In social psychology, social defeat is the negative experience of being excluded from the majority group. The term is used in the study of the physiological and behavioral effects of hostile interactions among either animals or humans, in either a dyadic or in a group-individual context, potentially greatly affecting control over resources, access to mates, and social positions.
Research on social stress has accumulated a useful body of knowledge, providing perspective on the effects of detrimental social and environmental interaction on the brain. Research and experimentation suffer from many methodological difficulties: usually a lack of ecological validity (similarity with natural conditions and stressors) or are not amenable to scientific investigation (difficult to test and verify).
Social psychology approaches to human aggression have developed a multitude of perspectives, based on observations of human phenomena like bullying, physical and verbal abuse, relational and indirect aggression, etc. Despite the richness of theories developed, the body of knowledge generated has not satisfied scientific requirements of testability and verifiability.
Animal studies of within-species aggression developed in 2 main branches: A) approaches based on laboratory experiments, on controlled conditions, allowing the measurement of behavioral, endocrine and neurological variables, but with the shortcoming of applying unnatural stressors (such as foot-shocks and restraint stress) in unnatural conditions (laboratory cages rarely approximate native habitats); B) approaches based on observations of animals in naturalistic settings, which avoided artificial environments and unnatural stresses, but usually not allowing the measurement of physiological effects or the manipulation of relevant variables.
In real life situations, animals (including humans) have to cope with stresses generated within their own species, during their interactions with conspecifics, especially due to recurrent struggles over the control of limited resources, mates and social positions (Bjorkqvist, 2001; Rohde, 2001; Allen & Badcock, 2003).
Social defeat is a source of chronic stress in animals and humans, capable of causing significant changes in behaviour, brain functioning, physiology, neurotransmitter and hormone levels, and health (Bjorkqvist, 2001; Rohde, 2001; Allen & Badcock, 2003).
History
The social defeat approach was originated from animal experiments, using the "resident-intruder" paradigm, in which an animal was placed in the cage of another animal or group of animals of the same species, in a manner that allowed a non-lethal conflict. It has been documented to produce anxiety-like and depressive-like behavioral declines in susceptible mice, for instance.[1]
If animals are allowed to fight on a single occasion only, it is usually regarded as a model of acute stress; if they are allowed to fight on several occasions, on different days, consecutive or not, it is regarded as a model of chronic stress. After the defeat or in the interval between fights, the subordinate animal may also be exposed to threats from the dominant one, by having to stay in a cage or compartment beside or nearby the dominant, exposed to its visual or olfactory cues.
Later, the social defeat approach was also applied to observations of animal within-species aggression, in the wild, which suggested that the hypotheses generated on artificial laboratory settings can also be applied in observed in natural settings, confirming the predictions of the model.
The social defeat model has been extended to include observations of human aggression, bullying, relational aggression, chronic subordination and humiliation. The social defeat model attempts to extend animal studies to include human behaviour as well, in contrast to the social psychology study of aggression, in which comparisons are drawn exclusively from experiments involving humans (Bjorkqvist, 2001; Rohde, 2001).
Bullying has interesting parallels with animal models of social defeat, the bully being equivalent to the dominant animal and the victim the subordinate one. At stake are possessions of material objects, money, etc., social position in the group, represented by in-group prestige, and the consequent lack of access to mates, including for socio-sexual behaviors like copulation. Human victims typically experience symptoms like low self-esteem (due to low regard by the group), feelings of depression (due to unworthiness of efforts), social withdrawal (reduced investments in the social environment), anxiety (due to a threatening environment), and they can also be shown to experience a plethora of physiological effects, e.g. increased corticosterone levels, and also a shift towards sympathetic balance in the autonomic nervous system (Bjorkqvist, 2001).
Research about human aggression, usually conducted by psychologists or social psychologists, resembles to a great extent the research about social defeat and animal aggression, usually conducted by biologists or physiological psychologists. However, there is the problem of the use of different terminologies for similar concepts, which hinders communication between the two bodies of knowledge (Bjorkqvist, 2001).
Similarly, research on depression has employed similar constructs, such as learned helplessness, although that theory is focused on the perceived inability to escape any sort of negative stimuli rather than on social factors.
Social defeat is a very potent stressor and can lead to a variety of behavioral effects, like social withdrawal (reduced interactions with conspecifics), lethargy (reduced locomotor activity), reduced exploratory behavior (of both open field and novel objects), anhedonia (reduced reward-related behaviors), decreased socio-sexual behaviors (including decreased attempts to mate and copulate after defeat), various motivational deficits, decreased levels of testosterone (due to a decline in the functionality of the Leydig cells of the testes), increased tendencies to stereotyped behaviours and self-administration of drugs and alcohol (Rygula et alli, 2005; Huhman, 2006).
