Sunday, July 27, 2014

Sarah Kovac - Spanking the Gray Matter Out of Our Kids

New research shows that spanking or other forms of corporal punishment can alter children's brains, particularly manifested in decreased gray matter in prefrontal cortexes, areas of the brain that are linked to depression, addiction, and executive function.

I was spanked both at home and in school (in Oregon, not Southern California), actually more often at school than at home. I wonder what impact that had on some of my addiction issues as a teen and young adult.

Spanking the gray matter out of our kids

By Sarah Kovac, Special to CNN
Wed July 23, 2014

The more you physically punish your children for their lack of self-control, the less they have, Sarah Kovac says.

  • Spanking or other forms of corporal punishment can alter children's brains, research shows
  • Kids who were regularly spanked had less gray matter in prefrontal cortexes, studies say
  • These areas of the brain have been linked to depression, addiction
Editor's note: Sarah Kovac is a motivational speaker and author of "In Capable Arms: Living a Life Embraced by Grace." The opinions expressed are solely the author's.

(CNN) -- How to discipline the next generation is a hotly debated topic. In 2012, a national survey showed more than half of women and three-quarters of men in the United States believe a child sometimes needs a "good hard spanking."

Science tells a different story. Researchers say physical punishment actually alters the brain -- not only in an "I'm traumatized" kind of way but also in an "I literally have less gray matter in my brain" kind of way.

"Exposing children to HCP (harsh corporal punishment) may have detrimental effects on trajectories of brain development," one 2009 study concluded.

Harsh corporal punishment in the study was defined as at least one spanking a month for more than three years, frequently done with objects such as a belt or paddle. Researchers found children who were regularly spanked had less gray matter in certain areas of the prefrontal cortex that have been linked to depression, addiction and other mental health disorders, the study authors say.

The researchers also found "significant correlations" between the amount of gray matter in these brain regions and the children's performance on an IQ test.

Several other studies support these findings. A 2010 study published in Pediatrics found that frequent -- more than twice in the previous month -- spanking when a child was 3 was linked to an increased risk for higher levels of child aggression when the child was 5.

Another, from the Journal of Aggression, Maltreatment and Trauma, found that corporal punishment doled out from the mother was independently related to a decrease in cognitive ability relative to other children. Corporal punishment had the largest effect on children 5 to 9.

Behind all this science-speak is the sobering fact that corporal punishment is damaging to children. That gray matter we've been spanking out of them? It's the key to the brain's ability to learn self-control.

"The more gray matter you have in the decision-making, thought-processing part of your brain (the prefrontal cortex), the better your ability to evaluate rewards and consequences," write the authors of a 2011 study that appeared in the Journal of Cognitive Neuroscience.

The sad irony is that the more you physically punish your kids for their lack of self-control, the less they have. They learn how to be controlled by external forces (parents, teachers, bosses), but when the boss isn't looking, then what?

Elizabeth Gershoff, an associate professor at the University of Texas at Austin, has been studying corporal punishment for 15 years, and is known as the leading researcher on spanking in the United States today. Over the years, Gershoff has done a systematic review of the hundreds of studies on the effects of corporal punishment.

"There's no study that I've ever done that's found a positive consequence of spanking," Gershoff said. "Most of us will stop what we're doing if somebody hits us, but that doesn't mean we've learned why somebody hit us, or what we should be doing instead, which is the real motive behind discipline."

Initially it was believed that spanking, at the very least, was associated with immediate compliance in children, and that parental warmth would buffer any harmful effects.

But the finding that spanking produced compliance "was overly influenced by one study," Gershoff said; it turns out spanking "doesn't make your kids better behaved. You think it does. ... It doesn't."

What is spanking associated with? Aggression. Delinquency. Mental health problems. And something called "hostile attribution bias," which causes children, essentially, to expect people to be mean to them.

This bias makes the world feel especially hostile. In turn, children are on edge and ready to be hostile back. Over time, across cultures and ethnicities, the findings are consistent: Spanking is doing real, measurable damage to the brains of our children.

And yet in 19 states, Gershoff notes, it is still legal for schools to paddle children.

For those thinking, "I was spanked, and I turned out fine," or, "I spank my kids and they're great!" consider that you don't know who you would be or how your children would behave in a world without spanking.

It could be that your children are thriving not because you spank, but in spite of it.


Kansas lawmaker pushes spanking bill

Study: Spanking may cause mental issues

Does corporal punishment work?

* * * * *

This is an older study (2009) that showed the same basic results in young adults as were shown in younger children in the new study.

Corporal punishment needs to be abolished completely.

Full Citation:
Tomoda, A,  Suzuki, H, Rabi, K,  Yi-Shin Sheu, YS, Polcari, A, and Teicher, MH. (2009, Mar). Reduced Prefrontal Cortical Gray Matter Volume in Young Adults Exposed to Harsh Corporal Punishment. Neuroimage; 47(Suppl 2): T66–T71. doi:  10.1016/j.neuroimage.2009.03.005

Reduced Prefrontal Cortical Gray Matter Volume in Young Adults Exposed to Harsh Corporal Punishment

Akemi Tomoda, MD, PhD, Hanako Suzuki, MA, Keren Rabi, MA, Yi-Shin Sheu, BS, Ann Polcari, PhD, and Martin H. Teicher, MD



Harsh corporal punishment (HCP) during childhood is a chronic, developmental stressor associated with depression, aggression and addictive behaviors. Exposure to traumatic stressors, such as sexual abuse, is associated with alteration in brain structure, but nothing is known about the potential neurobiological consequences of HCP. The aim of this study was to investigate whether HCP was associated with discernible alterations in gray matter volume (GMV) using voxel-based morphometry (VBM).


1,455 young adults (18–25 years) were screened to identify 23 with exposure to HCP (minimum 3 years duration, 12 episodes per year, frequently involving objects) and 22 healthy controls. High-resolution T1-weighted MRI datasets were obtained using Siemens 3T trio scanner.


GMV was reduced by 19.1% in the right medial frontal gyrus (medial prefrontal cortex; MPFC, BA10) (P = 0.037, corrected cluster level), by 14.5% in the left medial frontal gyrus (dorsolateral prefrontal cortex; DLPFC, BA 9) (P = 0.015, uncorrected cluster level) and by 16.9% in the right anterior cingulate gyrus (BA 24) (P < 0.001, uncorrected cluster level) of HCP subjects. There were significant correlations between GMV in these identified regions and performance IQ on the WAIS-III.


Exposing children to harsh HCP may have detrimental effects on trajectories of brain development. However, it is also conceivable that differences in prefrontal cortical development may increase risk of exposure to HCP.

