René Girard and the Mimetic Nature of Eating Disorders

French historian and literary critic René Girard (1923–2015), most widely known for the concepts of mimetic desire and scapegoating, also engaged in the discussion of the surge of eating disorders in his 1996 essay Eating Disorders and Mimetic Desire. This article explores Girard’s ideas on the mimetic nature and origin of eating disorders from a clinical psychiatric perspective and contextualizes them within the field of eating disorders research as well as in relation to broader psychological, sociological and anthropological models of social comparison and non-consumption. Three main themes in Girard’s thinking on the topic of eating disorders are identified and explored: the ‘end of prohibitions’ as a driving force in the emergence of eating disorders, eating disorders as a phenomenon specific to modernity, and the significance of ‘conspicuous non-consumption’ in the emergence of eating disorders.     

The Circadian System and Affective Disorders: Clocks or Rhythms?

There have been a number of proposals that a pathology of the circadian system involving clock functioning underlies the affective disorders. It is argued that neither current findings from research into the neurophysiological substrates of the affective disorders, recent clinical findings regarding these illnesses or their phenomenology support such a contention. This does not mean however that there is not a primary pathological disturbance of the circadian system at the heart of the affective disorders. The same neurophysiological, phenomenological and clinical evidence can be offered in favour of a disturbance of circadian rhythms in the presence of grossly normal clock functioning. The research and remedial implications of this alternative are outlined briefly.     

Acid Base Disorders—The Clinical Use of the Astrup Method of Determining pH. pCO2 and Base Excess

The Astrup method for determination of arterial pH, pCO₂, and “base excess” provides a simple and accurate means for quantitation of acid-base disorders. The “base excess” value, a measure of metabolic acidosis or alkalosis, gives the clinician a valuable tool with which to estimate electrolyte replacement. The pCO₂ is a measure of respiratory acidosis or alkalosis. The pH is used as a measure of the adequacy of compensation. Several representative cases illustrate the use and interpretation of the test.     

Drug-Related Disorders and the Criminal and Clinical Background of the Prison Population of S?o Paulo State,Brazil

Objective

To analyze the association between drug (DAD) and alcohol (AAD) abuse and dependency and criminal and clinical background by gender of prisoners in São Paulo, Brazil.

Method

Cross-sectional study, random sample stratified by administrative district, from which prisons and prisoners were selected via random, multistage sampling. Psychiatric diagnoses were made with the CIDI 2.1. Lifetime prevalence and 95% CI were calculated and adjusted via analysis of complex samples. Multinomial logistic regression analysis was carried out with four categories of dependent variables: presence AAD; presence DAD; presence of another mental disorder; no mental disorders. For female alcohol and drug abuse and dependency (ADAD) were combined into a single category.

Results

The sample was composed by 1809 interviewed prisoners (1192 men and 617 women). Prevalence of DAD and AAD was 25.2% and 15.6%, respectively, among female prisoners, and 26.5% and 18.5% among males. Male prisoners with DAD were more likely to have a criminal record as an adolescent (OR 2.17), to be a repeat offender (OR 2.85), and to have committed a property crime (OR 2.18). Prisoners with AAD were repeat offenders (OR 2.18). Among female prisoners, ADAD was associated with repeat offenses (OR 3.39), a criminal record as an adolescent (OR 9.24), a clinical or infectious condition (OR 5.09), another health problem (OR 3.04), and violent crime (OR 2.5).

Conclusion

The study confirmed an association between drug-use disorders and the criminal and clinical background in the study population. Prisoners with such disorders were more likely to be repeat offenders and to have a criminal record as adolescents. Among female prisoners disorders were also associated with violent crime and health problems, while among males they were associated with property crime. These patterns in clinical and criminal backgrounds illustrate the need for social rehabilitation programs and specific medical treatment for prison populations.     

Sleep Related Breathing Disorders and Inflammation — The Missing Link? A Cohort Study Evaluating the Interaction of Inflammation and Sleep Related Breathing Disorders and Effects of Treatment

Introduction

Sleep related breathing disorders (SRBD) are associated with both obesity and systemic inflammation. While the relationship between obesity and SRBD is established, the causality between inflammation and SRBD remains unclear. In this study we investigated the relation between SRBD and C-reactive protein (CRP) as a parameter of inflammation and the influence of SRBD treatment on CRP with additional regard to changes in metabolic and cardiovascular parameters.

Methods

Polysomnography (PSG) and laboratory data of patients diagnosed with SRBD over a period of 5 years were prospectively collected in a database and retrospectively analysed regarding the association of SRBD (according to apnoea-hypopnoea- index (AHI), duration of events and extent of desaturation) to CRP, blood pressure, cholesterol, fasting plasma glucose, HbA1c, quality of life measured via a visual analogue scale (VAS 0–100%), and the effects of SRBD therapy on these parameters.

