Resilience in mental health: linking psychological and neurobiological perspectives

Abstract

Objective: To review the literature on psychological and biological findings on resilience (i.e. the successful adaptation and swift recovery after experiencing life adversities) at the level of the individual, and to integrate findings from animal and human studies.

Method: Electronic and manual literature search of MEDLINE, EMBASE and PSYCHINFO, using a range of search terms around biological and psychological factors influencing resilience as observed in human and experimental animal studies, complemented by review articles and cross-references.

Results: The term resilience is used in the literature for different phenomena ranging from prevention of mental health disturbance to successful adaptation and swift recovery after experiencing life adversities, and may also include post-traumatic psychological growth. Secure attachment, experiencing positive emotions and having a purpose in life are three important psychological building blocks of resilience. Overlap between psychological and biological findings on resilience in the literature is most apparent for the topic of stress sensitivity, although recent results suggest a crucial role for reward experience in resilience.

Conclusion: Improving the understanding of the links between genetic endowment, environmental impact and gene-environment interactions with developmental psychology and biology is crucial for elucidating the neurobiological and psychological underpinnings of resilience.

Fig. 1

Model of resilience (a) and trajectories of risk and resilience (b). (a) Provides a model for illustrating the level of an individual's mental wellbeing over time and illustrates a decline of mental wellbeing in response to a severe adversity such as exposure to trauma followed by recovery in mental wellbeing. An individual may vary in i) the level of mental wellbeing before the exposure, ii) The speed and severity of mental health disturbance in response to the exposure, iii) The speed and timing of mental health recovery and iv) level of mental health and wellbeing after the exposure-related disturbance and recovery. (b) four different trajectories (grey full, grey dashed, black full and black dashed lines) of individuals' risk and resilience for developing psychopathology in response to exposure to a severe stressor/trauma. The grey full line depicts an individual with a positive level of mental health preceding the exposure, a consistent decline in mental health following the exposure without subsequent recovery. The grey dashed line depicts an individual with a positive level of mental health preceding the exposure (a more positive mental health than the others), with a temporary and relatively brief decline in mental health following the exposure followed by swift recovery up to a somewhat higher level of mental health than before the exposure. The full black line depicts an individual with a positive level of mental health preceding the exposure, a consistent decline in mental health following the exposure that recovers quickly to preexposure levels of mental health after a certain delay period in which the individual expresses psychopathology. The dashed black line depicts an individual with a positive level of mental health preceding the exposure, a consistent decline in mental health following the exposure that recovers quickly to preexposure levels of mental health and continues to increase thereby surpassing preexposure levels of mental health (this can be seen as post-traumatic growth).

Fig. 2

Brain circuitries involved in the stress response and reward experience. Key brain regions involved in the response to stress and reward experience. (a) Hypothalamus–pituitary–adrenal axis. Psychological and physiological stressors are known to activate the hypothalamus–pituitary–adrenal (HPA) axis, leading to corticotrophin releasing hormone (CRH) production by the hypothalamus and adrenocorticotropic hormone (ACTH) release from the anterior pituitary (indicated by the black arrows). ACTH induces glucocorticoid hormone release from the adrenal cortex into the circulation (indicated by the grey arrows). Moreover, GCs exert a negative feedback on the activation of the HPA activation, via GR in the hippocampus, therefore controlling their own release. Cortisol has important regulatory functions on the amygdala (AMYGD), hippocampus and prefrontal cortex (indicated by the grey arrows). Besides cortisol, another adrenal steroid hormone released under stress is (dehydroepiandrosterone) DHEA (indicated by dashed arrows). DHEA is released synchronously with cortisol from the adrenal glands. It has antiglucocorticoid and antiglutamatergic characteristics in the brain, and is – in general – related to inhibition of the HPA axis. (b) Norepinephrine and sympathetic nervous system (SNS).Next to activation of the HPA axis, stress increases norepinephrine release from the LC (locus coeruleus) to its projecting neurons in the amygdala, PFC and hippocampus (indicated by the long dashed arrows). As a result, the PFC is inhibited both by the LC itself and the amygdala (indicated by the black arrow), thereby favouring instinctive responses over complex thinking. Moreover, the amygdala stimulates brainstem autonomic centres (BAC). During stress, the sympathetic autonomous nervous system (SNS) releases epinephrine and NE. (c) Mesolimbic reward pathway. Activation of the hippocampus, amygdala and PFC also activates the mesolimbic reward pathway. These three structures have glutamatergic projections to the (nucleus accumbens) NAC (indicated by the long dashed arrows). The strength of the synapse is modulated by dopamine signalling that modulates glutamate release. A reward stimulus leads to phasic dopamine release from the VTA (indicated by short dashed arrows). GABAergic neurons in the NAc in turn exert negative feedback on the VTA, thereby controlling dopamine release, and dopaminergic signalling to the PFC. Integration of signals of the VTA, hippocampus (learned behaviour) and amygdala (emotional behaviour) by the PFC underlies the sensation of the reward feeling. In addition, BDNF is produced in the VTA and transported to the NAc via its dopaminergic afferent. It is likely that BDNF, when administered in the VTA-NAc also activates the GABAergic neurons in the NAc, thus inhibiting dopaminergic input from the VTA, possibly underlying blunted responses to emotional stimuli or symptoms of anhedonia.