Race, plaque and disease

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Neutrophil Response to Dental Plaque by Gender and Race:

The inflammatory response, which has both genetic and environmental components, is a central mechanism linking oral and systemic diseases. We hypothesized that dental plaque accumulation over 21 days in the experimental gingivitis model would elicit systemic inflammatory responses [change in white blood cell (WBC) count and neutrophil activity], and that these responses would differ by gender/race. We recruited 156 healthy young adults, including black and white males and females. Plaque Index (PI), Gingival Index (GI), systemic WBC counts, and peripheral neutrophil oxidative activity were recorded. Overall, 128 participants completed the study. During the experimental phase, the correlation between PI and GI was 0.79. Total WBC and neutrophil counts did not change. Neutrophil activity increased in blacks but not whites, suggesting that there may be racial differences in the inflammatory response to dental plaque accumulation.

Don’t genes like DARC track the nature of inflammatory response? And don’t those genes exhibit a lot of African/non-African difference? Pointers, corrections and thoughts welcome in the comments.

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  1. Well, there’s this SNP, which makes a stop codon – the *less* inflammatory variant is only found in Africa. I think I learned about that one in the Cochran & Harpending book. 
     
    Even if one had a clear idea about which had a bigger fitness burden from infection, Africa or Eurasia (and had it for more millennia) – I’m not necessarily sure what that would lead you to predict… inflammation being a delicate balance between effective aggression, and collateral damage.  
     
    Also, some pathogens have a stratagem of dampening inflammation, such as Entamoeba, and others seem to egg it on. (I’m not quite as clear on this subject, though.) The superantigens of staph and strep seem to produce inflammation while jamming the adaptive immune system – it may be that these varmints fear the adaptive system but can deal with the general heat from the innate immune system that their superantigens create. Presumably it’s a genetically *less* active innate system, if anything, that would reduce their ability to do what they do. 
     
    There’s also the fitness burden from autoimmune diseases to consider, all the moreso if ultra-common diseases like depression turn out to be autoimmune in some cases.

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