Keywords: corporal punishment (CP), harsh corporal punishment (HCP), voxel-based morphometry (VBM), gray matter volume (GMV), medial prefrontal cortex (MPFC), dorsolateral prefrontal cortex (DLPFC), anterior cingulate gyrus (AC), MRPFC (medial rostral prefrontal cortex)


Corporal punishment (CP) has been defined as “the use of physical force with the intention of causing a child to experience pain but not injury for the purpose of correction or control of the child’s behavior” (Straus et al., 1997). However, such discipline (or its excessive use) has been considered as a type of child maltreatment and has been identified as having various negative psychological and physiological consequences. A history of exposure to severe CP is reportedly associated with aggression, delinquency (Gershoff, 2002), antisocial and violent behaviors (Ambati et al., 1998; Ohene et al., 2006; Slade and Wissow, 2004; Straus et al., 1997), depression (Banks, 2002; Straus and Kantor, 1994), suicidal behavior (Straus and Kantor, 1994), and other psychiatric disorders such as PTSD (Medina et al., 2001) and substance abuse (Lau et al., 2005). Furthermore, CP is related to the intergenerational transmission of intimate partner and family violence (Deater-Deckard et al., 2003; Muller et al., 1995; Schwartz et al., 2006) and is associated with risk of being victim of physical abuse and risk of abusing one’s own child or spouse (Gershoff, 2002).

Exposure to various forms of childhood abuse, including physical abuse, sexual abuse and neglect have been associated with alterations in brain structure (e.g., (Andersen et al., 2008; Bremner et al., 1997; De Bellis et al., 1999; De Bellis et al., 2002; De Bellis and Kuchibhatla, 2006; Richert et al., 2006; Teicher et al., 2004; Teicher et al., 1997)). Diffusion tensor differences have also been observed in young adults with high-level exposure to parental verbal abuse (Choi et al., 2008).

Is exposure to parental CP a sufficiently severe developmental stressor to be associated with discernible effects on brain morphometry? To address this question we chose to examine exposure to a form of CP that is widely considered to be excessive and unacceptable. The American Academy of Pediatrics (AAP) considers spanking with an open hand for the purpose of behavior modification to be an acceptable form of punishment. However, this form of punishment becomes unacceptable if it involves use of an object, extends to regions beyond buttocks and extremities, is conducted out of anger, or results in injury. We defined harsh CP (HCP) as a severe form of CP, in which an object (e.g., belt, paddle, hair brush) was used on occasion for the purpose of disciplining a child, provided it did not extend beyond the buttocks, was not conducted out of anger, and did not result in injury. We focused on HCP rather than ordinary CP, which is much more common, hypothesizing that HCP would be associated with a stronger signal and more discernible effects. If associations emerged between imaging findings and HCP it would justify studies in a larger group of subjects exposed to ordinary CP.

This study was designed to evaluate GMV using an unbiased, whole-brain, voxel-by-voxel approach in a non-clinical sample of late adolescents/young adults exposed to HCP during childhood. Our sample was screened to exclude extraneous factors (e.g., substance abuse, head injury, fetal drug exposure, exposure to physical, sexual or emotional abuse) that might have influenced brain development. We hypothesized that exposure to childhood HCP might alter the developmental trajectory of brain regions involved in regulating emotion, aggression, attention, and cognition.


1. Participants and procedure

The McLean Hospital Institutional Review Board approved all procedures. Participants in the study were recruited from the community through an advertisement entitled “Memories of Childhood”. Screenings were conducted on 1,455 volunteers using a detailed online assessment instrument with 2,342 entry fields that provided a vast array of information regarding childhood history, development, and symptomatology. The questionnaire also included demographic information, such as subjects’ and parents’ educational levels, annual household income, and race/ethnicity. In addition, a scale was included to assess subjects’ perception of financial stress while they were growing up. Known as ‘perceived financial sufficiency’ and based on a 5-point Likert scale, subjects rated their family’s financial situation while growing up, which ranged from 1 (much less than enough money for our needs), to 5 (much more enough money for our needs). Subjects provided written informed consent prior to completing the online instrument, and again before interviews and imaging.

Eligible subjects were invited for three visits. The first visit constituted a face-to-face interview to elicit subjects’ developmental history and history of psychiatric disorders using Structured Clinical Interviews for DSM-IV Axis I and II Disorders (SCID-I, II) (First et al., 1997). The second visit consisted of standardized psychometric testing such the Wechsler Adult Intelligence Scale III (WAIS-III) (Wechsler, 1997), the Woodcock-Johnson Test, and the Memory Assessment Scale (Golden et al., 1999). Finally, we recruited 45 individuals (23 subjects with CP and 22 controls) for MRI evaluation.

The HCP group contained 23 young adults (15 males, 8 females; mean age, 21.7 years, SD, 2.2 years) with a history of exposure to CP in early childhood (Table 1) that occasionally involved use of objects. The control group comprised 22 young adults (6 males, 16 females; mean age, 21.7 years; SD, 1.8 years) with neither a current nor past DSM-IV-TR Axis I disorder (based on the SCID-I). Controls had no history of abuse nor exposure to traumatic events, HCP, or more than minimal exposure to ordinary CP. Subjects were excluded who had any history of substance abuse, any recent substance use, head trauma with loss of consciousness, significant fetal exposure to alcohol or drugs, perinatal or neonatal complications, neurological disorders, or medical conditions that might adversely affect growth and development. All participants were right-handed and unmedicated. HCP and controls were matched as closely as possible for degree of alcohol and substance use.
Table I
Table I - Demographics and subject characteristics for VBM Comparisons (click the link to enlarge)
2. Measure

2.1. Harsh Corporal punishment and other trauma

History of exposure to CP was obtained using the Life Experiences Questionnaire (LEQ) as part of the on-line assessment and through the face-to-face interview. The LEQ consisted of 34 items that screen for exposure to traumatic events in general (e.g., witnessing gang violence, nearly drowning). Questions about parental CP are included in this questionnaire (e.g., “Have you ever been punished with spankings from your parents’ open hand?” “Have you ever been punished with spankings with a belt, paddle, or stick?”). The LEQ was used to identify potential subjects. Degree of exposure was evaluated through a detailed semi-structured interview, which explored the ways in which they were disciplined throughout childhood. The criteria for inclusion in the HCP group was CP that began prior to their 12th birthday and lasted for at least 3 years, with a frequency of about 12 episodes or more per year. Additionally, an object such as belt, strap, hairbrush, or paddle was used for punishment more or less annually. HCP subjects must have experienced these punishments from a primary disciplinarian who was a custodial adult. Subjects who either had never received CP or had only minimal exposure, and were never struck with objects were classified into the control group. Moreover, we were careful to exclude instances of physical abuse, emphasizing that CP had to occur specifically for discipline, with parents in emotional control, and not striking out in anger. Any intentional injury that received, or should have received medical attention, or left a scar was considered abuse. So was any painful physical contact other than to the buttocks or extremities, save potentially for a rare open handed slap to the face. A panel of three doctoral-level psychiatric clinicians with extensive experience treating children, who were blind to any of the neuroimaging results, reviewed the disciplinary history of each subject. Assignments were made to groups by full consensus.

