Characterizing the natural selection of complex traits is important for
understanding human evolution and both biological and pathological mechanisms.
We leveraged genome-wide summary statistics for 870 polygenic traits and
attempted to quantify signals of selection on traits of different forms in European ancestry across 4 periods in human history and evolution.
We found that 88% of these traits underwent polygenic change in the past 2,000–3,000 years. Recent selection was associated with ancient selection signals in
the same trait. Traits related to pigmentation, body measurement and nutritional intake exhibited strong selection signals across different time scales. Our
findings are limited by our use of exclusively European data and the use of genome-wide association study data, which identify associations between genetic
variants and phenotypes that may not be causal.
In sum, we provide an overview of signals of selection on human polygenic traits and their characteristics across human evolution, based on a European subset of
human genetic diversity. These findings could serve as a foundation for further population and medical genetic studies.
…As shown in Figure 1, we focus on 2 primary goals. First, we describe the selection pressure on each trait at 4 different time scales
(Figures 2–5). This is achieved using various metrics derived from different statistical models (Mendelian randomization (MR), singleton density score, ancient genome analysis and so on),
each fitting a specific timeframe or form of selection. Second, we integrate these metrics to explore the association among selection pressures, trait
characteristics and functional genomic patterns (Figures 6–8), using linear regression and unsupervised clustering.
…Body measurements and contemporary reproductive success: Our analysis started by exploring natural selection pressure at the present time. We
hypothesized that the current natural selection of a trait is relevant to whether it could causally impact human reproductive success (that is, number of
offspring) and mating success (for this, we used the proxy of number of overall sexual partners). To quantify these causal effects, we applied MR on GWAS summary statistics between tested
traits and reproductive success, as well as between tested traits and mating success. At the statistical-significance cutoff of |zMR| > 4
(Methods), we found that 7.4% of traits with valid MR results (that is, traits passing sensitivity analysis) (40 out of 539) had a causal effect on the number of
offspring of males, whereas 5.9% (32 out of 542) of traits with valid MR results impacted the number of offspring of females (Supplementary
Table 2). Separating the traits into 15 categories (Figure 2A, Figure 2B), we observed that 52% (23⁄44) of
anthropometric body measurement traits such as height (zMR = 8.09, p = 3.33 × 10−16 in males; zMR =
4.91, p = 4.55 × 10−7 in females) were causally related to the number of offspring of males. By contrast, only 30% (14⁄47) of body measurement
traits were causally related to the number of offspring of females. In addition, the effect of another type of body measurement (dermatology traits such as skin
colour) on reproductive success also exhibited sex specificity: 38% (5⁄13) of dermatology traits influenced the number of offspring of males, but none affected the
number of offspring of females. However, when testing for 112 complex conditions such as schizophrenia11 and stroke15, polygenic risks showed
no statistically-significant causal effect on the numbers of offspring for
either males or females (nominal p > 0.05/112). The distribution of effect direction was also similar between disease and non-disease traits
(Fisher p = 0.40 for males, p = 0.71 for females).
For mating success (Supplementary
Figure 2), body measurement traits also had an impact: 44% of body measurement traits impacted the number of sexual partners of males, compared
with 12% affecting the number of sexual partners of females. Interestingly, among all 112 tested polygenic disease traits, schizophrenia (zMR =
7.37, p = 8.53 × 10−14) and attention-deficit hyperactivity disorder (zMR = 4.62, p = 1.92 × 10−6) increased the number of sexual
partners of males, in line with previous findings that increased genetic liability for schizophrenia does not confer a fitness advantage but does increase mating
success16. For males, the impact on
reproductive success of a trait was positively correlated with its impact on mating success (Supplementary Figure 2; Pearson correlation coefficient(PCC) 0.47, 95% CI 0.39 to 0.55,p = 9.30 × 10−31). However, this was not true for females, for whom the impact
on reproductive success of a trait was negatively correlated with its impact on mating success (Supplementary Figure 2; PCC −0.10, 95% CI −0.20 to 0,p = 0.02). This discrepancy is consistent with the evolutionary psychology theory that males and females adopt distinct sexual
strategies that shape assortative selection17.
Next, we investigated whether the trait impact on reproductive success and mating would differ between the sexes. In general, trait impact on human reproductive
success was similar for males and females (Figure 2c; PCC 0.38, 95% CI 0.32 to 0.44,p = 6.85 × 10−31). Trait impacts of mating success were also similar between the sexes (Supplementary Figure 2;
PCC 0.64, 95% CI 0.58 to 0.70,p = 9.18 × 10−106). Notably, high intelligence trait
statistically-significantly reduced the number of offspring in both females and males (zMR = −7.55, p = 2.18 × 10−14 in
females, zMR = −5.13, p = 1.45 × 10−7 in males), and increased the expected number of sexual partners for females
(zMR = 7.05, p = 8.97 × 10−13) (Supplementary Figure 1).
In addition, we applied causal analysis using summary effect estimates18
to all MR results to analyse the role of genetic correlation. We found that
most of the results were explained mainly by causal effects instead of genetic correlation. Using another GWAS19
dataset and applying MR bias estimation20, we again showed that our results were not explained by GWAS sample
overlap (‘MR analysis details’ in Supplementary Information).
…Widespread polygenic adaptation in the past 2,000–3,000 years: At the statistical-significance threshold of p < (0.05/870 = 5.7
× 10−5), we found that 88% (761⁄870) of polygenic traits had a statistically-significant correlation between the GWASp-value and tSDS (ρSDS; Supplementary Table 3). Previous analysis has found that population stratification of UK Biobank might bias the estimated polygenic adaptation22.
