Editing Psychology (section)

=== Genes and environment ===
{{Main|Behavioural genetics}}

All researched psychological traits are influenced by both [[genes]] and [[social environment|environment]], to varying degrees.<ref>{{cite journal |doi=10.1038/ng.3285 |pmid=25985137 |title=Meta-analysis of the heritability of human traits based on fifty years of twin studies |journal=Nature Genetics |volume=47 |issue=7 |pages=702–709 |year=2015 |last1=Polderman |first1=Tinca J C. |last2=Benyamin |first2=Beben |last3=De Leeuw |first3=Christiaan A. |last4=Sullivan |first4=Patrick F. |last5=Van Bochoven |first5=Arjen |last6=Visscher |first6=Peter M. |last7=Posthuma |first7=Danielle |s2cid=205349969 |url=https://espace.library.uq.edu.au/view/UQ:364460/UQ364460_OA.pdf }}</ref><ref>{{cite journal |doi=10.1111/1467-8721.00084 |title=Three Laws of Behavior Genetics and What They Mean |journal=Current Directions in Psychological Science |volume=9 |issue=5 |pages=160–164 |year=2000 |last1=Turkheimer |first1=Eric |s2cid=2861437 }}</ref> These two sources of influence are often confounded in observational research of individuals and families. An example of this confounding can be shown in the transmission of [[Depression (mood)|depression]] from a depressed mother to her offspring. A theory based on environmental transmission would hold that an offspring, by virtue of their having a problematic rearing environment managed by a depressed mother, is at risk for developing depression. On the other hand, a hereditarian theory would hold that depression risk in an offspring is influenced to some extent by genes passed to the child from the mother. Genes and environment in these simple transmission models are completely confounded. A depressed mother may both carry genes that contribute to depression in her offspring and also create a rearing environment that increases the risk of depression in her child.<ref>{{cite journal | doi=10.1001/jamanetworkopen.2020.8783 | title=Risk of Depression in the Adolescent and Adult Offspring of Mothers with Perinatal Depression | date=2020 | last1=Tirumalaraju | first1=Vaishali | last2=Suchting | first2=Robert | last3=Evans | first3=Jonathan | last4=Goetzl | first4=Laura | last5=Refuerzo | first5=Jerrie | last6=Neumann | first6=Alexander | last7=Anand | first7=Deepa | last8=Ravikumar | first8=Rekha | last9=Green | first9=Charles E. | last10=Cowen | first10=Philip J. | last11=Selvaraj | first11=Sudhakar | journal=JAMA Network Open | volume=3 | issue=6 | pages=e208783 | pmid=32602910 | pmc=7327545 }}</ref>

Behavioral genetics researchers have employed methodologies that help to disentangle this confound and understand the nature and origins of individual differences in behavior.<ref name="Behavior Genetics" /> Traditionally the research has involved [[twin studies]] and [[adoption study|adoption studies]], two designs where genetic and environmental influences can be partially un-confounded. More recently, gene-focused research has contributed to understanding genetic contributions to the development of psychological traits.

