Evolution, the Immune System, and the Health Consequences of Socioeconomic Inequality

Rook, G. A. W.

doi:10.1128/msystems.01438-21

Cited by 7 publications

(5 citation statements)

References 189 publications

(220 reference statements)

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“…In agreement with the current work, Fowler et al [32] discounted the importance of ethnicity per se as a risk factor for the CMV infection. Similar conclusions were reached by Lantos et al [54], Rook [55], and Dowd et al [56,57].…”

Section: Discussionsupporting

confidence: 80%

Guilty in absentia ‒ Cytomegalovirus seropositivity relates inversely to cancer incidence in race/ethnicity groups and worldwide: is latent viral infection oncopreventive?

Janković

Milićević

Todorović-Balint

et al. 2023

Preprint

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Background. Race and ethnic disparities in cancer incidence rates and the prevalence of cytomegalovirus (CMV) are known to exist in the United States (U.S.) but also across broad geographic expanses. The prevalence of CMV seems to inversely contrast rates of tumor incidence both in ethnic groups and globally. Is there a biological link between cancer and CMV infection? Methods. Global cancer data were retrieved from the World Health Organization (WHO) database. Incidence of cancer and CMV seroprevalence (73 countries) were subjected to Spearman’s correlation test. The Bayesian framework was adopted for CMV seropositivity variables. Cancer incidence and CMV pervasiveness in the U.S. were extracted from publications based on the Surveillance, Epidemiology, and End Results (SEER) registries and the National Health and Nutrition Examination Surveys (NHANES), 1988-2004. Results. An inversely directed coupling between cancer and CMV seropositivity across diverse ecologies and cultural domains suggest a global oncoprotective effect of the CMV (Spearman’s ρ = -0.732; p<0.001). Rates of all cancers combined and CMV seropositivity show an opposite association ( p<0.001) among the races and foremost U.S. ethnic groups. Conclusion. The racial/ethnic incidence of cancers and CMV seropositivity are inversely proportional both in the U.S. and globally. This would support a view that CMV is a potential driver against tumorigenesis. An absence of CMV infection abrogates protection against malignant clones afforded by the virus to an infected host. Abating CMV seroprevalence may relate causally to the buildup of malignancies in U.S. and the West world countries with thriving hygiene and healthcare systems.

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Section: Discussionsupporting

confidence: 80%

Guilty in absentia ‒ Cytomegalovirus seropositivity relates inversely to cancer incidence in race/ethnicity groups and worldwide: is latent viral infection oncopreventive?

Janković

Milićević

Todorović-Balint

et al. 2023

Preprint

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“…In a classic study the difference in life expectancy in some parts of the British isles between wealthy and deprived areas was as high as 27 years ( 189 ). We and others have argued recently that much of this SES-associated health deficit might be secondary to inappropriate microbial exposures and inappropriate microbiota ( 190 – 192 ). We need to find out how much of the health deficit is mediated in this way because this might inspire new ways to combat the SES-linked health deficit.…”

Section: Causes Of Failed Microbial Exposures; Links To Diet Ses and ...mentioning

confidence: 99%

The old friends hypothesis: evolution, immunoregulation and essential microbial inputs

Rook

2023

Front. Allergy

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In wealthy urbanised societies there have been striking increases in chronic inflammatory disorders such as allergies, autoimmunity and inflammatory bowel diseases. There has also been an increase in the prevalence of individuals with systemically raised levels of inflammatory biomarkers correlating with increased risk of metabolic, cardiovascular and psychiatric problems. These changing disease patterns indicate a broad failure of the mechanisms that should stop the immune system from attacking harmless allergens, components of self or gut contents, and that should terminate inappropriate inflammation. The Old Friends Hypothesis postulates that this broad failure of immunoregulation is due to inadequate exposures to the microorganisms that drive development of the immune system, and drive the expansion of components such as regulatory T cells (Treg) that mediate immunoregulatory mechanisms. An evolutionary approach helps us to identify the organisms on which we are in a state of evolved dependence for this function (Old Friends). The bottom line is that most of the organisms that drive the regulatory arm of the immune system come from our mothers and family and from the natural environment (including animals) and many of these organisms are symbiotic components of a healthy microbiota. Lifestyle changes that are interrupting our exposure to these organisms can now be identified, and many are closely associated with low socioeconomic status (SES) in wealthy countries. These insights will facilitate the development of education, diets and urban planning that can correct the immunoregulatory deficit, while simultaneously reducing other contributory factors such as epithelial damage.

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“…Another growing body of human microbiome research focuses on the broader structural inequities of racialized uneven development (Amato et al 2021; Renson et al 2020). The premise of this research is that disparities in human microbiomes provide evidence of the way minoritized people face more pollutants, have unequal access to education and good food (e.g., food deserts), and overall face more stressors across housing, learning, and working environments than non-racialized peoples (Ishaq et al 2021; Rook 2022).…”

Section: Anti-racism 1: Environmental In/justicementioning

confidence: 99%

Anti-racism, racism, and the microbiome: A review

Rawson

2024

Progress in Environmental Geography

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Debates about the relationship between racism, anti-racism, and the new life sciences calls for further inquiry into the growing popularity of microbiome science. Scientists define human microbiomes as unique communities of microorganisms that vary across body-sites, lifespan, location, and lifestyle. As new biomarkers for human diversity, scientists argue that microbiomes environmentally mediate development and health, which also reframes classical models of disease. In the small subset of literature that engages the stakes for race, the implications of human microbiome science are posed in terms of paradoxically reifying racism and empowering anti-racist science. To illustrate this duality, I first review the two most pervasive critiques of explicitly and implicitly reproducing racial categories in human microbiome science. Then, I show how some of the same critics embrace other versions of microbiome science as a tool to fight for environmental justice and de-essentialize race. However, in the next section, I challenge this distinction by arguing that even the most promising aspect of microbiome science as biosocial “becoming” can reproduce racial hierarchies too. In sketching limits in the current literature, I conclude by suggesting that critical engagements with biosocial formations of race need to further examine the relational formation of whiteness and that such inquiry requires elevating Black and Indigenous scholars.

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Evolution, the Immune System, and the Health Consequences of Socioeconomic Inequality

Cited by 7 publications

References 189 publications

Guilty in absentia ‒ Cytomegalovirus seropositivity relates inversely to cancer incidence in race/ethnicity groups and worldwide: is latent viral infection oncopreventive?

Guilty in absentia ‒ Cytomegalovirus seropositivity relates inversely to cancer incidence in race/ethnicity groups and worldwide: is latent viral infection oncopreventive?

The old friends hypothesis: evolution, immunoregulation and essential microbial inputs

Anti-racism, racism, and the microbiome: A review

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