4.4.2 Abnormalities in Foetal Development
Minor physical anomalies (MPAs) can occur in some individuals, such as having a curved fifth finger, a single palmar crease, low-seated ears or a furrowed tongue, which are thought to arise from abnormalities in foetal development. These may have a genetic basis, but they might also be due to anoxia, bleeding or infection (Guy, Majorski, Wallace, & Guy, 1983). Studies have indicated that there is a correlation between MPAs and aggressive behaviours in children as young as three years of age (e.g., Waldrop, Bell, McLauglin, & Halverson, 1978). There is also an increased prevalence of MPAs in school-aged boys exhibiting behavioural problems (e.g., Halverson & Victor, 1976); specifically, MPAs identified at age 14 predict violence at age 17 (Arsenault, Tremblay, Boulerice, & Saucier, 2002). Pine, Shaffer, Schonfield, and Davies (1997) found that the presence of MPAs significantly interacted with other adverse life experiences (see Box 4.4), such as marital conflict and poverty leading to physical neglect, to predict conduct problems in adolescence. As for the relationship with adult offending, Brennan, Mednick, and Raine (1997), in a study of 72 male offspring of psychiatrically ill parents, found that those with both MPAs and family adversity, had especially high rates of adult violent offending.
4.4.3 Other Prenatal Risk Factors
4.4.3.1 Maternal alcohol, tobacco and drug use
The estimated rate of drug use for pregnant women in the US is 13.8% for alcohol, 17.7% for tobacco, and 3.4% for illegal drugs (Lester, Andreozzi & Appiah, 2004). We will now examine the effects of these teratogens on the foetal brain, and the research that suggests a link with these perinatal risk factors and offending sequalae.
Foetal alcohol sydrome (FAS)/foetal alcohol spectrum disorder (FASD) can arise due to excessive alcohol use in pregnancy, as alcohol is clearly a teratogen.
The term teratogen describes any agent that disturbs the development of an embryo or foetus. Teratogens may cause a birth defect in the child. Teratogens include maternal infections, chemicals, and alcohol, tobacco and illegal drugs.
Full blown FAS does not arise in all children exposed in utero, but children who do not display the full FAS syndrome can still have some of the functional deficits characteristic of the syndrome (Schonfeld, Mattson, & Riley, 2005), and there are a range of problems. Foetal alcohol spectrum disorder (FASD) is the umbrella term used to describe this spectrum of abnormalities, with FAS lying at the most severely affected end of the spectrum. FASD arises because the developing foetus does not process alcohol the same way as an adult, and hence it is more concentrated in the foetus. This concentration of alcohol can prevent enough nutrition and oxygen from getting to the foetus’ vital organs, particularly the brain. Particular areas that are the most vulnerable include the hippocampus (an area of the brain to do with memory), the basal ganglia and the corpus callosum (the band of fibres that connect the two cerebral hemispheres).
FASD, as well as having physical effects, also produces major psychological problems such as: behavioural and emotional regulation problems (outbursts, rigidity, defiance, depression, anxiety, attachment issues and generally being difficult); attentional problems (i.e. inattention, hyperactivity and poor impulse control); intellectual disability (ranging from mild to severe); immaturity (here overall performance can be equivalent to children of half the individual’s age); language delays (e.g., poor receptive language, slowness of processing verbal instructions); memory issues; and executive functioning issues (i.e. a lack of abstract reasoning and linking actions to consequences, poor problem-solving skills). Alcohol appears to be most harmful to the foetus during the first trimester, when a woman might not yet know that she is pregnant. The risk increases if the mother is a heavy drinker; in fact, binge drinking (6+ units of alcohol, which equates to two glasses of wine, is defined as binge drinking) is a particular risk factor. However, consumption of alcohol at any time during pregnancy can be harmful.