History of exposure to no other forms of abuse were confirmed using the semi-structured Traumatic Antecedents Interview (Herman et al., 1989). Exposure to childhood verbal abuse was assessed with the Parental Verbal Aggression Scale (PVAS). Subjects with PVAS scores ≥ 40, indicative of exposure to substantial and deleterious levels verbal abuse (Teicher et al., 2006), were excluded.

2.2. Psychiatric symptoms and well-being

Self-report ratings of dissociation, ‘limbic irritability’, depression, anxiety and anger-hostility were obtained using the Dissociative Experience Scale, (Bernstein and Putnam, 1986) limbic system checklist – 33 (LSCL-33) (Teicher et al., 1993), and Kellner’s Symptom Questionnaire (Kellner, 1987), respectively. Scores on these scales are elevated by exposure to other forms of childhood stress (Teicher et al., 2006), and have been found in previous studies to correlate with regional alterations in structure or function associated with maltreatment (Anderson et al., 2002; Choi et al., 2008). Hence, we used these ratings in an exploratory manner to delineate potential functional correlates of regions of reduced GMV.

3. MRI acquisition and analysis

Image analysis was performed on high-resolution T1-weighted MRI datasets, which were acquired on a Trio Scanner (3 T; Siemens AG). An inversion prepared 3D MPRAGE sequence was used with an eight-element phased-array RF reception coil (Siemens AG). The GRAPPA acquisition and processing was used to reduce the scan time, with a GRAPPA factor of 2. Scan parameters were: the sagittal plane, TE/TR/TI/flip = 2.74 ms/2.1 s/1.1 s/12 deg; 3D matrix 256 × 256 × 128 on 256 × 256 × 170 mm field of view; bandwidth 48.6 kHz; scan time 4:56.

VBM was performed using SPM5 for imaging processing (MATLAB 6.5; The MathWorks Inc., Natick, MA, USA). As a fully automated whole-brain morphometric technique, VBM detects regional structural differences between groups on a voxel-by-voxel basis (Good et al., 2001a; Good et al., 2001b). Briefly, images were segmented into gray matter, white matter, cerebrospinal fluid, and skull/scalp compartments, then normalized to standard space and re-segmented. Any volume change that was induced by normalization was adjusted. The spatially normalized segments of gray and white matter were smoothed using a 12-mm full-width half-maximum isotropic Gaussian kernel. Statistical analysis of regional differences between groups was performed using a permutation test for decreased probability of a particular voxel containing gray or white matter. Potential confounding effects of age, gender, score on the PVAS, parental education, perceived financial sufficiency, and whole segment GMV were modeled. Variances attributable to them were excluded from analyses. The significance levels for statistics estimated by permutation tests were set at P = 0.05, corrected for multiple comparisons.

4. Statistical analysis

Significant sociodemographic differences between HCP and control group complicated the exploration of post-hoc functional correlates between VBM identified regions with significantly reduced GMV, and symptom ratings and IQ measures. Hence, multiple regression analysis was used to assess whether there were statistically significant associations (standardized beta weights and overall r-value) between GMV in identified regions and ratings, taking into account differences attributable to gender, parental education and perceived financial sufficiency. Multiple regression analysis was performed on the entire sample, as there were no significant group differences on most measures of interest. When a significant association was found, we also ascertained whether it was present in the HCP group alone, to help assure that the relationship was not an artifact of group differences. This approach reduced the number of cross-correlations examined by a factor of three. A multiple regression r value ≤ 0.01 was required for significance, to compensate for the number of tested associations. Statistical analyses were performed using SPSS statistical software (SPSS Inc., Chicago, IL).


HCP subjects reported mean duration of exposure to CP of 8.5 ± 3.5 years. Thirty-six percent of controls had limited exposed to ordinary CP, with an average exposure duration of 1.8 ± 3.0 years. Average age of onset and offset of CP in the HCP group was 3.9 ± 2.3 and 11.4 ± 2.5 years, respectively. HCP began almost concurrently with CP (4.2 ± 2.3 years). Subjects in the HCP group were predominantly male (65%), whereas controls were predominantly female (73%; Table I). Parents of HCP subjects had, on average, two years less education than parents of controls (P = 0.004), and HCP subjects experienced a somewhat greater degree of financial stress growing up (P = 0.01). HCP subjects were exposed to significantly higher levels of parental verbal aggression than controls (P < 0.0001), though no subjects were exposed to levels that we had previously defined as abusive (Choi et al., 2008; Teicher et al., 2006). Differences in gender ratio, parental education, perceived financial stress and exposure to parental verbal aggression were controlled for in subsequent analyses. HCP and control subjects did not differ in years of formal education. Control subjects had superior verbal IQ scores, which were about 10 points higher than in subjects with HCP (P = 0.058). There were no differences between groups in performance IQ (PIQ) or symptom ratings, except for ‘contendedness’ (5.8 ± 0.7 vs 5.0 ± 1.1; F = 7.13, df = 1,42, P = 0.01), which is a wellness item indicating freedom from depression and ability to experience happiness, joy and satisfaction. One subject in the HCP group met criteria for lifetime history of ADHD, none met criteria for conduct disorder.

The most prominent finding was a significant reduction in GMV in the right medial frontal gyrus (medial prefrontal cortex, MPFC) in individuals exposed to CP (BA 10; Talairach’s coordinates x= 14, y= 47, z= 1, cluster size = 402, P = 0.037, corrected cluster level) (Fig. 1). A 19.1% lower average GMV was found in these regions of the CP subjects than in healthy controls.
Fig. 1
Fig. 1 - Significant differences between corporal punishment (CP) subjects and controls. Significantly lower gray-matter densities in CP subjects were measured in the right medial frontal gyrus (medial prefrontal cortex, BA10). Crosshairs placed at x= 14, y= 47, ... (click the link to enlarge)
Using lower criteria for statistical significance revealed 14.5% reduction in GMV in the left medial frontal gyrus (dorsolateral prefrontal cortex; DLPFC) (BA 9; Talairach’s coordinates x= 10, y= 40, z= 20, cluster size = 283, P = 0.015, uncorrected cluster level) and 16.9% reduction in GMV in the right anterior cingulate gyrus (BA 24; Talairach’s coordinates x= 10, y= 30, z= 15, cluster size = 124, P < 0.001, uncorrected voxel level). No other areas of reduction were found with a corrected cluster probability value that approached significance.

No significant correlations emerged between the GMV in those regions and symptom ratings (all P > 0.10). However, multiple regression analysis revealed that GMV in these identified regions was significantly correlated with PIQ on the WAIS-III (Table II). Overall, there was a 0.634 correlation between GMV and covariates of interest and PIQ for the entire group of subjects (n=45). There was also a significant correlation within the HCP (r = 0.754) group alone. As indicated in Table II, there were strong reciprocal correlations between GMV in right BA 10 region and left BA 9 and PIQ. Overall, there was a direct correlation between GMV in left BA9, and an inverse correlation between right BA10, and PIQ.
Table II
Table II - Multiple regression analysis between prefrontal cortex gray matter volume and performance IQ scores. (Click the link to enlarge)


This study examined the association between exposure to HCP and brain structure. HCP includes occasional use of objects to induce pain, and is considered an unacceptable form of punishment by the AAP. Results from this study apply to HCP, they do not apply to exposure to ordinary forms of CP that the AAP considers acceptable (but less effective than alternative forms of discipline).

