become sensitized to the presence of aggression.

The HPA system is also altered in animals that become domesticated. As we saw earlier, domestication produces changes in behaviour and the brain. Domesticated animals are less fearful, less aggressive and have elevated levels of serotonin²⁷ – a neurotransmitter associated with prosocial activity.²⁸ Normally wild fox pups become fearful of humans at around forty-five days and are less likely to explore their environments as their natural fight-or-flight response kicks in. In contrast, this fearful response is not observed in domesticated pups of the same age and they continue to explore their environments. For domesticated foxes, the period of socialization is significantly longer and play activity extends into adulthood.²⁹

Don’t feel nervous, feel excited!

The relationship between body and mind is critical to understanding emotion. One of the first accounts of this relationship was William James’s proposal that emotions were produced by the body’s response to a stressful encounter.³⁰ When we see a bear, our fight-or-flight response immediately kicks in to deal with the threat and only afterwards do we feel the emotion of fear. That’s the way it should be, as a good evolutionary strategy, because it is better to act first and ask questions later when you are in potential danger. James argued that we needed to react before we had time to ponder the situation. You don’t want to be sitting around considering how you feel about the bear.

Most of us rarely encounter bears in the modern world, but we have all had that act-now, think-later experience. Maybe it was a sudden fright when someone jumped out at you or possibly an unexpected threat. Our heart rate and breathing surges as adrenaline pumps around our body in preparation. Road rage is a classic aggression scenario triggered by a perceived threat before we have had time to evaluate the actual threat.

James’s account of emotions following responses failed to take into consideration situations where the body responds more slowly to stressful situations than our thought processes.³¹ Also, people are not always sensitive to the changes in their body in stressful situations. Sometimes emotions can precede bodily changes, which is why we can feel embarrassment before we blush. Maybe you burped in public accidentally, looked around at others and then felt your cheeks burning bright red with heat as the emotional significance of your faux pas sunk in. The thought was almost immediate but the change in blood flow took longer. So which is it? Does fleeing cause fear or do we run away because we are frightened?

The answer is both. In some situations, the need to respond as fast as possible trumps the need to think (the sudden bear attack), whereas in others we need to consider the situation and respond accordingly (blushing in public). However, in both situations, experience and expectations play a role. If we know that the bear is actually stuffed, then we are less likely to be frightened. If we are among family when we burp, we do not feel so socially awkward.

As these different examples reveal, there are fast and slow pathways to emotion that depend on the circumstances and how we interpret the situation.³² Our emotions are also largely influenced by others. In a classic study of the importance of social context,³³ naïve subjects were given an injection of adrenaline and told they were receiving vitamins that would boost performance on a visual test. This was all a sham to get at the real purpose of the study – how do those around us influence emotional experiences? Some of the participants were correctly informed that the injection would make their hands tremble, give them a flushed face and increase their heart rate. Others were told incorrect symptoms of a mild headache and itching skin.

While the participants sat around in the waiting room, they were asked to fill out mood questionnaires. Seated among them was an experimenter who acted in one of two ways. This confederate had not been injected with adrenaline but behaved either negatively, complaining about the study, or positively, by saying how much they were enjoying the experience and acting up playfully.

Meanwhile, in the real participants, the adrenaline triggered their HPA axis and produced the bodily symptoms associated with the fight-or-flight response. Suddenly they had these sensations, but what did they make of them? Those who had been warned correctly about the effects of adrenaline interpreted their sensations correctly (‘I’m feeling a little revved up because of the shot’). But those who did not expect the increased heart rate and tremors were in a state of ignorance and needed to make sense of the signals their bodies were sending them. This is where others play a critical role. The emotions experienced by the naïve participants depended on the influence of the stooge in the room. Those seated with the playful experimenter rated their mood much more positive compared to those seated with the irritated experimenter. They were using the social context of others to interpret their own bodily sensations. Whether we are enjoying a rock concert, a football game or a day at the funfair, our emotional experience depends heavily on how others respond.