There is a great deal of evidence that FASD predisposes individuals to antisocial behaviour (e.g., Olson et al., 1997; Roebuck, Mattson, & Riley, 1999). For example, Streissguth, Barr, Kogan, and Bookstein (1996), in a study of 400 adolescents and adults with FASD, found that 60% had been in trouble with the law and 50% exhibited (unwanted) sexual behaviour, while 30% reported alcohol/drug problems. Other evidence suggests that individuals with FASD are at high risk of coming into repeated contact with the criminal justice system both as victims and offenders (e.g., Boland, Chudley & Grant, 2002; Chartrand & Forbes-Chilibeck 2003; Streissguth & Kanter 1997). As for the prevalence of these problems in forensic populations, the lifetime prevalence of FASD in incarcerated populations was 32% for adolescents, and 42% for adults (Streissguth & Kanter 1997), in the USA, while the prevalence of FASD among a sample of adult male offenders entering a federal correctional facility in Canada was 10% in a study reported by MacPherson and Chudley (2007).
PHOTO 4.2 The greater the amount of smoking by the mother during pregnancy, the greater the risk of criminality for the child in later life.
Source: © Zurijeta/Shutterstock
In terms of maternal smoking, extensive human and animal studies have noted that the 7000+ chemicals contained in cigarettes can easily cross the placental barrier and hence have a harmful effect upon the foetus’ brain (e.g., British Medical Association, 2004; Rogers, 2009). Specifically, Hackshaw, Rodeck, & Boniface (2011) note that in the UK 3,759 babies were born with non-chromosomal congenital abnormalities associated with smoking in 2008, while maternal smoking is an established risk factor for miscarriages, perinatal mortality, low birth weight and premature birth (Hackshaw et al., 2011). The specific mechanisms are that cigarette smoke interferes with normal placental function, acting as a vasoconstrictor to reduce uterine blood flow. Hence, the foetus is deprived of oxygen and nutrients (Ganapathy, Prasad, Ganapathy & Leibach, 2000). Cigarette smoke also acts as a neuroteratogen (i.e. specifically affecting the nervous system). Nicotine targets the nicotinic acetylcholine receptors in the foetus’s brain to change the pattern of cell proliferation and differentiation (synaptogenesis/synaptic pruning), and causes abnormalities in the development of synaptic activity. Additionally, the by-products of smoking (such as hydrogen cyanide and carbon monoxide) may affect the brain’s dopaminergic and noradrenergic systems (Muneoka et al., 1997), as well as glucose metabolism, (Eckstein, Shibley, Pennington, Carver, & Pennington, 1997). Maternal smoking can also have an affect upon various brain structures including the cerebral cortices (Olds, 1997; Raine, 2002).
There is a significant body of evidence that demonstrates that maternal smoking predisposes children toward developing antisocial behaviour (Wakschlag, Pickett, Cook, Benowitz, & Leventhal, 2002). For example, prenatal smoking predicts externalising behaviours in childhood, and criminal behaviour in adolescence (Fergusson, Woodward, & Horwood, 1998; Orlebeke, Knol, & Verhulst, 1997; Wakschlag et al., 1997). Researchers have also identified a clear dose-dependent relationship between smoking and later criminal behaviour, in that a high level of smoking during pregnancy predicts higher risk of criminality in later life for the child (Brennan, Grekin, & Mednick, 1999; Maughan, Taylor, Caspi, & Moffitt, 2004).
4.4.3.2 Prenatal malnutrition
Although most studies have focused on nutrition in the post-natal period, one study investigated the role of malnutrition in the prenatal period. Here, Neugebauer, Hoek, and Susser (1999) examined the children of women who were pregnant during the German food blockade of Dutch cities in World War II. The blockade produced near starvation and severe food shortages at the time. The researchers found that the male offspring of women who were in the first and second trimesters of pregnancy during this time had 2.5 times the rate of antisocial personality disorder than the offspring of women who were not affected by food shortages. Another study of prenatal nutrition, reported by Hibbeln et al. (2007), examined a sample of 11,875 pregnant women, and their consumption of fatty acids. Adequate intake of omega-3 fatty acids such as eicosapentaenoic acid and docosahexaenoic acid, and vita
min D, are all important for cognitive functioning (Perica & Delas, 2011; Przybelski & Binkley, 2007). Pregnant women who ate food less rich in omega-3 fatty acids (i.e. less than 340 grams a week), had children that demonstrated significantly lower scores on a number of neurodevelopmental outcomes, including more antisocial behaviour, than the children of mothers who consumed more omega-3 rich food.