Both animal and human studies suggest that the social environment has a strong influence on the consequences of stresses. This finding seems to be especially true in the case of social stresses, like social defeat (Bjorkqvist, 2001; Rygula et alli, 2005; de Jong et alli, 2005).
In animal studies, animals housed collectively showed reduced symptoms after defeat, in comparison with those housed alone; and animals that live in more stable groups (with stable hierarchies, less intra-group aggression) exhibit reduced effects after a defeat, in comparison with those housed in a more unstable group (de Jong et alli, 2005). In separate studies, defeat behaviors can be modulated by acetylcholine (Smith et al., 2015).[2]
In human studies, individuals with greater support seem to be protected against excessive neuroendocrine activation, thereby reducing the adverse effects of stresses in general, and especially stresses of social origin.
This apparent confusion, in which social defeat generates behavioral and neuroendocrine effects, both of which depending on social contextual variables, raises the question of how to interpret this data. A useful concept is the concept of “causal chain”, in which recurrent evolutionary events, in this case intra-specific competition, generates selective pressures that last for thousands of generations, influencing a whole species. This way physiological phenomena may evolve, in this case the referred neuro-endocrine phenomena, to facilitate adaptive patterns of action by individuals, in this case the referred behavioral effects. According to this framework, selective pressures generated by intra-specific competition can be considered as the ultimate cause, the neuroendocrine phenomena can be considered to be the proximate causes (sometimes also called mechanisms or moderators) and the observed behavioral alterations are considered the effects (the end events in the causal chain)(Gilbert et alli, 2002; Allen & Badcock, 2003; Rygula et alli, 2005).
Some authors, for example Randolph Nesse, warn us that patterns of behavior commonly considered inappropriate or even pathological may well have adaptive value. Evolutionary psychology provides several possible explanations for why humans typically respond to social dynamics in the way that they do, including possible functions of self-esteem in relation to dominance hierarchies. In a synchronic[check spelling] perspective behaviors considered abnormal may in fact be part of an adaptive response to stressors in modern or at least in old environments, for example social stressors from chronic subordination or interpersonal conflicts (Gilbert et alli, 2002; Allen & Badcock, 2003). Similarly, from a diachronic perspective various behaviors related to intra-species competition or predator-prey relationships may have played a role in the evolution of human abilities, for example defensive immobilization is hypothesized to have played a role in the evolution of both human parent-child attachment[3] and theory of mind.[4]
Fear is an intensely unpleasant primal emotion in response to perceiving or recognizing a danger or threat. Fear causes psychological changes that may produce behavioral reactions such as mounting an aggressive response or fleeing the threat. Fear in human beings may occur in response to a certain stimulus occurring in the present, or in anticipation or expectation of a future threat perceived as a risk to oneself. The fear response arises from the perception of danger leading to confrontation with or escape from/avoiding the threat, which in extreme cases of fear can be a freeze response.
Serotonin or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter. Its biological function is complex, touching on diverse functions including mood, cognition, reward, learning, memory, and numerous physiological processes such as vomiting and vasoconstriction.
Aggression is a behavior aimed at opposing or attacking something or someone. Though often done with the intent to cause harm, it can be channeled into creative and practical outlets for some. It may occur either reactively or without provocation. In humans, aggression can be caused by various triggers. For example, built-up frustration due to blocked goals or perceived disrespect. Human aggression can be classified into direct and indirect aggression; whilst the former is characterized by physical or verbal behavior intended to cause harm to someone, the latter is characterized by behavior intended to harm the social relations of an individual or group.
Stress, whether physiological, biological or psychological, is an organism's response to a stressor such as an environmental condition. Stress is the body's method of reacting to a condition such as a threat, challenge or physical and psychological barrier. There are two hormones that an individual produces during a stressful situation, well known as adrenaline and cortisol. There are two kinds of stress hormone levels. Resting (basal) cortisol levels are normal everyday quantities that are essential for standard functioning. Reactive cortisol levels are increases in cortisol in response to stressors. Stimuli that alter an organism's environment are responded to by multiple systems in the body. In humans and most mammals, the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis are the two major systems that respond to stress.