Chronic exposure to HCP was associated with a marked reduction in GMV in the right medial frontal gyrus (MPFC, BA10). There were also possible associations between HCP and reduced GMV in left medial frontal gyrus (DLPFC, BA 9) and the right anterior cingulate gyrus (BA 24). Other imaging studies have found those regions to be involved in aspects of addiction (Crockford et al., 2005; Drexler et al., 2000), suicidal behavior and/or depression (Bar et al., 2007; Liotti and Mayberg, 2001; Raust et al., 2007), post-traumatic stress disorder (PTSD) (Bremner, 2003; Fennema-Notestine et al., 2002; Geuze et al., 2007; Hou et al., 2007; Liberzon et al., 2003), dissociative disorders (Veltman et al., 2005), and depression (Fitzgerald et al., 2008). HCP may be an aversive and stressful event for human beings that potentially alters the developmental trajectory of some brain regions in which abnormalities have been associated with major forms of psychopathology.

The regions identified with reduced GMV are part of the medial rostral prefrontal cortex (MRPFC). Recent studies have pointed to the MRPFC as a region of the human brain that plays a crucial role in social cognition as well as functional organization (Amodio and Frith, 2006; Gilbert et al., 2007). In particular, medial BA10 and BA32 appear to be involved with self-knowledge, person perception and mentalizing (Amodio and Frith, 2006). At its most basic level, self-knowledge involves the ability to differentiate the self from other objects and to recognize attributes and preferences related to oneself. The ability to represent another person’s psychological perspective is referred to as mentalizing, and this capacity allows us to predict the behavior of others. Person perception involves judgments about the attributes and behaviors of others. BA24, in contrast appears to be involved in the internal monitoring of our actions to ensure that they are consistent with intentions and the current situational context (Amodio and Frith, 2006). The more posterior portion of the MRPFC (primarily BA 8 and 9) is activated by cognitive tasks, such as those designed to engage action monitoring and attention. For example, left BA9 is activated in young adults during working memory retrieval tasks (Sun et al., 2005).

It is interesting that individuals exposed to high levels of HCP had reduced GMV in right BA10 and possibly in right BA24. HCP is administered ostensibly to correct behavior. Children may increase their risk of exposure to CP, or HCP, if they have an inadequate ability to internally monitoring their own actions (BA24), or if they have deficits in self-perception, person perception, or mentalizing (BA10). Being able to predict how parents will react, and being able infer their parents’ state of mind is probably quite adaptive. Hence, it is conceivable that differences observed in regional GMV were preexisting abnormalities that increased their risk of exposure to HCP. However, exposure to CP began at about 3.9 years of age, when prefrontal cortex is quite immature. BA10 has a particularly protracted pattern of dendritic development (Travis et al., 2005), and medial prefrontal cortex and other components of the ‘social brain’ undergo structural development, including synaptic reorganization, during adolescence (Blakemore, 2008). Nevertheless, this region of the brain is not quiescent during early development, as episodic memory and episodic future thinking (which requires involvement of medial prefrontal cortex) emerges at about 4 years of age (Weiler and Daum, 2008). It is perhaps most reasonable to assume that the use of CP or HCP for disciplining of young children is strongly dictated by parental experience and beliefs. However, continuing development of MRPFC regions may make it easier for a child to avoid exposure to physical punishment. An inherited lag in the development of the MRPFC may lead to the intergeneration transmission of HCP.

Conversely, exposure to HCP may have attenuated development of these regions. It is conceivable that exposure to HCP produced conflicts in perception and self-monitoring that were difficult to reconcile, and these conflicts attenuated or suppressed development. For example, it may be challenging to integrate perceptions of a parental figure as caring and loving on one hand, and critical and intentionally hurtful on the other. Similarly, there may be a disconnect between a child’s self-monitored impression that he did not do much if anything wrong, versus a parental judgment that he needed to be severely punished for his mistakes. In short, HCP may create a mismatch between internal and external perceptions of one’s actions or one’s beliefs about others. In doing so, it may attenuate or arrest important components of social cognition.

It is interesting that left BA9 GMV was positively correlated with PIQ, while right BA10 was negatively correlated. GMV in BA9 and BA10 were found in a previous study to be two cortical regions most strongly associated with general intelligence (Haier et al., 2005). However, there were substantial gender differences in that study, with BA9 showing a greater correlation in males, and BA10 correlating more significantly in females. As seen in Table II, gender did not significantly affect associations in the present study. The observation that GMV in right BA10 was negatively correlated with PIQ was confusing, but understandable, as IQ may relate even more strongly to white matter volume (or gray/white matter ratio) in BA10 than to GMV alone (Haier et al., 2005).

VBM studies provided an unbiased, even-handed, assessment of regional alterations in GMV. However, these studies have a significant number of limitations. Care was taken to make sure that there were no issues with alignment. Subjects inthe two groups were of almost identical age, and selected from a narrow age range to minimize any potential developmental differences in template registration. All subjects were scanned on the same machine over the same time-period. Unfortunately, there were significant differences between groups in gender ratio, parental education level and perceived financial stress, which can independently affect brain development. These factors were controlled for statistically, but these findings will need to be confirmed in samples that are better matched for gender and sociodemographic variables. Our primary concern in this study was to equate the two groups for degree of drug and alcohol use. Although no subject in the study had a history of drug or alcohol abuse, we found that subjects exposed to HCP used these substances to a much greater extent than controls recruited for other studies. The primary finding of reduced GMV in right MPFC was observed with corrected P < 0.05. Additional findings of reduced GMV in left DLPFC and right ACC were found to be highly significant at the uncorrected cluster level. There is no guarantee that these were not false-positive results or that all relevant brain areas were identified.

One potential confounding factor is that children with ADHD may have an increased degree of exposure to CP or HCP, though recent studies do not support this association in the USA {Burke, 2008 #5973; Whitmore, 1993 #5972}. Excluding the one child with ADHD in the study did not alter the results. ANCOVA analyses confirmed that there were marked differences in GMV in the three identified regions between HCP subjects and controls when the HCP subject with ADHD was excluded (BA 10: F1,37 = 77.277 p < 10−9; DLPFC: F1,37 = 61.409 p < 10−8; ACC: F1,37 = 49.825 p < 10−7).

