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From stress to inflammation and major depressive disorder: a social signal transduction theory of depression - PubMed
Source: pubmed.ncbi.nlm.nih.gov
Article summary:
1. The innate immune system developed to counter physical threats from predatory animals and hostile conspecifics in the ancestral environment.
2. Exposure to modern-day social, symbolic, anticipated, and imagined threats can activate a conserved transcriptional response to adversity (CTRA), leading to increased risk for several inflammation-related conditions, including depression.
3. The hypothalamic–pituitary–adrenal (HPA) axis and inflammatory system coordinate to keep an individual physically safe and biologically healthy, but prolonged activation of the HPA axis and inflammatory response caused by persistent actual or perceived threat is biologically costly and can increase a person’s risk for several inflammation-related conditions.
Article analysis:
The article “From stress to inflammation and major depressive disorder: a social signal transduction theory of depression” is generally reliable in its presentation of information regarding the link between stress, inflammation, and major depressive disorder. The article provides evidence for its claims through citations of relevant research studies as well as figures that illustrate key points. Additionally, the article does not appear to be biased towards any particular point of view or opinion; rather it presents both sides of the argument in an evenhanded manner.
However, there are some areas where the article could be improved upon in terms of trustworthiness. For example, while the article does provide evidence for its claims through citations of relevant research studies, it does not explore any potential counterarguments or alternative explanations for its findings. Additionally, while the article does present both sides of the argument in an evenhanded manner, it does not provide any evidence for its claims regarding potential risks associated with prolonged activation of the HPA axis and inflammatory response caused by persistent actual or perceived threat. Finally, while the article does provide figures that illustrate key points related to cortisol and proinflammatory cytokine responses to social cues indicating possible danger as well as neuro-inflammatory sensitization to adversity, these figures do not include any labels or descriptions that explain what they are depicting which could make them difficult for readers who are unfamiliar with this topic area to understand.