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In genetic epidemiology, an envirome the total set of environmental factors, both present and past, that affect the state, and in particular the disease state, of an organism.[1] The study of the envirome and its effects is termed enviromics. The term was first coined in the field of psychiatric epidemiology by J.C. Anthony in 1995.[2][3] More recently, use of the term has been extended to the cellular domain, where cell functional enviromics studies both the genome and envirome from a systems biology perspective.[4]

Envirome classification[edit]

While there can be both positive and negative effects of the envirome on the organism, negative effects are often emphasized in discussing disease. A typology of envirome health hazards suggested by McDowall is natural physico-chemical, man-made physico-chemical, biological/organic, natural or man-made, macrosocial, micro- or psychosocial.[3]

The time-scale of the envirome hazard is another possible dimension of classification; an envirome hazard are said to be a sudden change (such as a disaster), a rapid environmental change, or a slow change or a static situation.[3] In twin studies, envirome influences are often decomposed into shared environmental factors, common to both twins and non-shared environmental factors that differ between the twins.[5]

Gene-environment correlation and interaction[edit]

The effect of an envirome on an organism can be potentially modulated by its genetic makeup, i.e., its genome. The two main ways genes and environment may interact is through genotype-environment correlation and interaction.[5] Genotype-environment correlation occurs because, for example, children both inherit genes from their parents and live under the influence of their parents.[5] In the context of genetic epidemiology, interaction refers to the genes and the environment both participating in a causal way that departs from a simple additive model of the effects.[3] An example of a gene environment interaction is the increased risk of getting Alzheimer disease following a head injury in persons carrying the APOE allele.[6]


Some researchers see envirome as a renaming of the already well-established nurture component of the nature vs. nurture dichotomy in explaining psychological behavior.[3] Steven Rose has argued that in psychiatry, it is time to abandon the genome-envirome dichotomy altogether in favor of an integrative view of a person's life course.[7]

See also[edit]


  1. ^ "-Omes and -omics glossary & taxonomy". Cambridge Healthtech Institute. Retrieved 25 April 2013. 
  2. ^ Shayne Cox Gad (2008). Preclinical Development Handbook: Toxicology. John Wiley & Sons. p. 778. ISBN 9780470249048. 
  3. ^ a b c d e Cooper, Brian (2001). "Nature, nurture and mental disorder: old concepts in the new millennium". The British Journal of Psychiatry. 178 (suppl. 40): 91–102. doi:10.1192/bjp.178.40.s91. 
  4. ^ Teixeira, Ana P.; ML Dias, João; Carinhas, Nuno; Sousa, Marcos; J Clemente, João; E Cunha, António; von Stosch, Moritz; M Alves, Paula; JT Carrondo, Manuel; Oliveira, Rui (2011). "Cell functional enviromics: Unravelling the function of environmental factors". BMC Systems Biology. 5: 92–108. doi:10.1186/1752-0509-5-92. Retrieved 25 April 2013. 
  5. ^ a b c NEIDERHISER, JENAE M. (2001). "Understanding the roles of genome and envirome: methods in genetic epidemiology". The British Journal of Psychiatry. 178 (suppl. 40): s12–s17. doi:10.1192/bjp.178.40.s12. 
  6. ^ Nicoll, J.A.; Roberts, G. W.; Graham, D. I. (1996). "Amyloid beta-protein, APOE genotype and head injury (review)". Annals of the New York Academy of Sciences. 777: 271–275. doi:10.1111/j.1749-6632.1996.tb34431.x. 
  7. ^ Rose, S. (2001). "Moving on from old dichotomies: beyond nature ^ nurture towards a lifeline perspective". British Journal of Psychiatry. 178 (suppl. 40): s3–s7. doi:10.1192/bjp.178.40.s3.