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The Neural Garden

Sophie lies awake in bed. Tonight sleep has been slow in coming. She mulls over the day’s events in her mind, wincing at each commitment she willfully piled onto her already overburdened schedule. At every request, absurd promises rise to her lips: offers to tutor Timmy McManus two nights a week until his math grade improves, to take over coaching the girls’ volleyball team, to meet with Mr. and Mrs. Deluca again about their spoiled son. Dwelling on it now is pointless and painful and will only delay her getting the sleep she desperately needs; but Sophie can’t help herself. Her brain returns to it again and again like a tongue to a sore tooth, poking and prodding despite the pain.

For a moment the pressure becomes a physical thing, its weight on her chest malicious and unbearable. Sophie’s heart beats faster, her hands clench, her breath freezes into a cold, hard clump in the back of her throat. She takes slow, measured breaths, counting each one off as her therapist taught her until she gets to 10. Her heart rate slows. Her hands loosen, revealing angry half-moon marks where her fingernails bit into her palms. She heaves a heavy sigh of mingled exhaustion and relief.

We tend to think of panic as a primarily psychological response to stress or fear. The physical symptoms we associate with it — sweaty palms, trembling fingers, shortness of breath — seem like superficial manifestations of a much deeper mental anguish. Stress response, we feel, is all about mindset. But much like the outmoded concept of nature versus nurture, assuming that stress must be either a wholly physical or a wholly mental condition creates a false dichotomy between the two. Your mind and body are not separate parties ruling over you through coalition; they are very much linked. Those seemingly superficial cues — the sweating, the trembling, the rattling breath — betray a deeper and far more complex physiological response, one that engages an elaborate series of glands, nerves, and neurons called the hypothalamic-pituitary-adrenal (HPA) axis.

The HPA axis consists of three segments: the hypothalamus, the pituitary gland, and the adrenal glands. The hypothalamus is a tiny part of the brain — in humans, the entire thing is roughly the size of an almond — located just above the brain stem. Despite its small size, the hypothalamus’s duties are manifold, though its most vital function is facilitating communication between the nervous system and the endocrine system. The nervous system links the brain to the rest of the body, allowing it to move muscles and receive sensory input through the transmission of electrochemical signals. The endocrine system comprises a series of glands that secrete hormones responsible for regulating a number of important bodily functions, including internal temperature, hunger, thirst, circadian rhythm (or sleep cycle), and, most germane to our current discussion, response to stress.

The HPA axis is itself an endocrine system, which is why its first junction is the hypothalamus. When our body acquires sensory data (captured by our eyes, ears, nose, tongue, and sense of touch) indicating a potential threat, the hypothalamus takes that information — brought to it by the nervous system in the form of electrochemical impulses — and translates it into a chemical-based language that the HPA axis can understand. It does this by secreting a hormone called “corticotropin-releasing hormone,” or CRH, which travels from the hypothalamus to the nearby pituitary gland, where it stimulates the release of — you guessed it — corticotropin. However, this was apparently too self-evident for anatomists, who reissued corticotropin a clunkier and less intuitive name: adrenocorticotropic hormone, or ACTH.

The pituitary gland is even smaller than the hypothalamus: about the size of a pea in humans and weighing less than a gram. Like the hypothalamus, its duties are manifold. Though most renowned for its role in human sexual development, the pituitary gland is also a vital part of our stress response system. As we’ve mentioned, it secretes the hormone ACTH, which travels through the bloodstream to a pair of glands perched atop the kidneys. Here, at the adrenal cortex, we have reached the final stop along the HPA axis. This is where we truly get down to business.

Upon receiving a dose of ACTH, the adrenal cortex instructs its glands to secrete a pair of hormones responsible for implementing our physiological stress response. The first of the two is adrenaline, a name you’ve probably heard before. We attribute to adrenaline the “rush” we feel in the face of danger, the jackhammering heart and sweaty palms and manic burst of wide-eyed energy. Yet adrenaline is only one half of an integral stress response partnership. It’s other half is a far less celebrated hormone, but one that is no less important: cortisol.

Cortisol’s main role in responding to stress is redistributing energy (in the form of glucose, or sugar) to the parts of the body that need it most in a time of crisis — the brain for making snap decisions, the major muscle groups to carry those decisions out, and the heart to provide the muscles with the surplus oxygen they need to work at full capacity. Cortisol acts as a kind of override switch, drawing power from other areas of the body (such as digestion, immune system response, and gamete production) and allowing us to make full use of our adrenaline. Adrenaline rushes headlong into battle, ramping up our heart rate and boosting our muscle tone and readying our fight-or-flight response, which is why it tends to get all the glory. But cortisol is no less vital. It provides a critical support role in the stress response system, overseeing our glucose supplies and keeping the troops well-nourished for the duration of the battle.

It’s easy to see how a stress response system can come in handy. When fleeing from a sabre-tooth tiger or defending your village from a warring tribe, the ability to dip into the reserves and muster up that extra bit of energy could make the difference between life and death. But eventually the threat passes, at which point our energy is no longer well-spent on muscle tone and a hammering heart. The surplus glucose needs to be returned to the systems from which it was initially drawn, or else we’ll have escaped from whatever triggered our stress response system in the first place only to die from malnutrition or disease, as our digestive and immune systems failed to shift back into gear. Fortunately, our HPA axis has a nifty way of returning to business as usual. Once cortisol reaches a certain concentration in the bloodstream, it makes its way up to the hypothalamus and pituitary gland, where it dampens the production of CRH and ACTH, respectively. As our stress hormone levels drop, the amount of cortisol in the bloodstream gradually decreases until the body returns to its original, pre-stress state. This is called a feedback loop, and it’s an incredibly valuable trait. In essence, it’s like having your bathwater reach up and shut off the tap before the tub gets too full and floods the washroom.

