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Inflammation and the aging process: devil or angel

PainSci » bibliography » Gauldie 2007
Tags: inflam-sys

One article on PainSci cites Gauldie 2007: Chronic, Subtle, Systemic Inflammation

PainSci summary of Gauldie 2007: ?This page is one of thousands in the bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.

This is a short and technical exploration of reasons not to demonize inflammation. There is some evidence that it might actually be a relatively innocent bystander to the some pathologies it has been blamed for. Otherwise, the article is mainly just a reminder that inflammation is synonymous with immune function and dazzlingly complex, and suppressing it in general is best avoided unless absolutely necessary (which is not wrong, but also so obvious I wonder if it actually needed to be said).

~ Paul Ingraham

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Inflammation is often viewed as a pathologic mechanism leading to tissue damage and interference with function, such as the process of chronic tissue scarring or fibrosis. However, it is important to note that inflammation is a crucial component of normal tissue repair as well as being fundamental to the body's defense against infection. Considering inflammation as a "causative agent in aging" belies the underlying mechanisms whereby the acute inflammatory response is necessary for survival, and efforts to reduce and control the inflammatory response leave the host susceptible to infectious agents and improper healing. Chronic inflammation inevitably has initiating mechanisms that include immune, autoimmune, and metabolic pathways, leading to the activation and presence of the host-protective response. It is more appropriate to target the underlying initiating conditions than the inflammatory process that ensues and treat the basic mechanisms of disease rather than interfere in a very important protective mechanism of the host.

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