Thus, to exclude this potential confound in our analyses, we applied another method with a different statistical model, which involves reconstructing the history
of polygenic scores(RHPS)23, based on RELATE24 (RHPS-RELATE, Methods). We set the reference panel as all European participants of 1000 Genomes to avoid population stratification. As shown in Supplementary
Table 3, the polygenic risk score (PRS) alteration in the past 100 generations (roughly equivalent to
2,800 years (ref. 24)) was mostly in accordance with ρSDS(PCC 0.25, 95%
CI 0.18 to 0.32,p = 3.96 × 10−13). Among 755 traits with statistically-significant non-zero ρSDS, 13.8% (104⁄755) showed a consistent statistically-significant alteration of PRS
(p for ‘Tx test’ from RHPS < 0.05/870, Methods), and 26.1% (197⁄755) showed a nominally
statistically-significant alteration (p for Tx test < 0.05). Notably, our RHPS-RELATE results also
highlighted those traits with the highest ρSDS, such as ease of skin tanning (p for ρSDS <10−100; p for Tx test
<10−100) and raw vegetable intake (p for ρSDS <10−100; p for Tx test
2.69 × 10−51) (Supplementary Table 3). In general, the results of RHPS-RELATE were
consistent with the ρSDS analysis, albeit at lower statistical power. Thus, we conclude that the ρSDS results are credible and can truly reflect
recent adaptation prevalence…by utilizing simulations of genetic drift and
demographic isolation strategies, our results suggest that population stratification did not drive a systematic bias on ρSDS. We consequently propose that the observed bias on height might not represent the majority of traits.
…When analysing all traits, we observed that dermatology traits generally showed the most statistically-significant selection signals (median
|ρSDS| = 0.69, Figure 3A, B), followed by nutrition intake (median |ρSDS| = 0.48; Supplementary Figure 4) and reproduction-related traits (median |ρSDS| = 0.30; Supplementary Figure 4). Ease of skin tanning was the trait with the most statistically-significant
adaptation (ρSDS = 0.96, p < 10−100; Figure 3c). Ever been drinkers
(ρSDS = −0.82, p < 10−100) and sitting height (ρSDS = 0.84, p < 10−100) were also among traits with an extreme adaptation signal (|ρSDS| > 0.8), which made up 3.3% of all traits (Supplementary Figure 4). Neurological traits such as brain
structures exhibited the least polygenic adaptation (median |ρ| = 0.05).
In contrast to non-disease traits, the adaptive pressure on polygenic disease traits was generally negative (median ρSDS = −0.08; permutation p = 3.22 × 10−6), especially for early-onset conditions such as autism spectrum disorder (median ρSDS =
−0.12; Supplementary Figure 5). The greatest evidence of negative adaptation was found for high cholesterol (ρSDS = −0.66, p < 10−100; Supplementary Figure 5). Still, we found evidence of positive
adaptation for a few diseases such as skin cancer and inflammatory bowel disease (ρSDS
> 0.2, p <10−100; Supplementary Figure 5), and even some early-onset conditions such as attention deficit hyperactivity
disorder (ρSDS = 0.20, p <2.16 × 10−24) and anorexia nervosa (ρSDS = 0.16, p =
1.24 × 10−19) (Supplementary Table 3). This result suggested that some of the disease traits might be by-products of other positive
…As shown in Figure 4a and Supplementary Table 5, after controlling for covariances (for example, latitude, longitude and
genotyping coverage) and multiple tests, the polygenic burden of 78 traits was statistically-significantly associated with the percentage of hunter-gatherer
ancestry (HG%). By contrast, another 6 traits, such as denture usage, were associated with
time in at least one of 3 datasets. 7 of 13 dermatology traits were most predominantly associated with HG% (Figure 4a), with ‘ease of skin
tanning’ as the most statistically-significant example (regression tHG = 20.3, p = 1.74 × 10−38; Figure 4b). In the
Near East dataset, we observed that signals of selection on skin tanning varied by latitude (Figure 4c), with signals of positive selection
observed in regions of low latitude (latitude < 50°; t = 4.12, p = 1.91 × 10−5), but signals of negative selection observed at high latitudes (t = 4.95,
p = 3.80 × 10−7). After controlling for the impact of latitude, we observed a general ascending trend for ‘ease of skin tanning’ for the Near
East dataset, suggesting overall positive selection (regression tNear East = 5.81, p = 2.29 × 10−8; Figure
4c). We also found a nominally statistically-significant increment for ease of skin tanning in the pre-Neolithic period (regression tpre-Neolithic = 4.25, p = 1.11
× 10−5), but not in the Neolithic period (regression tNeolithic = 0.92, p = 0.18; Supplementary Figure
…although all the above possibilities explained a proportion of disease heritability, there is still room for another ‘trivial explanation’: natural selection
was indeed eliminating the risk alleles but simply not fast enough, due to the small effect of each allele and the small effective population size at the risk loci8,46
Using data from the first Census data set that includes complete measures of male biological fertility for a large-scale probability sample of the U.S.
population (the 2014 wave of the Study of Income and Program ParticipationN = 55,281), this study shows that:
high income men are more likely to marry, are less likely to divorce, if divorced are more likely to remarry, and are less likely to be childless than low
income men. Men who remarry marry relatively younger women than other men, on average, although this does not vary by personal income. For men who divorce who have
children, high income is not associated with an increased probability of having children with new partners. Income is not associated with the probability of
marriage for women and is positively associated with the probability of divorce.
High income women are less likely to remarry after divorce and more likely to be childless than low income women. For women who divorce who have children, high
income is associated with a lower chance of having children with new partners, although the relationship is curvilinear.
These results are behavioral evidence that women are more likely than men to prioritize earning capabilities in a long-term mate and suggest that high income
men have high value as long-term mates in the U.S.
[Keywords: evolutionary psychology, fertility, marriage, childlessness, divorce, sex differences]
We assess the impact of exogenous variation in oral contraceptives prices—a year-long decline followed by a sharp increase due to a documented collusion case—on
fertility decisions and newborns’ outcomes. Our empirical strategy follows an interrupted time-series design, which is implemented using multiple sources of
administrative information. As prices skyrocketed (45% within a few weeks), the Pill’s consumption plunged, and weekly conceptions increased (3.2% after a few
We show large effects on the number of children born to unmarried mothers, to mothers in their early twenties, and to primiparae women. The incidence of low
birth weight and fetal/infant deaths increased (declined) as the cost of birth control pills rose (fell). In addition, we document a disproportional increase in
the weekly miscarriage and stillbirth rates. As children reached school age, we find lower school enrollment rates and higher participation in special education
Our evidence suggests these “extra” conceptions were more likely to face adverse conditions during critical periods of development.