The importance of interpretation explains why some of us feel anxious and some of us feel excited. We learn to interpret situations based on experiences that we accumulate over our lifetime. This is why children raised in an environment where there is excessive conflict come to expect this as normal. If there is one thing that is predictable in conflict households, it is anger. When there is anger, violence soon follows, which is why abused children tend to see anger earlier in faces and interpret faces as being angrier whereas they show no higher sensitivity for other emotional expressions. Having a bias for interpreting anger means that children can be prepared for fight-or-flight.

Knowing this enables us to change the way troubled teenagers behave. Colleagues in my department at Bristol produced a series of computer-generated faces made up from morphed real faces that varied on a continuum from happy through neutral to anger.³⁴ The teenagers, most already with criminal convictions and attending a programme for high-risk repeat offenders, saw the ambiguous faces as more aggressive. However, in a clever twist, half of the teenagers were given false feedback on a task where they had to judge the expression, which eventually shifted their bias away from angry faces. In other words, after training, they were much more likely to see ambiguous faces as happy and happy faces as even happier.

The psychologists were able to shift the teenagers’ perception to a more positive interpretation. More remarkably, the effect was long lasting and altered their behaviour in general. The teenagers kept diaries and were evaluated by staff who were unaware of which condition each teenager had been in. After only two weeks, those teenagers who had their anger bias shifted were happier, less aggressive and involved in less conflict incidents as rated by the staff.

Domestic violence

We all need someone from the very start. This imperative to have someone in your life explains the paradox of children’s attachment to abusive parents and why domestic violence can persist. According to the UK’s National Society for the Prevention of Cruelty to Children statistics published in 2012, one in four young adults were severely maltreated as children. You would think that we have evolved brains that learn to avoid danger, yet when social workers, doctors, or police officers attempt to rescue these victims from an abusive situation, the child will often lie to protect the parents. Harry Harlow also demonstrated similar phenomena in his rearing studies, when frightened infant rhesus monkeys would cling to a surrogate mother made of wire, cloth and a plastic head. Even when they were punished for this attachment with an aversive puff of air, they would still hang on for dear life. How can we understand such strange love?

Regina Sullivan, a neuroscientist who studies the neurobiological basis of attachment, believes an answer might be found by looking at rat pups.³⁵ Rats are smart and can quickly learn what is painful. They can learn to associate an odour with a painful shock. Surprisingly, the brain area responsible for fear and avoidance learning is turned off by the presence of the mother. Even though rat pups can associate a smell with a painful shock, they do not avoid the odour when the mother is present and will in fact approach the smell associated with punishment. Somehow the presence of the mother switches avoidance into approach behaviour in painful situations. The explanation for this masochistic behaviour is that learning about painful situations requires the activity of the rat’s equivalent of the stress hormone, corticosterone, but the presence of the mother turns this off in the young pups in the nest.

Outside the nest, when they are older, exploratory rats will avoid potential dangers but they do this by returning to the nest for comfort and safety.³⁶ This response is social buffering and we see it in humans faced with stressful situations where the presence of a loved one makes the experience more bearable. Even having the photograph of a loved one is sufficient to alleviate pain.³⁷ The problem arises when that loved one is also the source of pain and danger. When rats return to their nest, their corticosterone mechanisms are switched off and they forget what a monster their mother can be. So unpredictable environments are stressful but less stressful than consistently abusive situations. For some, uncertainty of the future is worse than the predictability of the current situation, albeit abusive, which is the origin of the saying ‘Better the devil you know’.

Clearly early domestic violence can leave a lasting impression, but not everyone responds to adversity in the same way and not everyone develops stress-related illness. Not everyone stays in an abusive situation. Given our understanding of stress as a biological phenomenon, how is it that individuals can respond to it so differently?