Results

716 patients were included in the study, 171 with mild SRBD (AHI ≥5 to <15/h), 209 with moderate SRBD (AHI 15 to <30/h), 336 with severe SRBD (AHI ≥30/h). Results according to severity of SRBD. Severe SRBD was significantly associated with elevated levels of CRP (3.7 [1.8–7.0] mg/l, vs. moderate (p = 0.001), and mild SRBD (p<0.001), and higher prevalence of hypertension as compared to moderate and mild SRBD (p<0.001, respectively). Results in highly successful treatment. If SRBD treatment was highly successful (AHI <5/h), CRP and quality of life improved significantly (p = 0.001 and p = 0.002), as did blood pressure (p<0.001 for systolic and diastolic values), although BMI increased (p<0.001). Results in partially successful treatment. If success was defined as reduction of AHI of ≥50%, CRP also decreased (p<0.001), as did blood pressure (p<0.001). Again, BMI increased (p<0.001).

Conclusion

This is the first study to show an association of SRBD and CRP independently of BMI in a large cohort. The SRBD therapy-induced CRP decrease was not associated with BMI changes or metabolic changes but rather with the magnitude of AHI improvement.     

A Role for the PKC Signaling System in the Pathophysiology and Treatment of Mood Disorders: Involvement of a Functional Imbalance?

Mood disorders, such as bipolar and major depressive disorders, are frequent, severe, and often disabling neuropsychiatric diseases affecting millions of individuals worldwide. Available mood stabilizers and antidepressants remain unsatisfactory because of their delayed and partial therapeutic efficacy. Therefore, the development of targeted therapies, working more rapidly and being fully effective, is urgently needed. In this context, the protein kinase C (PKC) signaling system, which regulates multiple neuronal processes implicated in mood regulation, can constitute a novel therapeutic target. This paper reviews the currently available knowledge regarding the role of the PKC signaling pathway in the pathophysiology of mood disorders and the therapeutic potential of PKC modulators. Current antidepressants and mood stabilizers have been shown to modulate the PKC pathway, and the inhibition of this intracellular signaling cascade results in antimanic-like properties in animal models. Disrupted PKC activity has been found both in postmortem brains and platelet from patients with mood disorders. Finally, the PKC inhibitor tamoxifen has recently demonstrated potent antimanic properties in several clinical trials. Overall, emerging data from preclinical and clinical research suggest an imbalance of the PKC signaling system in mood disorders. Thus, PKC may be a critical molecular target for the development of innovative therapeutics.     

Understanding the Impact of Brain Disorders: Towards a ‘Horizontal Epidemiology’ of Psychosocial Difficulties and Their Determinants

Objective

To test the hypothesis of ‘horizontal epidemiology’, i.e. that psychosocial difficulties (PSDs), such as sleep disturbances, emotional instability and difficulties in personal interactions, and their environmental determinants are experienced in common across neurological and psychiatric disorders, together called brain disorders.

Study Design

A multi-method study involving systematic literature reviews, content analysis of patient-reported outcomes and outcome instruments, clinical input and a qualitative study was carried out to generate a pool of PSD and environmental determinants relevant for nine different brain disorders, namely epilepsy, migraine, multiple sclerosis, Parkinson’s disease, stroke, dementia, depression, schizophrenia and substance dependency. Information from these sources was harmonized and compiled, and after feedback from external experts, a data collection protocol including PSD and determinants common across these nine disorders was developed. This protocol was implemented as an interview in a cross-sectional study including a convenience sample of persons with one of the nine brain disorders. PSDs endorsed by at least 25% of patients with a brain disorder were considered associated with the disorder. PSD were considered common across disorders if associated to 5 out of the 9 brain disorders and if among the 5 both neurological and psychiatric conditions were represented.

Setting

The data collection protocol with 64 PSDs and 20 determinants was used to collect data from a convenience sample of 722 persons in four specialized health care facilities in Europe.

Results

57 of the PSDs and 16 of the determinants included in the protocol were found to be experienced across brain disorders.

Conclusion

This is the first evidence that supports the hypothesis of horizontal epidemiology in brain disorders. This result challenges the brain disorder-specific or vertical approach in which clinical and epidemiological research about psychosocial difficulties experienced in daily life is commonly carried in neurology and psychiatry and the way in which the corresponding health care delivery is practiced in many countries of the world.     

Erratum: Human Demography in the Pleistocene: Do Mitochondrial and Nuclear Genes Tell the Same Story? Evol. Anthropol. 8: 81–86.

