So far in this class, we have studied the concept of phenotypic plasticity in the terms of animal models such as rodents and amphibians. This makes perfect sense, as these animal models can be made the subject of experimentation with the goal of understanding the genetic and environmental factors and mechanisms that drive phenotypic plasticity. However, I'd like to look at this concept from a different scope; while humans are not used for experimentation of this kind for obvious reasons, they can still make for useful models by applying geographical and physiological data into a framework.
One paper by Zaccone et al. (2006) reviews the genetic and environmental evidence for the increased rates of autoimmune disorders in highly developed countries. Using the Hygiene Hypothesis, which suggests that parasites have been instrumental in the development and fine-tuning of the human immune system, Zaccone et al. cites the use of sanitation techniques and antibiotic use as a possible reason for the increased prevalence of autoimmune disorders in industrialized countries. Using data from the International Diabetes Federation, the review establishes a link between greater incidences of Type 1 Diabetes (T1D) and ease of access to sanitation and clean water by country. It is acknowledged that this can be explained somewhat by the introduction of insulin treatment in the 1920s, thus conserving T1D susceptibility genes, but this can only account for a small portion of the increased rate of T1D in highly developed countries.
The review goes on to detail the effects of helminth infection on the immune system. In Non-Obese Diabetic (NOD) mice, which are bred to spontaneously develop T1D, individuals kept under germ-free conditions developed T1D much faster than those kept under conventional conditions, lending support to the Hygiene Hypothesis (Zaccone et al. 2006).
In an effort to synthesize the environmental factors that contribute to the increased incidence of autoimmune disorders in highly developed countries, Zaccone et al. (2006) suggest a link between the greater prevalence of helminth infections, particularly that of Schistosoma mansoni, and the seemingly supplementary effect of this infection during host development on host immune function. Antigens produced by S. mansoni increased Treg populations, thus promoting self-tolerance maintenance by increasing the effectiveness of the Th-2 response (Zaccone et al. 2006). With their rich diversity of glycosylated molecules, S. mansoni and other schistosomes are able to "train" the immune system by activating natural killer T cells at an early age while the immune system is developing (Zaccone et al. 2006).
While the conclusion of this review discussed the potential applications and treatments as a result of these findings, I found that it provided a different model for understanding phenotypic plasticity in an unusual model: humans. By comparing immunological reaction norms from more developed countries and less developed countries, and providing evidence for both the genetic (antibiotic use and decreased selection pressure) and environmental factors (increased sanitation lowering prevalence of parasite infection) contributing to the difference, a reaction norm framework can be established using the Hygiene Hypothesis. While the reality of differences in immune system development is likely much more complex than differences in rates of parasite infection, I believe it is a useful way to understand phenotypic plasticity in a more relatable and cultural sense.
Zaccone, P., Fehervari, Z., Phillips, J. M., Dunne, D. W., & Cooke, A. (2006). Parasitic worms and inflammatory diseases. Parasite immunology, 28(10), 515–523. https://doi.org/10.1111/j.1365-3024.2006.00879.x
This is very interesting to think about. It made me think of a way we attempt to study evolution in species by comparing the same or similar species across landscape gradients. To understand how a species of owl might respond to a change in the environment, we can take a look at the owl in a different region that has already undergone in a sense that change in environment. Comparing differences in distance or in your example, culture, we can estimate adaptation.
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