Two peas in a pod

I have a collection of rare postcards from the sideshow era that I described in the opening to this chapter. They fascinate me since they are a reminder of how social history and attitudes can change so dramatically. One of the cards is a rare photograph of Daisy and Violet Hilton as babies. Daisy and Violet were Siamese twins – two identical sisters conjoined at the hips. They were born in 1908 in Brighton and immediately rejected by their unmarried mother, who thought they were a curse from God for being born out of wedlock. Daisy and Violet were adopted by their midwife and raised to be talented musicians who went on to achieve fame and even appeared in the movies, most notably Tod Browning’s infamous production of Freaks in 1932.

Identical twins occur when a fertilized egg splits in two soon after conception. In the rare cases of conjoined twins, that separation is incomplete. Identical twins share all their genes whereas non-identical twins, who come from two separate fertilized eggs, share only half of their genes. Like Tweedledum and Tweedledee from Alice in Wonderland, identical twins look the same, behave the same and often think the same thoughts. There is even a popular myth that twins are telepathically connected and read each other’s minds.

Studying twins is important for working out the roles of genes and environment in shaping the course of development. Like Daisy and Violet, twins are sometimes adopted, but unlike conjoined twins, they can be fostered out to different households. By comparing twins, identical and non-identical, raised in the same or different households, you can estimate how similar they are and then work out the relative contribution of genes and the relative contribution of the environment.

These adoption studies show that identical twins raised separately are more similar than non-identical twins raised by different families. This proves that aspects of personality and intelligence must be heritable. But identical twins are not identical. Even as conjoined twins, Daisy and Violet had marked differences in personality and allegedly even different sexual orientations, but they were hardly the same person.³⁸ When it comes to personality and intelligence, heritability only accounts for, at best, half of the overall similarity. This is an important point that Judith Rich Harris draws our attention to in her book No Two Alike³⁹. We are so used to thinking of identical twins as being identical, we fail to realize how different they actually can be. If you think about it, Daisy and Violet Hilton not only shared the same genes but they literally shared the same environment. How could they be so different?

Most people believe that one of the main reasons that individuals can be so different is because they were raised in different homes. The history of parenting is full of advice about how best to raise children and the bookstores have whole sections dedicated to parenting manuals. This comes from an understandable concern to look after our offspring and give them the best start in life as well as deep-seated beliefs about the forces that shape individual development. We have all grown up in a variety of households with different experiences that have shaped us, which is why there is a common assumption that we are what we are because of the way we were raised. When we blame delinquent children, we typically look to the parents. However, Harris spent many years surveying the fields of developmental psychology and concluded that when it comes to psychological outcomes such as intelligence and personality, neither genes nor the household environment can predict how we will turn out.

Ironically, that is a message that most parents probably do not want to hear, but they should be the first to agree with Harris. Any parent should be able to confirm that no matter how much they try to treat their various children equally, they end up very different. In fact, when the proper measurements are done, two siblings raised in the same household are not much more similar than two randomly selected individuals of roughly the same age plucked from the same population. Despite what most parents want to believe and parenting manuals promote, the home environment plays a relatively minor role in shaping the development of children.

If it isn’t the home environment and it cannot all be the genes, then what explains individuality? Harris argues that the major determinant of a child’s intellect and personality is the influence of their peer group – other children. While the child may behave according to their parents’ expectations in the home, they put on a different face in the playground and shopping mall. Children act and respond to others differently in different situations. This is why children of immigrants do not learn their parents’ accents when learning English, but adopt the local dialects and accents of the neighbourhood kids.

Harris’s thesis is highly controversial as it goes against the modern trend for parenting expertise. It is also leaves out the extreme environments of Romanian orphanages and depressed mothers who have been shown to affect long-term development. Moreover, parents indirectly influence which peer groups children are exposed to because they choose the neighbourhoods and schools that their children end up in. That said, the goalposts are likely to shift again when one considers the pervasive role that social networking sites such as Facebook and Twitter now play in teenagers’ lives. However, even if today’s extensive networks outside the home play a greater role in shaping children, this cannot explain why Daisy and Violet, who shared the same genes, the same environment and the same peers, were still different. Perhaps it’s because people treat identical twins, even those conjoined at the waist, differently so as to distinguish them. That seems plausible, but a more likely explanation is in itself unlikely – and that is the role of random events in development: an area of research known as epigenetics.