4.4.4 Perinatal Risk Factors
There are a number of risk factors that can happen around the period of childbirth. These include: maternal pre-eclampsia (a medical condition in which hypertension arises in pregnancy); premature birth; low birth weight: use of forceps in delivery leading to anoxia (absence of oxygen to the brain) and hence transfer to a neonatal intensive care unit; and low Apgar scores.
An Apgar score (developed by Virginia Apgar, 1953) is a measure of the physical condition of a newborn infant. It is obtained by adding points (0, 1, 2) for: (a) heart rate, (b) respiratory effort, (c) muscle tone, (d) response to stimulation and (e) skin coloration. A score of 10 represents the best possible condition of the infant.
Such maternal complications have been shown to have deleterious effects on neonatal brain function in that newborn babies who suffer obstetrical complications are also more likely to exhibit externalising behaviours at age 11 than those without complications (Liu 2004; Liu & Wuerker, 2005).
Obstetric complications were found to mediate the relationship between low IQ and externalising behaviours (Liu, Raine, Wuerker, Venables, & Mednick, 2009). For example, Raine, Brennan, and Mednick (1994) investigated a cohort of 4,269 Danish men and found that obstetrical complications significantly interacted with severe maternal rejection (such as efforts to terminate the pregnancy, reporting the pregnancy as unwanted, or attempting to give up custody of the baby) to predict violent crime in adolescence. These findings have since been replicated in the United States, Sweden, Finland and Canada, where it has been also been found that birth complications interact with a number of psychosocial risk factors, and are related to later antisocial behaviours (e.g., Hodgins, Kratzer, & McNeil, 2001; Kemppainen, Jokelainen, Jarvelin, Isohanni, & Rasanen, 2001; Tibbetts & Piquero, 1999).
4.4.5 Post-natal/childhood Risk Factors
These risk factors can include a high level of adverse childhood experiences, poor nutrition, and traumatic brain injury. We will now examine these.
4.4.5.1 Poor nutrition
Poor nutrition has been investigated as a risk factor for criminal behaviour (Breakey, 1997; Werbach, 1995). The exact mechanism by which malnutrition later affects antisocial behaviour is not well understood, but it is hypothesised that proteins, or minerals, may either regulate neurotransmitters and hormones, or ameliorate neurotoxins (Liu & Raine, 2006). Studies have also shown that deficiencies in nutrients such as proteins, zinc, iron and docosahexaenoic acid (a component of omega 3 fatty acid) can lead to impaired brain functioning and a predisposition to antisocial behaviour in childhood and adolescence. Liu and Raine (2006), found that children with protein, iron or zinc deficiencies at age 3 had significantly more aggressive and hyperactive behaviour at the age of 8, more antisocial behaviour at age 11, and more excessive motor activity and conduct disorder at age 17, compared to controls. Significantly, this study also found a dose-dependent relationship between the extent of malnutrition and the extent of later behaviour problems. While longitudinal studies have also shown that malnutrition in infancy is associated with aggressive behaviour, and attentional deficits in childhood (e.g., Galler & Ramsey, 1989; Galler, Ramsey, Solimano, & Lowell, 1983).
4.4.5.2 Adverse childhood experiences (ACEs)
Ten adverse childhood experiences (ACEs) have been formally defined by Felitti et al. (1998) as being predictive of chronic disease / s in adulthood, and in offenders. These are shown in Box 4.4.
BOX 4.4 ADVERSE CHILDHOOD EXPERIENCES (ACES)
Recurrent physical abuse
Recurrent emotional abuse
Contact sexual abuse
There is substance abuse taking place within the home
A household member is in prison
Household mental illness
Family violence (typically to the mother from a partner)
Parental separation/divorce
Physical neglect
Emotional neglect
An ACE score of 1 is given if the ACE is present, and zero for its absence, therefore a maximum ACE score will be 10. People with high ACE scores are more likely to be violent and to have more marriages, more broken bones, more drug prescriptions, more depression and more autoimmune diseases. Having an ACE score of 4 increases the risk of suicide by a factor of 12, and high ACE scores have also been linked with risky sexual behaviours, such as engaging in sexual activity prior to the age of 15, teenage pregnancy and/or having 50 or more sexual partners (Hillis et al., 2004).