Neurobiological research on the effects of early stress has the potential to recast our thinking about the role of early experience in the development of psychopathology (e.g. (Teicher et al., 2002; Teicher et al., 2003)). HCP or excessive CP have been found to be associated with emergence of depression, addiction and aggressive behaviors (Ambati et al., 1998; Banks, 2002; Deater-Deckard et al., 2003; Gershoff, 2002; Lau et al., 2005; Muller et al., 1995; Ohene et al., 2006; Schwartz et al., 2006; Slade and Wissow, 2004; Straus and Kantor, 1994; Straus et al., 1997). These associations may be viewed in a new light, if it turns out to be true that HCP attenuates the development of brain regions crucial for self-knowledge, person perception, mentalizing, and internal monitoring of our actions. Results from this study raise the possibility that exposure to HCP acts as a chronic sub-traumatic stressor that alters the developmental trajectory of MRPFC. If so, it underscores efforts to prevent children from receiving CP or HCP from parents or other adults. It should be emphasized that CP received by these subjects was excessive. It involved more than open hand slaps to the buttocks, and in all cases persisted past their 6th birthday. How detrimental (or beneficial) spanking is depends a great deal on the age of the subject, frequency of administration, race, who administers the spanking, family context, and whether it is used as a primary means of discipline, or as a ‘backup’ strategy (Gunnoe and Mariner, 1997; Larzelere, 1996; Larzelere and Kuhn, 2005). These findings do not necessarily generalize to milder, less frequent, and less persistent episodes of spanking ending before age 6. Further, we must emphasize again the possibility that reduced GMV in the identified regions may have been a risk factor for persistence (or escalation) of CP, rather than a consequence of exposure. Prospective longitudinal studies will be required to validate and untangle the nature of the relationship.


This study was supported by RO1 awards from the U.S.A. National Institute of Mental Health (MH-53636, MH-66222) and National Institute of Drug Abuse (DA-016934, DA-017846) to MHT. We thank Dr. H. Tanabe, National Institute for Physiological Sciences, Aichi, Japan for his assistance with data analyses.

References available at the PMC site.

Life, Art, and Therapy - To the Best of Our Knowledge

This week on NPR's To the Best of Our Knowledge, the topic is psychoanalysis - whatever happened to it? Sadly, the question they ask refers more to Freudian psychoanalysis, and not any of the relational, object-relations, or intersubjective systems models that have emerged from the charred remains of Freudian analysis over the last several decades (beginning especially with the object-relations school in England and Kohut's Self Psychology in the U.S.).

Still, there is some interesting stuff here.

Life, Art, and Therapy



Whatever happened to psychoanalysis? It used to be the most influential science of the mind, but today its founder, Sigmund Freud, just looks like a sex-obsessed old man. Analyst Adam Phillips says we got Freud all wrong; he remains a radical thinker if we know how to read him. This hour explores the connections between therapy and art.

Producer(s): Steve Paulson
Related Link(s):
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Rethinking Freud - Adam Phillips


Extended Interview

Psychoanalyst Adam Phillips says we've gotten Freud all wrong. He wasn't a scientist; he was a great writer and countercultural figure. And his insights still have the power to dazzle us.

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Growing Up Freudian - Erin Clune


What's it like to grow up with a mom who's a Freudian therapist? Commentator Erin Clune has a few personal observations.

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Cartooning & Psychotherapy - Alison Bechdel

Extended Interview

Acclaimed cartoonist Alison Bechdel has written two brutally honest memoirs about her parents. She tells Steve Paulson about her complicated relationship with her mother and how it inspired her as an artist.

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Art as Therapy - Alain de Botton


Maybe you're familiar with art therapy - making art to cope with pain. Philosopher Alain de Botton has a different idea. He thinks just looking at great art can be therapeutic.

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BookMark: Nic Pizzolatto


"True Detective" creator and writer Nic Pizzolatto recommends "Absalom, Absalom" by William Faulkner.

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On Our Minds: James McBride


James McBride won the National Book Award for "The Good Lord Bird," his novel about the abolitionist John Brown. He explains why he doesn't like most fictional portraits of slavery and how he tried to tell a different story.

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Related Books:

Becoming Freud
(Adam Phillips)

Are You My Mother?
(Alison Bechdel)

Art as Therapy
(Alain de Botton, John Armstrong)

The Good Lord Bird
(James McBride) 

Saturday, July 26, 2014

A $650 Million Dollar Donation for Psychiatric Research - Misguided? 
The Broad Institute of MIT and Harvard

This was big news last week, when late on Monday, the Broad Institute, a biomedical research center, announced a $650 million donation for psychiatric research from the Stanley Family Foundation — one of the largest private gifts ever for scientific research.

This news broke the same day as a new article in the journal Nature - Biological insights from 108 schizophrenia-associated genetic loci - revealed research that identified an additional 83 genes linked to schizophrenia, as well as confirming 25 previously identified genes - now a total of 108 genes are linked to schizophrenia.

With 108 possible genes linked to schizophrenia, we know little about the specific combinations of genes, their epigenetic triggers, their environmental factors (both physiological and relational) that may turn off or on specific genes, and a lot of other variables.

For example, we know that physical and emotional neglect is more linked to psychosis and schizophrenia than is physical and sexual abuse. For more background on a relational view, see A relational view of causality in normal and abnormal development (2002).

Anyway, this article is about the generous donation given to the Broad Institute. It's wonderful that they gave such a huge sum in support of research, however, by giving it to an organization that focuses on psychiatric research (psychopharmacology and genetics) rather than a wider bio-psycho-social model.

Spark for a Stagnant Research

A $650 Million Dollar Donation for Psychiatric Research

By Carl Zimmer and Benedict Carey
July 21, 2014

“You’re talking to a guy who went from psychotic to normal with some pills,” said Jonathan Stanley, who was found to have bipolar disorder in the 1980s. The donation of a foundation started by his father is one of the largest private gifts ever for scientific research. Credit Max Reed for The New York Times
ONE DAY IN 1988, a college dropout named Jonathan Stanley was visiting New York City when he became convinced that government agents were closing in on him.

He bolted, and for three days and nights raced through the city streets and subway tunnels. His flight ended in a deli, where he climbed a plastic crate and stripped off his clothes. The police took him to a hospital, and he finally received effective treatment two years after getting a diagnosis of bipolar disorder.

“My son’s life was saved,” his father, Ted Stanley, said recently. When he himself was in college, he added, “those drugs didn’t exist; I would have had a nonfunctioning brain all the rest of my life.”

The older Mr. Stanley, 84, who earned a fortune selling collectibles, created a foundation to support psychiatric research. “I would like to purchase that happy ending for other people,” he said.

Late on Monday, the Broad Institute, a biomedical research center, announced a $650 million donation for psychiatric research from the Stanley Family Foundation — one of the largest private gifts ever for scientific research. Audio

It comes at a time when basic research into mental illness is sputtering, and many drug makers have all but abandoned the search for new treatments.

Despite decades of costly research, experts have learned virtually nothing about the causes of psychiatric disorders and have developed no truly novel drug treatments in more than a quarter century.