Epigenetics

What do the sex of a clownfish and the spread of the common cold have in common? A strange question maybe, but both are examples of epigenetic phenomena that are triggered by social behaviour. They both depend on the interaction of biology and the influence of others. Epigenetics is the study of the mechanisms of interaction between the environment and genes – the way that nature and nurture work together.

Epigenetics provides answers to the sorts of common questions we all ask ourselves. Are we born mad, bad or sad, or is our personality determined by events in our lives? Why are our children so different when we try to treat them equally? These questions are at the heart of how best to create the societies we wish to live in; often shaped and controlled by government policies and laws. The answers people prefer to give to these questions come from deep personal opinions and reflect their political persuasion about the role of the individual in society. However, epigenetics offers a new perspective to understand human development that combines our biology with our experiences.

As we noted earlier, genes are the strings of DNA molecules, found in every living cell, that instruct the cell what to become. They do this by building proteins from amino acids, which in turn are made from combinations of atoms of carbon, hydrogen, oxygen and nitrogen. Every cell in the body has thousands of proteins and DNA determines what type a cell is and how it operates by regulating the production of proteins. Genes are like books in a library that contain information that needs to be read or transcribed in order to build the proteins. The proteins instruct the cell to become something, such as hair follicles, while others can turn them into neurons. This is a very simplistic account and there is considerably more to the story of the mechanism of genes, but for the level of discussion here, it is sufficient to know that genes are like sequences of computer code within the cell that control its operation.

Genes build humans and humans are very complex animals. Each body is made up of trillions of cells and the initial speculation was that humans must have a considerable number of genes to code for all the different arrangements of cells in our bodies. In 1990, scientists working on the human genome project began to map the entire sequence of genes for our species, using sophisticated technology that enabled computers to read off the sequences as strings of code. Very soon, it appeared that initial estimates of over 100,000 genes had been way off. Although the project is still continuing, at the last count it would appear that humans have only 20,500 different genes. That may still sound like quite a few but when you consider that the humble fruit fly, drosophila, has 15,000 genes, humans look decidedly puny in the genetic endowment department. In fact, much simpler living things like the banana or the rather revolting roundworm have more genes than humans and, as if that were not enough, the organisms that have the highest and lowest numbers of genes are both sexually transmitted diseases, trichomonas vaginalis with 60,000 and mycoplasma genitalium with 517.

So the number of genes does not reflect the complexity of the animal. The reason we initially overestimated the number of genes for humans was because the role of epigenetics was not yet fully appreciated. Moreover, it turns out that there is more information encoded in the few genes we have than is ever actually used. Only 2 per cent of genes appear to be related to building proteins. This information is only activated when the gene becomes expressed and geneticists now understand that only a fraction of genes are expressed. In fact, gene expression is the exception and not the rule. The reason is that genes are sets of IF–THEN instructions that are activated by experiences. These experiences operate through a number of mechanisms, but genetic methylation is typically one that silences a gene and is believed to play a major role in long-term changes that shape our development. If you think about genes like books in a library and the library is the full genome, then each gene can be read to build proteins. Methylation acts a bit like moving a book out of reach so the information to build proteins cannot be read, or blocking access to it by placing some furniture in front of the book.

DNA may instruct cells how to form and organize themselves to build our bodies but these instructions unfold within environments that modulate their instructions. For example, the African butterfly bicyclus anyana comes in two different varieties, either colourful or drab, depending on whether the larvae hatch in the wet or the dry season. The genes do not know in advance, so are simply switched on by the environment.