…This paper quantifies the Pill’s role in fertility and child outcomes using a sequence of events in which unexpected shocks affected the access to oral
contraceptives. In particular, we exploit a well-established case of anticompetitive behavior in the pharmaceutical market, which—after a year-long price war
between the 3 largest pharmaceutical retailers in Chile—triggered a sharp and unexpected increase in the prices of birth control pills.
The price war took place during 2007, and it effectively reduced the prices of medicines across the board. In particular, prices of oral contraceptives fell by
24% during that year. By the end of 2007, the 3 largest pharmacies agreed to end the price war and engaged in a collusion scheme in which they strategically
increased the prices of 222 medicines. Oral contraceptives were included in this group, experiencing price increases ranging from 30 to 100% in just a few weeks
(45% on average in the first 3 weeks). We use daily information on prices and quantities sold in the country by the 3 companies from almost 40 million transactions
to determine the date when the price changes for birth control pills took place. Using these data, we implement an interrupted time-series analysis (Bloom, 2003;
Cauley & Iksoon 1988), which takes into account the seasonality of births, the general trends of fertility, as well as dynamics that arise because it takes
time for the menstrual cycle to be fully regulated after discontinuing the Pill’s intake. We complement the pharmacies’ transaction data with administrative
information from birth and death certificates collected between 2005 and 2008 and administrative records on school enrollment from 2013 to 2016. Our empirical
strategy considers 2 different treatments: one stemming from a sustained and steady decline in prices (2007) and another one from a massive and sudden increase
(first weeks of 2008).
Changes in mean intelligence test scores were minimal in Denmark in 2006–2019 [2006–2010: 111.5, 111.1, 110.8, 110.7, 110.6, | 2011–2019: 109.1, 109.2,
109.0, 109.1, 109.3, 109.2, 109.1, 108.7, 108.8].
A change in the format of the intelligence test resulted in a sudden drop in scores.
Neither changes in parental age, dysgenics, or immigration can explain the findings.
Changes in sample composition may conceal a true decline in intelligence test scores.
The present register-based study investigated the secular trend of intelligence test scores during the period from 2006 through 2019 in a Danish
population-representative sample, as well as whether the observed trend could be explained by changes in parental age, dysgenics, and immigration or changes in the
format of the intelligence test and sample characteristics.
The study population consisted of all Danish men appearing before a draft board during the study period (n = 400,288). Intelligence test scores were
obtained by the use of Børge Priens Prøve, typically at age 19. For each of the included draft board cohorts, the intelligence test score mean and standard
deviation were estimated.
The results showed that changes in mean intelligence test scores were minimal during the study period. A slight decline was observed from 2006 to 2010.
Furthermore, there was a drop of 1.5 IQ points from 2010 to 2011, which coincided with the change in the format of the intelligence test from paper-and-pencil to
computer-based, but there was essentially no change after 2011. Neither changes in parental age, dysgenics, or immigration seem to have influenced the
observations. However, changes in sample composition may conceal a true decline in intelligence test scores given that a larger proportion of individuals with low
intelligence seems to be exempted from testing.
In conclusion, the study findings suggest no systematic change in intelligence test scores during the last decade, but due to changes in sample composition, it
cannot be excluded that there has been a negative secular trend.
…A slight decline in mean IQ score was observed from 2006 to 2010, which can be seen as a continuation of the decline previously reported between 1998 and 2004
(Teasdale & Owen 2008)…We have had the opportunity to rescale the mean intelligence test scores from the Danish draft board examinations reported by Teasdale
& Owen 2008 against our baseline year 1960 to compare them with our observations. The rescaled mean IQ scores are as follows: 1988: 111.0 (SD: 13.0);
1998: 112.4 (SD: 12.7); 2003–4: 111.1 (SD: 12.8). As can be seen, there was an increase from 1988 to 1998 followed by a small decline from 1998 to 2003–4. The mean
IQ score in 1998 remains the highest recorded using Danish draft board data, whereas the mean IQ score in 2003–4 is comparable with our mean intelligence test
score in 2006. As such, there has been a decline of 1.8 IQ points during the period from 1998 through 2010 followed by a drop of 1.5 IQ points which is probably
due to the change in the format of the intelligence test and virtually no change from 2011 through 2019. However, the variance has declined statistically-significantly
throughout the study period, corresponding to a decline of 0.15 SD per year (p < 0.001). A previous study has suggested that the negative secular trend
observed in developmental test performances may be rooted in declining performances of the top percentiles (Flynn & Shayer 2018), leading to declining variances. If this is also true in our study where the
proportion of individuals with low test intelligence scores who were exempted from testing has increased over time, this might explain our observation of no change
in mean intelligence test scores, but a declining variance.
Age at first sexual intercourse (AFS) and age at first birth (AFB) have
implications for health and evolutionary fitness. In the largest genome-wide association study to date (AFS,n= 387,338; AFB,n = 542,901), we identify 370 independent signals, 11 sex-specific, with a
5–6% polygenic score (PGS) prediction. Heritability of AFB shifted from 9% [CI
= 4–14] for women born in 1940 to 22% [CI = 19–25] in 1965. Signals are driven by the genetics of reproductive biology and externalizing behaviour, with key genes
related to follicle stimulating hormone (FSHB), implantation (ESR1), infertility,
and spermatid differentiation. Polycystic Ovarian Syndrome leads to later AFB, linking with infertility. Late
AFB is protective against later-life disease and associated with parental longevity. Higher childhood
socioeconomic circumstances and those in the highest PGS decile (90%+) experience markedly later reproductive onset.
Results are relevant for improving teenage and late-life health, for understanding longevity, and guiding experimentation into mechanisms of infertility.
bioRxiv; author discussion: 1, 2, 3.] Natural selection has been documented in contemporary
humans, but little is known about the mechanisms behind it. We test for natural selection through the association between 33 polygenic scores and fertility, across
two generations, using data from UK Biobank (n = 409,629
British subjects with European ancestry).