Broad Institute officials hope that Mr. Stanley’s donation will change that, and they timed their announcement to coincide with the publication of the largest analysis to date on the genetics of schizophrenia.

The analysis, reported by the journal Nature on Monday, identified more than 100 regions of DNA associated with the disease. Many of them contain genes involved in just a few biological functions, like pumping calcium into neurons, that could help guide the search for treatments.

“For the first time, there’s a clear path forward,” said Eric Lander, the president of the Broad Institute.

Experts not affiliated with the institute or the new paper agreed that the news on both fronts was good, but characterized the research as a first step in a long process. “The signals they found are real signals, period, and that is encouraging,” said David B. Goldstein, a Duke University geneticist who has been critical of previous large-scale projects. “But at the same time, they give us no mechanistic insight, no targets for drug development. That will take a lot more work.”

Jonathan Stanley, now 48, cannot explain why he suddenly developed bipolar disorder at 19. All he knows is that his brain responded well to lithium. He was eventually able to return to college, complete law school and become a lawyer. “You’re talking to a guy who went from psychotic to normal with some pills,” he said.

When scientists began to discover psychiatric drugs like lithium in the mid-20th century, they did so mostly by accident, not out of an understanding of the biology of the diseases they hoped to cure. For many years, they worked backward, hoping that by figuring out the action of the drugs, they could understand the causes of the diseases. But they came up empty.

Some researchers argued that a better strategy would be to find the genes involved in psychiatric disorders. This approach would give them new molecular targets for drugs they could test.

Yet the staggering complexity of the brain has yielded few secrets. More than 80 percent of the roughly 20,000 genes in human DNA are active in the brain.

In the 1990s, many scientists argued that the best approach to find “mood genes” was top-down. They would identify promising genes based on their biological properties and then survey their variants in people with and without a diagnosis.

But this approach was something like trying to find a thief in a crowd, based on a hunch of what he or she might look like. The research was “pretty much completely useless,” Dr. Lander said. “It turns out we are terrible guessers.”

By the early 2000s, the ability to decode human DNA had vastly improved, and scientists could look across our complete complement of genetic material, known as the genome, comparing samples from ever-larger groups of people. Ted Stanley’s first donation to the Broad Institute — $100 million in 2007, to found the Stanley Center for Psychiatric Research — went to support precisely such research.

Yet these studies were disappointing, too, and many researchers thought they were a dead end. “We were saying, ‘Maybe it isn’t the right way to go,’ ” Dr. Lander said.

Soon, the Broad Institute joined forces with scores of other research groups to form a consortium that could pool tens of thousands of subjects for analysis. In 2011, the consortium reported five genetic markers associated with schizophrenia. The group added more people to its studies and found even more genetic links.

The new paper in Nature is a culmination of the effort to date. The consortium analyzed 37,000 people who had schizophrenia and 114,000 who did not. It found 83 regions of the genome linked to the disorder that had not been previously flagged, and confirmed 25 previously identified ones, bringing the total to 108.

Dr. Lander cautioned that each variant accounts for only a tiny portion of the risk of developing schizophrenia. “It shouldn’t be used for a risk predictor,” he said.

Still, Dr. Samuel Barondes, a professor of neurobiology and psychiatry at the University of California, San Francisco, who was not involved in the study, called the findings encouraging. Even though schizophrenia is a “diverse disorder, with a horribly complicated genetic basis,” he said, “it is possible to pick up a reliable genetic signal if you have enough people.”

Other research teams are making progress on other conditions, such as bipolar disorder and autism, and finding that some mutations are rare while others are common variants.

On Sunday, an international team of scientists reported a study in Nature Genetics in which they compared 466 autistic people to 2,580 others. They found that most of the genetic risk of autism involved common mutations.

But these studies of brain disorders are also revealing a deep complexity that could pose an obstacle to rapid progress to effective drugs.

For example, recent research has found that mutations in the very same gene can cause a wide range of brain disorders, including autism, schizophrenia and epilepsy. “We are implicating the exact same genes across really different neuropsychiatric disorders,” Dr. Goldstein said. “We have no idea at all about why that is, and the only way to find out is to do some hard biology — to find out not only which genes matter, but what about them matters.”

That will take time and will probably produce plenty of reversals and spurious predictions. “Expect no grand-slam home runs,” said Dr. Allen Frances, professor emeritus of psychiatry at Duke and author of “Saving Normal,” a critique of psychiatric diagnosis. “There will be lots of strikeouts and only occasional singles.” The new study in Nature found that many risk variants clustered around specific body functions, like the immune system and calcium transmission in brain cells.

To understand their underlying biology, Broad researchers plan to grow neurons with mutations in the genes they have discovered, to see how they differ from normal cells. They will engineer mice with some of the mutations to see how their brains are affected. The scientists hope these experiments will lead them to hypotheses about the biology underlying psychiatric disorders — which they will test by giving mice drugs that target specific molecules in the brain.

These studies will be expensive, which is where the Stanley foundation comes in. Last year, after the death of his wife, Vada, Mr. Stanley, the founder of MBI, began considering what he would do with his fortune. He decided that his first gift to Broad Institute was not enough.

“After I’m gone,” he said, “I just want the money to flow to them as it would if I was still alive.”

John Martin Fischer - How Does a Belief in Immortality Affect the Way We Live Now?

Immortality seems to me to be morally indefensible. The Earth is right now at 7 billion people, so let's say we develop immortality in 10-15 years, when the population will be at 8 billion or more. So none of those people die, and yet people keep reproducing, forever. Imagine the Earth with 15 billion people, or 25 billion. We have already overpopulated the planet. How would we feed these people, where would we get fresh water (as of now, 780 million people lack clean drinking water and 2.3 billion lack basic sanitation), and what about the lack of natural resources for homes, and so on.

Personally, the idea of immortality is abhorrent. Where and how would we find purpose in life if we never die? Boredom would eventually set in, so the only choice would be suicide. Even in the modern vampire stories, creatures who are immortal, many of the oldest vampires express their sense of exhaustion with existence, their "living" malaise. The fact that this idea turns up even in our myths suggests that it is a commonly held belief.

Anyway - this article sets out a philosophical argument for how the idea of immortality might affect how we live our lives today.

How Does a Belief in Immortality Affect the Way We Live Now?

By John Martin Fischer
July 8, 2014

image: Getty

I was asked to address the question,” "How does a belief in immortality affect the way we live now?" I am going to break this into two separate questions that are related to (if not identical to) it. The first question is, “How would the recognition of extreme longevity or even living forever change the way we would behave (or should behave)?” Then I’ll turn to how a belief in an afterlife would (or should) affect our behavior.

First: imagine that you knew that you would live for a very, very long time. We can simplify and imagine that you know that you will live forever. How would or should this hypothetical supposition affect your behavior? Well, it depends! It depends at least on certain background assumptions about the conditions of your envisaged life. Let’s make the “rosy” assumptions that you are in good health, that your body is not deteriorating, that you are comfortable financially, that you have friends and loved ones who are also immortal (in the sense of living forever). These are, of course, big assumptions; but to ask a really big question, sometimes we have to make big assumptions.

