26 I. THEORETICAL  PERSPECTI vES AND  CONCEPT uAL uNITS
all lifetime reproductive success (Alvergne 
et al., 2010; Hutteman, Bleidorn, Penke, & 
Denissen, 2013; Jokela, Alvergne, Pollet, & 
Lummaa, 2011; Jokela, Hintsa, Hintsanen, 
& Keltikangas-  Järvinen, 2010; Jokela & 
Keltikangas-  Järvinen, 2009). Selective neu -
trality is therefore unlikely to be an impor -
tant explanation for many or most heritable 
individual differences in personality.
Mutation–Selection  Balance
The models we have presented thus far are 
based on two different classes of mutations. 
The first class refers to those mutations that 
are advantageous and therefore favored by 
selection, whether in the form of directional 
selection for universal psychological adapta -
tions or by balancing selection. The second 
class refers to those mutations that do not 
have an impact on reproductive success— 
selectively neutral mutations. There is a 
third and final class of mutations: those 
mutations that are deleterious and therefore 
selected against. Despite their detrimental 
effects, these mutations cannot be entirely 
eliminated from the population, because se -
lection cannot work fast enough to do so.
Research suggests that each human is 
born with approximately two new deleteri -
ous mutations (Keightley, 2012). However, 
few of these mutations are so harmful that 
they are selected out immediately. Although 
selection eventually weeds out harmful mu -
tations (see Fu et al., 2012), those that are 
only mildly harmful can take many genera -
tions for selection to purge. Consequently, 
these heritable mutations can accumulate 
across generations despite their deleteri -
ous effects. Conservative estimates suggest 
that the average human carries at least 500 
brain-  disruptive mutations (Fay, Wyckoff, 
& Wu, 2001; Keller & Miller, 2006).
Nonetheless, the number of mildly harm -
ful mutations that individuals carry—  called 
their “mutation load”—varies tremendously 
across individuals (Penke et al., 2007). Re -
cent work suggests that individual differenc -
es in mutation load might be able to explain 
the heritability of some individual differ -
ences, such as general intelligence (Penke et 
al., 2007; Deary, Penke, & Johnson, 2010), 
and some harmful mental disorders, such as 
schizophrenia and autism (Keller & Miller, 2006), although these hypotheses require 
further empirical verification.
Molecular Genetics Evidence Consistent 
with Mutation–  Selection Balance . The last 
few years have seen an explosion of molecu -
lar genetics findings relevant to evolutionary 
models of personality. The most significant 
change was from analyzing individual or 
small sets of genomic markers to genome -
wide approaches that use hundreds of thou -
sands of genetic markers. More recently, 
there has been another shift to whole-  genome 
sequencing of all the nucleotide letters in the 
DNA of studied individuals. While the ex -
isting evidence is not yet conclusive and a 
detailed review is beyond the scope of this 
chapter, we provide a short summary of the 
current state of the evidence here.
The last decade has greatly altered our 
view of the molecular genetics associated 
with personality variation. Meta-  analyses 
of individual genes, such as the dopamine 
receptor gene DRD4  or the serotonin trans -
porter gene 5HTT,  have yielded negative or 
weak results at best (Munafo & Flint, 2011). 
At the same time, sufficiently powered ge -
nomewide association studies (GWAS) have 
shown that there are no common (i.e., fre -
quent in the population) genetic variants 
that explain more than 1% of the genetic 
variance associated with broad personality 
traits such as those in the five-  factor model 
(de Moor et al., 2012; Verweij et al., 2012). 
This means that there are either thousands 
of genetic variants, each with very small ef -
fects on personality trait levels, or many dif -
ferent rare mutations that account for sub -
stantial proportions of genetic variation in 
personality (Penke, 2011).
Recent research has also attempted to es -
timate how much of the additive heritability 
of traits can be explained by all the common 
genetic variants used in a GWAS in total, 
regardless of how much individual variants 
explain. Interestingly, while this approach 
is able to explain almost all of the genetic 
variance in traits such as height (Yang et 
al., 2010), only a very small percentage of 
the genetic variance in Cloninger’s (Verweij 
et al., 2010) and Eysenck’s (Vinkhuyzen et 
al., 2012) personality traits can be explained 
this way. Some researchers (e.g., Verweij et 
al., 2012) take this as evidence for personal -