Consistently over time, polygenic scores associated with lower (higher) earnings, education and health are selected for (against). Selection effects are
concentrated among lower SES groups, younger parents, people with more lifetime sexual partners, and people not living with a partner. The direction of natural
selection is reversed among older parents (22+), or after controlling for age at first live birth. These patterns are in line with economic theories of fertility,
in which higher earnings may either increase or decrease fertility via income and substitution effects in the labour market.
Studying natural selection can help us understand the genetic architecture of health outcomes: we find evidence in modern day Great Britain for multiple natural
selection pressures that vary between subgroups in the direction and strength of their effects, that are strongly related to the socio-economic system, and that
may contribute to health inequalities across income groups.
I test the assumptions of the Malthusian model at the individual, cross-sectional level for France, 1650–1820. Using husband’s occupation from the parish
records of 41 French rural villages, I assign three different measures of status. There is no evidence for the existence of the positive check; infant deaths are
unrelated to status. However, the preventive check operates strongly, acting through female age at first marriage. The wives of rich men are younger brides than
those of poorer men. This drives a positive net-fertility gradient in living standards. However, the strength of this gradient is substantially weaker than it is
in pre-industrial England.
Ageing may be due to mutation accumulation across the lifespan, leading to tissue dysfunction, disease, and death. We tested whether germline autosomal mutation
rates in young adults predict their remaining survival, and, for women, their reproductive lifespans. Age-adjusted mutation rates (AAMRs) in 61 women and 61 men from theUtah CEPH (Centre d’Etude du Polymorphisme Humain)
families were determined. Age at death, cause of death, all-site cancer incidence, and reproductive histories were provided by the Utah Population Database,
Utah Cancer Registry, and Utah Genetic Reference Project. Higher AAMRs were statistically-significantly associated with
higher all-cause mortality in both sexes combined. Subjects in the top quartile of AAMRs experienced more than
twice the mortality of bottom quartile subjects (hazard ratio [HR], 2.07; 95% confidence interval [CI], 1.21–3.56; p = 0.008; median survival
difference = 4.7 years). Fertility analyses were restricted to women whose age at last birth (ALB) was ≥ 30 years, the
age when fertility begins to decline.Women with higher AAMRs had statistically-significantly fewer livebirths and a younger ALB. Adult germline mutation accumulation rates are established in adolescence, and later
menarche in women is associated with delayed mutation accumulation. We conclude that germline mutation rates in healthy young adults may provide a measure of both
reproductive and systemic ageing. Puberty may induce the establishment of adult mutation accumulation rates, just when DNA repair systems begin their lifelong decline.
Identifying genetic determinants of reproductive success may highlight mechanisms underlying fertility and also identify alleles under present-day selection.
Using data in 785,604 individuals of European ancestry, we identify 43 genomic loci associated with either number of children ever born (NEB) or childlessness. These loci span diverse aspects of reproductive biology across the life course, including puberty timing, age
at first birth, sex hormone regulation and age at menopause. Missense alleles in ARHGAP27 were associated with
increased NEB but reduced reproductive lifespan, suggesting atrade-off between reproductive ageing and
intensity. As NEB is one component of evolutionary fitness, our identified associations indicate loci under present-day
natural selection. Accordingly, we find that NEB-increasing alleles have increased in frequency over the past two
generations. Furthermore, integration with data from ancient selection scans identifies a unique example of an allele—FADS1/2 gene locus—that has been under selection for thousands of years and remains under selection today. Collectively, our
findings demonstrate that diverse biological mechanisms contribute to reproductive success, implicating both neuro-endocrine and behavioural influences.
Recent years have seen the birth of sociogenomics via the infusion of molecular genetic data. We chronicle the history of genetics, focusing particularly on
post-2005 genome-wide association studies, the post-2015 big data era, and the emergence of polygenic scores. We argue that understanding polygenic scores,
including their genetic correlations with each other, causation, and underlying biological architecture, is vital. We show how genetics can be introduced to
understand a myriad of topics such as fertility, educational attainment, intergenerational social mobility, well-being, addiction, risky behavior, and longevity.
Although models of gene-environment interaction and correlation mirror agency and structure models in sociology, genetics is yet to be fully discovered by this
discipline. We conclude with a critical reflection on the lack of diversity, non-representative samples, precision policy applications, ethics, and genetic
determinism. We argue that sociogenomics can speak to long-standing sociological questions and that sociologists can offer innovative theoretical, measurement, and
methodological innovations to genetic research.
The timing of reproductive behaviour—age at first sexual intercourse (AFS) and age at first birth (AFB)—has implications for reproductive health, adolescent development and evolutionary fitness. In the largest genome-wide
association study to date (AFS,n = 387,338; AFB,n =
542,901), we identify 370 independent signals, 11 which are sex-specific, with a 5–6% polygenic score prediction. Heritability shifted from 10% for those born in
1940 to 23% for the 1965 birth cohort. Using Genomic SEM, we show that signals are largely driven by the genetics
of reproductive biology and externalizing behaviour. This is supported by extensive biological follow-up that isolates key genes related to follicle
stimulating hormone (FSHB), implantation (ESR1), infertility (endometriosis,
spontaneous abortion) and spermatid differentiation, morphogenesis and binding (KLF17, ZPBP). Later AFB is protective against later-life disease (type 2 diabetes, cardiovascular) and
associated with longevity. Those from higher childhood socioeconomic circumstances and polygenic scores in the highest deciles (90%+) experience markedly later
reproductive onset. Results are relevant for interventions in teenage sexual, reproductive and mental health, deepen our understanding of the drivers of later-life
health and longevity, and fuel infertility and functional follow-up experiments.
In many species, the offspring of related parents suffer reduced reproductive success, a phenomenon known as inbreeding depression. In humans, the importance of this
effect has remained unclear, partly because reproduction between close relatives is both rare and frequently associated with confounding social factors. Here, using genomic inbreeding
coefficients (FROH) for >1.4 million individuals, we show that FROH is statistically-significantly associated (p < 0.0005) with apparently deleterious changes in 32 out of 100
traits analysed. These changes are associated with runs of homozygosity (ROH), but not with common varianthomozygosity, suggesting that genetic variants
associated with inbreeding depression are predominantly rare. The effect on fertility is striking: FROH
equivalent to the offspring of first cousins is associated with a 55% decrease [95% CI 44–66%] in the odds of having children. Finally, the effects of
FROH are confirmed within full-sibling pairs, where the variation in FROH is independent of all environmental confounding.
