Tag Archives: trauma

CHILDHOOD TRAUMA AND MENTAL ILLNESS. Overcoming Childhood Trauma, Beyond the smoke – Johann Hari.

Depression isn’t a disease; depression is a normal response to abnormal life experiences.

For every category of traumatic experience you go through as a kid, you are radically more likely to become depressed as an adult. The greater the trauma, the greater your risk of depression, anxiety, or suicide.

Chronic adversities change the architecture of a child’s brain, altering the expression of genes that control stress hormone output, triggering an overactive inflammatory stress response for life, and predisposing the child to adult disease.

Emotional abuse especially, is more likely to cause depression than any other kind of trauma, even sexual molestation. Being treated cruelly by your parents is the biggest driver of depression, out of all categories.

Vincent Felitti didn’t want to discover just a sad fact, he wanted to discover a solution. He was the doctor who uncovered the startling evidence about the role childhood trauma plays in causing depression and anxiety later in life. He proved that childhood trauma makes you far more likely to be depressed or severely anxious as an adult. He traveled across the United States explaining the science, and there is now a broad scientific consensus that he was right. But for Vincent, that wasn’t the point. He didn’t want to tell people who’d survived trauma that they were broken and doomed to a diminished life because they were not properly protected as kids. He wanted to help them out of this pain. But how?

He had established these facts partly by sending a questionnaire to every single person who received health care from the insurance company Kaiser Permanente. It asked about ten traumatic things that can happen to you as a kid, and then matched them against your current health. It was only after he had been doing this for more than a year, and the data was clear, that Vincent had an idea.

What if, when a patient checked that they had suffered a trauma in childhood, the doctor waited until they next came in for health care of any kind, and asked the patient about it? Would that make any difference?

So they began an experiment. Every doctor providing help to a Kaiser Permanente patient, for anything from hemorrhoids to eczema to schizophrenia, was told to look at the patient’s trauma questionnaire, and if the patient had suffered a childhood trauma, the doctors were given a simple instruction. They were told to say something like: “I see you had to survive X or Y in your childhood. I’m sorry that happened to you, it shouldn’t have. Would you like to talk about those experiences?” If the patient said she did, the doctor was told to express sympathy, and to ask: Do you feel it had negative long-term effects on you? Is it relevant to your health today?

The goal was to offer the patient two things at the same time. The first was an opportunity to describe the traumatic experience, to craft a story about it, so the patient could make sense of it. As this experiment began, one of the things they discovered almost immediately is that many of the patients had literally never before acknowledged what happened to them to another human being.

The second, just as crucial, was to show them that they wouldn’t be judged. On the contrary, as Vincent explained to me, the purpose was for them to see that an authority figure, who they trusted, would offer them real compassion for what they’d gone through.

So the doctors started to ask the questions. While some patients didn’t want to talk about it, many of them did. Some started to explain about being neglected, or sexually assaulted, or beaten by their parents. Most, it turned out, had never asked themselves if these experiences were relevant to their health today. Prompted in this way, they began to think about it.

What Vincent wanted to know was, would this help? Or would it be harmful, stirring up old traumas? He waited anxiously for the results to be compiled from tens of thousands of these consultations.

Finally, the figures came in. In the months and years that followed, the patients who had their trauma compassionately acknowledged by an authority figure seemed to show a significant reduction in their illnesses, they were 35 percent less likely to return for medical help for any condition.

At first, the doctors feared that this might be because they had upset the patients and they had felt shamed. But literally nobody complained; and in follow-ups, a large number of patients said they were glad to have been asked. For example, one elderly woman, who had described being raped as a child for the first time, wrote them a letter: “Thank you for asking,” it said simply. “I feared I would die, and no one would ever know what had happened.”

In a smaller pilot study, after being asked these questions, the patients were given the option of discussing what had happened in a session with a psychoanalyst. Those patients were 50 percent less likely to come back to the doctor saying they felt physically ill, or seeking drugs, in the following year.

So it appeared that they were visiting the doctor less because they were actually getting less anxious, and less unwell. These were startling results. How could that be? The answer, Vincent suspects, has to do with shame. “In that very brief process,” he told me, “one person tells somebody else who’s important to them something [they regard as] deeply shameful about themselves, typically for the first time in their life. And she comes out of that with the realization, ‘I still seem to be accepted by this person.’ It’s potentially transformative.”