The availability of [[microarray]] [[molecular genetics|molecular genetic]] or [[genome sequencing]] technologies allows researchers to measure participant DNA variation directly, and test whether individual genetic variants within genes are associated with psychological traits and [[psychopathology]] through methods including [[genome-wide association studies]]. One goal of such research is similar to that in [[positional cloning]] and its success in [[Huntington's]]: once a causal gene is discovered biological research can be conducted to understand how that gene influences the phenotype. One major result of genetic association studies is the general finding that psychological traits and psychopathology, as well as complex medical diseases, are highly [[polygenic]],<ref>{{cite journal |doi=10.1016/j.ajhg.2011.11.029 |pmid=22243964 |pmc=3257326 |title=Five Years of GWAS Discovery |journal=The American Journal of Human Genetics |volume=90 |issue=1 |pages=7–24 |year=2012 |last1=Visscher |first1=Peter M. |last2=Brown |first2=Matthew A. |last3=McCarthy |first3=Mark I. |last4=Yang |first4=Jian}}</ref><ref>{{cite journal |doi=10.1038/nature13595 |pmid=25056061 |pmc=4112379 |title=Biological insights from 108 schizophrenia-associated genetic loci |journal=Nature |volume=511 |issue=7510 |pages=421–427 |year=2014 |bibcode=2014Natur.511..421S |last1=Ripke |first1=Stephan |last2=Neale |first2=Benjamin M. |last3=Corvin |first3=Aiden |last4=Walters |first4=James T. R. |last5=Farh |first5=Kai-How |last6=Holmans |first6=Peter A. |last7=Lee |first7=Phil |last8=Bulik-Sullivan |first8=Brendan |last9=Collier |first9=David A. |last10=Huang |first10=Hailiang |last11=Pers |first11=Tune H. |last12=Agartz |first12=Ingrid |last13=Agerbo |first13=Esben |last14=Albus |first14=Margot |last15=Alexander |first15=Madeline |last16=Amin |first16=Farooq |last17=Bacanu |first17=Silviu A. |last18=Begemann |first18=Martin |last19=Belliveau |first19=Richard A. |last20=Bene |first20=Judit |last21=Bergen |first21=Sarah E. |last22=Bevilacqua |first22=Elizabeth |last23=Bigdeli |first23=Tim B. |last24=Black |first24=Donald W. |last25=Bruggeman |first25=Richard |last26=Buccola |first26=Nancy G. |last27=Buckner |first27=Randy L. |last28=Byerley |first28=William |last29=Cahn |first29=Wiepke |last30=Cai |first30=Guiqing |display-authors=29 }}</ref><ref>{{cite journal |doi=10.1038/ng.1108 |pmid=22344220 |pmc=3327879 |title=Estimating the proportion of variation in susceptibility to schizophrenia captured by common SNPs |journal=Nature Genetics |volume=44 |issue=3 |pages=247–250 |year=2012 |last1=Lee |first1=S Hong |last2=Decandia |first2=Teresa R. |last3=Ripke |first3=Stephan |last4=Yang |first4=Jian |last5=Sullivan |first5=Patrick F. |last6=Goddard |first6=Michael E. |last7=Keller |first7=Matthew C. |last8=Visscher |first8=Peter M. |last9=Wray |first9=Naomi R. }}</ref><ref>{{cite journal |doi=10.1038/nrg3240 |pmid=22777127 |pmc=4110909 |title=Genetic architectures of psychiatric disorders: The emerging picture and its implications |journal=Nature Reviews Genetics |volume=13 |issue=8 |pages=537–551 |year=2012 |last1=Sullivan |first1=Patrick F. |last2=Daly |first2=Mark J. |last3=O'Donovan |first3=Michael }}</ref><ref>{{cite journal |doi=10.1001/jamapsychiatry.2015.0554 |pmid=25993607 |pmc=4667957 |title=Meta-analysis of Genome-wide Association Studies for Neuroticism, and the Polygenic Association with Major Depressive Disorder |journal=JAMA Psychiatry |volume=72 |issue=7 |pages=642–50 |year=2015 |last1=De Moor |first1=Marleen H. M. |last2=Van Den Berg |first2=Stéphanie M. |last3=Verweij |first3=Karin J. H. |last4=Krueger |first4=Robert F. |last5=Luciano |first5=Michelle |last6=Arias Vasquez |first6=Alejandro |last7=Matteson |first7=Lindsay K. |last8=Derringer |first8=Jaime |last9=Esko |first9=Tõnu |last10=Amin |first10=Najaf |last11=Gordon |first11=Scott D. |last12=Hansell |first12=Narelle K. |last13=Hart |first13=Amy B. |last14=Seppälä |first14=Ilkka |last15=Huffman |first15=Jennifer E. |last16=Konte |first16=Bettina |last17=Lahti |first17=Jari |last18=Lee |first18=Minyoung |last19=Miller |first19=Mike |last20=Nutile |first20=Teresa |last21=Tanaka |first21=Toshiko |last22=Teumer |first22=Alexander |last23=Viktorin |first23=Alexander |last24=Wedenoja |first24=Juho |last25=Abecasis |first25=Goncalo R. |last26=Adkins |first26=Daniel E. |last27=Agrawal |first27=Arpana |last28=Allik |first28=Jüri |last29=Appel |first29=Katja |last30=Bigdeli |first30=Timothy B. |display-authors=29 }}</ref> where a large number (on the order of hundreds to thousands) of genetic variants, each of small effect, contribute to individual differences in the behavioral trait or propensity to the disorder. Active research continues to work toward understanding the genetic and environmental bases of behavior and their interaction.