Family and Parenting 3-Book Bundle. Michael Reist
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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