In many countries where companion dogs are popular, owners are strongly encouraged to neuter their dogs. Consequently, millions of dogs are neutered each year.
In recent times considerable attention has been paid to the possible effects of such procedures on canine health and welfare. Less scrutinized are the potential
ramifications of widespread neutering on the breeding of dogs and their continued success as human companions. This paper summarizes research investigating factors
influencing the breeding and rearing of dogs most suited to companionship roles in contemporary, typically high-density, communities, and briefly reviews current
breeder practices. It then argues that a fundamental shift to promote inclusion of “proven” companion dogs in the gene pool, as opposed to dogs meeting
conformation or working/sporting standards, is required to successfully meet the needs of modern urban dog owners. A new model is proposed, whereby responsible
owners and breeders work together to produce dogs most suited for life as human companions.
…The demonstrated importance of genetics and early environment in determining behavioral predispositions makes it imperative to consider where companion dogs
come from. Prior to the widespread introduction of neutering practices, dogs often bred indiscriminately, and people typically obtained their dogs for free from
neighbors whose bitch had produced a litter (47). While this was problematic in terms of creating dog overpopulation, it meant that most of the dogs who produced
offspring were well suited to the demands of the lives they were expected to lead. Those who weren’t well-suited were disposed of. Today, strong demand for
companion dogs, coupled with rapid urbanization, increased concern regarding the welfare of animals, particularly companion dogs, and high neutering rates, has
resulted in a multimillion-dollar industry involving the selective breeding and selling of puppies (48). Widespread neutering means that humans intentionally
control nearly all dog breeding in developed countries…As described previously, in many developed countries, neutering companion dogs is considered an important
aspect of responsible ownership. Hence, the very best companion dogs in the general community, those owned by responsible citizens who choose their dogs carefully
and ensure they are reared correctly, are almost certainly those most likely to be neutered. Conversely, it is those companion dog owners who fail to perform the
“responsible” behavior of neutering their dog who are perhaps most likely to breed. These “breeders” may also choose not to perform other “responsible” behaviors,
such as selecting their dog carefully, testing it for genetic disorders, or evaluating the dog’s suitability as a companion prior to allowing it to reproduce. In
other words, they may not thoroughly consider the genetic and environmental factors known to be critical to optimal puppy development.
Second, we advocate that all dogs should be independently tested for suitability before being bred—much as breeders now advertise that their puppies’ parents
are successful show dogs, or that they are free from known genetic disorders, so they should be encouraged to advertise that independent testing has shown their
breeding dogs to be well-suited behaviourally to life as human companions. We anticipate that responsible breeders would be willing to pay for this independent
certification, much as they presently pay for genetic tests, eye screening and tests for hip dysplasia. Several behavioral tests exist to measure specific traits,
such as the Socially Acceptable Behavior test (64), which measures aggression, or the Dog Mentality Assessment test (65), which examines levels of playfulness,
curiosity, aggression, sociability, and chase-proneness. In the USA, the Canine Good Citizen program, administered
by the American Kennel Club, takes <30 min to administer and is designed to identify dogs that meet ten objectives consistent with being a good companion dog.
Any one of these tests could be used as a basis for developing an assessment suited to breeding dogs—dogs that are not themselves good companions are less likely
to produce puppies able to excel at this role.
Heritable variation in fitness—survival and reproduction—is the fuel of evolution by natural selection. Many human societies have dramatically reduced mortality
before and during the prime reproductive years, making fertility a reasonably good proxy for the whole of fitness in much of our species. For this reason,
empirical knowledge regarding the genetics of fertility must be an essential part of any framework for understanding past and ongoing trends in human adaptive
evolution. Here we use R. A. Fisher’s analysis of human fertility as a starting point and find strong support from more recent research for his main contentions:
fertility is a moderately heritable trait, where much of the genetic influences are shared with psychological characteristics.
Using newly available polygenic scores for educational attainment and cognitive ability, this paper investigates the possible presence and causes of a negative
association between IQ and fertility in the Wisconsin Longitudinal Study sample, an issue that Retherford and Sewell first addressed 30 years ago. The effect of
the polygenic score on the sample’s reproductive characteristics was indirect: a latent cognitive ability measure, comprised of both educational attainment and IQ,
wholly mediated the relationship. Age at first birth mediated the negative effect of cognitive ability on sample fertility, which had a direct (positive) effect on
the number of grandchildren. statistically-significantly greater impacts of cognitive ability on the sample’s fertility characteristics were found among the female
subsample. This indicates that, in this sample, having a genetic disposition toward higher cognitive ability does not directly reduce number of offspring; instead,
higher cognitive ability is a risk factor for prolonging reproductive debut, which, especially for women, reduces the fertility window and, thus, the number of
children and grandchildren that can be produced. By estimating the effect of the sample’s reproductive characteristics on the strength of polygenic selection, it
was found that the genetic variance
component of IQ should be declining at a rate between −0.208 (95% CI [−0.020, −0.383]) and −0.424 (95% CI [−0.041, −0.766]) points per decade, depending on
whether GCTA-GREML or classical behavior genetic estimates of IQ heritability are used to correct for ‘missing’ heritability.
The relationship between general cognitive ability and reproduction is reviewed.
There is an inverse relation between cognitive ability and number of children.
The effect is stronger among females than males.
The effect appears to be increasing in strength over time.
Notable limitations of the current literature are reviewed.
