The biology of trust is the study of physiological mechanisms involved in mediating trust in social attachments. It has been studied in terms of genetics, endocrinology and neurobiology.[1]
Trust is the intentional choice to believe the input of strangers because one believes they know the truth and have one's best interest at heart.[2] Trust is important in creating social attachments.
Social bonds is a characteristic present in many mammals and other vertebrae species.[3] However, there exists a paradox in the formation of social bonds in humans- while there are benefits, drawbacks, such as judgment, vulnerabilities to harmful physical and emotional hurt do exist.[4] And overarching all of this is trust, which is marked by the intentional choice to rely on another individual for an underlying purpose, despite drawbacks- a factor in social bonds with biological implications.[2]
Neural Mechanisms edit
Neuropeptides, specifically oxytocin (OT) and arginine-vasopressin (AVP), have been shown to be involved in physiological mechanisms of social behavior.[5] Sex hormones, have also been correlated.[5] The involvement of OT and AVP in trust and social attachment can be attributed the fact that both molecules can be released as neurotransmitters or hormones throughout the body.[5] OT and AVP act as neurotransmitters when released directly by the hypothalamus; they act as neurohormones when released peripherally by the pituitary gland.[5] So, both AVP and OT are peripheral (functioning throughout the body) and central (functioning within the brain).[5][6]
Both social bonding and social attachment involve OT.[6] In female rats that had OT injected directly into the brain, studies found that the OT rats exhibited full maternal behavior towards foster pups.[6] In studies involving human subjects, increases in OT were observed in subjects who received intentional trust signals in a controlled trust game.[5] When an OT receptor antagonist was injected in rats, it was found that there was a decrease in social recognition and decreased social bonding.[5] In a similar study, injection of central or peripheral OT in the lateral septum or main olfactory bulbs showed an increase in social recognition and interaction.[5] Studies have also shown the integration of OT with Dopamine (DA) and AVP in social bonding.[3] Function of DA neurons on OT receptors bound in the striatum strengthen social attachment by directing the reward pathways in which DA is involved with towards behavioral trust.[3]
Social recognition memory also involves AVP.[5] In a study conducted on Brattleboro rats that carried a mutation inhibiting AVP production, injection of central and peripheral AVP was correlated with an improvement in social recognition.[5] As with OT, injection of AVP receptor antagonist was followed by impaired social bonding and recognition. In male titi monkeys, injection of AVP increased social behavior towards their female partner.[5] In human studies, AVP has also shown to increase pro-social behavior towards their significant other.[5] The effects of AVP are reinforced by its integration with OT.[6] In a study in which rats received increased peripheral or central OT and AVP, the rats with increased OT or AVP exhibited an increase in huddling and sharing food with other rats.[5]
Social bonding is mediated several brain areas which respond to OT, AVP, and DA.[3] Studies using fMRI have been used in research to assess associated brain areas in human attachment based on auditory and visual stimuli responses of the brain to attachment target.[3] These studies found that the ventral tegmental area (VTA) and ventral striatum in the brain were activated during responses to attachment target.[3] Further research in fMRI studies have shown that the amygdala, nucleus accumbens (NA), hypothalamus, sub-cortical and cortical reward neural networks are also involved mediating social attachment.[3] These networks and pathways contain receptors that allow OT, AVP, and DA to exert their effects in high and low level processes in the brain that provide a foundation for social trust.[5] In studies with human subjects who experienced social isolation, there was an increase in activity in the hypothalamic-pituitary-adrenal (HPA) axis-a neural network involved in the release of cortisol, a stress-response hormone.[4] This same research showed a deactivation in brain regions associated with OT and AVP.[4]
References edit
- ^ Riedl, Rene; Javor, Andrija (2011). "The Biology of Trust: Integrating Evidence From Genetics, Endocrinology, and Functional Brain Imaging". Journal of Neuroscience, Psychology, and Economics. 5 (2): 63. doi:10.1037/a0026318.
- ^ a b Sciences, Roundtable on Public Interfaces of the Life; Sciences, Board on Life; Studies, Division on Earth and Life; Education, Board on Science; Education, Division of Behavioral and Social Sciences and; The National Academies of Sciences, Engineering (2015-09-23). What Is Trust. National Academies Press (US).
- ^ a b c d e f g Feldman, Ruth (2017). "The Neurobiology of Human Attachments". Trends in Cognitive Sciences. 21 (2): 80–99. doi:10.1016/j.tics.2016.11.007. PMID 28041836. S2CID 3651287.
- ^ a b c Annual review of psychology. Volume 66, 2015. Fiske, Susan T.,, Schacter, Daniel L.,, Taylor, Shelley E. Palo Alto, California. 1953. ISBN 9780824302665. OCLC 897575784.
{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: others (link) - ^ a b c d e f g h i j k l m n Lieberwirth, Claudia; Wang, Zuoxin (2014). "Social bonding: regulation by neuropeptides". Frontiers in Neuroscience. 8: 171. doi:10.3389/fnins.2014.00171. ISSN 1662-453X. PMC 4067905. PMID 25009457.
- ^ a b c d Churchland, Patricia S.; Winkielman, Piotr (2012). "Modulating social behavior with oxytocin: How does it work? What does it mean?". Hormones and Behavior. 61 (3): 392–399. doi:10.1016/j.yhbeh.2011.12.003. PMC 3312973. PMID 22197271.