Sometimes those switches are social in nature. For many fish, the social environment can play a fundamental role in shaping how genes operate, even to the extent of switching sex. Clownfish live in social groups that are headed up by the top female. What Pixar’s film Finding Nemo did not tell the audience is that clownfish have the potential for transsexuality. When the dominant female in a school of clownfish dies, the most dominant male changes into a female and takes over. Or consider the humble grasshopper. When the population of grasshoppers becomes overcrowded, they change colour, increase in size and become gregarious and socially sensitive to other locusts. This transformation from a solitary grasshopper within a swarm is triggered simply by the amount of physical contact they have with others.⁴⁰

Social environments can trigger a metamorphosis in a number of different species, but is there any evidence that social environments regulate human genes in a similar way? The example of the common cold helps to address the question. Social environments increase our susceptibility to the common cold but also influence how we fight it. Colds are more common in the winter months, not because of the lower temperatures (contrary to popular belief) but through the transmission of the virus between people. One reason why the virus may be more prevalent in the winter months is that we tend to congregate closer as the nights draw in, enabling the virus to transmit more readily from one to another. Viruses are small packets of DNA made up of about 10–100 genes that enter our cells and hijack the protein production to make copies of themselves. As this infection multiplies, the normal function of the cells and ultimately the whole of the body comes under attack. However, a virus’s ability to express and duplicate its own DNA is regulated by our own body’s reaction to social stress.

Social stress and isolation have long been known to affect viral infections, which is why we can all do with a little TLC along with our chicken soup when it comes to nursing a cold.⁴¹ All this sounds like common sense, but what this folk wisdom reflects is an increasing understanding of the role of social factors in illness. An analysis of the DNA in the white blood cells or leukocytes of lonely adults revealed different levels of gene expression in comparison to adults who were not lonely.⁴² Specifically, the genes responsible for producing antibodies to infection were downgraded, making their immune response less effective. This may explain why lonely adults are more vulnerable to diseases. What is remarkable is that the different gene expression is only found in those individuals who feel they are lonely and is not related to the actual number of social contacts they have. Even some of the most popular people can still be the loneliest in a crowd because it is how they feel that is more important, rather than the extent of their actual social circles.

If social factors can regulate the expression of viral genes, then our own complement of roughly 20,000 genes is likely to be regulated in biologically significant ways by social factors as well.⁴³ It is not only our biology but also our psychology that affects how we cope with illness.

Lamarck’s daft idea

What is the evidence for epigenetic processes in humans? After all, humans do not spontaneously change sex when a dominant female leaves the group, but critical events can trigger changes in how our genes operate and sometimes the resulting changes in behaviour can be passed on to subsequent offspring. This is an astonishing idea but is not new. In the early nineteenth century a minor French noble, Jean-Baptiste Lamarck, proposed that characteristics acquired during a lifetime could be passed on to the next generation.

In support of this idea, he showed that the sons of blacksmiths had larger arm muscles than the sons of weavers before they ever took part in the family business, which he interpreted as an inherited characteristic. As another example, he suggested that giraffes’ necks became long through their constant reaching up to high branches to eat leaves – a physical trait that they then passed on to their young.

Contrast this Lamarckian notion to Darwinian natural selection. In Darwin’s theory there are two mechanisms that lead to change. The first is spontaneous mutation that generates variations among members of the group. Today, we now understand that this variation arises from genetic processes. Second, the environment operates to select those variations that endow the individual with a competitive advantage to breed and pass on the variation. With successive generations, the variant becomes stable in the population. In the case of giraffes, those born with a mutation that resulted in them having longer necks were more successful in breeding. It was not the experience of trying to reach leaves that was passed on to the offspring, but rather the genes that increased the length of the neck.

Darwin originally suggested that long necks would provide an advantage for reaching more leaves, but it turns out that there are a number of competing explanations.⁴⁴ What is known is that the mechanism of inheritance is not Lamarckian. Rather, long necks originated as a genetic mutation that was passed on while giraffes with short necks did not get the same opportunity to reproduce for some reason. Lamarckian theory has been roundly denounced as daft in scientific circles but epigenetics is casting new light on his ideas. Maybe experiences during a lifetime can influence the biology of the next generation.