What this suggests is it’s not just the childhood trauma in itself that causes these problems, including depression and anxiety, it’s hiding away the childhood trauma. It’s not telling anyone because you’re ashamed. When you lock it away in your mind, it festers, and the sense of shame grows. As a doctor, Vincent can’t (alas) invent time machines to go back and prevent the abuse. But he can help his patients to stop hiding, and to stop feeling ashamed.

There is a great deal of evidence that a sense of humiliation plays a big role in depression. I wondered whether this was relevant here, and Vincent told me: “I believe that what we’re doing is very efficiently providing a massive reduction in humiliation and poor self-concept.” He started to see it as a secular version of confession in the Catholic Church. “I’m not saying this as a religious person because I’m not [religious, but confession has been in use for eighteen hundred years. Maybe it meets some basic human need if it’s lasted that long.”

You need to tell somebody what has happened to you, and you need to know they don’t regard you as being worth less than them. This evidence suggests that by reconnecting a person with his childhood trauma, and showing him that an outside observer doesn’t see it as shameful, you go a significant way toward helping to set him free from some of its negative effects.

“Now, is that all that needs to be done?” Vincent asked me. “No. But it’s a hell of a big step forward.”

Can this be right? There is evidence, from other scientific studies, that shame makes people sick. For example, closeted gay men, during the AIDS crisis, died on average two to three years earlier than openly gay men, even when they got health care at the same point in their illness. Sealing off a part of yourself and thinking it’s disgusting poisons your life. Could the same dynamic be at work here?

The scientists involved are the first to stress that more research needs to be done to find out how to build on this encouraging first step. This should only be the start. “Right now, I think that is waiting to happen, in terms of the science of it,” Vincent’s scientific partner, Robert Anda, told me. “What you’ve asked about is going to require a whole new thinking, and a generation of studies that has to put all this together. It hasn’t been done yet.”

I didn’t talk at all about the violence and abuse I survived as a child until I was in my mid-twenties, when I had a brilliant therapist. I was describing the course of my childhood to him, and I told him the story I had told myself my whole life: that I had experienced these things because I had done something wrong, and therefore I deserved it.

“Listen to what you’re saying,” he said to me. At first I didn’t understand what he meant. But then he repeated it back to me. “Do you think any child should be treated like that? What would you say if you saw an adult saying that to a ten-year-old now?”

Because I had kept these memories locked away, I had never questioned the narrative I had developed back then. It seemed natural to me. So I found his question startling.

At first I defended the adults who had behaved this way. I attacked the memory of my childhood self. It was only slowly, over time, that I came to see what he was saying.

And I felt a real release of shame.

Also on TPPA = CRISIS

CHILDHOOD TRAUMA AND MENTAL ‘ILLNESS’. Beyond the smoke

Johann Hari

Depression isn’t a disease; depression is a normal response to abnormal life experiences.

The medical team, and all their friends, expected these people, who had been restored to health to react with joy. Except they didn’t react that way. The people who did best, and lost the most weight were often thrown into a brutal depression, or panic, or rage. Some of them became suicidal.

Was there anything else that happened in your life when you were eleven? Well, Susan replied that was when my grandfather began to rape me.

“Overweight is overlooked, and that’s the way I need to be.”

What we had perceived as the problem, major obesity, was in fact, very frequently, the solution to problems that the rest of us knew nothing about. Obesity, he realized, isn’t the fire. It’s the smoke.

For every category of traumatic experience you go through as a kid, you are radically more likely to become depressed as an adult. The greater the trauma, the greater your risk of depression, anxiety, or suicide.

Emotional abuse especially, is more likely to cause depression than any other kind of trauma, even sexual molestation. Being treated cruelly by your parents is the biggest driver of depression, out of all these categories.

We have failed to see depression as a symptom of something deeper that needs to be dealt with. There’s a house fire inside many of us, and we’ve been concentrating on the smoke.

CHILDHOOD TRAUMA AND MENTAL ‘ILLNESS’. Beyond the smoke – Johann Hari

from

Lost Connections. Uncovering the Real Causes of Depression and the Unexpected Solutions

by Johann Hari

get it at Amazon.com

OUR EARLIEST EXPERIENCES SHAPE WHO WE ARE. Babies, Their Wonderful World – Dr Guddi Singh * The Six Faces of Maternal Narcissism – Karyl McBride Ph.D.

