Editing Twin study (section)

=== Gene × environment interactions ===

Gene effects may often be dependent on the environment. Such interactions are known as ''G×E interactions'', in which the effects of a gene allele differ across different environments. Simple examples would include situations where a gene multiplies the effect of an environment: perhaps adding 1&nbsp;inch to height in high nutrient environments, but only half an inch to height in low-nutrient environments. This is seen in different slopes of response to an environment for different genotypes.

Often researchers are interested in changes in [[heritability]] under different conditions: In environments where [[alleles]] can drive large phenotypic effects (as above), the relative role of genes will increase, corresponding to higher heritability in these environments.

A second effect is ''G × E correlation'', in which certain alleles tend to accompany certain environments. If a gene causes a parent to enjoy reading, then children inheriting this allele are likely to be raised in households with books due to GE correlation: one or both of their parents has the allele and therefore will accumulate a book collection ''and'' pass on the book-reading allele. Such effects can be tested by measuring the purported environmental correlate (in this case books in the home) directly.

Often the role of environment seems maximal very early in life, and decreases rapidly after [[compulsory education]] begins. This is observed for instance in reading<ref>{{Cite journal | last1 = Byrne | first1 = Brian | last2 = Wadsworth | first2 = Sally | last3 = Corley | first3 = Robin | last4 = Samuelsson | first4 = Stefan | last5 = Quain | first5 = Peter | last6 = Defries | first6 = John C. | last7 = Willcutt | first7 = Erik | last8 = Olson | first8 = Richard K. | doi = 10.1207/s1532799xssr0903_3 | title = Longitudinal Twin Study of Early Literacy Development: Preschool and Kindergarten Phases | journal = [[Scientific Studies of Reading]] | volume = 9 | issue = 3 | pages = 219–235 | year = 2005 | url = http://psych.colorado.edu/~willcutt/pdfs/Byrne_2007.pdf | access-date = 2015-08-28 | archive-url = https://web.archive.org/web/20160304111352/http://psych.colorado.edu/~willcutt/pdfs/Byrne_2007.pdf | archive-date = 2016-03-04 | url-status = dead | citeseerx = 10.1.1.530.7555 | s2cid = 144069119 }}</ref>
as well as intelligence.<ref>{{Cite journal | last1 = Deary | first1 = Ian J.| last2 = Spinath | first2 = Frank M.| last3 = Bates | first3 = Timothy C.| doi = 10.1038/Sj.Ejhg.5201588 | title = Genetics of intelligence | journal = [[European Journal of Human Genetics]]| volume = 14 | issue = 6 | pages = 690–700 | year = 2006 | pmid =  16721405| doi-access = free }}</ref> This is an example of a G*Age effect and allows an examination of both GE correlations due to parental environments (these are broken up with time), and of G*E correlations caused by individuals actively seeking certain environments.<ref>{{Cite journal | last1 = Plomin | first1 = Robert| last2 = Daniels | first2 = Denise| doi = 10.1017/S0140525X00055941 | title = Why are children in the same family so different from one another? | journal = [[Behavioral and Brain Sciences]] | volume = 10 | issue = 3| pages = 1–16| year = 1987| pmc = <!--none-->}}<br />''revisited in: <!-- or possibly republished as-->'' {{Cite journal | last1 = Plomin | first1 = R.| last2 = Daniels | first2 = D.| doi = 10.1093/ije/dyq148 | title = Why are children in the same family so different from one another? | journal = [[International Journal of Epidemiology]] | volume = 40 | issue = 3 | pages = 563–582 | date=June 2011 | pmid = 21807642| pmc = 3147063 }}</ref>

==== Norms of reaction ====
Studies in plants or in [[animal breeding]] allow the effects of experimentally randomized [[genotypes]] and environment combinations to be measured. By contrast, human studies are typically observational.<ref>{{Cite journal | last1 = Kempthorne | first1 = Oscar| title = Heritability: uses and abuses| journal = [[Genetica]]| volume = 99 | issue = 2–3| pages = 109–112 | doi = 10.1007/bf02259514 | year = 1997 | pmid = 9463066| s2cid = 23266944}}</ref><ref>{{Cite journal | last1 = Kendler | first1 = K. S.| last2 = Gruenberg | first2 = A. M.| doi = 10.1001/archpsyc.1984.01790170029004 | title = An Independent Analysis of the Danish Adoption Study of Schizophrenia: VI. The Relationship Between Psychiatric Disorders as Defined by DSM-III in the Relatives and Adoptees | journal = [[Archives of General Psychiatry]]| volume = 41 | issue = 6 | pages = 555–564 |date=June 1984 | pmid =  6732417}}</ref> This may suggest that [[norms of reaction]] cannot be evaluated.<ref>{{cite book | last1 = Kamin | first1 = Leon J. | last2 = Rose | first2 = Steven R. | last3 = Lewontin | first3 = Richard C. | title = Not in Our Genes: Biology, Ideology and Human Nature | publisher = Penguin Books | location = New York | year = 1984 | isbn = 978-0-14-022605-8 | title-link = Not in Our Genes }}</ref><ref>{{Cite journal | last1 = Rose | first1 = Richard J.| title = Separated Twins: Data and Their Limits | doi = 10.1126/science.215.4535.959 | journal = [[Science (journal)|Science]] | volume = 215 | issue = 4535 | pages = 959–960 | year = 1982 | pmid =  17821364| bibcode = 1982Sci...215..959F}}</ref>

