Search Results (6)

Depression is one of the most disabling of all disorders across the community, yet many aspects of the disorder remain contentious. Psychosocial and biological perspectives are often placed in opposition to one another, which in part reflects a failure of our explanatory frameworks. The active inference account of brain function breaks down this dualism, demonstrating that bodily processes are deeply integrated with the social world. It shows us that there is no contradiction in understanding depression as a product of the social environment at the same time as having a brain basis and manifesting in biological symptoms. From an active inference perspective, depression can be thought of as a synaptopathy: a disorder that arises from alterations to the excitatory-inhibitory balance enacted at the synapse, reflecting the interoceptive precision-weightings that have changed in the context of psychosocial instability. Therapies that alleviate depressive symptoms act at different levels of the active inference framework to re-weight precision estimates and the confidence we have in our predictions: this is true for psychotherapies, lifestyle interventions and antidepressant medications. Their effectiveness is often only partial, and while different treatment modalities can complement one another, there is a need for continued development of new and better treatment options. Full article

Allostatic self-efficacy (ASE) represents a computational theory of fatigue and depression. In brief, it postulates that (i) fatigue is a feeling state triggered by a metacognitive diagnosis of loss of control over bodily states (persistently elevated interoceptive surprise); and that (ii) generalization of low self-efficacy beliefs beyond bodily control induces depression. Here, we converted ASE theory into a structural causal model (SCM). This allowed identification of empirically testable hypotheses regarding causal relationships between the variables of interest. Applying conditional independence tests to questionnaire data from healthy volunteers, we sought to identify contradictions to the proposed SCM. Moreover, we estimated two causal effects proposed by ASE theory using three different methods. Our analyses identified specific aspects of the proposed SCM that were inconsistent with the available data. This enabled formulation of an updated SCM that can be tested against future data. Second, we confirmed the predicted negative average causal effect from metacognition of allostatic control to fatigue across all three different methods of estimation. Our study represents an initial attempt to refine and formalize ASE theory using methods from causal inference. Our results confirm key predictions from ASE theory but also suggest revisions which require empirical verification in future studies. Full article

Interoceptive dysfunctions are increasingly implicated in a number of physical and mental health conditions. Accordingly, there is a pertinent need for therapeutic interventions which target interoceptive deficits. Heartrate and heartrate variability biofeedback therapy (HR(V)-BF), interventions which train individuals to regulate their cardiovascular signals and constrain these within optimal parameters through breathing, could enhance the functioning of interoceptive pathways via stimulation of the vagus nerve. Consequently, this narrative systematic review sought to synthesise the current state of the literature with regard to the potential of HR(V)-BF as an interoceptive intervention across behavioural, physiological and neural outcome measures related to interoception. In total, 77 papers were included in this review, with the majority using physiological outcome measures. Overall, findings were mixed with respect to improvements in the outcome measures after HR(V)-BF. However, trends suggested that effects on measures related to interoception were stronger when resonance frequency breathing and an intense treatment protocol were employed. Based on these findings, we propose a three-stage model by which HR(V)-BF may improve interoception which draws upon principles of interoceptive inference and predictive coding. Furthermore, we provide specific directions for future research, which will serve to advance the current knowledge state. Full article