Eugene E. Harris and Jody Hey (1999). Human Demography in the Pleistocene: Do Mitochondrial and Nuclear Genes Tell the Same Story? Evol. Anthropol. 8: 81–86. On page 84 at the end of 1st paragraph of the 2nd column should read “. . .intergenetic variation Xq 13.3 to about 535,000 years,³⁹. . .” On page 84 in the 2nd paragraph of the 3rd column should read “. . .and seem to indicate widespread or restricted gene flow among populations.”^19,48,49 On page 85 in the 2nd paragraph of the 1st column should read “. . .united by gene flow at zones of overlap.”⁵³     

Which Neurodevelopmental Disorders Get Researched and Why?

Aim

There are substantial differences in the amount of research concerned with different disorders. This paper considers why.

Methods

Bibliographic searches were conducted to identify publications (1985–2009) concerned with 35 neurodevelopmental disorders: Developmental dyslexia, Developmental dyscalculia, Developmental coordination disorder, Speech sound disorder, Specific language impairment, Attention deficit hyperactivity disorder, Autistic spectrum disorder, Tourette syndrome, Intellectual disability, Angelman syndrome, Cerebral palsy, Cornelia de Lange syndrome, Cri du chat syndrome, Down syndrome, Duchenne muscular dystrophy, Fetal alcohol syndrome, Fragile X syndrome, Galactosaemia, Klinefelter syndrome, Lesch-Nyhan syndrome, Lowe syndrome, Marfan syndrome, Neurofibromatosis type 1, Noonan syndrome, Phenylketonuria, Prader-Willi syndrome, Rett syndrome, Rubinstein-Taybi syndrome, Trisomy 18, Tuberous sclerosis, Turner syndrome, Velocardiofacial syndrome, Williams syndrome, XXX and XYY. A publication index reflecting N publications relative to prevalence was derived.

Results

The publication index was higher for rare than common conditions. However, this was partly explained by the tendency for rare disorders to be more severe.

Interpretation

Although research activity is predictable from severity and prevalence, there are exceptions. Low rates of research, and relatively low levels of NIH funding, characterise conditions that are the domain of a single discipline with limited research resources. Growth in research is not explained by severity, and was exceptionally steep for autism and ADHD.     

Autistic Disorders and Schizophrenia: Related or Remote? An Anatomical Likelihood Estimation

Shared genetic and environmental risk factors have been identified for autistic spectrum disorders (ASD) and schizophrenia. Social interaction, communication, emotion processing, sensorimotor gating and executive function are disrupted in both, stimulating debate about whether these are related conditions. Brain imaging studies constitute an informative and expanding resource to determine whether brain structural phenotype of these disorders is distinct or overlapping. We aimed to synthesize existing datasets characterizing ASD and schizophrenia within a common framework, to quantify their structural similarities. In a novel modification of Anatomical Likelihood Estimation (ALE), 313 foci were extracted from 25 voxel-based studies comprising 660 participants (308 ASD, 352 first-episode schizophrenia) and 801 controls. The results revealed that, compared to controls, lower grey matter volumes within limbic-striato-thalamic circuitry were common to ASD and schizophrenia. Unique features of each disorder included lower grey matter volume in amygdala, caudate, frontal and medial gyrus for schizophrenia and putamen for autism. Thus, in terms of brain volumetrics, ASD and schizophrenia have a clear degree of overlap that may reflect shared etiological mechanisms. However, the distinctive neuroanatomy also mapped in each condition raises the question about how this is arrived in the context of common etiological pressures.     

The Rise of Eating Disorders in Japan: Issues of Culture and Limitations of the Model of “westernization”

As the first non-Western nation in contemporary history to become a major industrialized economic power, Japan is central to the debate on cultural relativism in psychiatric nosologies, and the study of eating disorders in Japan contributes to the complex discussion of the impact of culture and history on the experience, diagnosis and treatment of such disorders (R. Gordon 2001; Palmer 2001). Without question, the rise in eating disorders in Japan correlated with increasing industrialization, urbanization, and the fraying of traditional family forms following World War II. While the case of Japan confirms that the existence of eating disorders appears to be linked with these broader social transformations, it also points to the importance of specific cultural and historical factors in shaping the experience of eating disorders. In this article, we explore two particular dimensions of culture in contemporary Japan: (1) gender development and gender role expectations for females coming of age; and (2) beauty ideals and the role of weight and shape concerns in the etiology of eating disorders. Our analysis of these dimensions of culture, and the data accruing from empirical and qualitative research, reveal limitations to the model of Westernization and call for a more culturally sensitive search for meaning in both describing and explaining eating disorders in Japan today.