Love and attention.

One of the most important things that we know about early brain development is that the first two years of life are crucial.

Our brains are literally built on experience from the moment we are born. Experiences help build strong neural pathways between brain cells and allow brain material to expand.

Strong initial attachment bonds are crucial to making a happy secure adult.

Babies aren’t just eating and sleeping machines. Instead, we know they are like mini computers taking in everything that is going on around them.

In the first few months of life, personality traits start to show like caution, or bravery.

Babies who are not exposed to enough stimulation in their environment do not have the chance to develop the ‘hardware’ they need to be effective adults. Our brains are literally built on experience from the moment we are born. Experiences help build strong neural pathways between brain cells and allow brain material to expand. Stress and neglect can also inhibit brain growth because high levels of the stress hormone cortisone inhibits brain cells, although ironically it may encourage the over development of areas that are involved in the fight or flight response, increasing the likelihood that an individual will be prone to anxiety.

When it comes to smart phones and screens in baby cots, the issue is not so much that technology inhibits brain growth but that it causes a problem when it is a stand-in for parental involvement and love. That’s when we see problems when mobile phones and screens are used as babysitters for long periods while carers divert their attention elsewhere. From observational studies, it seems that it interferes with normal attachment and socialisation as well as inhibiting sleep, and the brain needs sleep for normal growth.

Babies who have siblings may benefit from socialisation and to a baby, nothing is funnier than a sibling. But single children can also be stimulated in a busy, challenging environment where they can still get this type of input including in a nursery environment.

The strongest evidence we have about developmental milestones early in life surround attachment theory. It has been shown time and time again that strong initial attachment bonds are crucial to making a happy secure adult. This is why paediatricians advocate close skin to skin contact in the early days and weeks of life. And we know that babies who are separated from a strong parental figure early on can have all sorts of emotional and social problems later in life.

However, that figure does not have to be the parent but can be someone from an extended family or even the community. It is really helpful to look at different cultures and how they parent their kids, there isn’t a one perfect solution and it can be done in different ways. In the west, there is a fetishisation of biological bonds, but adopted or looked after children can benefit from this strong bond as long as it includes love and attention.

Hippocratic Post

Dr Guddi Singh is a paediatrician based at East London NHS Foundation Trust. She is one of the advisers on the new BBC 2 series, Babies – Their Wonderful World. She is a member of the Royal Society of Medicine’s Paediatrics and Child Health Section Council.

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Also on TPPA = CRISIS

The Six Faces of Maternal Narcissism – Karyl McBride Ph.D.

“We Will Change The World , Starting From The Very Beginning.” Building Babies Brains . Criança Feliz, Brazil’s Audacious Plan To Fight Poverty – Jenny Anderson

Life After Severe Childhood Trauma . I Think I’ll Make It. A True Story Of Lost And Found – Kat Hurley

Chronic Childhood Stress And A Dysfunctional Family – Kylie Matthews * Different Adversities Lead To Similar Health Problems – Donna Jackson Nakazawa

How Our Brains Grow – Ruby Wax

The Deepest Well. Healing The Long Term Effects Of Childhood Adversity – Dr Nadine Burke Harris

Childhood Adversity Can Change Your Brain. How People Recover From Post Childhood Adversity Syndrome – Donna Jackson Nakazawa * Future Directions In Childhood Adversity and Youth Psychopathology – Katie A. McLaughlin

Childhood Disrupted . How Your Biography Becomes Your Biology , And How You Can Heal – Donna Jackson Nakazawa * The Origins Of Addiction . Evidence From The Adverse Childhood Experiences Study – Vincent J. Felitti MD.

LOOKING BACK FROM DEATH ROW. A Gunman’s Regret – R. Douglas Fields * Study: Violent aggression predicted by multiple pre-adult environmental hits – Molecular Psychiatry.

Alternative Title: Adverse Childhood Experiences cause Epigenetic changes in the developing young Brain, leading to mental illness, depression, anger management issues, violent crime, incarceration and a multi generational vicious cycle of hopelessness and despair.

With only 5 percent of the world’s population, the United States has 25 percent of the world’s prison population. Why?

This study is the first to provide sound evidence, based on 6 separate cohorts, of a disease independent relationship between accumulation of multifaceted pre-adult environmental hits and violent aggression.