Thanks to the feedback loop, there’s nothing unhealthy about experiencing occasional bouts of stress. This is a good thing, as it’s a very fortunate few who can live their entire lives without succumbing to feelings of anxiety, frustration, or fear. When we do experience these unpleasant sensations, our body provides us with the extra energy needed to respond to them, then dials us back down to a state of hormonal equilibrium called homeostasis. Homeostasis is our body’s natural resting point, where internal temperature, pH, and hormone levels coexist in perfect harmony. An organism in homeostasis is functioning optimally — in utilitarian terms, it is expending the least possible amount of energy to perform the most work. Less waste means a more efficient conversion of food into energy, greater production of gametes (or sex cells), a more disciplined and well-staffed immune system, and a smarter, sleeker, swifter brain. An organism in homeostasis is, in short, better equipped to survive, which is why our bodies have a number of mechanisms in place designed to make homeostatic harmony sturdy and, in the event of a shakeup, easy to re-obtain. The HPA cortisol feedback loop is one of them.

Think of cortisol as a kind of hormonal ballast, keeping our bodies on an even keel in calm or choppy waters. Only sometimes the waters are more than just choppy. Sometimes life steers us into the arms of a raging hurricane. If the waves of stress and fear batter us too intensely, allowing no chance for us to rest and recalibrate, our ballast may shift. At this point, our body is no longer able to manage itself effectively. With our homeostatic equilibrium compromised, our beleaguered ship begins to sail at an uneven keel. Stress sloshes onto our decks, and our poor vessel is suddenly at risk of sinking. The captain calls all hands on deck in a desperate attempt to keep our ship afloat. The cook stops cooking. The navigator abandons his charts. The ship doctor closes his clinic. Our body’s many systems, suppressed by cortisol in a desperate attempt to weather the storm, stop working. Our immune system shuts down, increasing our risk of contracting diseases and reducing our ability to fight them. Our digestion and sleep schedules become interrupted, weakening us further still.

This is bad enough in adulthood. During early childhood, when the bulk of our energy should be directed toward our physical and mental growth, excessive stress can have disastrous lifelong consequences. Chronic exposure to high levels of stressful stimuli — called toxic stress — among children corrodes the very foundation of human development. And when the groundwork is poorly set, everything built atop it risks collapse. Problems we associate with adulthood or even old age — heart disease, diabetes, alcoholism, etc. — all have their roots in early childhood.

We should clarify that toxic stress is very different from the mild anxieties, injuries, and upsets that comprise a normal and healthy childhood. Your child stubbing their toe or being scolded for colouring on the walls or throwing a tantrum in the supermarket are not signs of toxic stress sinking its poisonous fangs into their defenceless minds. A little stress isn’t a bad thing; in fact, it can actually be good from a developmental standpoint.

Stress, as defined by experts in child trauma, comes in three levels. The first, called positive stress, is a normal part of growing up. Every child gets stressed out at some point, and moments of mild frustration, anger, or anxiety serve to calibrate their stress response system, giving their HPA axis a sort of trial run in order to get the kinks worked out and prepare it for more serious crises later in life. A child is dropped off at daycare, or gets a booster shot, or pinches his finger in a cupboard. He cries, his heart rate rises, cortisol circulates through his bloodstream. A few moments later his mother comforts him, and after a bit of coddling and gentle reassurance, the child is tottering happily through the house again, his discomfort forgotten and his cortisol levels back to baseline.

The second level, called tolerable stress, occurs when a child undergoes a significant traumatic event. She breaks her leg, survives a major earthquake, or loses her grandmother to cancer. These experiences are not part of an ideal childhood, but they aren’t prescriptions for lifelong hardship, either. If they occur infrequently, and if the child has in her life a supportive and nurturing adult presence to help her through it, she’ll almost certainly recover with no negative long-term effects.

However, when stress is severe and ongoing and the necessary parental support is not present, the stress becomes toxic. Aside from extreme circumstances like war and famine, the parental support, or lack thereof, is really the key distinction between tolerable and toxic stress. For the first six months of a child’s life, the HPA axis isn’t very reliable. It needs to learn to do its job, and it can’t do so if it’s constantly bludgeoned with stressful stimuli at levels that would challenge even a grown adult. Mastering hormonal self-regulation under conditions of toxic stress would be like trying to teach a child the rules of touch football by pitting him against an NFL linebacker. It’s not a fair fight. Children need shelter from the storm of stress, and parents are the ones to provide it. For the first six months of your child’s life, you are the HPA axis. Any stress they experience filters through you first, and the better equipped your own stress response system is for metabolizing adverse stimuli, the more effectively you’ll be able to shield your child from the emotional fallout of life’s many traumas.

When a parent isn’t up to the task, due either to their own malfunctioning HPA axis or an overpowering flood of adverse stimuli (no parent, no matter how well-adjusted, could protect their child from the abominable brunt of the Holocaust if its nefarious agents kicked down their door), toxic stress bleeds through. And as its name suggests, toxic stress is dangerous stuff. It poisons children, weakening their immune systems and adversely affecting their emotional, physical, and intellectual development. Children raised in environments rife with toxic stress suffer disproportionately from a vast and deeply troubling array of conditions. Worst of all, a hyperactive stress response system undermines the body’s attempts to build a strong neural framework. Cortisol is neurotoxic, meaning it kills brain cells. If excess cortisol is present in infancy, the time when brain cells are rapidly growing and connecting, the brain doesn’t develop as it should. It becomes weaker, its neurons less densely packed, its operational capacity compromised.

