Abstract:Background: The quality and quantity of individuals' social relationships has been linked not only to mental health but also to both morbidity and mortality.
“…Likewise, viewing social stress or social isolation as a physiological phenomenon, as well as a psychological phenomenon, may help us to better understand the robust relationships between social ties and health (Holt-Lunstad et al, 2010). A better understanding of the co-regulation of inflammation and social behavior may bring us a step closer to these goals.…”
Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threatrelated neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed.
“…Likewise, viewing social stress or social isolation as a physiological phenomenon, as well as a psychological phenomenon, may help us to better understand the robust relationships between social ties and health (Holt-Lunstad et al, 2010). A better understanding of the co-regulation of inflammation and social behavior may bring us a step closer to these goals.…”
Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threatrelated neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed.
“…Romantic love is one of the most powerful motivators of human behavior and has been linked to physical and mental health (Holt-Lunstad et al, 2010). Grief over the loss of a partner is considered a major adverse life event associated with an elevated risk for stress-related psychiatric disorders (Lundin, 1984;Keyes et al, 2014), acute myocardial infarction in men (Mostofsky et al, 2012) and breast cancer in women (Lillberg et al, 2003;Lin et al, 2013).…”
The hypothalamic peptide oxytocin (OXT) has been identified as a key modulator of pair-bonding in men, but its effects in women are still elusive. Moreover, there is substantial evidence that hormonal contraception (HC) influences partner preferences and sexual satisfaction, which constitute core domains of OXT function. We thus hypothesized that OXT effects on partner-related behavioral and neural responses could be significantly altered in women using HC. In this functional magnetic resonance imaging study involving 40 pair-bonded women, 21 of whom were using HC, we investigated whether a 24-IU nasal dose of OXT would modulate brain reward responses evoked by the romantic partner's face relative to the faces of familiar and unfamiliar people. Treatment with OXT increased the perceived attractiveness of the partner relative to other men, which was paralleled by elevated responses in reward-associated regions, including the nucleus accumbens. These effects of OXT were absent in women using HC. Our results confirm and extend previous findings in men that OXT interacts with the brain reward system to reinforce partner value representations, indicating a common OXT-dependent mechanism underlying partner attraction in both sexes. This mechanism may be disturbed in women using HC, suggesting that gonadal steroids could alter partner-specific OXT effects.
“…Research has shown that loneliness can worsen health-related problems (Hawkley and Cacioppo 2010;Sugisawa et al 1994;Thurston and Kubzansky 2009). Indeed, one study showed that lonely people have a 45% higher mortality rate than people who are not lonely (Holt-Lunstad et al 2010). How does the pursuit of an entrepreneurial career influence healthrelated loneliness?…”
Section: Health and Entrepreneurial Motivationmentioning
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