Being subject to a number of ACEs has also been identified with immediate negative consequences such as structural and functional changes in the developing brain. Structural changes can include reduced size of the mid-portions of the corpus callosum and attenuated development of the left neocortex, hippocampus and amygdala (Teicher et al., 2003), while functional consequences include increased “electrical irritability” in the limbic structures of the brain (Teicher et al., 2003). Other evidence suggests that chromosomal damage can also occur due to the effects of ACEs, such as telemore erosion (associated with cellular aging, disease and morality in later life) (Shalev et al., 2013).
Telomeres are an essential part of human cells that affect how our cells age, and are the caps at the end of each strand of DNA that protect chromosomes, rather like the plastic tips at the end of shoelaces.
As for the incidence of ACEs in offender populations, recent data from the Ministry of Justice in England and Wales (Williams, Papadopoulou, & Booth, 2012), based on 1,435 newly sentenced prisoners (in the years 2005 and 2006) are shown in Box 4.5, together with ACE indications.
BOX 4.5 OFFENDERS’ PROBLEMATIC CHILDHOODS
Nearly a third of all prisoners (29%) reported that they had experienced some form of abuse/neglect in childhood (ACE 1, 2, 9, 10).
A number (41%) had observed violence in the home as a child – particularly those who stated that they had a family member with an alcohol or drug problem (ACE 7).
18% stated that as a child they had a family member with an alcohol problem (ACE 4).
14% stated that as a child they had a family member with a drug problem (ACE 4).
Over a third (37%) reported having family members who had been convicted of a serious crime, of whom 84% had been in prison or a young offenders’ institution (ACE 5).
24% said that they had been in care at some point during their childhood (aspect of ACE 8).
It can be seen from Box 4.5, that all of the ACEs (apart from a family member being chronically depressed, and being subject to contact sexual abuse) can be seen in this sample. Specifically, we would note that: nearly a third of the sample reported having experienced some sort of abuse in childhood; nearly half had observed violence in the home where they were brought up; 20% had a family member with an alcohol problem; and 14% had a family member with a drug problem. Similar results have been found in a study of 64,329 juvenile offenders in Florida, USA by Baglivio et al. (2014). They found that two-thirds of the sample reported family violence, parental separation and household member incarceration (ACEs 1, 5, 8). There was also a clear relationship with the number of ACEs and the number of negative outcomes, in terms of level of offending. Case Study 4.1 provides an example of a young man who committed a homicide in the United States, whose background clearly shows evidence of many of the ACEs outlined in Box 4.5
CASE STUDY 4.1 D.P.
A young woman was murdered in her own home in the United States, after a brutal physical assault. The murderer was identified as D.P., a 24-year-old man with a prior history of violent crime. His defence team did not deny that he committed the murder, but argued that the crime was impulsive and opportunistic. Afte
r the jury found D.P. guilty of first- degree murder, information was provided at the sentencing portion of his hearing to try to mitigate the sentence in order to avoid execution by lethal injection. Information from D.P.’s history reported at least six adverse childhood risk factors (ACEs), in that:
he was born to a single, teenage mother (ACE 8: one parent)
he had been admitted five times in the first two years of his life to hospital for injuries related to having been shaken violently for crying too much (ACE 1: recurrent physical abuse)
he was noted to have eaten paint chips as a baby (ACE 9: physical neglect)
his later childhood medical history revealed treatment for severe physical and sexual abuse (ACE 1 & 3: recurrent physical/contact sexual abuse)
social services records reported that his mother was frequently absent (ACE 10: emotional neglect)
he often slept in abandoned buildings in a dangerous, inner-city environment as a child (ACE 9: physical neglect).
As for the consequences of these ACEs, neuropsychological testing revealed that D.P. had notable executive functioning deficiencies, due to dramatic reductions in activity in his bilateral prefrontal cortices. Due to the combined influence of these biopsychosocial risk factors, D.P. was spared the death sentence and was instead given a life sentence.
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