The Neural Garden

Infancy and early childhood encompass a period of unparalleled brain growth. Neurons are rapidly generated by neuronal stem cells, and the connections between them multiply frantically. Each neuron releases a mad tangle of tiny filaments called dendrites, microscopic cables connecting one neuron to the next. The brain grows thick with them, a jungle canopy teeming with electrochemical impulses. And as in the jungle, Darwinian selection looms ever-present. When neural connections are used often they flourish, their wispy dendrites growing into sturdy trunks. Meanwhile, dendrites that go unused atrophy — a process called pruning — until the jungle of neural connections becomes sparser and more cultivated, a garden of the mind.

This in itself is not cause for concern; dendritic pruning is an integral part of neurological development. It might seem somewhat inefficient — why waste precious energy growing dendrites when you’re just going to till them under? — but an initial surplus of synapses (or neural connections) gives our brains a certain amount of wiggle room during our early years. We call this feature of our brains “neural plasticity,” and it is vital to our ability to adapt to diverse and changing environments. By providing a dense network of synapses, our brains allow for every contingency. Once in place, the connections go on a kind of probation. If a dendrite is used often, the brain assumes it must be valuable and reinforces it. If a connection is used rarely or not at all, the brain assumes our circumstances don’t require that particular informational pathway and lets it wither. By the time we are adolescents, our brains have turned from lumps of unformed clay into highly individualized sculptures, shaped by the deft and meticulous hands of our early rearing environment. It is for this reason that children pick up new skills — especially languages — with an ease that leaves most adults flummoxed. Their brains are more pliant than ours and new abilities can be incorporated easily into the folds of their neocortex, while our synapses are far more set in their ways.

Dendritic pruning is a highly effective early learning system, but it has one major drawback. Growing all those dendrites takes a lot of energy. Under normal conditions this isn’t a problem, but if some other part of the body starts demanding the bulk of the resources — an overactive stress response system, say — then the dendrites aren’t able to grow at an ideal rate. And if the stress response system continues to tap the body’s energy reserves at an unsustainable rate, many useful dendrites will wither alongside their unused peers. Those that do manage to survive will languish in impoverished neural soil, their stalks sickly and weak. To make matters worse, an environment rife with toxic stress isn’t likely to provide children with a lot of intellectual stimulation; not only is the child starved for physical resources, but the environment is simultaneously failing to stimulate his brain in a meaningful way. With both biological and sociological factors stacked against them, these children are effectively fighting a war on two fronts. Nurture bombards them with adverse stimuli while nature besieges them, cutting them off from the resources they need to feed their growing brains.

Rodent Rules

In 1957, a young researcher named Seymour Levine observed a strange phenomenon among the rats in his laboratory. He took newborn rat pups and, at regular daily intervals for the first several weeks of their lives, separated them from their mothers for 15-minute periods. The separated mice spent their brief diasporas exploring the confines of a small, unadorned cage. When the 15 minutes were up they were returned unharmed to their mothers. This procedure is called handling, and though it may not seem like much of an occurrence, it has a significant impact on a rat’s stress response system. Handled pups, when compared to their non-handled peers, react to stressful stimuli in a far more relaxed manner. The effect is both behavioural and physiological. When presented with a novel environment, handled rats are much calmer than non-handled rats, and their cortisol levels don’t surge nearly as high.

The opposite effect can also be achieved. Should you for some reason — be it scientific or sadistic — want to produce rats with highly sensitive stress response systems, simply separate them from their mothers for more prolonged periods. An hour or two will do it. Repeat the process — called, appropriately enough, “maternal separation” — a dozen or so times, and the rats in question will grow into neurotic, fretful creatures rife with cortisol, their HPA axes pumping loads of the stuff into their bloodstreams long after their handled brethren have already returned to homeostasis.

A number of established scientists repeated Levine’s results. As the studies piled up, not only was the efficacy of handling and maternal separation confirmed, but the reason why it worked became clear. Handling and maternal separation weren’t changing anything about the rats directly. Rather, these practices changed the way their mothers treated them. The real cause was a series of affectionate and nurturing actions collectively called licking, grooming, and arched-back nursing[34] behaviour, or LG-ABN. Rat dams (mothers) who engaged in high LG-ABN — those who licked, groomed, and nursed their offspring more often than usual — produced rat pups with tempered, easy-going stress response systems. Meanwhile, low LG-ABN mothers — those who spent little time licking and grooming their young, and made little effort to nurse them — produced jittery, easily agitated offspring with hyperactive stress response systems. Handling, it turns out, increases LG-ABN behaviour, while maternal separation decreases it. Levine’s findings remained accurate, but the context surrounding them suddenly changed. Handling and maternal separation were catalysts, not causes.

LG-ABN behaviour is highly heritable. When the pups became mothers themselves, those raised by low LG-ABN mothers acted cold and distant to their offspring while those raised by high LG-ABN mothers became warm and affectionate parents. This led scientists to question whether LG-ABN behaviour really altered rats’ stress response systems at all. Perhaps, they thought, LG-ABN was just an extension of rats’ genetically preprogrammed HPA behaviour, and handling and maternal separation were, at most, enhancing behaviours that would have appeared regardless.

To counter this claim, researchers Michael Meaney and Moshe Szyf of McGill University in Montreal performed a cross-fostering study. Pups of high LG-ABN dams were given to low LG-ABN mothers, who raised them as their own. In turn, pups of low LG-ABN mothers were given to high LG-ABN mothers. Additionally, some pups were cross-fostered to mothers of the same type — low LG-ABN pups to low LG-ABN mothers and high LG-ABN pups to high LG-ABN mothers — to confirm that the act of cross-fostering pups wasn’t itself causing a change in stress behaviour.