The name “correctional facility” is accurate from society’s perspective, but it is a delusional euphemism from the perspective of most inmates. According to the National Institute of Justice, three quarters of prisoners will be rearrested within five years of their release.

We lock up 7.16 out of 1,000 people in the United States, the highest rate of incarceration in the world.

The explosion of senseless mass violence in places that were once society’s most cherished communal places, schools, concert stadiums, public transportation and even houses of worship, is ripping apart the social fabric of American life.

The roots of violence at the level of brain biology need to be understood so that violence can be prevented.

Researchers have found a high incidence of genetic factors that increase impulsivity and anger in the violent prison population, and also an increased incidence of neurological abnormalities detectable with brain imaging. Studies of twins show that heredity accounts for over 60 percent of the risk for aggression.

The perpetrators of violent crime are almost always male. Humans have evolved through the survival-of-the-fittest struggle in the wild, evolved brain and bodily attributes that equip and predispose them to engage in aggression to provide and protect. This biological drive in males for aggression still exists in modern civilization.

Changes in society and in traditional male roles must be accompanied by new approaches to channel male aggression positively.

This can be reached by a path guided by neuroscience. Males have this biology of aggression for a reason, but it must be adapted to our current environment.

A new study finds that exposure to certain adverse events in early life, while the brain is undergoing maturation, greatly multiplies the odds of being institutionalized as an adult for violent aggression. They include poverty, social rejection from peer groups, cannabis and alcohol abuse, living in an urban environment, traumatic brain injury, immigration, conflict and violence in the home, and physical or sexual abuse.

. . . Scientific American

Molecular Psychiatry: Study

Violent aggression predicted by multiple pre-adult environmental hits.

Early exposure to negative environmental impact shapes individual behavior and potentially contributes to any mental disease. We reported previously that accumulated environmental risk markedly decreases age at schizophrenia onset. Follow up of matched extreme group individuals unexpectedly revealed that high risk subjects had 5 times greater probability of forensic hospitalization.

In line with longstanding sociological theories, we hypothesized that risk accumulation before adulthood induces violent aggression and criminal conduct, independent of mental illness. We determined in 6 independent cohorts (4 schizophrenia and 2 general population samples) pre adult risk exposure, comprising urbanicity, migration, physical and sexual abuse as primary, and cannabis or alcohol as secondary hits. All single hits by themselves were marginally associated with higher violent aggression.

Most strikingly, however, their accumulation strongly predicted violent aggression. An epigenome wide association scan to detect differential methylation of blood-derived DNA of selected extreme group individuals yielded overall negative results. Conversely. detemination in peripheral blood mononuclear cells of histone deacetylasel mRNA as ‘umbrella mediator’ of epigenetic processes revealed an increase in the high risk group, suggesting lasting epigenetic alterations.

Together, we provide sound evidence of a disease independent unfortunate relationship between well defined pre adult environmental hits and violent aggression, calling for more efficient prevention.

Introduction

Early exposure to external risk factors like childhood maltreatment, sexual abuse or head trauma, but also living in urban environment or migration from other countries and cultures, have long been known or suspected to exert adverse effects on individual development and socioeconomic functioning. Moreover, these environmental risk factors seem to contribute to abnormal behavior and to severity and onset of mental illness, even though different risk factors may have different impact, dependent on the particular neuropsychiatric disease in focus. On top of these ‘primary factors‘ that are rather inevitable for the affected, ‘secondary’, avoidable risks add to the negative individual and societal outcome, namely cannabis and alcohol abuse.

Adverse experiences in adulthood, like exposure to violence, traumatic brain injury, or substance intoxication, can act as single triggers to increase the short term risk of violence in mentally ill individuals as much as in control subjects.

However, comprehensive studies, including large numbers of individuals and replication cohorts, on pre-adult accumulation of environmental risk factors and their long term consequences on human behavior do not exist.

In a recent report we showed that accumulation of environmental risks leads to a nearly 10 year earlier schizophrenia onset, demonstrating the substantial impact of the environment on mental disease, which by far outlasted any common genetic effects. To search for epigenetic signatures in blood of carefully matched extreme group subjects of this previous study we had to re-contact them. This reconnect led to the unforeseen observation that high risk subjects had 5 times higher probability to be hospitalized in forensic units compared to low risk subjects.