As in other fields such as [[instrumental variable|economics]] and [[Mendelian randomization|epidemiology]], several designs have been developed to capitalise on the ability to use differential gene-sharing, repeated exposures, and measured exposure to environments (such as children social status, chaos in the family, availability and quality of education, nutrition, toxins etc.) to combat this confounding of causes. An inherent appeal of the classic twin design is that it begins to untangle these confounds. For example, in identical and fraternal twins shared environment and genetic effects are  not confounded, as they are in non-twin familial studies.<ref name=ATK>{{Cite journal | last1 = Martin | first1 = Nicholas| last2 = Boomsma | first2 = Dorret| last3 = Machin | first3 = Geoffrey| doi = 10.1038/ng1297-387 | title = A twin-pronged attack on complex traits | url = http://genepi.qimr.edu.au/contents/p/staff/CV190Martin_UQ_Copy.pdf| journal = [[Nature Genetics]] | volume = 17 | issue = 4 | pages = 387–392 | year = 1997 | pmid =  9398838| hdl = 1871/2733| s2cid = 2028886}}</ref> Twin studies are thus in part motivated by an attempt to take advantage of the random assortment of genes between members of a family to help understand these correlations.

While the twin study tells us only how genes and families affect behavior within the observed range of environments, and with the caveat that often genes and environments will covary, this is a considerable advance over the alternative, which is no knowledge of the different roles of genes and environment whatsoever.<ref name=Neale1996>M. C. Neale and H. H. Maes. (1996). Methodology for genetics studies of twins and families. ''Journal''.</ref> Twin studies are therefore often used as a method of controlling at least one part of this observed variance: Partitioning, for instance, what might previously  have been assumed to be family environment into shared environment and additive genetics using the experiment of fully and partly shared genomes in twins.<ref name=Neale1996 /> Additional information is available outside the classic twin design. [[Adoption Study|Adoption designs]] are a form of natural experiment that tests norms of reaction by placing the same genotype in different environments.<ref>{{Cite journal | last1 = Petrill | first1 = S. A.| last2 = Deater-Deckard | first2 = K.| title = The heritability of general cognitive ability: A within-family adoption design | doi = 10.1016/j.intell.2004.05.001 | journal = [[Intelligence (journal)|Intelligence]] | volume = 32 | issue = 4 | pages = 403–409| date=July–August 2004 }}</ref> Association studies, e.g.,<ref>{{Cite journal | last1 = Steer | first1 = C. D.| last2 = Davey Smith | first2 = G.| author-link2=George Davey Smith| last3 = Emmett | first3 = P. M.| last4 = Hibbeln | first4 = J. R.| last5 = Golding | first5 = J.| editor1-last = Penha-Goncalves | editor1-first = Carlos | title = FADS2 Polymorphisms Modify the Effect of Breastfeeding on Child IQ | doi = 10.1371/journal.pone.0011570 | journal = [[PLoS ONE]] | volume = 5 | issue = 7 | pages = e11570 | date=July 2010 | pmid =  20644632| pmc = 2903485 | bibcode = 2010PLoSO...511570S| doi-access = free}}</ref> allow direct study of allelic effects.  [[Mendelian randomization]] of alleles also provides opportunities to study the effects of alleles at random with respect to their associated environments and other genes.<ref>e.g. {{Cite journal | last1 = Davey Smith | first1 = G.| author-link1=George Davey Smith| title = Capitalizing on Mendelian randomization to assess the effects of treatments | doi = 10.1177/014107680710000923 | journal = [[Journal of the Royal Society of Medicine]]| volume = 100 | issue = 9 | pages = 432–435 | date=September 2007 | pmid =  17766918| pmc = 1963388 }}</ref>