The hypothalamic–pituitary–adrenal axis is a complex set of direct influences and feedback interactions among three components: the hypothalamus, the pituitary gland, and the adrenal glands. These organs and their interactions constitute the HPA axis.
Psychoneuroimmunology (PNI), also referred to as psychoendoneuroimmunology (PENI) or psychoneuroendocrinoimmunology (PNEI), is the study of the interaction between psychological processes and the nervous and immune systems of the human body. It is a subfield of psychosomatic medicine. PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.
Irritability is the excitatory ability that living organisms have to respond to changes in their environment. The term is used for both the physiological reaction to stimuli and for the pathological, abnormal or excessive sensitivity to stimuli.
Vasopressin V1b receptor (V1BR) also known as vasopressin 3 receptor (VPR3) or antidiuretic hormone receptor 1B is a protein that in humans is encoded by the AVPR1B gene.
Allostatic load is "the wear and tear on the body" which accumulates as an individual is exposed to repeated or chronic stress. The term was coined by Bruce McEwen and Eliot Stellar in 1993. It represents the physiological consequences of chronic exposure to fluctuating or heightened neural or neuroendocrine response which results from repeated or prolonged chronic stress.
Tend-and-befriend is a behavior exhibited by some animals, including humans, in response to threat. It refers to protection of offspring (tending) and seeking out their social group for mutual defense (befriending). In evolutionary psychology, tend-and-befriend is theorized as having evolved as the typical female response to stress.
Chronic stress is the physiological or psychological response induced by a long-term internal or external stressor. The stressor, either physically present or recollected, will produce the same effect and trigger a chronic stress response. There is a wide range of chronic stressors, but most entail relatively prolonged problems, conflicts and threats that people encounter on a daily basis. And several chronic stressors, including "neighbourhood environment, financial strain, interpersonal stress, work stress and caregiving.", have been identified as associated with disease and mortality.
Animal psychopathology is the study of mental or behavioral disorders in non-human animals.
Wim E. Crusio is a Dutch behavioral neurogeneticist and a directeur de recherche with the French National Centre for Scientific Research in Talence, France.
Animal models of depression are research tools used to investigate depression and action of antidepressants as a simulation to investigate the symptomatology and pathophysiology of depressive illness or used to screen novel antidepressants. These models provide insights into molecular, genetic, and epigenetic factors associated with depression. Criteria for valid animal models include face, construct, and predictive validity. Endophenotypes, such as anhedonia, behavioral despair, changes in appetite, neuroanatomical alterations, neuroendocrine disturbances, alterations in sleep architecture, and anxiety-related behaviors, are evaluated in these models. Antidepressant screening tests are employed to assess the effects of genetic, pharmacological, or environmental manipulations. Stress models, including learned helplessness, chronic mild stress, and social defeat stress, simulate the impact of stressors on depression. Early life stress models, psychostimulant withdrawal models, olfactory bulbectomy, and genetically engineered mice contribute to a comprehensive understanding of depression's etiology and potential therapeutic interventions.
Social stress is stress that stems from one's relationships with others and from the social environment in general. Based on the appraisal theory of emotion, stress arises when a person evaluates a situation as personally relevant and perceives that they do not have the resources to cope or handle the specific situation.
Addiction vulnerability is an individual's risk of developing an addiction during their lifetime. There are a range of genetic and environmental risk factors for developing an addiction that vary across the population. Genetic and environmental risk factors each account for roughly half of an individual's risk for developing an addiction; the contribution from epigenetic risk factors to the total risk is unknown. Even in individuals with a relatively low genetic risk, exposure to sufficiently high doses of an addictive drug for a long period of time can result in an addiction. In other words, anyone can become an individual with a substance use disorder under particular circumstances. Research is working toward establishing a comprehensive picture of the neurobiology of addiction vulnerability, including all factors at work in propensity for addiction.
Behavioral endocrinology is a branch of endocrinology that studies the Neuroendocrine system and its effects on behavior. Behavioral endocrinology studies the biological mechanisms that produce behaviors, this gives insight into the evolutionary past. The field has roots in ethology, endocrinology and psychology.
Cognitive bias in animals is a pattern of deviation in judgment, whereby inferences about other animals and situations may be affected by irrelevant information or emotional states. It is sometimes said that animals create their own "subjective social reality" from their perception of the input. In humans, for example, an optimistic or pessimistic bias might affect one's answer to the question "Is the glass half empty or half full?"
Aggression in cattle is usually a result of fear, learning, and hormonal state, however, many other factors can contribute to aggressive behaviors in cattle.