Meaney and Szyf have performed dozens, if not hundreds, of these studies. The results have been consistent and profound. Again and again, rat pups adopted the stress response system of the mothers who raised them, both on a behavioural level, in their nervousness or lack thereof, and a physiological level, in the degree of stress hormones found in their bloodstream. Regardless of the disposition of their birth mothers, rat pups raised by high LG-ABN mothers were calm and self-assured, and displayed a measured and stable hormonal stress response, while those raised by low LG-ABN mothers were invariably timid, edgy, and rife with cortisol. And these effects didn’t go away after a single generation. Pups cross-fostered to low or high LG-ABN mothers raised their “children” in the same manner as their adoptive parents, perpetuating the cycle of low or high stress response.

So what is causing this physiological change? The answer appears to be epigenetics. To demonstrate, let’s follow the development of two rats, one born of a low LG-ABN mother and one of a high LG-ABN mother. From fertilization to birth — spanning a period of about 22 days — our two subjects are essentially identical. Most germane to our interests, their stress response genes[35] are free of any methyl molecule tags that might impede their function. In rats of both high and low LG-ABN mothers, these genes are switched on and ready to make proteins. However, shortly after birth, the region becomes methylated (or turned off) in both rats and remains so until the pups are six days old, at which point our two subjects’ genomes diverge. In pups raised by high LG-ABN mothers, the sequence switches back on, shedding the shackles of its methyl molecules and resuming the ability to produce proteins. In pups of low LG-ABN mothers, the methyl tags remain in place, locking down the gene and restricting its ability to operate. Importantly, this divergence always occurs at precisely the same time when mothers start really licking and grooming their young and the differences between high and low LG-ABN mothers become readily apparent.

We are beginning to see evidence of these same effects in humans. Unfortunately, the highly invasive nature of cross-fostering studies makes them impractical (not to mention unethical) to perform on human beings — it is a rare mother indeed who would willfully allow her newborn daughter to be taken from her arms and replaced with a squalling infant born of strangers. Understandably, human studies have been less invasive and more roundabout. Yet they do occur.

In 2011, Dr. Marilyn Essex approached participants in the long-running Wisconsin Study of Families and Work, which began following an initial 570 pregnant women and their partners beginning in 1990 and continues to the present day, albeit with reduced numbers. Of the original 570, many were ineligible for Essex’s study, and still others declined the offer to participate. All told, 109 mothers and their children participated in Essex’s study. Not a huge number, but big enough for her purposes.

Poring through stacks of medical data, Essex traced the rise and fall of stressful life events occurring in each participant’s household during their children’s early years, noting every death, car accident, divorce, nervous breakdown, and any other unfortunate occurrence that could have conceivably raised the stress levels of the affected family. She then genotyped those children — now in their teens — and noted the patterns of methylation present on a number of key genes, particularly those pertaining to the stress response system. Her hypothesis was that traumatic events in parents’ lives, if they occurred at a certain critical period of development, would alter the patterns of methylation found on their children’s genomes. As it turned out, they did. Adult stress and child methylation synced up in complex, surprising, and remarkably consistent ways.

Essex found that if stressful events occurred during certain trigger periods in a child’s life, they would leave an epigenetic imprint on that child’s genes. These trigger periods, though consistent, were not cut and dried across the entire population of the study. Rather, they were highly dependent on the gender of both the affected child and his or her parent. The parent’s gender determined the time at which their stressful experience had the most bearing on the methylation patterns present in their children. For mothers, the period was during their child’s infancy. Mothers who reported experiencing a great deal of stress when their children were just babies — be it from losing a job, relationship trouble, or grieving the loss of a loved one — had children who displayed a distinct and unconventional pattern of methylation in certain target genes. Fathers produced a different but no less distinct methylation pattern, but only when stressed during their children’s preschool years, and only in their daughters. Sons showed no abnormal patterns of methylation regardless of their father’s stress patterns. Mothers, on the other hand, impacted the methyl patterns of their sons and daughters equally.

What does all this mean? From a short-term standpoint, admittedly not all that much. If you were hoping for a silver bullet solution, a lone methyl tag placed at a critical moment in childhood responsible for all of our problems, then we’re about to disappoint you. None of the genes Essex monitored in her study have a direct link to heart disease, cancer, depression, or any other genetically modified malady. A panacea bearing Essex’s moniker is, sadly, not forthcoming. However, to the more far-seeing among us, Essex’s findings are truly groundbreaking. A profound truth about the power of motherhood, proven again and again in Meaney and Szyf’s rodents, has now been officially seen in humans. And where one epigenetic influence goes, others will surely follow. There is no telling what shocking and far-reaching discoveries the next decade of epigenetic research will bring.

Conduits

Bruce Perry could be called a Hobbesian, though that would perhaps be uncharitable. Like the dour 17th-century philosopher Thomas Hobbes, Perry believes that humankind, despite great leaps forward in social structure, quality of life, and technological innovation, has not ventured far from the jungle from whence it came. Yet Perry does not believe bloodshed to be an innate part of human behaviour, which is where he and Hobbes differ. Hobbes could not have known about genes, having died almost 200 years before Gregor Mendel had so much as planted his garden, but had he the ability to learn of DNA, he would almost certainly believe violence to be tangled up in there somewhere. Perry, however, rejects this fatalist notion. To him, violence is a learned behaviour, a tragic legacy passed down through a thousand generations. It may be our birthright, however much we may begrudge those who gave it to us, but it is not innate.

