We examine the impact of winning/success and defeat/failure, on individual and family functioning. Defeat, at both the individual and family level, triggers an array of psychological and physiological reactions that, while adaptation on the one hand, may trigger or perpetuate problems. We explore these mechanisms along with broader evolutionary forces operating on the family. A number of therapeutic interventions are offered, designed to deactivate the mechanisms triggered by failure/defeat, disrupt maladaptive cycles, and overcome resistance to change.
We draw on an article published in 1973 in this journal. We described how we taught “Geoff,” a 6-year old boy with autism, an elementary form of sign language during the course of 24 one-hour sessions held over a 12-week period (Webster et al. in J Autism Child Schizophr 3:337–346, 1973; Fruchter in Autism: new directions in research and education, pp 184–186, 1980). Here, we describe how it is that Geoff has maintained the vestiges of what we taught him (and indeed what he taught us) over the long span. This basic communication strategy has endured well and continues to contribute to his enjoyment of life.
Child maltreatment is a prevalent societal problem that has been linked to a wide range of social, psychological, and emotional difficulties. Maltreatment impacts on two putative evolved psychobiological systems in particular, the attachment system and the social rank system. The maltreatment may disrupt the child's ability to form trusting and reassuring relationships and also creates a power imbalance where the child may feel powerless and ashamed. The aim of the current article is to outline an evolutionary theory for understanding the impact of child maltreatment, focusing on the interaction between the attachment and the social rank system. We provide a narrative review of the relevant literature relating to child maltreatment and these two theories. This research highlights how, in instances of maltreatment, these ordinarily adaptive systems may become maladaptive and contribute to psychopathology. We identify a number of novel hypotheses that can be drawn from this theory, providing a guide for future research. We finally explore how this theory provides a guide for the treatment of victims of child maltreatment. In conclusion, the integrated theory provides a framework for understanding and predicting the consequences of maltreatment, but further research is required to test several hypotheses made by this theory.
OBJECTIVE:This study examined the direct and indirect outcomes of a social skills group intervention for children with high functioning autism spectrum disorders and their parents.METHOD:Thirty-five children and their parents participated in the program evaluation. Children and parents completed measures of child social skills and problem behaviors. Children reported on their self-concept, and parents reported on their psychological acceptance and empowerment.RESULTS:Results indicate significant increases in overall child social skills according to parent and child report, in child general self-worth, and in parent service empowerment and psychological acceptance.CONCLUSION:While past program evaluations of social skills groups highlight changes in social competence, taking a broader perspective on the types of positive outcomes suggests potential benefits for both child and parent.
OBJECTIVE:To examine the connection between winning and losing and family functioning. We do this by hypothesizing a link between successful outcomes in individual competition and in functional family interaction. This enables us to show how therapeutic interventions can be directed toward the attachment system, by lowering anxiety and fostering mutual trust, and toward the social rank system, by promoting success and feelings of empowerment.METHOD:A search of online databases was conducted with key search terms related to winning and losing, and their effects on attachment patterns and family interactions.RESULTS:Winning in agonistic encounters has been associated with lowered dysphoria, anxiety, and hostility. These affective states trigger positive patterns of family interaction through their effect on the social rank and attachment systems.CONCLUSION:Continued success promotes adaptive cycles of interaction, whereas inability to accept loss has the reverse effect. Early humans, who were more successful in competition, were better able to promote the survival and well-being of other family members, which would have accelerated our phylogenetic adaptation.
Objective: To advance a new evolutionary model that examines the effects of winning and losing on mood and physiological variables. Previous studies have focused on the involuntary defeat strategy in de-escalating conflict. Here, we propose that there also exists an involuntary winning strategy (IWS) that is triggered by success and characterized by euphoria and increased self-confidence. It motivates efforts to challenge, and promotes reconciliation. Method: Previous studies are presented, including data on student athletes, demonstrating the impact of winning and losing on mood. Results: Winning is consistently shown to be related to physiological changes such as increased testosterone and serotonin levels in primates. It reliably leads to mood changes that serve to motivate winners to continue their competitive efforts. Conclusion: When the IWS functions optimally, success leads to success in an adaptive cycle. Over time, the initial differences between the winners and losers of agonistic encounters become magnified in a process known as difference amplification. As a result of assortative mating, the children of people who have entered into an adaptive cycle will inherit traits from both parents that will, in turn, give them an increased competitive advantage. In this manner, difference amplification could have accelerated human evolution by natural selection. Vignettes of clinical interventions are also used to illustrate therapeutic strategies designed to disrupt maladaptive cycles and promote adaptive behaviour.
