Affiliative bonds are the hallmark of human sociability, having evolved to support survival, reproduction, and nurturing of the offspring. Social relationships are associated with security and comfort. Such feelings could serve as safety signals, promoting incentive motivation towards social bonding. Building up on the seminal work by Jaak Panksepp and colleagues, recent genetic studies suggest that different neurochemicals including dopamine, oxytocin, and particularly opioid peptides regulate different aspects of sociability (Pearce et al, 2017). Human positron emission tomography (PET) studies have highlighted that the endogenous opioid system, best known for its role in pain and reward, supports also social bonding in humans. Prosocial behavior, such as social laughter, triggers endogenous opioid release in thalamus and insular cortex concurrently with increased calmness and amusement (Manninen et al, 2017). Such group-level opioid release via contagious laughter, rather than time-consuming dyadic bonding, may have allowed humans to significantly extend their social sphere. Yet conversely, also social rejections or losses may trigger similar endogenous opioid activation as social bonding (Hsu et al, 2013), paralleling the contribution of the opioid system to processing of purely sensory pleasure and pain in humans. Thus, the opioid system seems to modulate both motivation towards social contacts and support, and away from solitude.

Capacity for vicarious experience is a key feature of human sociability: feeling others’ pain in our own mind may create a strong urge to help others in distress. Fusion imaging work combining PET with functional magnetic resonance imaging shows that the more opioid receptors humans have in their brain, the more strongly their frontocortical areas respond to seeing others’ distress (Karjalainen et al, 2017). Similarly, placebo analgesia (modulated by the opioid system) also reduces empathy-related brain responses towards others’ distress (Rutgen et al, 2015). Accordingly, the physical and vicarious pain might share the same neuromolecular basis, and opioidergic neurotransmission may facilitate more complex prosocial motivation than just social bonding.

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