Category Archives: Justice & Prisons

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

The way we punish crime adds to our prison bill – Julia Fyers.

Only the US has more of its population locked up per capita than New Zealand. Opting for more home detention would save a lot of money.

New Zealand has the second highest rate of imprisonment in the world. The only country with more of its population behind bars per capita is the USA and they’ve acknowledged it’s a problem. We are on par with third world countries with our population of prisoners.

This should be a source of great international shame for our country. Importantly though, the problem is not crime, it’s punishment.

Penal populism drives the social and financial disaster that is our prison problem. Criminal justice policies have escalated wildly in response to voters’ supposed desire for increased punishment of crime.

As tax payers, how our money is being spent should be of importance to us. The costs of running New Zealand’s 18 prisons are enormous. The public need to know the actual cost of prisons and imprisonment, and make an informed decision on whether a “tough on crime” stance is worth it.

Here’s some numbers: The operational cost of keeping one person in prison for one year is in excess of $120,000. Currently, we have 10,695 prisoners. This means the cost of our prisons is more than $1.28 billion a year.

Then there are the added capital costs of building and maintaining prisons. To give one recent example, the proposed expansion to Waikeria Prison is forecast to cost $1 billion.

Perhaps more importantly though, there are the inter-generational health and social costs of having a system that doesn’t work.

It is a common misconception that prison deters crime and that the best approach to offending is to “lock them up and throw away the key”. Lobby groups such as the highly unsensible Sensible Sentencing Trust appeal to that sentiment.

Thankfully, current sentencing laws don’t make this possible (much to the relief of the New Zealand taxpayer). Inevitably, prisoners are released back into the community.

However, in addition to the costs of incarceration, further avoidable social and health costs occur after release. Convicted criminals have the stigma of a criminal record, potential media attention around their offending and a gap in their employment history.

Although the Government spent $181 million on prisoner reintegration in 2017, it is unsurprising that, after 12 months of release, 31.2 per cent were back in prison.

We can’t stop crime, but we can change the way we punish it.

Two thirds of prisoners have addiction issues which remain untreated in prison. Rehabilitation programmes in prison don’t work because they are not transferable to a community setting.

Prisoners are released with $350 from Winz, no job, no home, no transferable life skills and nowhere safe to go. It doesn’t take a rocket scientist to work out what is likely to happen next.

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If we want to make our communities safer, we need to give offenders the tools they need to stop the cycle of crime.

Compare the cost of all this to the cost of keeping one person on electronic monitoring for one year around $40,000.

Home detention is no walk in the park. You are confined to the perimeters of your property 24/7. As your sentence progresses, you may earn the right to attend drug and alcohol counselling for a couple of hours a week or to go to the gym for two hours a week.

Besides that, you are confined to the four walls of your home. Towards the end of your sentence, you may be allowed four hours of social leave a fortnight. Some electronic monitoring has the capability to alert probation if drugs (including alcohol) are being consumed. Your every move is monitored by a GPS tracker.

Another benefit of this type of sentencing is that the offender is able to work, if he or she is lucky enough to find a supervisor to vouch for him. This means actual reparation can be made to victims, as opposed to $2 per week from a prisoner. Community sentences have the benefit of allowing an offender to stay within society whilst ensuring the public are kept safe, at a fraction of the price.

To deter crime, people need tools that enable them to reconnect with society. Downsizing prisons will free up money to be redirected to where it will help reduce the continuing cost of people who have been damaged and marginalised by the prison system. Remember, one third are back in prison within 12 months of release.

Addiction causes crime, and the opposite of addiction is connection. Offenders need to be reconnected to society with jobs, social inclusion, positive relationships and help with the issues that caused them to offend in the first place.

Decreasing the prison population will not increase crime or risk to public safety. It is time to stop the nonsense, end the war on drugs and create evidence based policies. Rather than more prisons and prisoners, increased management of electronically monitored offenders could help reduce recidivism. An extension of clean slate legislation could remove the stigma which can prevent an offender’s economic reconnection.

You wouldn’t buy a billion dollar house if it was eventually going to fall off a cliff, so why are we willing to make an investment that we know is going to fail?


Julia Fyers has a masters degree in law and is a legal researcher, working on issues of human rights and drug and prison policy reform.

Dr Jarrod Gilbert: Bill English faces tough job shifting the ‘lock ’em up’ penal policy

For a number of years Bill English has quietly championed a prison reform approach that should appeal to fiscal conservatives and social liberals alike. As prime minister, he now needs to sell it.

At stake is a billion dollar spend on a new prison caused by a prison population that recently hit 10,000. With an election year on the doorstep, that’s money English would rather employ elsewhere.

In 2012, the government and the Department of Corrections set a bold target of reducing reoffending by 25per cent by 2017.

They are going to fall well short. Undoubtedly, many people will make a big deal of that failure, and perhaps that’s reasonable, but it ought be applauded for its bold intent.

It was the ambition of the target that challenged corrections staff – from policy analysts to prison guards – to fundamentally rethink what they were doing. Instead of simply containing prisoners until their release, they were instructed to think about creating an environment and initiatives that rehabilitate them.

NZ Herald