Beyond often being associated between with one another, both<unk>  and inflammation are similarly sensitive to external stressors, something which has been used to further argue in favor of their connection. Of the possible types of stressors, those involving social adversity tend to be the most likely to result in<unk>  and are significant predictors of inflammation levels in both experimental and observational studies. This is often seen short term, with inflammation markers often being found to be elevated in response to negative social outcomes and throughout the course of one's<unk> , with bereaved individuals often experiencing greater inflammation than non-grieving individuals. Both one's risk of<unk>  and inflammation levels have also been found to be higher in adults who experienced childhood adversity. Similarly, these individuals also face increased risk of autoimmune diseases, which are both indicative of greater inflammatory responses and risk factors for<unk> . As with the relationship between<unk>  and inflammation as a whole, this relationship is thought to be bidirectional with both<unk>  increasing one's risk of autoimmune disease and autoimmune disease increasing one's risk of<unk> . However, it is also likely that this connection is also due in part to<unk>  and inflammation sharing many risk factors that may contribute to both conditions. Social support as a protective factor Similar to their shared risk factors, social support has been found to reduce the risk of both<unk>  and pro-inflammatory phenotypes. This is seen with relatively high levels of social support being found to be associated with decreased risk of<unk>  as well as asthma and heart disease, while also being associated with decreased levels of inflammatory markers as a whole following negative social interactions.
Depression and immune function
Brain and Behavior
Sleep and metabolism
Sexual motivation and hormones
Cancer immunology
Nutrition and Cancer
Nutrition and cognition
Breastfeeding and fertility