Earlier this chapter, we discussed how the infant brain develops: a fecund flourishing of dendritic foliage thick as a jungle canopy, pruned and harvested and organized by our earliest experiences into something more orderly and productive, a kind of intellectual agriculture. We select the dendrites we use most and tend to them closely, watering them and weeding them and fertilizing their soil. The dendrites we don’t use we yank free in order to provide greater resources to our more desirable neurological crops. But managing such an immense and complex garden takes work, and work takes energy. The body accounts for this under normal conditions — infants don’t have much to do with their energy besides learn and grow. But when we are besieged by ever-present toxic levels of stress, our stores are gradually depleted. Tending to our intellectual nourishment is put on hold in favour of our more immediate survival, and gradually our garden begins to wither. The soil becomes parched, its dendrites weak and wilted. Weeds choke the life from our desired neurons, filling our heads with bitter, spiny synapses from which we in no way benefit. Dr. Perry is fascinated with this unfortunate process, though intellectual stimulation is not his chief concern. He is far more interested in the effects of emotional stimulation on a child’s life, studying how a supportive adult presence filters the toxins from otherwise toxic stress, and how that same parent’s absence allows those toxins to flow unimpeded.

Perry is no stranger to trauma. A senior fellow of the Child Trauma Academy, he has served as an expert witness on many high-profile cases in which children and adolescents were traumatized, including the siege of the Branch Davidian compound in Texas, the Columbine High School massacre, and the Oklahoma City bombing. He stood on the front lines of mental health support during Hurricane Katrina and 9/11, assisting children and adults who suffered from post-traumatic stress disorder, depression, and other emotional fallout. His research has informed our modern understanding of how young minds respond to violence, and the profound effect parents have on moderating, or exacerbating, this response.

Certainly, neglectful parenting has an adverse effect on children’s development. Our neural gardens need more than fresh soil to truly flourish. They need pruning and weeding and watering. An untended garden may grow thick and green if the sun is shining and rain comes often enough, but it will be a wild, chaotic patch of earth, fruitful perhaps, but also cluttered and choked with weeds. The same goes with young minds. Infants need more than food and warmth and safety; they need stimulation and interaction and play, and the more of it they get, the better they’ll be at thinking and reasoning and, above all, feeling. Emotional intelligence and intellectual intelligence (what we generally mean when we just say “intelligence”) are closely connected attributes, but they are not identical. Perry gives a chilling example of this point in his 1997 paper on the cycle of violence.

Six o’clock in the evening in inner-city Baltimore. A 15-year-old boy named William sees a classmate shooting hoops on the neighbourhood basketball court. It’s twilight and the city feels deserted. There are no pedestrians on the sidewalks, no cars on the streets, no conversations drifting though open windows. The classmate dribbles his way up the court, the thwack of his ball on the pavement echoing off the nearby tenements. William’s eyes drift from the basketball to his classmate’s shoes. Air Jordans, their vamps and laces an immaculate white, the fresh rubber of their soles squeaking against the tarmac with each step. William approaches his classmate, who eyes him nervously.

“Hey,” the classmate says.

“Gimme your shoes,” says William.

“What? No way.”

William lifts up his jersey and pulls a handgun from the waistband of his pants. He’d been wearing the gun for no particular reason except that it felt good against his stomach. It feels even better in his hand, he notes. The classmate’s eyes go wide. He raises his hands, backing up slowly.

“The shoes,” says William.

“Y-yeah, okay, sure,” the classmate stammers. Very slowly, he bends down and unties his laces. He takes off the shoes and hands them to William, who takes them with an approving smile. He holds them up to his face and looks them over, the gun still trained on his classmate.

“Cool. Thanks,” he says, and pulls the trigger. The classmate collapses. Blood speckles William head to toe, staining the leather of his new shoes a splotchy red. He puts them on anyway, not bothering to wipe them clean. On his walk home, he tosses his old shoes over a fence.

The stains are what undo him. Them and the gun, which confirms the story his bloody shoes had already told. The police take William into custody, where a stone-faced officer questions him for an hour. Most of his questions concern what happened and why, but near the end of their interview he asks the boy something different.

“Son, if you could do it all over again, would you do anything differently?”

William thinks about it for some time. Finally, he responds.

“I would have cleaned my shoes.”

Consider William’s reply. There is regret imbedded in his statement, but it is of a purely intellectual sort. He regrets his actions because they led to him being caught, not because they caused the death of an innocent human being. In that respect, the boy couldn’t care less. He is capable of regret, an intellectual response, but not remorse, an emotional one. Perry’s story highlights this distinction. We are all familiar with the concept of mental retardation, but children can also suffer from emotional retardation, in which their capacity for empathy is stunted or missing entirely. And while mental retardation is often the result of genetic conditions, emotional retardation is almost exclusively learned. Just as a child raised by wolves never learns how to speak, a child raised without love never learns to form the emotional bonds necessary to empathize with other people.

Over the past few decades, we have blamed this problem on a large and shifting cast of bogeymen. Poverty, single parenthood, television, heavy metal music, video games: each has at some point faced the ignominious spotlight cast by the media as a rogue and a villain, the blood of uncountable children on its hands. And in truth, it’s unlikely that any of these factors serve to decrease problem behaviour in children. Being poor means more financial stress in the home, fewer opportunities for children to go to good schools or participate in extracurricular programs, and greater odds of living in a violent neighbourhood bereft of strong role models. Single parenthood doubles the burden placed on the mother (or father) and reduces the amount of time children can interact with them — somebody’s got to pay the bills, after all, and it’s a rare parent who can work productively and attend to their kid’s needs at the same time. And there is evidence that an overexposure to violent media can to a certain extent inoculate children to its horrors, making them, if not more violent, then at least less repulsed by the concept of violence. Yet all of these factors pale in comparison to the true root cause of emotional malnourishment: relational poverty. Not to be confused with poverty of the socioeconomic sort, relational poverty refers to a lack of supportive adults in a child’s life. Though a family may be well-off financially, their children can still suffer from emotional impoverishment if they have limited contact with parents, grandparents, and other friendly faces.

