https://archive-ouverte.unige.ch/unige:101745/ATTACHMENT01

The role of testosterone in social interaction

Although there are dozens of books on cognitive therapy of depression, a majority are edited volumes and relatively few are distinguished by the comprehensive mastery of the material and clarity of exposition apparent in this book by Clark, Beck, and Alford. This volume offers a relatively up-to-date (circa 1999) and scholarly review of the phenomenology of depressive disorders from the cognitive perspective, along with detailed evaluations of the literature pertaining to the key hypotheses of the cognitive model of depression.

The book is well written, but it is not for the cognitive therapy neophyte. It is rather lengthy and detailed. Moreover, as might be expected, the discussions of criticisms of the cognitive model are somewhat partisan, and the authors consistently present the cognitive model as dynamic and organic (as opposed to static) in response to new and at times contradictory data. Nevertheless, it provides a valuable source companion to the classic but outdated treatment manual originally published in 1979 by Dr. Beck and colleagues (Cognitive Therapy of Depression) and the excellent how-to book by Dr. Judith Beck, Cognitive Therapy: Basics and Beyond, which was published in 1995.

Subheads, periodic summaries, and statements of key points within each chapter focus the reader's attention and enhance comprehension; the authors are, after all, expert cognitive therapists. There is a minimum of redundancy across the 11 chapters, and although the copyediting is not infallible (e.g., influential early behaviorist Charles Ferster is referred to as “Fester” in both the text and the reference list), typographical errors are few.

As a treatment researcher, I was disappointed that the authors did not devote at least one chapter to reviewing the comparative outcome research studies of CT. Outcomes data has been one of the key aspects of the scientific foundation of CT for nearly 25 years.1 This is a shortcoming, particularly in view of work linking early evidence of CT's superiority (over other therapies) to strong allegiance effects2 and the increasing number of studies in which CT has not performed so well under more “neutral”3,4 or even potentially “allegiance-disadvantaged”5–7 conditions. Ultimately, the most pragmatic benefit of an elegant, scientifically strong model of psychopathology is the ability to translate such knowledge into greater or more enduring benefits for our patients. In this regard, it is not yet clear that the elaborate suprastructure of schema theory actually adds such benefits relative to simpler behavioral5 or interpersonal6 models of intervention.

Scientific Foundations of Cognitive Theory and Therapy of Depression

Gene-Stress-Epigenetic Regulation of FKBP5: Clinical and Translational Implications.

Mismatch or cumulative stress: toward an integrated hypothesis of programming effects.

We provide a theoretical and empirical basis for the claim that individual differences exist in developmental plasticity and that phenotypic plasticity should be a subject of study in its own right. To advance this argument, we begin by highlighting challenges that evolutionary thinking poses for a science of development and psychopathology, including for the diathesis-stress framework that has (fruitfully) guided so much empirical inquiry on developmental risk, resilience, and dysregulation. With this foundation laid, we raise a series of issues that the differential-susceptibility hypothesis calls attention to, while highlighting findings that have emerged over just the past several years and are pertinent to some of the questions posed. Even though it is clear that this new perspective on Person × Environment interaction is stimulating research and influencing how hypotheses are framed and data interpreted, a great many topics remain that need empirical attention. Our intention is to encourage students of development and psychopathology to treat phenotypic plasticity as an individual-difference construct while exploring unknowns in the differential-susceptibility equation.

/pdf/beyond-risk-resilience-and-dysregulation-phenotypic-1hq90d27n4.pdf

Beyond risk, resilience, and dysregulation: Phenotypic plasticity and human development

There is a growing body of data suggesting that gene-environment interaction is critical in the characterization of personality traits; however, previous studies have not taken into consideration variability in parental rearing as an environmental factor. In this study, we examined the effects of the interaction between the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and parental rearing on personality traits in 710 healthy Japanese subjects. Perceived parental rearing was assessed by the Parental Bonding Instrument (PBI), which consists of the care and protection factors. Assessment of personality traits was performed by the temperament and character inventory (TCI), which has seven dimensions, i.e. novelty seeking, harm avoidance, reward dependence, persistence, self-directedness, cooperativeness and self-transcendence. Parental rearing has significant main effects on some TCI dimensions, but no significant main effects of the BDNF genotype on the TCI scores were found. The interaction between the BDNF genotype and maternal care of the PBI had significant effects on harm avoidance and self-directedness of the TCI. Post hoc analyses showed that decreased maternal care was correlated with increased harm avoidance and decreased self-directedness, and for both personality traits the partial correlation coefficient was highest in the Met/Met genotype group and lowest in the Val/Val genotype group and the value of the Val/Met genotype group was in the middle. Data from this study suggest that the BDNF Val66Met polymorphism modulates the effects of parental rearing, especially maternal care, on harm avoidance and self-directedness in healthy subjects.

The brain-derived neurotrophic factor Val66Met polymorphism modulates the effects of parental rearing on personality traits in healthy subjects

Association study between a functional polymorphism of FK506-binding protein 51 (FKBP5) gene and personality traits in healthy subjects.

The effects of dysfunctional parenting styles on interpersonal sensitivity were studied in 640 Japanese volunteers. Interpersonal sensitivity was assessed by the Interpersonal Sensitivity Measure (IPSM), and perceived parental rearing was evaluated by the Parental Bonding Instrument (PBI), which is consisted of care and protection factors. Parental rearing was classified into 4 types, i.e., optimal parenting (high care/low protection), affectionate constraint (high care/high protection), neglectful parenting (low care/low protection), and affectionless control (low care/high protection). Males with paternal affectionless control showed higher total IPSM scores than those with paternal optimal parenting (p = 0.022). Females with maternal affectionate constraint (p = 0.001), neglectful parenting (p = 0.022), and affectionless control (p = 0.003) showed higher total IPSM scores than those with maternal optimal parenting. In males and females, dysfunctional parenting styles by the opposite-sex parents did not affected total IPSM scores. The present study suggests that in both males and females interpersonal sensitivity is increased by dysfunctional parenting styles by the same-sex parents.

Dysfunctional parenting styles increase interpersonal sensitivity in healthy subjects.

Parental overprotection increases interpersonal sensitivity in healthy subjects.

Background
It has been suggested that interpersonal sensitivity, a personality trait associated with depression and anxiety disorders, is linked with attachment insecurity. To confirm this link, we studied the correlations of interpersonal sensitivity with working models of the self and other.

/pdf/correlations-of-interpersonal-sensitivity-with-negative-3z5yqrr668.pdf

Yoshihiko Matsumoto

Papers

The brain-derived neurotrophic factor Val66Met polymorphism modulates the effects of parental rearing on personality traits in healthy subjects

Association study between a functional polymorphism of FK506-binding protein 51 (FKBP5) gene and personality traits in healthy subjects.

Dysfunctional parenting styles increase interpersonal sensitivity in healthy subjects.

Parental overprotection increases interpersonal sensitivity in healthy subjects.

Correlations of interpersonal sensitivity with negative working models of the self and other: evidence for link with attachment insecurity.