This finding stimulated the present work: Having the longstanding concepts of sociologists and criminologists in mind, we hypothesized that early accumulation of environmenml risk factors would lead to increased violent aggression and social rule-breaking in affected individuals, independent of any mental illness. To test this hypothesis, we explored environmental risk before the age of 18 years in 4 schizophrenia samples of me GRAS (Göttingen Research Association for Schizophrenia) data collection. Likewise, risk factors were assessed as available in 2 general population samples.

In all cohorts, accumulation of pre-adult environmental hits was highly significantly associated with lifetime conviction for violent acts or high psychopathy and aggression hostility scores as proxies of violent aggression and rule breaking.

As a first small hint of epigenetic alterations in our high risk subjects, histone deacelylasel (HDACI) mRNA was found increased in peripheral blood mono nuclear cells (PBMC).

Fig. 1 Multiple environmental hits before adulthood predict violent aggression in mentally ill subjects as well as in the general population. Results from 6 independent samples.

a – Distribution of forensic hospitalization in the discovery sample (see results) suggested a substantial impact of environmental risk accumulation on violent aggression, a finding replicated in the remaining GRAS sample (GRAS I males and females minus extreme group subjects of the discovery sample). Note the ‘stair pattem’ upon stepwise increase in risk factors; stacked charts illustrate risk factor composition in the respective groups (including all risk factors of each individual in the respective risk group), Each color represents a panicular risk (same legend for dg and jk); b – Brief presentation of the violent aggression severity score, VASS, ranging from no documented aggression to lethal consequences of violent aggression with relative weight given to severity of aggression and number of registered re occurrences. c – Highly significant intercorrelation of violent aggression measures used in the present paper. d – Application of VASS to risk accumulation in the discovery sample; Kmskal Wallis H test (two sided). e-g – Schizophrenia replication cohorts 1: ‘stair pattem‘ of aggression proxy in risk accumulation groups: all 12 test (one sided). h – Comparative presentation of subjects (%) with violent aggression in risk accumulation groups across schizophrenia cohorts. i – Comparative presentation of subjects (%) with violent aggression before (pre morbid, ‘early’) or after schizophrenia onset (‘late‘) vs. individuals without evidence of aggression (‘no’) in risk accumulation groups of the discovery sample. j-k – General population replication cohorts IV and V: ‘stair pattern‘ of aggression proxies, LSRP secondary psy chopathy score (j) and aggression hostility factor of ZKFQ 50 CC (k) in risk accumulation groups; Kruskal Wallis 1 test (one sided). l – HDACI mRNA levels in PBMC of male extreme group subjects as available for analysis; Student‘s t test (one sided).

Discussion

The present work was initiated based on the observation in a schizophrenia cohort that accumulation of environmental risk factors before adulthood promotes the likelihood of later forensic hospitalization, interpreted as indicator of violent aggression. This interpretation and the effect of risk accumulation were consolidated using direct scoring of aggression over lifetime or, as aggression proxies, forensic hospitalization and conviction for battery, sexual assault, manslaughter or murder. or respective psychopathology measures in 4 independent schizophrenia cohorts and 2 general population samples. Importantly, our data support the concept of a disease independent development of violent aggression in subjects exposed to multiple pre adult environmental risk factors.

Whereas a vast amount of literature on single environmental risk factors reports consequences for abnormal behavior and mental illness, publications on pre-adult risk accumulation are scarce and mostly based on closely interrelated social/familial risk factors. Also, risk and consequence are often not clearly defined. Studies including larger, comprehensively characterized datasets and replication samples do not exist.

The present work is the first to provide sound evidence, based on 6 separate cohorts, of a disease independent relationship between accumulation of multifaceted pre-adult environmental hits and violent aggression.

The overall societal damage is enormous, and we note that mentally ill individuals who re-enter the community from prison are even more at risk for unemployment, homelessness, and criminal recidivism. These results should encourage better precautionary measures, including intensified research on protective factors which is still underrepresented.

In the psychosociological literature, the so called externalizing behavior in childhood includes hostile and aggressive physical behavior toward others, impulsivity, hyperactivity, and noncompliance with limit setting. The respective risk factors are all highly plausible, yet often theoretical, and derived from 4 broad domains: child risk factors (e.g., adverse temperament, genetic and gender risk), sociocultural risks (e.g., poverty, stressful life events), parenting and caregiving (e.g., confiict and violence at home, physical abuse), and children’s peer experiences (e.g., instable relationships, social rejection). A full model of the development of conduct problems has been suggested to include at least these 4 domains.