Angela J. Grippo is an American neuroscientist and health psychologist known for her research on stress, mood disorders, and cardiovascular disease. She is an associate professor of psychology at Northern Illinois University.
References
↑ Lehmann, Michael L, Poffenberger, Chelsie N, Elkahloun, Abdel G, Herkenham, Miles. Analysis of cerebrovascular dysfunction caused by chronic social defeat in mice. Brain, Behavior, and Immunity. 2020;88. 735-747. doi:10.1016/j.bbi.2020.05.030.
Rohde, P. (2001). "The relevance of hierarchies, territories, defeat for depression in humans –hypotheses and clinical predictions". Journal of Affective Disorders. 65 (3): 221–230. doi:10.1016/S0165-0327(00)00219-6. PMID11511402.
Laviola, G.; Adriani, W.; Rea, M.; Aloe, L.; Alleva, E. (2004). "Social withdrawal, neophobia, and stereotyped behavior in developing rats exposed to neonatal asphyxia". Psychopharmacology. 175 (2): 196–205. doi:10.1007/s00213-004-1800-3. PMID14985924. S2CID24682349.
Bartolomucci, A; Palanza,P.; Sacerdote,P.; Panerai,A.E.; Sgoifo,A.; Dantzer,R.; Parmigiani, S (2005). "Social factors and individual vulnerability to chronic stress exposure". Neuroscience and Biobehavioral Reviews. 29 (1): 67–81. doi:10.1016/j.neubiorev.2004.06.009. PMID15652256. S2CID38146908.
Marinia, F; Pozzatob, C.; Andreettab, V.; Janssonc, B.; Arbanb, R.; Domenicic, E.; Carbonic, L. (2006). "Single exposure to social defeat increases corticotropin-releasing factor and glucocorticoid receptor mRNA expression in rat hippocampus". Brain Research. 1067 (1): 25–35. doi:10.1016/j.brainres.2005.10.002. PMID16360122. S2CID36113304.
Gilbert, P; Allan, S.; Brough, S.; Melley, S.; Miles, J.N.V. (2002). "Relationship of anhedonia and anxiety to social rank, defeat and entrapment". Journal of Affective Disorders. 71 (1–3): 141–151. doi:10.1016/S0165-0327(01)00392-5. PMID12167510.
Van Reeth, O; Weibel, L.; Spiegel, K.; Leproult, R.; Dugovic, C.; Maccari, S. (2000). "Physiology of sleep (review) - Interactions between stress and sleep; from basic research to clinical situations". Sleep Medicine Reviews. 4 (2): 201–219. doi:10.1053/smrv.1999.0097.
Rygula, R.; Abumaria, N.; Flugge, G.; Fuchs, E.; Ruther, E.; Haveman-Reinecke, U. (2005). "Anhedonia and motivational deficits in rats: Impact of chronic social stress". Behavioural Brain Research. 162 (1): 127–134. doi:10.1016/j.bbr.2005.03.009. PMID15922073. S2CID20487773.
Allen, N. B.; Badcock, P.B. (2003). "The Social Risk Hypothesis of Depressed Mood: Evolutionary, Psychosocial, and Neurobiological Perspectives". Psychological Bulletin. 129 (6): 887–913. doi:10.1037/0033-2909.129.6.887. PMID14599287.
Sloman, L.; Farvolden, P.; Gilbert, P.; Price, J. (2006). "The interactive functioning of anxiety and depression in agonistic encounters and reconciliation". Journal of Affective Disorders. 90 (2–3): 93–99. doi:10.1016/j.jad.2005.12.001. PMID16442166.
Sgoifo, A.; Costolia, T.; Meerlob, P.; Buwalda, B.; Pico'-Alfonsoa, M.A.; De Boerc, S.; Mussoa, E.; Koolhaas, J. (2005). "Individual differences in cardiovascular response to social challenge". Neuroscience and Biobehavioral Reviews. 29 (1): 59–66. doi:10.1016/j.neubiorev.2004.07.001. hdl:11381/1445989. PMID15652255. S2CID42806161.
de Jong JG, van der Vegt BJ, Buwalda B, Koolhaas JM (January 2005). "Social environment determines the long-term effects of social defeat". Physiol. Behav. 84 (1): 87–95. doi:10.1016/j.physbeh.2004.10.013. PMID15642611. S2CID45384785.
T. Steckler; N. H. Kalin; J. M. H. M. Reul (2005). Handbook of Stress and the Brain (part 2). pp.113+. ISBN978-0-444-51823-1.
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