There are so many problems and errors with Lamarck’s evidence that it would be all too easy to consign the notion to the dung heap of bad ideas. Moreover, Darwin’s theory of evolution by natural selection is simply better at explaining and predicting the data. And yet aspects of Lamarck’s daft idea have been resurrected with the rise of epigenetics. Sometimes events during one’s lifetime can affect the next generation. Epigenetics explains how environmental signals change the activity of genes without altering the underlying sequence of the DNA. The process of natural selection will ultimately correct any epigenetic influences of the environment. Rather, the effects are more to do with the switches that are being flipped by epigenetic processes. So Lamarck may have gained a minor battle, but Darwin has won the war in explaining how we pass on characteristics from one generation to the next. Epigenetics may even explain why humans traumatized as infants grow up with an emotional legacy that can stay with them for the rest of their lives. Once again, studies of the rearing practices of generations of laboratory rats have shown how early experiences shape the bond between mother and daughters.

Licking rats

What could be worse than licking a rat? For many people, rats are disgusting abhorrent pests associated with poverty, disease and death. This is rather unfair, as the female rat is an intelligent and social animal with a strong maternal instinct. When she is rearing her pups in the nest, the female rat will invest time licking and grooming her brood like an attentive mother. Some mother rats are much more conscientious, with very high rates of licking, whereas others are less so – a trait these mothers share with all their sisters.⁴⁵

What is remarkable is that if you take female pups from a low-licking mother and have them raised in the litter of a high-licking mother, they will acquire this attentive trait. Likewise, if you cross-foster in the opposite direction, you get the opposite effect.⁴⁶ Is this rat example simply a case of learning how to raise your pups? There is more to it than that. Grooming and licking appears to regulate the baby rat’s response to stress. Those mothers with a high licking rate produce offspring who cope much better with stress than those from a low-licking mother. They also grow up into more resilient adult rats and, if female, pass this behavioural trait on to the next generation.⁴⁷ They are better adapted to reproduce.

You can even generate this effect if rat pups are reared by humans and given different levels of handling during the early days. This activity changes the baby rats’ HPA response by altering their reactivity to stress. The grooming and licking releases the ‘feel-good’ neurotransmitter serotonin that regulates the gene that controls for GR in the hippocampus. In contrast, this gene is switched off in the under-stimulated pups, whereas it is almost never methylated in the pups of high-licking grooming mothers. With higher levels of GR expressed in the hippocampus, the rat is better able to regulate the HPA effectively. Even though DNA methylation patterns tend to be stable, if you cross-foster the pups of high- and low-licking mothers during the critical period, you can reverse the methylation of the gene in the hippocampus. In short, the early grooming experience is turning the genes on or off.⁴⁸

This may be all well and good for rats, but what of humans? Is there any evidence of biological embedding of early experiences later in life? Post-mortem examination of suicide victims revealed that GR expression in the hippocampus was reduced in those with a history of early abuse compared to those without this childhood trauma.⁴⁹ What makes this finding all the more incredible is that it was not the stress of events that ultimately led them to take their own lives that produced this genetic difference, but rather events during their childhood that were responsible for silencing the genes.

It should be noted that there is not just one gene responsible and there are a multitude of different types of stress that affect individuals differently. In a recent study⁵⁰ of teenagers whose parents had reported stress during their child’s upbringing, methylation of environmental stressor genes was investigated. The effects of the mother’s stress were only evident if that stress had occurred when the child was still an infant. Fathers also produced methylation in stress-related genes but only when the child was older, during the preschool years. More intriguing was the finding that this effect was restricted to the girls in the study. It has been reported for some time that absent or deadbeat fathers have a greater influence on their daughters than their sons, but this study is some of the first evidence to point the finger of suspicion at epigenetics.