The risk factors analyzed in the present study are perhaps somewhat clearer defined but partially related to and overlapping across these domains. Urbanicity, migration, cannabis and alcohol reflect sociocultural input but also peer experience, and physical or sexual abuse belong to the parenting/caregiver aspect.

Certainly, there are many more, still undiscovered risk and numerous protective factors, potentially explaining why ‘only’ 40-50% of high risk individuals in our schizophrenia samples fulfill criteria of violent aggression.

We note that this study does not include genetic data analysis or correction for any genetic impact. The genetic influence on aggression, however, may be of considerable relevance for the individual, even though highly heterogeneous as for essentially all behavioral traits. Heritability of aggression, estimated from twin studies, reaches >60%. In fact, 50% of individuals with violent aggression upon pre-adult risk accumulation in the present study means another 50% without detectable aggression. This consistent finding across samples likely indicates that genetic predisposition is prerequisite for whichever behavioral consequence. Individuals without genetic predisposition and/or with more protective factors (genetic and environmental) may not react with violent aggression to accumulated environmental risk.

Importantly, the obvious gender effect may be a matter of degree rather than of pattern. In fact, the etiology of externalizing behavior problems is similar for girls and boys, as is the consequence of risk accumulation in the present study for males and females.

The risk factors of the sociological domains seem to be stable predictors over time, to some degree interchangeable, pointing to many pathways leading to the same outcome (principle of equifinality). The interchangeability is highly interesting also with respect to potential biological mechanisms. It appears that any of the here investigated hits alone, independent of its kind, can be compensated for but that higher risk load increases the probability of violent aggression.

Also for that reason, we are weighing risk factors equally in the present study. This could theoretically create some bias. However, to be able to estimate the true effect size of each specific factor separately on violent aggression and subsequently weigh all factors in a more proper way, much larger samples sizes would be needed that are presently not available anywhere in the world.

In contrast to the marginal influence of genome wide association data on mental disease in GRAS, the accumulated environmental impact on development of violent aggression is huge, reflected by odds ratios of >10. When striking at a vulnerable time of brain development, namely around/before puberty, the environmental input may ‘non specifically’ affect any predisposed individual. The hypothetical biological mechanisms underlying this accumulation effect in humans may range from alterations in neuroendocrine and neurotransmitter systems, neuronal/ synaptic plasticity and neurogenesis to changes in the adaptive immune system and interference with developmental myelination, affecting brain connectivity and network function.

Our approach to detect methylation changes in blood using an epigenome wide association scan was unsuccessful despite matched extreme group comparison, likely due to the small sample size, and perhaps the etiological/pathogenetic complexity of accumulated risks. Changes in brain, not accessible here for analysis, can certainly not be excluded. Interestingly, however, HDAC1 mRNA levels in PBMC of male extreme group subjects were increased in the high risk compared to the low risk group. This finding confirms peripheral HDAC1 mRNA levels as a more robust readout of epigenetic alterations in relatively small sample sizes, as compared to specific methylation sites in epigenome wide association scans or even in candidate genes. To gain further mechanistic insight and thereby develop in addition to prevention measures novel individualized treatment concepts, animal studies modeling risk accumulation seem unavoidable.

To conclude, this study should motivate sociopolitical actions, aiming at identifying individuals at risk and improving precautionary measures. Effective violence prevention strategies start early and include family focused and school based programs. Additional risk factors, interchangeable in their long term consequences, like urbanicity, migration, and substance abuse, should be increasingly considered. Health care providers are essential for all of these prevention concepts. More research on protective factors and resilience should be launched. Animal studies need to be supported that model risk accumulation for mechanistic insight into brain alterations leading to aggression, and for developing new treatment approaches, also those targeting reversal of epigenetic alterations. As a novel concept, scientific efforts on ‘phenaryptyping of the environment’, should be promoted to achieve more fundamental risk estimation and more effective prevention in the future.

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Read the complete study here: Violent aggression predicted by multiple pre-adult environmental hits

BULLYING! This is my child – Carrie Golledge.