How do your genes and the environment interact?
The first instance of debate occurred between Ronald Fisher and Lancelot Hogben. Fisher sought to eliminate interaction from statistical studies as it was a phenomenon that could be removed using a variation in scale.
Hogben believed that the interaction should be investigated instead of eliminated as it provided information on the causation of certain elements of development.
A similar argument faced multiple scientists in the s.
Lewontin and Layzer argued that in order to conclude causal mechanisms, the gene-environment interaction could not be ignored in the context of the study while Jensen defended that interaction was purely a statistical phenomenon and not related to development.
Rothman supported the use of a statistical definition for interaction while researchers Kupper and Hogan believed the definition and existence of interaction was dependent on the model being used.
In contrast to previous debates, Moffitt and Caspi were now using the statistical analysis to prove that interaction existed and could be used to uncover the mechanisms of a vulnerability trait.
Contention came from Zammit, Owen and Lewis who reiterated the concerns of Fisher in that the statistical effect was not related to the developmental process and would not be replicable with a difference of scale. Tabery  has labeled them biometric and developmental interaction, while Sesardic  uses the terms statistical and commonsense interaction.
The biometric or statistical conception has its origins in research programs that seek to measure the relative proportions of genetic and environmental contributions to phenotypic variation within populations. Biometric gene—environment interaction has particular currency in population genetics and behavioral genetics.
Biometric interaction is relevant in the context of research on individual differences rather than in the context of the development of a particular organism. Developmental interaction is not seen merely as a statistical phenomenon.
Model A describes a genotype that increases the level of expression of a risk factor but does not cause the disease itself. For example, the PKU gene results in higher levels of phenylalanine than normal which in turn causes mental retardation.
The risk factor in Model B in contrast has a direct effect on disease susceptibility which is amplified by the genetic susceptibility. Model C depicts the inverse, where the genetic susceptibility directly effects disease while the risk factor amplifies this effect. In each independent situation, the factor directly effecting the disease can cause disease by itself.
Model D differs as neither factor in this situation can effect disease risk, however, when both genetic susceptibility and risk factor are present the risk is increased.
For example, the G6PD deficiency gene when combined with fava bean consumption results in hemolytic anemia. This disease does not arise in individuals that eat fava beans and lack G6PD deficiency nor in G6PD-deficient people who do not eat fava beans.
Lastly, Model E depicts a scenario where the environmental risk factor and genetic susceptibility can individually both influence disease risk. When combined, however, the effect on disease risk differs.
The models are limited by the fact that the variables are binary and so do not consider polygenic or continuous scale variable scenarios. Additionally, adopted individuals are compared to their adoptive family due to the difference in genes but shared environment.the idea that nature "selects", or allows to survive and reproduce, those members of a species whose genes permit them to adapt to their enviornment.
Misunderstandings about “nature versus nurture” remain prevalent in biology and psychology as well as in the public sphere. As D. S. Moore (hereafter, Moore) points out in The Dependent Gene, contributing to the problem are the common cultural assumptions that (a) genes program for many traits, with the environment in a subordinate role; and that (b) genetic and environmental contributions.
Jul 13, · Genes, Behavior, the Environment, and Health For over years, NIH has supported biomedical research to enhance health, lengthen life, and reduce the burdens of illness and disability. Read the stories of research discovery, current treatment status, and future expectations for the prevention and treatment of diseases and .
Genes and Environment is an open access, peer-reviewed journal that aims to accelerate communications among global scientists working in the field of genes and environment.
The journal publishes articles across a broad range of topics including environmental mutagenesis and carcinogenesis, environmental genomics and epigenetics, molecular. traits influenced by multiple pairs of genes, interacting with environmental factors, rather than by a single pair of genes Mutation a change in teh structure or arrangement of one or more genes that produces a new phenotype.
The main ingredient in aspirin, salicin, is the oldest pain reliever in history, but it took time and science before it became the drug we recognize today.