Warrior genes

On 16 October 2006, Bradley Waldroup sat in his truck drinking heavily and reading the Bible. He was waiting for his estranged wife to arrive with their four kids for the weekend. When his wife, Penny, turned up with her friend Leslie Bradshaw, a fight broke out and Waldroup went berserk. He shot the friend eight times and then chased after his wife before hacking her to death with a machete. It was one of the worst, most bloody crime scenes that Tennessee police officers had ever dealt with. What makes this horrific crime stand out, apart from its sheer brutality, was that it was one of the first cases where defence lawyers successfully argued that Waldroup should not be given the ultimate punishment of the death sentence because of his genetic make-up. They argued that Bradley Waldroup had a biological disposition towards extreme violence because he carried a warrior gene.

This gene was discovered in the Netherlands in 1993 by a geneticist, Hans Brunner, who had been approached by a group of Dutch women who were concerned that the males in their family were prone to violent outbursts and criminal activity including arson, attempted rape and murder.⁵¹ They wanted to know if there was some biological explanation. Brunner soon found that they all possessed a variant of the monoamine oxidase A, or MAOA gene located on the X chromosome. In the following years, evidence mounted to support the link between patterns of aggression and low-activity MAOA. The condition would have remained known as the rather lame ‘Brunner Syndrome’ if it had not been for the columnist Ann Gibbons, who christened it the ‘warrior gene’.⁵² The emotive name is a bit of a misnomer as it is more of a lazy gene because it fails to do its main job, which is to break down the activity of neurotransmitters.

With the discovery of the warrior gene, soon everyone was looking for this biological marker in the underclass of society. Male gang members were more likely to have the warrior gene and four times more likely to carry knives. In one particularly inflammatory report⁵³ based on a very small sample of males, New Zealand’s indigenous Maoris, famous for their warrior past, were found to have the gene. Not surprisingly, this report created a public outcry.

One of the problems with these sorts of studies is that they relied on self-report questionnaires, which are often inaccurate. One ingenious study⁵⁴ tested the link between the warrior gene and aggressive behaviour by getting males to play an online game where they could dish out punishment in the form of administering chilli sauce to the other anonymous player. In fact, they were playing against a computer that was rigged to deliver a win to itself despite the best efforts of the male participants. Those with the low-activity MAOA gene wanted revenge and were significantly more likely to deal out punishments in retribution.

The warrior gene may be linked to aggressive behaviour, but as Ed Yong, the science writer, puts it, ‘The MAOA gene can certainly influence our behaviour, but it is no puppet-master.’⁵⁵ One of the main difficulties in explaining violent behaviour like that of Bradley Waldroup is that around one in three individuals of European descent carry this gene, but the murder rate in this population is far less. Why don’t the rest of us with the gene go on a bloody rampage?

The answer could come from epigenetics. Genes operate in environments. Individuals are more likely to develop antisocial problems if they carry the low-activity MAOA-L and were abused as children. Researchers studied over 440 New Zealand males with the low-activity MAOA gene and discovered that over eight out of ten males who had the deficit gene went on to develop antisocial behaviours, but only if they had been raised in an environment where they were maltreated as children.⁵⁶ Only two out of ten males with the same abnormality developed antisocial adult behaviour if they had been raised in an environment with little maltreatment. This explains why not all victims of maltreatment go on to victimize others. It is the environment that appears to play a crucial role in triggering whether these individuals become antisocial.

As for Bradley Waldroup, was it right for him to be treated more leniently? He certainly had an abusive childhood, but probably no greater than other males in that trailer park in a socially deprived area of Tennessee. A third of them presumably also carried the gene. At the time, Waldroup was drunk and we know that alcohol impairs our capacity to regulate rage and anger arising from the limbic system. But was he accountable for his actions?