This is the second edition of a multidisciplinary approach to the pervasive developmental disorders (PDD). PDD encompasses autism, which ranges from profound mental retardation to people with average IQ or above and Aspergers syndrome, which is limited to those with average IQ or above. However, the distinction between autism and Asperger syndrome is very blurred. Though PDD is heterogeneous, one common feature is a problem in reciprocal social interaction. Even people with average IQ or above often have learning disabilities and sensory anomalies, possibly involving all of the perceptual modes. The lack of uniformity of criteria for diagnosing these conditions has contributed to contradictory findings. The first chapter provides a helpful guide to diagnosis. However, one would have welcomed a discussion of the numerous diagnostic questionnaires in use.
Structural variation (copy number variation [CNV] including deletion and duplication, translocation, inversion) of chromosomes has been identified in some individuals with autism spectrum disorder (ASD), but the full etiologic role is unknown. We performed genome-wide assessment for structural abnormalities in 427 unrelated ASD cases via single-nucleotide polymorphism microarrays and karyotyping. With microarrays, we discovered 277 unbalanced CNVs in 44% of ASD families not present in 500 controls (and re-examined in another 1152 controls). Karyotyping detected additional balanced changes. Although most variants were inherited, we found a total of 27 cases with de novo alterations, and in three (11%) of these individuals, two or more new variants were observed. De novo CNVs were found in similar to 7% and similar to 2% of idiopathic families having one child, or two or more ASD siblings, respectively. We also detected 13 loci with recurrent/overlapping CNV in unrelated cases, and at these sites, deletions and duplications affecting the same gene(s) in different individuals and sometimes in asymptomatic carriers were also found. Notwithstanding complexities, our results further implicate the SHANK3-NLGN4-NRXN1 postsynaptic density genes and also identify novel loci at DPP6-DPP10-PCDH9 (synapse complex), ANKRD11, DPYD, PTCHD1, 15q24, among others, for a role in ASD susceptibility. Our most compelling result discovered CNV at 16p11.2 (p = 0.002) (with characteristics of a genomic disorder) at similar to 1% frequency. Some of the ASD regions were also common to mental retardation loci. Structural variants were found in sufficiently high frequency influencing ASD to suggest that cytogenetic and microarray analyses be considered in routine clinical workup.
Difference amplification was the process whereby the difference in fitness between two competing individuals in early man was magnified by the results of the competition. It arises from adaptive and maladaptive cycles (characterized by depression and anxiety) that are initiated by winning and losing agonistic encounters. Those who were most successful were likely to find mates that were also successful and vice versa. This would have contributed to well-endowed progeny and accelerated phylogenetic evolution. The adaptive and maladaptive cycles of the difference amplification model are also a feature of the social rank and attachment models. Ineffective operation of social rank and attachment systems is associated with anxiety and depression. This paper introduces the notion that the efficient operation of these two systems in hierarchical encounters accelerates the phylogenetic adaptation of the individual’s genetic line. This suggests an adaptive function of attachment and social rank mechanisms that has not been previously described. Social rank, attachment and difference amplification should be viewed as different aspects of a comprehensive evolutionary model of depression and anxiety. This new model has psychotherapeutic implications.