The purpose of this study is to conduct a systematic review of the literature on the relationship between general cognitive ability and fertility among modern
humans. Our goals were to (a) evaluate the state of the extant literature, and (b) provide a quantitative summary of effect sizes to the extent possible (given the limitations of the
literature). A thorough search identified 17 unique datasets that passed the inclusion criteria. Using a Random Effects Model to evaluate the data, the
overall weighted effect was r = −0.11, although the data also indicated a sex effect (stronger correlations among females than males), and a race effect
(stronger correlations among Black and Hispanic populations compared to Whites). Importantly, the data suggest the correlation has been increasing in strength
throughout the 20th century (and early 21st). Finally, we discovered several notable limitations of the extant literature; limitations that
currently prohibit a psychometric meta-analysis. We
discuss these issues with emphasis on improving future primary studies to allow for more effective meta-analytic
The rate of evolution of population mean fitness informs how selection acting in contemporary populations can counteract environmental change and genetic
degradation (mutation, gene flow, drift, recombination). This rate influences population increases (eg. range expansion), population stability (eg. cryptic
eco-evolutionary dynamics), and population recovery (ie. evolutionary rescue). We review approaches for estimating such rates, especially in wild populations. We
then review empirical estimates derived from two approaches: mutation accumulation (MA) and additive genetic variance in fitness (IAw). MA studies
inform how selection counters genetic degradation arising from deleterious mutations, typically generating estimates of <1% per generation. IAw
studies provide an integrated prediction of proportional change per generation, nearly always generating estimates of <20% and, more typically, <10%.
Overall, considerable, but not unlimited, evolutionary potential exists in populations facing detrimental environmental or genetic change. However, further studies
with diverse methods and species are required for more robust and general insights.
Previous research has found a genetic component of human reproduction and childlessness. Others have argued that the heritability of reproduction is
counterintuitive due to a frequent misinterpretation that additive genetic variance in reproductive fitness should be close to zero. Yet it is plausible that
different genetic loci operate in male and female fertility in the form of sexual dimorphism and that these genes are passed on to the next generation. This study
examines the extent to which genetic factors influence childlessness and provides an empirical test of genetic sexual dimorphism. Data from the Swedish Twin
Register (n = 9942) is used to estimate a classical twin model, a genomic-relatedness-matrix restricted maximum likelihood (GREML) model on twins and estimates polygenic scores of age at first birth on childlessness. Results show that the variation in
individual differences in childlessness is explained by genetic differences for 47% in the twin model and 59% for women and 56% for men using the
GREML model. Using a polygenic score (PGS) of age at first birth(AFB), the odds of remaining childless are around 1.25 higher forindividuals with 1 SD higher score on the
AFB PGS, but only for women. We find that different sets of genes influence childlessness in men and in women. These
findings provide insight into why people remain childless and give evidence of genetic sexual dimorphism.
The genomes of ancient humans, Neandertals, and Denisovans contain many alleles that influence disease risks. Using genotypes at 3180 disease-associated loci,
we estimated the disease burden of 147 ancient genomes. After correcting for missing data, genetic risk scores were generated for nine disease categories and the
set of all combined diseases. These genetic risk scores were used to examine the effects of different types of subsistence, geography, and sample age on the number
of risk alleles in each ancient genome. On a broad scale, hereditary disease risks are similar for ancient hominins and modern-day humans, and the
GRS percentiles of ancient individuals span the full range of what is observed in present day individuals. In addition,
there is evidence that ancient pastoralists may have had healthier genomes than hunter-gatherers and agriculturalists. We also observed a temporal trend whereby
genomes from the recent past are more likely to be healthier than genomes from the deep past. This calls into question the idea that modern lifestyles have caused
genetic load to increase over time. Focusing on individual genomes, we find that the overall genomic health of the Altai Neanderthal is worse than 97% of present
day humans and that Ötzi the Tyrolean Iceman had a genetic predisposition to gastrointestinal and cardiovascular diseases. As demonstrated by this work, ancient
genomes afford us new opportunities to diagnose past human health, which has previously been limited by the quality and completeness of remains.
Epidemiological studies suggest that educational attainment is affected by genetic variants. Results from recent genetic studies allow us to construct a score
from a person’s genotypes that captures a portion of this genetic component. Using data from Iceland that include a substantial fraction of the population we show
that individuals with high scores tend to have fewer children, mainly because they have children later in life. Consequently, the average score has been decreasing
over time in the population. The rate of decrease is small per generation but marked on an evolutionary timescale. Another important observation is that the
association between the score and fertility remains highly statistically-significant after adjusting for the educational attainment of the individuals.
Epidemiological and genetic association studies show that genetics play an important role in the attainment of education. Here, we investigate the effect of
this genetic component on the reproductive history of 109,120 Icelanders and the consequent impact on the gene pool over time. We show that an educational
attainment polygenic score, POLYEDU, constructed from results of a
recent study is associated with delayed reproduction (p < 10−100) and fewer children overall. The effect is stronger for women and remains
highly statistically-significant after adjusting for educational attainment. Based on 129,808 Icelanders born between 1910 and 1990, we find that the average
POLYEDU has been declining at a rate of ~0.010 standard units per decade,
which is substantial on an evolutionary timescale. Most importantly, because POLYEDU only captures a fraction of the overall underlying genetic component the latter could be declining at a rate that is two to three
The genetic architecture of human reproductive behavior—age at first birth (AFB) and number of children ever born
(NEB)—has a strong relationship with fitness, human development, infertility and risk of neuropsychiatric disorders.
However, very few genetic loci have been identified, and the underlying mechanisms of AFB and NEB are poorly understood. We report a large genome-wide association study of both sexes including 251,151 individuals for
AFB and 343,072 individualsfor NEB. We identified 12 independent loci that
arestatistically-significantly associated with AFB and/or NEB in aSNP-based genome-wide association study and 4 additional loci associated in a gene-based effort. These loci harbor
genes that are likely to have a role, either directly or by affecting non-local gene expression, in human reproduction and infertility, thereby increasing
understanding of these complex traits.