What is clear is that it was the evidence for a warrior gene that persuaded members of the jury to find Waldroup not guilty of murder even though it is clear that they did not fully understand the nature of gene-environment interactions. After the Waldroup outcome, one might think that raising the presence of the warrior gene and abusive childhood would make for a good defence strategy in the law courts. However, there is another way of seeing the argument. One could argue that those with a genetic predisposition towards violent crime should not be let off more lightly but rather punished more severely. This is because they are more likely to reoffend and so the deterrent should be even harsher. Warrior genes and abusive childhoods are risk factors that make some more inclined to violence, but then again, punishment and retribution are also factors that reduce the likelihood of committing crimes. The decisions we make throughout our life represent the interaction of biology, environment and random events. Deciding which is more important is the job of society operating through its laws and policies, but it would be wrong to think that the answer is simple.

The landscape of life

It is a cliché but we often talk about life as a journey with many forks and turnings. Just think about where you are today and how you got here. Did you know ten years ago where you would be today? Although some things in life are certain (death and taxes) and some are likely, many events are unpredictable. And some leave a lasting impression.

As we develop from a simple ball of cells into an animal made up of trillions of cells, the process is guided by instructions shaped by natural selection over the course of evolution and encoded in our genes. However, the genome is not a blueprint for the final body but rather a script that can vary depending on events that take place during development. These are not only events outside the womb, but also those within the unfolding sequence of body building, which explains why identical twins end up different despite sharing the same genes. They may start out with the same genome, but random events can set them off on different pathways as the body is being constructed. This explains why there are increasing differences observed in genetic methylation for identical twins the older they become. Even cloned fruit flies raised in the same lab-controlled environment should be absolutely identical and yet have different arrangements in their brains. When you consider the complexity of neural networks and the explosion of synapses with googols of connections, it seems obvious that no two brains could ever be the same.

Despite the diversity in brains that is inevitable during development, evolution still produces offspring that resemble their parents more than they resemble another species. The majority of genetic information must be conserved and yet remain flexible enough to allow for individual variation arising from events that occur during the developmental process. One way to consider the influence of genes and environment is to think about the journey through life as an epigenetic landscape.

In 1940, the brilliant British polymath Conrad Waddington used a metaphor of a ball rolling down a corralled landscape made of up troughs and valleys of different depth. The diagrams overleaf represent two paths of development in two individuals (A and B) who have the same starting genotype, as in the case of identical twins. These two individuals therefore inherit the same probability of developing a certain phenotype – the expression of those genes into characteristics that emerge over one’s lifetime. However, they may have different actual phenotypic end points, determined by chance events and environmental effects, especially at critical points. At each junction, development can take a different path but whether it stays on course depends on the depth of the gully. Some gullies or canals are very deep, so the ball has no option but to follow that trajectory and it would take a mighty upheaval to set it on another course. These are the genetic pathways that produce very little variation in the species. Other canals are shallower, so that the path of the ball could be more easily set on another route by a slight perturbation. These are aspects of development that may have a genetic component but outcomes can be easily shifted by environmental events.

Figure 7: Waddington’s epigenetic landscape

(After Kevin Mitchell, PL.S Bristol © 2007)

Waddington’s metaphor of canalization helps us to think about development as a probabilistic rather than deterministic process. Most of us end up with two arms and two legs but it is not inevitable. Something dramatic during foetal development could produce a child with missing limbs, as happened during the 1960s when the drug thalidomide was given to pregnant women to prevent morning sickness. Other individual differences are much more susceptible to the random events in life that can set us off on a different course. This can happen at every level, from a chance encounter with a virus as a child to growing up in an abusive household.

Unravelling the complexity of human development is a daunting task and it is unlikely that scientists will ever be able to do so for even one individual, because the interactions of biology and environment are likelihoods and not certainties. There are just too many ways that the cards could stack up. More importantly, as the vernacular saying goes, ‘Shit happens’, which is a very succinct and scientifically accurate way of saying that random events during development can change the course of who we become in unpredictable ways.