We trace the development of ideas about the relation of mood to social rank and territory. We suggest that elevated mood enabled a person to rise in rank and cope with the increased activities and responsibilities of a leadership role, while depressed mood enabled a person to accept low rank and to forego the rewards associated with high rank. This led to the concept of a trio of agonist/investor strategy sets, each consisting of escalating and de-escalating strategies, one set at each of the three levels of the triune forebrain. Depressed mood can be seen as a de-escalating (appeasement) strategy at the lowest (reptilian) level; this should facilitate de-escalation at the highest (rational) level, but sometimes this rational level de-escalation is blocked (e.g., by stubbornness, courage, pride or ambition) and then clinical depression may ensue. These evolved psychobiological mechanisms survived the partial transition from agonistic to prestige competition. We discuss difficulties which have arisen with our ideas, and their implications for clinical work and research.
This paper explores the well-known overlap of anxiety and depressive symptoms in mood and anxiety disorders. We suggest that the regulation of both negative and positive affects has served important adaptive functions (especially for coping with threats, losses, failures and defeats), and that in some contexts both affect systems require regulation at the same time (e.g. increased anxiety coupled with low positive affect). Here we will focus on how low positive and high negative affect in the individual experiencing losses and defeats regulates their competitive and acquisitive behaviors and in some cases may prevent, de-escalate, and possibly terminate on-going agonistic (hierarchical) encounters. When high negative affect (anxiety) and low positive affect (depression) fail to fulfill their adaptive roles, they tend to persist and often intensify. This may lead each affect control system to stimulate specific types of anxiety and depressive disorders, exhibiting features reminiscent of the original adaptive function of the behavior. Furthermore, as these different systems tend to operate in a synchronous fashion, the psychiatric syndromes they generate are often comorbid.
This article suggests that, in prehistoric man, the results of competition magnified the effect of small genetic differences between competing individuals, thereby increasing the differential in their relative reproductive success (difference amplification). This had the effect of accelerating the evolution of early man. The differential effect of success and failure on competing individuals led to “difference amplification”. These mechanisms can still be observed today. This model is relevant to psychotherapy with depressed clients.
Selective mutism (SM) occurs when a child persistently lacks speech in some social situations but not in others, despite the ability to use and comprehend language. While considered to be related to anxiety, SM is poorly understood and studies of SM children are often based on parent reports. This study developed a unique, non-verbally based assessment protocol for SM children in order to better characterize their clinical profile, language abilities, and learning abilities. A comparison was done with a group of children of similar age, with social phobia (SP) but no SM, to search for characteristics that might distinguish SM from other anxiety disorders. Twenty-three children participated in the study (14 SM and 9 SP). The assessment protocol included standardized anxiety rating scales, cognitive and academic tests, and a speech and language assessment. SM and SP groups showed similar levels of anxiety and academic ability, but the SM group showed some language impairments relative to the SP group. Though requiring replication with a larger sample and nonclinical comparison group, the results suggest that SM children can be assessed by non-verbal means and that their disorder is characterized by anxiety and subtle language impairments. (C) 2003 Wiley-Liss, Inc.
Evolved mechanisms underpinning attachment and social rank behavior may be the basis for some forms of major depression, especially those associated with chronic stress. We note the heterogeneity of depression, but suggest that some of its core symptoms, such as behavioral withdrawal, low self-esteem and anhedonia, may have evolved in order to regulate behavior and mood and convey sensitivity to threats and safety. Focusing on the evolved mental mechanisms for attachment and social rank helps to make sense of (1) depression's common early vulnerability factors (e.g., attachment disruptions, neglect and abuse), (2) the triggering events (e.g., loss of close relationships, being defeated and/or trapped in low socially rewarding or hostile environments), and (3) the psychological preoccupations of depressed people (e.g., sense of unlovableness, self as inferior and a failure). This focus offers clues as to how these two systems interact and on how to intervene.
Sloman, Leon MRCS, LRCP, FRCPC*; Konstantareas, Mary PhD†; Remington, Gary MD, PhD, FRCPC* Author Information
The attachment and social rank systems are biological-evolutionary systems that can serve as models for conceptualizing family interaction. By exploring both their unique and interrelated impact on affect regulation, we can differentiate between processes that foster healthy growth and those leading to individual psychopathology. This perspective facilitates the integration of biological and psychological models, and has therapeutic implications. It also integrates well with other family therapy models.
North Bay Psychiatric Hospital Developmental Disabilities Program North Bay, Ontario P1B 8L1 Canada