Utilizing a newly released cognitive Polygenic Score (PGS) from Wave IV of Add Health (n = 1,886),
structural equation models (SEMs) examining the relationship between PGS and fertility (which is
approximately 50% complete in the present sample), utilizing measures of verbal IQ and educational attainment as potential mediators, were estimated. The results
of indirect pathway models revealed that verbal IQ mediates the positive relationship between PGS and educational
attainment, and educational attainment in turn mediates the negative relationship between IQ and a latent fertility measure. The direct path from PGS to fertility was
non-significant. The model was robust to controlling for age, sex and race, furthermore the results of a multi-group SEM revealed no statistically-significant differences in the estimated path coefficients across sex. These results
indicate that those predisposed towards higher IQ by virtue of higher PGS values are also predisposed towards
trading fertility against time spent in education, which contributes to those with higher PGS values producing
We describe dynamics in assortative mating and fertility patterns by polygenic scores associated with anthropometric traits, depression, and educational
attainment across birth cohorts from 1920 to 1955. We find that, for example, increases in assortative mating at the phenotypic level for education are not matched
at the genotypic level. We also show that genes related to height are positively associated with fertility and that, despite a widening gap between the more and
less educated with respect to fertility, there is no evidence that this trend is associated with genes. These findings are important to our understanding of the
roots of shifting distributions of health and behavior across generations in US society.
This study asks two related questions about the shifting landscape of marriage and reproduction in US society over the course of the last century with respect
to a range of health and behavioral phenotypes and their associated genetic architecture: (1) Has assortment on measured genetic factors influencing reproductive
and social fitness traits changed over the course of the 20th century? (2) Has the genetic covariance between fitness (as measured by total fertility)
and other traits changed over time? The answers to these questions inform our understanding of how the genetic landscape of American society has changed over the
past century and have implications for population trends. We show that husbands and wives carry similar loadings for genetic factors related to education and
height. However, the magnitude of this similarity is modest and has been fairly consistent over the course of the 20th century. This consistency is
particularly notable in the case of education, for which phenotypic similarity among spouses has increased in recent years. Likewise, changing patterns of the
number of children ever born by phenotype are not matched by shifts in genotype-fertility relationships over time. Taken together, these trends provide no evidence
that social sorting is becoming increasingly genetic in nature or that dysgenic dynamics have accelerated.
Family and twin studies suggest that up to 50% of individual differences in human fertility within a population might be heritable. However, it remains unclear
whether the genes associated with fertility outcomes such as number of children ever born (NEB) or ageat
first birth (AFB) are the same across geographical and historical environments. By not taking this into account,
previous genetic studies implicitly assumed that the genetic effects are constant across time and space. We conduct a mega-analysis applying whole genome methods
on 31,396 unrelated men and women from six Western countries. Across all individuals and environments, common single-nucleotide polymorphisms (SNPs) explained only ~4% of thevariance in NEB and AFB. We then extend these models to test whether genetic effects are shared across different environments or unique to them. For
individuals belonging to the same population and demographic cohort (born before or after the 20th century fertility decline), SNP-based heritability was almost five times higher at 22% for NEB and19% for
AFB. We also found no evidence suggesting that genetic effects on fertility are shared across time and space. Our
findings imply that the environment strongly modifies genetic effects on the tempo and quantum of fertility, that currently ongoing natural selection is
heterogeneous across environments, and that gene-environment interactions may partly account for missing heritability in fertility. Future research needs to
combine efforts from genetic research and from the social sciences to better understand human fertility.
Fertility behavior—such as age at first birth and number of children—varies strongly across historical time and geographical space. Yet, family and twin
studies, which suggest that up to 50% of individual differences in fertility are heritable, implicitly assume that the genes important for fertility are the same
across both time and space. Using molecular genetic data (SNPs) from over 30,000 unrelated individuals from six
different countries, we show that different genes influence fertility in different time periods and different countries, and that the genetic effects consistently
related to fertility are presumably small. The fact that genetic effects on fertility appear not to be universal could have tremendous implications for research in
the area of reproductive medicine, social science and evolutionary biology alike.
Mortality selection is a general concern in the social and health sciences. Recently, existing health and social science cohorts have begun to collect genomic
data. Causes of selection into a genomic dataset can influence results from genomic analyses. Selective non-participation, which is specific to a particular study
and its participants, has received attention in the literature. But mortality selection—the very general phenomenon that genomic data collected at a particular age
represents selective participation by only the subset of birth cohort members who have survived to the time of data collection—has been largely ignored. Here we
test the hypothesis that such mortality selection may significantly alter estimates in polygenic association studies of both health and non-health traits. We
demonstrate mortality selection into genome-wide SNP data collectionat older ages using the U.S.-based
Health and Retirement Study (HRS). We then model the selection process. Finally, we test whether mortality selection
alters estimates from genetic association studies. We find evidence for mortality selection. Healthier and more socioeconomically advantaged individuals are more
likely to survive to be eligible to participate in the genetic sample of the HRS. Mortality selection leads to
modest drift in estimating time-varying genetic effects, a drift that is enhanced when estimates are produced from data that has additional mortality selection.
There is no general solution for correcting for mortality selection in a birth cohort prior to entry into a longitudinal study. We illustrate how genetic
association studies using HRS data can adjust for mortality selection from study entry to time of genetic data
collection by including probability weights that account for mortality selection. Mortality selection should be investigated more broadly in genetically-informed
samples from other cohort studies.
Higher paternal age at offspring conception increases de novo genetic mutations (Kong et al 2012). Based on evolutionary genetic theory
we predicted that the offspring of older fathers would be less likely to survive and reproduce, i.e. have lower fitness. In a sibling control study, we find
clear support for negative paternal age effects on offspring survival, mating and reproductive success across four large populations with an aggregate N > 1.3
million in main analyses. Compared to a sibling born when the father was 10 years younger, individuals had 4–13% fewer surviving children in the four populations.
Three populations were pre-industrial (1670-1850) Western populations and showed a pattern of paternal age effects across the offspring’s lifespan.
In 20th-century Sweden, we found no negative paternal age effects on child survival or marriage odds. Effects survived tests for competing
explanations, including maternal age and parental loss. To the extent that we succeeded in isolating a mutation-driven effect of paternal age, our results can be
understood to show that de novo mutations reduce offspring fitness across populations and time. We can use this understanding to predict the effect of
increasingly delayed reproduction on offspring genetic load, mortality and fertility.