Children have in them a great capacity for resilience, but it is predicated upon the attention and support they receive from the adults around them. Parents act as a kind of psychological immune system, allowing children to deal with modest threats without suffering any long-term harm. Strip a child of this protection, and the smallest upset in her life — the emotional equivalent of a common cold — becomes a serious threat. Toxic stress is only toxic if children lack the means to combat it, just as a disease is only dangerous if a person lacks the necessary antibodies. Except with toxic stress, the antibodies are not internal. They come from outside of the child, delivered by the affection of parents, aunts, grandfathers, teachers, neighbours, and friends.

Parents are the conduits through which toxic stress must pass. This idea is both liberating and terrifying. On the one hand, it is comforting to know that a parent’s loving presence can supersede most any external hardship their children may encounter. Poverty, violence, mourning, disaster: all can be endured if the affected child has the support of his or her caregiver. But such responsibility puts a tremendous amount of pressure on parents. In the midst of a crisis, a hectored mom can add yet another worry to what is likely already a long and daunting list: don’t let stress trickle down to the children.

Still, Perry’s assertion isn’t something to fear. Good parenting doesn’t require a degree or tons of cash or a rigid adherence to any set rules. To quote Lennon and McCartney, all you need is love (though effort and a bit of common sense don’t hurt either). Happily, love is something that just about every parent has in abundant supply.

Bonding

In the grand sweep of human history, there is perhaps no force more powerful than the bond between parent and child. If you’re a parent, you’ve probably experienced it firsthand. The need to protect, nurture, and guide one’s offspring is deep, profound, and overwhelming, capable of circumventing even the most primal urges of self-preservation. Stories abound of mothers and fathers temporarily endowed with almost superhuman strength, speed, and endurance when their children are in peril, allowing them to lift up the back ends of cars with their bare hands and fight off violent criminals twice their size. Apocryphal and exaggerated many of these claims may be, but there is a grain of truth buried within them. From an evolutionary standpoint, it’s not hard to envision why this would be. Any sexually reproducing organism that made no effort to protect its offspring would be far less likely to extend its lineage to subsequent generations than one who defends its children tirelessly, even if doing so costs the organism its life. Though our genetic imperative is to survive, an even greater imperative is to preserve our genetic lineage, and our children are the vessels in which this lineage resides. As far as our genes are concerned, child trumps parent every time.

The parent-child bond and the forces that forge it form the crux of attachment theory, which we discussed in a previous chapter. We often think of the parent-infant bond as something originating from the minds of mothers, but proponents of attachment theory argue that the infant has a part to play as well. Mothers may set the tone, but their children respond accordingly. As a result, we have the three major classes of attachment behaviour (or four, if you subscribe to the Main and Solomon school of attachment theory),[36] each of which corresponds to a different type of parenting behaviour. Type B children are called securely attached, comfortable with short separations from their parents but eager to see them return. Their parents are consistent, supportive, and attentive to their children’s needs. Type A children are called avoidant, and true to their name, they tend to ignore their parents even when feeling insecure. Their parents are often inattentive, having never paid much heed to their cries, causing children to seek comfort in themselves rather than waste energy calling for their caregivers in vain. Type C children are called reactive/ambivalent, and they display a consistent yet curiously contradictory pattern of behaviour: though extremely agitated by short separations from their caregivers, they derive no comfort from them upon their return. Type C children cling to their parents while thrashing and crying, seemingly unsure whether they want to be comforted or left alone. This paradoxical reaction is the result of inconsistent caregiving; parents of Type C children may come running at their child’s first whimper in one instance only to let them cry unattended for hours in the next.

When attachment theory was first created, its conclusions were drawn solely from observation. Dr. Bowlby, the theory’s founder, knew maternal behaviour altered child attachment strategy because he’d seen it do so, but he didn’t know why. At the time, the question seemed almost irrelevant. The important thing was to observe the cause and effect relationship between parent and child; the engine driving it was a mysterious biochemical transaction, relied upon but not understood. Gradually, this has begun to change. Researchers have started mapping the neuroendocrine responses of new mothers to pregnancy, lactation, and childbirth, and have already found a vast network of hormonal signals responsible for “priming” mothers for motherhood. The epigenetic changes dutifully observed by Meaney and company do not flow unidirectionally from mother to child through mom’s nursing behaviour, as was once assumed. The child, simply by being born, triggers a number of profound changes in a mother’s brain, not the least of which being a surge of oxytocin production.

Oxytocin is a hormone responsible for our sense of camaraderie, our capacity for empathy, and our ability to bond with other humans. Not surprisingly, it is released in copious amounts during and immediately after childbirth. One can hardly blame mothers for providing themselves with a little chemical compensation, given the gruelling nature of childbirth (it’s called “going into labour” for a reason), but after the birth is over and the new baby has been swaddled and handed squalling to mom, oxytocin’s work is only just beginning. It floats through the mother’s bloodstream at elevated levels for months, its ebb and flow intimately tied to lactation. Each time a baby feeds, mom gets a fresh dose, a Pavlovian encouragement to keep it up. Oxytocin is the reason why a new mother will often report a profound sense of kinship with her children when breastfeeding; her brain is bribing her with tiny hits of bliss. It’s a cynical way of looking at things, perhaps, but such crude tactics are hardly limited to childbirth. Just about everything we do is the result of biochemical bribery or threat. We keep our bodies nourished, hydrated, and rested, and our brains reward us with dollops of dopamine. We procreate, and our thankful genes reward us with an even bigger burst of the stuff. We come across a fire or a steep ledge or a predator and our brain reprimands us before we do something foolish. “Don’t touch it,” our cerebellum warns, “or you’ll be sorry.” Should the memory of past pain not suffice and we prove ourselves in need of another lesson — by touching the fire or tottering gleefully over the ledge or prodding the large and irascible predator with a stick — the brain is all too willing to deliver. Pain is a warning, alerting us to a potential problem we must attend to (“Hey! You’re bleeding!”), but it’s also a threat. “Smarten up,” it growls, “or you’ll get another.”