Major depressive disorder (MDD) is associated with dysfunctional self-reported interoception (i.e., abnormal perception of the body’s physiological state) and systemic inflammation, both of which adversely affect treatment response. In this study, we explored associations between C-reactive protein (CRP) and self-reported interoception, to gain more insight into the pathophysiology of interoceptive impairments in MDD. We also aimed to replicate previous findings on the associations of depression and fatigue severity with CRP. The study included 97 depressed individuals, who completed self-administered questionnaires (Multidimensional Assessment of Interoceptive Awareness (MAIA-2); Beck Depression Inventory-II, Multidimensional Fatigue Inventory). CRP concentrations were analyzed in the serum using a particle-enhanced turbidimetric immunoassay. We applied Bayesian inference to estimate robust effect parameters from posterior distributions based on MCMC sampling, and computed Bayes factors (BF₁₀) as indices of relative evidence. The bivariate analysis supported evidence against associations between CRP and self-reported interoception (BF₁₀ ≤ 0.32), except for one dimension (Not-Distracting: r = 0.11, BF₁₀ > 0.43, absence of evidence). Positive correlations with overall depression (r = 0.21, BF₁₀ = 3.19), physical fatigue (r = 0.28, BF₁₀ = 20.64), and reduced activity (r = 0.22, BF₁₀ = 4.67) were found. The multivariate analysis showed moderate evidence that low-grade inflammation predicted higher scores on the MAIA-2 Not-Worrying scale (β = 0.28, BF₁₀ = 3.97), after controlling for relevant confounders. Inflammatory responses, as measured by CRP, may not be involved in the pathophysiology of dysfunctional self-reported interoception. However, systemic low-grade inflammation could potentially exert a protective effect against worries about pain or discomfort sensations. An immunological involvement in interoceptive impairments cannot be ruled out until future studies considering additional biomarkers of inflammation replicate our findings. Full article

Ecstatic epilepsy is a rare form of focal epilepsy in which the aura (beginning of the seizures) consists of a blissful state of mental clarity/feeling of certainty. Such a state has also been described as a “religious” or mystical experience. While this form of epilepsy has long been recognized as a temporal lobe epilepsy, we have accumulated evidence converging toward the location of the symptomatogenic zone in the dorsal anterior insula during the 10 last years. The neurocognitive hypothesis for the genesis of a mental clarity is the suppression of the interoceptive prediction errors and of the unexpected surprise associated with any incoming internal or external signal, usually processed by the dorsal anterior insula. This mimics a perfect prediction of the world and induces a feeling of certainty. The ecstatic epilepsy is thus an amazing model for the role of anterior insula in uncertainty and surprise. Full article

Drawing from both enactivist and cognitivist perspectives on mind, I propose that explaining teleological phenomena may require reappraising both “Cartesian theaters” and mental homunculi in terms of embodied self-models (ESMs), understood as body maps with agentic properties, functioning as predictive-memory systems and cybernetic controllers. Quasi-homuncular ESMs are suggested to constitute a major organizing principle for neural architectures due to their initial and ongoing significance for solutions to inference problems in cognitive (and affective) development. Embodied experiences provide foundational lessons in learning curriculums in which agents explore increasingly challenging problem spaces, so answering an unresolved question in Bayesian cognitive science: what are biologically plausible mechanisms for equipping learners with sufficiently powerful inductive biases to adequately constrain inference spaces? Drawing on models from neurophysiology, psychology, and developmental robotics, I describe how embodiment provides fundamental sources of empirical priors (as reliably learnable posterior expectations). If ESMs play this kind of foundational role in cognitive development, then bidirectional linkages will be found between all sensory modalities and frontal-parietal control hierarchies, so infusing all senses with somatic-motoric properties, thereby structuring all perception by relevant affordances, so solving frame problems for embodied agents. Drawing upon the Free Energy Principle and Active Inference framework, I describe a particular mechanism for intentional action selection via consciously imagined (and explicitly represented) goal realization, where contrasts between desired and present states influence ongoing policy selection via predictive coding mechanisms and backward-chained imaginings (as self-realizing predictions). This embodied developmental legacy suggests a mechanism by which imaginings can be intentionally shaped by (internalized) partially-expressed motor acts, so providing means of agentic control for attention, working memory, imagination, and behavior. I further describe the nature(s) of mental causation and self-control, and also provide an account of readiness potentials in Libet paradigms wherein conscious intentions shape causal streams leading to enaction. Finally, I provide neurophenomenological handlings of prototypical qualia including pleasure, pain, and desire in terms of self-annihilating free energy gradients via quasi-synesthetic interoceptive active inference. In brief, this manuscript is intended to illustrate how radically embodied minds may create foundations for intelligence (as capacity for learning and inference), consciousness (as somatically-grounded self-world modeling), and will (as deployment of predictive models for enacting valued goals). Full article