Some would say that, even under these very optimistic assumptions, our lives would be totally different—and unpleasant or even unrecognizable as choiceworthy human lives. Various reasons for this curmudgeonly conclusion have been offered, and we’ll consider just a few. First, some have argued that life under such circumstances would be intolerably and relentlessly boring. The idea is that what keeps us from being bored are our “projects”, and eventually we would run out of projects in an indefinitely long (or even just a very long) life.

I just don’t think this is true. That is, I don’t accept the conclusion that we would run out of projects in a very long (even an infinitely long life). Just consider, for starters, all of the scientific problems that remain to be solved. Focus, as a concrete starting point, on all of the diseases that plague human beings. The project of curing all the currently existing diseases would take a very, very long time. And, even assuming we can (given enough time), cure all existing diseases, by that time many new diseases will have popped up, offering new challenges. I just don’t think that it is obvious that we will ever get to the point where we will have cured all diseases (and palliated all human pain, suffering, and distress—both physical and mental). Simply having lots of time—even infinite time—doesn’t seem to imply that all of these challenges will successfully be met.

And we have just focused on a relatively tiny portion of all of the human challenges—the health challenges. How about all of the other scientific and technological challenges? How long will it take to answer certain fundamental questions of physics and cosmology? Even when they have been answered, if they ever are, there would remain the problems of connecting the abstract theories with all manner of practical problems.

Think, just for another set of concrete examples, of all of the challenges we face in preserving our planet from further environmental degradation. These are multifaceted and daunting. They will keep us busy for a long, long time (if we have that long). They could keep us going for a very long time in an infinitely long life.

So far we have considered just a few (admittedly central and important) scientific challenges that would generate projects in an immortal life. There are more where they came from. And think of all of the other kinds of projects: athletic, artistic, social. Consider the projects of writing poetry or novels or creating lovely paintings or sculptures. Or reading and appreciating novels. Why suppose that these projects would run out? Even if you had an infinite amount of time, why suppose that you would exhaust all of the novels worth reading? Suppose you were to read all of the novels currently worth reading. That would take a very, very long time. But (as with the diseases above) by the time you were finished, there would certainly be a new set of novels worth reading (novels that had been written during your very long process of reading). And why suppose that you could not find challenge and engagement in writing novels, even after a million or a billion years? (Of course, all of one’s projects would have to be distributed appropriately—reading or writing or anything can be boring if pursued without a break!).

The challenges and associated projects discussed above might be called “other-directed” projects. But there are also “self-directed” projects, such as eating delicious food, drinking fine wines, listening to music, enjoying art and natural beauty, sex, prayer, and meditation. These are “self-directed” projects in the sense that they aim at or crucially involve pleasant or agreeable mental states of the individual whose project it is. Again, you would have to distribute these projects properly in a very long or even infinitely long life. But why would a life that contained at least some of these projects necessarily be boring? Why couldn’t these activities be part of an overall life that is engaging and worthwhile?

Assuming that we would still have projects—other-directed and/or self-directed—in a very long or infinitely long life, would we have any motivation to pursue the projects? Some have thought that, given an infinite amount of time, all our activities and projects would lack “urgency”. They have even suggested that we would not have any motivation to do anything insofar as “there would always be time”. This is kind of a procrastinator’s nightmare (or perhaps dream!).

But I don’t have much sympathy for the contention that we would have no motivation in an immortal life. Consider, for example, the motivation to avoid pain—that would still exist in an immortal life. Similarly for the motivation to address other forms of limitation or impairment. We care about how we feel now; if we are now in pain or impaired, we will want to address those issues in a timely way. If I am in significant pain now, it is hardly comforting to know that I have forever to live and so eventually my pain will subside.

Similarly with loneliness. If am separated from someone I love or care about, or if I am just lonely now, I have reason to seek to reunite with the person or to find friendship, love, and companionship. The mere fact that I know that I have forever does not alleviate the suffering of loneliness now.

The curmudgeons about projects in an immortal life are too pessimistic. They are spoil-sports. They greatly underestimate the prospects for human engagement and fulfillment. They look at our projects as like books in a library; with infinite time, we can read all of the books. They forget that there will always be new books to read and even new perspectives to bring to the old books.

What about the second way of understanding our basic question? That is, what if we were to come to believe in immortality in an afterlife? How would (or should) this affect our behavior? Well, again, it depends. First, it depends on what conception of immortality we work with—a Buddhist or Hindu view of reincarnation? A Judeo-Christian conception of the afterlife in heaven or hell?

But let’s abstract away from details. In all plausible religious views, what matters crucially for your prospects after you die—your next life in the wheel of reincarnation or your place in heaven, hell, or perhaps purgatory—is the moral quality of your life here and now. That is, your prospects are enhanced by right action for the right reasons in this life. You need actually to care not just about yourself, but about others—you need to love others and to care about justice. If your actions manifest love of others and a dominant concern for justice, then you will be rewarded in the afterlife. It is key that you must act for the right reasons. And here it is important that the reason for your behavior must not be that it will enhance your prospects in the afterlife. You may of course understand and anticipate this fact. But it cannot be your reason for action. If it were, then your action would be motivated by self-interest and not morality. You would not be doing the right thing for the right reason. So there is a sense in which your behavior now should be focused on this world and the needs and interests of others here and now, even if one were to believe in an afterlife.

Discussion Questions:

1. Do you agree that you would not necessarily run out of other-directed projects in a very long life? An infinitely long life?

2. Do you agree that you could still have self-directed projects in a very long or infinitely long life? Or would such a life necessarily be boring?

3. Do you agree that, even if you believe in an afterlife, you should be concerned about your behavior and motivations here and now. Or do you thank that you should focus more on the life to come?

Related Questions  

Book - "Mind, Modernity, Madness: The Impact of Culture on Human Experience" by Liah Greenfeld,204,203,200_.jpg

Allan Young reviews Liah Greenfeld's final installment in her Nationalism trilogy, Mind, Modernity, Madness: The Impact of Culture on Human Experience (2013) for the summer issue of The Hedgehog Review.

This appears to be a very interesting book - although Young doesn't feel there is too much true innovation here. Here is a passage from the review below:

Greenfeld argues that culture is simultaneously a source of madness and a source of self-medication that attenuates the severity of madness. As pathogenic forces strengthen, she writes, self-medication grows equally more desperate and socially disruptive in an era of globalization:
“Paradoxically, the rate of severe (clinical) mental disturbance should, in general, be proportional to the possibility of engaging in ideologically motivated collective activism; that is, the rate of disturbance should necessarily be highest in individualistic nations, and higher in collectivistic civic nations than in ones organized on the basis of ethnicity. The most aggressive and xenophobic strains of nationalism—the worst kind for international comity—would be the best for the mental health of individual citizens in states where such virulence held sway.”
Based on the brief review, this book, having not read it yet, seems like the intellectual heir of Wilhelm Reich's The Mass Psychology of Facism. If so, it is an important book.