Therefore, it should come as no surprise that when we engage in something as evolutionarily beneficial as motherhood our brains praise our noble behaviour with a burst of mood-enhancing hormones. Oxytocin is one of them. Dopamine is another. Though both are pleasurable chemicals, oxytocin and dopamine have distinct characters, and thus serve different purposes. Oxytocin, as mentioned above, promotes bonding and empathy — feelings that, though pleasant, emphasize the importance of connecting with others. Dopamine is far more self-absorbed. It is the id molecule, hedonism concentrated into a few choice atoms and released in tiny, intoxicating doses. Which is not to say dopamine works solely to selfish ends; mothers get a taste of it simply by looking upon their child’s smiling face. Their varying characters make oxytocin and dopamine great partners in parental motivation. Oxytocin provides the softly harmonious sense of rightness about child-rearing, while dopamine offers ephemeral but potent moments of joy. Together, they comprise the parent-child bond studied by attachment theorists and are thus largely responsible for the continued existence of our species.

But sometimes these bonds loosen or break. The hormonal adhesives binding parent to child weaken, dissolved by competing chemicals that change the way a mother’s brain responds to her infant’s laughs, cries, and gurgles. A lot of things can derail mother-child attachment, but perhaps no force is as destructive and insidious in this regard as addiction.

Neural Solvents

No one would argue that drug addiction makes for better parenting. We’ve all heard horror stories of children living in squalid apartments, playing on a floor littered with syringes while their junky parents sprawl unconscious across the couch, of mothers leaving babies in trash cans, incapable of caring for them and afraid of putting them up for adoption lest the authorities cast a disapproving glance their way, of fathers murdering their children in a drug-fuelled rage. Such actions seem to us unconscionable, nefarious, and downright evil. How could a parent treat an innocent child that way? We resist the very thought of it, as if the idea itself was a rotten, repugnant, physical thing capable of dripping its slime onto the floors of our subconscious.

Mercifully, these are extreme examples, but addiction inarguably takes its toll on a person’s ability to be a successful parent. Mothers addicted to cocaine are more hostile, are less emotionally engaged in maternal activities (e.g., feeding, bathing, and playing with their babies), and exhibit little to no pleasure in interacting with their children. It’s as if their mothering gene had been switched off. Of course, we’ve learned enough about genes by now to realize that there is no mothering gene, just as there’s no gene for depression or gene for addiction. Yet certain neural switches are being thrown, and certain connections rerouted, causing a dramatic shift in the way addict mothers view, interact with, and respond to their offspring.

Remember Marcy and Melissa, the twins we discussed in chapter 6?[37] Let’s pay them another visit. Marcy, you’ll recall, was ushered into a life of wealth and privilege while Melissa wallowed in emotional neglect. Now in adulthood, the two sisters have both become mothers.

Marcy’s labour wasn’t easy, but when she first laid eyes on her baby girl the pain and frustration and fear of the past 12 hours washed away. Her heart seemed to swell, infused with a love more primal and pure than anything she’d experienced before. It was like a drug, Marcy thought — though having never tried any substance stronger than a glass of wine, she could only guess that this was true. She named the girl Chloe.

The first few months were a challenge, and the sleepless nights and 3:00 a.m. feedings took their toll. Marcy was a driven woman, married to her career as much as her husband, and the endless days spent at home sometimes felt more like a prison sentence than a well-paid six-month maternity leave. She missed the bustle of the hospital, the patients and the dizzy chaos and the rush of adrenaline she felt whenever she stepped into an operating room and snapped latex gloves onto her steady, talented hands. Those hands felt wasted changing diapers and scrubbing baby spit-up off of bibs. Sometimes she sat on her bed and cried. But as the months passed Chloe became less of a helpless, mewling thing. She began to smile, to babble joyful gibberish, to trace the movement of Marcy’s fingers with wonder. The tiniest giggle set Marcy’s heart ablaze with maternal warmth. She watched her daughter grow with an unceasing sense of amazement and gratitude. Her body surged with affection for the little girl. She’d spent three months pining for her office and her operating theatre, but as her maternity leave drew to a close the thought of leaving Chloe made her miserable. The child was an endless fountain of comfort and joy.

While Marcy was delivering her first child, Melissa had just come home from the hospital with her third. The delivery had been a non-issue, a few hours, a few squirts of Demerol, and there you have it, another screaming mouth to feed, another pair of chubby little hands clawing greedily at her starving, threadbare chequebook. Melissa brought her baby — a girl she named Britney — home and went through the motions of motherhood. She fed her, changed her, bathed her on occasion, but the whole thing was joyless and dull. Drugs were what kept her going, and she popped, sniffed, or smoked them any chance she got. The exact substance didn’t much matter; Melissa did whatever she could get her hands on.

The moments that followed these indulgences were sacred, her mounting bills and crappy job and wailing kids held at bay by a wall of inebriation. Then the high would fizzle and Melissa would trudge back to her duties, regarding her children with poorly disguised contempt.

