To explain human social sophistication, and proximal phylogenetic steps leading to it, Dunbar claims that mentalising expands to increasingly high levels of recursion. However, the evidential basis for this claim is weak, exposing both a limitation in Dunbar’s account and in the field’s current understanding of social sophistication.

Facial expression has evolved as a solution to the primate group living problem. A growing body of empirical evidence suggests that the evolution of facial expression has been driven by the need to bond. Dunbar’s theories of group cohesion are therefore key to understanding primate (including human) facial expression.

Specialised forms of social cognition enable primates to manage the stresses of group living by allowing for flexible and intentional communication. This is used to increase the predictability of conspecifics’ behaviour for both signallers and receivers. Intentional communication helps to overcome the stimulus-driven processing that may occur due to stress, enhancing attention allocation in receivers.

The current manuscript rightly points out that non-human primates evolved complex social cognitive skills to maintain weaker social ties. However, these capacities are likely more expansive than currently proposed: research shows that apes behave more socially to those with whom they experience similar things, suggesting that they possess some precursor of humans’ capacity to bond through shared experiences.

Dunbar explains primates group cohesion through cognitive and structural mechanisms like grooming and social cognition. We extend this by highlighting collective social niche construction, where emergent social properties arise from feedback loops, selection pressures, and self-organisation. Adaptive social networks evolve through multilevel selection, cultural transmission, and ontogenetic changes, shaping survival, cognition, and collective intelligence across species.

Primate species deploy a suite of behavioural and cognitive adaptations to offset the costs of group-living. Dunbar uses species-level comparisons to posit a series of cumulative steps that describe large-scale phylogenetic patterns in the evolution of sociality. Here, we highlight the value of population-level variation within species for empirically testing the predicted socio-ecological correlations that underpin Dunbar’s hypothesis.

Dunbar presents an intriguing analysis of variance in primate group sizes, and social glue’s (grooming) relationship to cognitive evolution. This focus on primates with consistent and stable grouping excludes perspectives on the evolution of grouping beyond predation and competition. The analysis raises important questions about variation, dynamic sizes, and the conservation implications of variance for primate population extinction vulnerabilities.

Human social networks are far larger than those of nonhuman primates. Maintaining cohesion in large networks requires a robust mechanism that can accommodate the dense webs of connections within communities. A parsimonious account of how humans achieve social cohesion is mental abstraction, which enables individuals to construct fuzzy network representations that facilitate information flow tracking and mitigate conflict.

Drawing on our previous work on human trust networks, we provide further evidence of how group structure can foster group cohesion. But this work also raises doubts about two central tenets of the target paper: (1) the role assigned to cognitive abilities in group cohesion and stabilization; and (2) the emphasis on group size as the critical variable.

Cyantraniliprole is a widely used insecticide that disrupts calcium homeostasis by binding to ryanodine receptors (RyRs) in the sarcoplasmic reticulum. Insects have a type of RyR with a 47% sequence homology to mammalian RyRs. Due to the high homology and strong affinity of cyantraniliprole for insect RyRs, concerns have been raised about potential adverse effects in mammals. This study aimed to evaluate the effects of cyantraniliprole on the liver and kidneys of male Wistar rat offspring exposed to a dose of 10 mg/kg during gestation and lactation. Thirty-three 80-day-old pregnant Wistar rats were randomly assigned to either a control group or a cyantraniliprole group (10 mg/kg). The treatment period lasted from the 5th gestational day to the 21st lactational day. The offspring were euthanized on postnatal day 55 (puberty) or 90 (adulthood). Blood samples were collected for biochemical assays, and liver and kidney samples were collected for histopathological analysis, oxidative stress biomarkers, and inflammatory profile assessment. The results indicated that exposure to cyantraniliprole caused vacuolation and vascular congestion in the pubertal and adult offspring, as well as significant morphological changes in the liver and kidneys. There was an increase in catalase and glutathione S-transferase activity in response to oxidative stress induced by the insecticide in the liver, with elevated levels of thiobarbituric acid reactive substances in the liver of adult animals and increased myeloperoxidase activity in pubertal animals. These findings suggest that exposure to cyantraniliprole induces significant damage to the organs involved in metabolism and excretion.

Saturated fatty acids, particularly palmitic acid (PA), promote inflammation and contribute to chronic diseases such as type 2 diabetes and cardiovascular disease. PA induces interleukin-1 beta (IL-1β) production in lipopolysaccharide (LPS)-primed macrophages via NLRP3 inflammasome activation; but the underlying mechanism remains unclear. This study investigates whether PA-induced IL-1β production involves cytosolic potassium (K+) depletion. In LPS-primed macrophages, treatment with PA conjugated to bovine serum albumin (PA-BSA) significantly reduced cytosolic K+ levels and increased IL-1β production 2.4-fold. Stearic acid-BSA produced similar effects, whereas BSA-bound oleic, linoleic and docosahexaenoic acids had minimal impact. Voltage-gated potassium (Kv) channel blockers, 4-aminopyridine and tetraethylammonium chloride, attenuated PA-BSA-induced K+ efflux and IL-1β production in LPS-primed macrophages, implicating Kv channels as key mediators. These findings reveal a novel inflammatory pathway in which PA-BSA promotes IL-1β production via Kv channel-dependent K+ efflux, highlighting a mechanistic link between saturated fatty acid exposure and inflammatory signalling.

Dunbar suggests structural, behavioral, and cognitive mechanisms to mitigate the costs of living in large groups. While we generally concur with the notion of group size effects on female productivity, we call for a more explicit treatment of how functional support alleviates social costs and disagree with the outright dismissal of ecological drivers and phylogenetic inertia.

Dunbar exclusively sees groups as arising through the aggregate relationships between individuals and thereby makes the serious omission of not considering the capacity of those individuals to categorize one another as ingroup versus outgroup members.

The paper of Dunbar (2025) on social stress is a strong demonstration that stress in itself can have a purely cognitive origin. The paper shows that the cognitive system can have profound impacts on the hypothalamus. As detailed in my commentary, this opens up new avenues of how to interpret psychiatric conditions, placebo, and other associations between perceptions and vegetative functions in the brain.

Grooming is one strong mechanism allowing primate groups to grow larger and more cohesive, but a reduction in reactive aggression responses can be expected to have contributed to this trend too. There is indeed a partial overlap between the neurobiology of grooming and the neurobiology of reactive aggression.