Mind, Modernity, Madness: The Impact of Culture on Human Experience

Liah Greenfeld
Cambridge, MA: Harvard University Press, 2013.

Reprinted from The Hedgehog Review; 16.2 (Summer 2014). This essay may not be resold, reprinted, or redistributed for compensation of any kind without prior written permission. Please contact The Hedgehog Review for further details.

Liah Greenfeld, a professor of sociology at Boston University, describes Mind, Modernity, Madness as the product of “a new—radically different—approach that has never been tried.” At 688 pages, it is a long book that ranges in its “interdisciplinarity” from the clinical epidemiology of bipolar depression to the historiography of romantic love in Shakespeare. But it has a clear, bold thesis: that the advent of madness is connected, as both cause and effect, to the rise of nations and nationalism.

More specifically, Greenfeld contends, the historical conditions that gave rise to the nation—a community of equals; a measure of individual autonomy, liberty, and mobility; and a declining acknowledgment of divine authority—make madness not only possible but inevitable. As the value of human life grows and becomes of paramount concern, self-invention and romantic love become popular ideals, and even common people are driven by ambition, aspiration, and the pursuit of happiness. “Modern culture,” Greenfeld writes, “leaves us free to decide what to be and to make ourselves. It is this cultural laxity that is anomie—the inability of a culture to provide the individuals within it with consistent guidance.”

The author’s evidence is historical and biographical. Her conceptual framework is sociological, inspired by Émile Durkheim’s 1897 book Suicide. Indeed, Greenfeld’s vision of modernity restates and broadens Durkheim’s view that social disintegration produces the anomie and alienation that can lead to self-destructive behavior and acts, including the taking of one’s own life. While Durkheim adduced higher rates of suicide in the anomic nations of later-nineteenth-century Protestant Europe, Greenfeld focuses on the worldwide epidemiology of schizophrenia, bipolar disorder, and major depression, which she regards as an overwhelming threat to Western civilization.

Greenfeld rejects the “constructivist” approach that she believes is prevalent “among Western social scientists—anthropologists, sociologists, and historians studying psychiatry—who conclude that madness is largely an invented problem… analogous to the equally false ‘social constructions’ of witchcraft and possession of other cultures, but dressed in a scientific garb and unjustifiably enjoying the authority of science in ours.” She derides the “poetic” excesses of Michel Foucault’s Madness and Civilization, but ignores constructivist conceptualizations of greater consequence, notably “idioms of distress” and “bio-looping,” which circulate freely within clinical psychiatry and can be found in the Diagnostic and Statistical Manual on Mental Disorders in appendixes on somatization syndromes and cultural psychiatry.

When Greenfeld accuses anthropologists of creating “false social constructions” of witchcraft and possession and repeating this effect on Western madness, she means that anthropologists have misconstrued how culture, mind, consciousness, brain, and madness are connected. Culture, in her view, is an ideational, symbolic, non-material phenomenon. Human consciousness is an emergent phenomenon, “logically consistent with the biological and physical laws but autonomous,” and irreducible to organic reality. The human mind comprises or contains a form of collective consciousness she calls “culture in the brain.”

These conceptions, Greenfeld says, run counter to the dominant “dual mind/body view of reality,” which attributes causal primacy to the “material” (the central nervous system) over the “spiritual” (consciousness, mind, culture). Culture and consciousness, in this paradigm, are epiphenomena of the material world: causation proceeds from brain to mind via identifiable mechanisms. In other words, culture can disguise the material nature of madness but cannot interfere with it. Constructionists are said to share these conventions.

Greenfeld emphatically rejects the dualist paradigm, contending that culture can and does cause biologically real (material) diseases, including madness. She believes that her thesis, being both counterintuitive and empirically proven, has revolutionary implications for how we understand and address the increasing prevalence of madness in our current era and culture. Furthermore, she believes that her thesis enables her to advance additional, counterintuitive claims concerning the historical origins and epidemiology of madness.

Yet it is unclear to me whether Greenfeld’s thesis is truly revolutionary. The difficulty comes in her proposal that culture causes biologically real diseases. There are two ways to interpret this claim. She could mean that “culture in the brain” is a source of distressful dilemmas, contradictions, and emotions that precipitate chains of physiological, molecular, neurological, and anatomical effects; that these changes in turn undermine the homeostasis underpinning normal functioning; and that, as a result, a pathogenic loop is created and sustained. This interpretation seems consistent with the process Greenfeld is proposing, and it is consistent with what she says about clinical psychiatry and research. This is a credible thesis, but it is far from being counterintuitive or revolutionary. Indeed, it is the prevailing approach among anthropologists and other social scientists interested in mind, brain, and psychopathology.

But Greenfeld may have something far more original in mind: “So long as there remains the unresolved philosophical mind-body problem, no significant advance in human neuroscience and, therefore, psychiatry would be possible.… The first order of the business is, therefore, to escape the mind-body quagmire.” If, in this book, she has found a way out of this 400-year-old problem, however, it is not at all obvious to this reader what it is.

Such matters occupy only two chapters. The remaining 500 pages are devoted to “madness.” According to Greenfeld, the term was coined in England in the early modern period (fifteenth and sixteenth centuries), then spread to France and Germany. Between 1880 and 1900, “madness” bracketed the maladies we know today as schizophrenia and bipolar disorder. (In psychiatry, there is currently renewed interest in reconnecting the two disorders on a single diagnostic spectrum.) The author further describes the history of the term in separate chapters on Europe and America.

In a brief but provocative epilogue, Greenfeld argues that culture is simultaneously a source of madness and a source of self-medication that attenuates the severity of madness. As pathogenic forces strengthen, she writes, self-medication grows equally more desperate and socially disruptive in an era of globalization:

“Paradoxically, the rate of severe (clinical) mental disturbance should, in general, be proportional to the possibility of engaging in ideologically motivated collective activism; that is, the rate of disturbance should necessarily be highest in individualistic nations, and higher in collectivistic civic nations than in ones organized on the basis of ethnicity. The most aggressive and xenophobic strains of nationalism—the worst kind for international comity—would be the best for the mental health of individual citizens in states where such virulence held sway.”

Mind, Modernity, Madness is the final volume in Greenfeld’s trilogy on nationalism. It provides readers with a provocative commentary on the sociocultural origins and psychopathological consequences of modernity. And it is a splendid antidote to the reckless application of the term “madness,” by both pundits and politicians, to the policies and persons of America's political opponents and the excesses of their nationalisms.

~ Allan Young, professor of anthropology at McGill University and author of The Harmony of Illusions: Inventing Posttraumatic Stress Disorder (1995), is completing a book on the social brain, psychopathology, and myths of empathy.