The smiles and giggles and wide-eyed glances that bought Marcy such joy meant little to Melissa. Often she would just as soon have Britney sulk as smile. At least sulking was quiet. Laughter was better than her wretched wailing, but it still got on Melissa’s nerves.

Each night after putting Britney to bed, Melissa got high, be it on pot, prescription pills, or simply cigarette after cigarette. Money was tight and drugs hard to come by, but she tried not to worry too much about it. She’d get more somehow. She always did. It was the only thing that mattered.

It’s easy to cast Marcy as the benevolent, selfless mother and Melissa as the self-absorbed, self-destructive addict, but the distinction between the two women runs deeper than that. Marcy isn’t entirely selfless — after all, caring for Chloe gives her joy, comfort, and a not unjustified sense of maternal pride. Without that burst of emotions, she would probably still do her duty as a primary caregiver, but would she be as good at it, or as dedicated to her daughter’s happiness? Probably not. She might not be as neglectful to her children as Melissa — her greater financial means and more driven personality give her an additional leg up, to be sure — but if Marcy was deprived of her daily oxytocin-dopamine cocktail, or if Melissa was provided with one, the gulf separating the two mothers would likely shrink considerably.

The brain is a complex network of electrochemical impulses, a synaptic switchboard on a truly galactic scale. Billions of neurons forge trillions of connections with one another, allowing for more combinations of neural signals than there are stars in the Milky Way, and substantially more processing power than the fastest computer on earth. Imagine that each of these connections, when activated, gives off a flicker of light. These tiny lights fizzle and flash and coalesce, providing a bioluminescent map of brain activity. The more vigorously a neural region is being used, the brighter it shines, while underused regions remain dark.

Can you see it? Good. Let’s take this concept and examine the phosphorescent cartography of Marcy and Melissa’s brains. When Marcy sees Chloe smile or hears the sound of her laughter, Marcy’s nucleus accumbens — the region of her brain associated with pleasure — lights up. Her dopamine receptors dazzle like flashbulbs, elevating her mood and forging a positive association between her and Chloe. Bolstered by her brain’s neurochemical response, Marcy becomes more affectionate, attentive, and nurturing. This in turn makes Chloe a more interactive and curious baby, which sets Marcy’s dopamine receptors glowing even brighter. Their synapses flash and sparkle in a glorious and highly synchronized display of neural fireworks. When mother and child interact, their nuclei accumbens display nearly identical patterns of activity — they light up in sync. They signal to one another, their brains and bodies engaged in what child development experts call a serve and return relationship. Chloe serves up a giggle or a smile and Marcy returns it, tickling Chloe’s neurons and encouraging her cognitive development. Together the two of them play a kind of cerebral tennis, except the muscles being exercised are not calves and quads, but the nucleus accumbens and the cerebral cortex. And the more they play, the stronger the bond between them grows.

Meanwhile, Melissa’s brain is a dim and listless thing. As far as her neurons are concerned, a smile from Britney is worth less than a candle in the wind. Her dopamine receptors fizzle. Try as she might, Britney can’t trigger a single one. The fault is not with her; her mother’s brain has been cruelly rewired. Cocaine has the reins now, and it is a savage and relentless master. The bursts of dopamine that should seal Melissa’s relationship with her daughter come instead through outside substances. Her ability to feel happiness without chemical stimulation grows muted and weak. Melissa’s brain only glows when she’s taking a fresh hit, and with each snort, her light shines dimmer and dimmer.

Drug use erodes a mother’s ability to derive pleasure from the very act of mothering. On a chemical level, parenting becomes a pursuit of diminishing returns. It’s easy to call these mothers selfish — and perhaps selfishness does come into it, to a certain extent — but there is much more to the problem than that. The little things that compensate for the seemingly unending trials of motherhood — the warm maternal glow, the tiny joys imbued in a toddler’s laughter — these pleasures no longer register. Drugs dissolve the bond between mother and child, and once that effortless, unconscious connection is gone, holding on becomes a deliberate and exhausting effort. Imagine devoting your every waking hour to a creature from which you derive no satisfaction, feel no love, and sense no fealty. Few addicts, admittedly, are this extreme, but the gradual numbing of maternal connection is a well-documented effect of substance abuse. Drugs (especially cocaine, though other narcotics are guilty as well) eat away at the bonds between mothers and children. They are neural solvents, dissolving warmth into want, happiness into hunger, love into cold, unfeeling sludge. Addict parents are often indifferent to, or even resentful of, their children’s needs. Their parenting behaviour waffles between extremes: harsh, over-involved authoritarianism juxtaposed with excessively permissive indifference. On the latter pole, mothers occasionally invert the parent-child relationship, begging support from a child developmentally unequipped to take on the role of parent.

Sadly, growing up in this sort of environment has a palpable effect on children. Neglect, both emotional and physical, are distressingly commonplace in addicts’ homes. And we know what emotional neglect hath wrought — think back to Bruce Perry’s relational poverty, to Meaney’s troubled low LG-ABN rats, to Sophie’s sleepless nights. Children deprived of emotional and intellectual nourishment are cruelly denied the chance to grow and learn unfettered. Their dendritic gardens become parched and withered. Promise rots on the vine. Fussy infants become troubled toddlers become angry, sullen teens. Their love-starved brains lurch hungrily toward stimulus, anything to fire their rusty, underused dopamine receptors — alcohol, sex, cocaine, heroin, gambling. Booze and narcotics are the most popular choice, but the “what” of it is almost immaterial. The real issue is the why, and the why never changes.

Hungry Ghosts