Because the worldwide demand for sperm donors is much higher than the actual supply available through fertility clinics, an informal online market has emerged
for sperm donation. Very little empirical evidence exists, however, on this newly formed market and even less on the characteristics that lead to donor success.
This article therefore explores the determinants of online sperm donors’ selection success, which leads to the production of offspring via informal donation. We
find that donor age and income play a statistically-significant role in donor success as measured by the number of times selected, even though there is no
requirement for ongoing paternal investment. Donors with less extroverted and lively personality traits who are more intellectual, shy and systematic are more
successful in realizing offspring via informal donation. These results contribute to both the economic literature on human behaviour and on large-scale
The social sciences have been reticent to integrate a biodemographic approach to the study of fertility choice and behaviour, resulting in theories and findings
that are largely socially-deterministic. The aim of this paper is to first reflect on reasons for this lack of integration, provide a review of previous
examinations, take stock of what we have learned until now and propose future research frontiers. We review the early foundations of proximate determinants
followed by behavioural genetic (family and twin) studies that isolated the extent of genetic influence on fertility traits. We then discuss research that
considers gene and environment interaction and the importance of cohort and country-specific estimates, followed by multivariate models that explore motivational
precursors to fertility and education. The next section on molecular genetics reviews fertility-related candidate gene studies and their shortcomings and on-going
work on genome wide association studies. Work in evolutionary anthropology and biology is then briefly examined, focusing on evidence for natural selection.
Biological and genetic factors are relevant in explaining and predicting fertility traits, with socio-environmental factors and their interaction still key in
understanding outcomes. Studying the interplay between genes and the environment, new data sources and integration of new methods will be central to understanding
and predicting future fertility trends.
[Keywords: fertility, age at first birth, number of children ever born, genetics, behavioural genetics, molecular genetics, natural
The present review aims to ascertain whether different infertility etiologies share particular genes and/or molecular pathways with other pathologies and are
associated with distinct and particular risks of later-life morbidity and mortality. In order to reach this aim, we use two different sources of information: (1) a
public web server named DiseaseConnect focused on the analysis of common genes and molecular mechanisms shared by
diseases by integrating comprehensive omics and literature data; and (2) a literature search directed to find clinical comorbid relationships of infertility
etiologies with only those diseases appearing after infertility is manifested. This literature search is performed because DiseaseConnect web server does not
discriminate between pathologies emerging before, concomitantly or after infertility is manifested. Data show that different infertility etiologies not only share
particular genes and/or molecular pathways with other pathologies but they have distinct clinical relationships with other diseases appearing after infertility
is manifested. In particular, (1) testicular and high-grade prostate cancer in male infertility; (2) non-fatal stroke and endometrial cancer, and likely non-fatal
coronary heart disease and ovarian cancer in polycystic ovary syndrome; (3) osteoporosis, psychosexual dysfunction, mood disorders and dementia in premature
ovarian failure; (4) breast and ovarian cancer in carriers of BRCA1/2 mutations in diminished ovarian reserve; (5)
clear cell and endometrioid histologic subtypes of invasive ovarian cancer, and likely low-grade serous invasive ovarian cancer, melanoma and non-Hodgkin
lymphoma in endometriosis; and (6) endometrial and ovarian cancer in idiopathic infertility. The present data endorse the principle that the occurrence of a
disease (in our case infertility) is non-random in the population and suggest that different infertility etiologies are genetically and clinically linked with
other diseases in single meta-diseases. This finding opens new insights for clinicians and reproductive biologists to treat infertility problems using a phenomic
approach instead of considering infertility as an isolated and exclusive disease of the reproductive system/hypothalamic-pituitary-gonadal axis. In agreement
with a previous validation analysis of the utility of DiseaseConnect web server, the present study does not show a univocal correspondence between common gene
expression and clinical comorbid relationship. Further work is needed to untangle the potential genetic, epigenetic and phenotypic relationships that may be
present among different infertility etiologies, morbid conditions and physical/cognitive traits.
Physical attractiveness has been associated with mating behavior, but its role in reproductive success of contemporary humans has received surprisingly little
In the Wisconsin Longitudinal Study(WLS; 1244
women, 997 men born between 1937 and 1940) we examined whether attractiveness assessed from photographs taken at age ~18 predicted the number of biological
children at age 53–56.
In women, attractiveness predicted higher reproductive success in a nonlinear fashion, so that attractive (second highest quartile) women had 16% and very
attractive (highest quartile) women 6% more children than their less attractive counterparts. In men, there was a threshold effect so that men in the lowest
attractiveness quartile had 13% fewer children than others who did not differ from each other in the average number of children. These associations were partly but
not completely accounted for by attractive participants’ increased marriage probability. A linear regression analysis indicated relatively weak directional
selection gradient for attractiveness (β = 0.06 in women, β = 0.07 in men).
These findings indicate that physical attractiveness may be associated with reproductive success in humans living in industrialized settings.
Scores on cognitive tests have been very widely reported to have increased through the decades of the last century, a generational phenomenon termed the
‘Flynn Effect’ since it was most comprehensively documented by James Flynn in the
1980s. There has, however, been very little evidence concerning any continuity of the effect specifically into the present century.
We here report data from a population, namely young adult males in Denmark, showing that whereas there were modest increases between 1988 and 1998 in scores on
a battery of 4 cognitive tests—these constituting a diminishing continuation of a trend documented back to the late 1950s—scores on all 4 tests declined between
1998 and 2003–2004. For 2 of the tests, levels fell to below those of 1988. Across all tests, the decrease in the 5–6 year period corresponds to approximately
1.5 IQ points, very close to the net gain between 1988 and 1998. The declines between 1998 and 2003–4 appeared amongst both men pursuing higher academic education
and those not doing so.
The so-called domestic cat occupies a unique position within the
truly domestic animals since it freely interbreeds with feral populations, and there is considerable gene flow in both directions. This is possible because the
likelihood of an individual cat forming a relationship with people is strongly affected by its experiences during the
socialisation period (3–8 weeks of age), although this does not preclude differences between owned and feral populations in the relative frequencies of alleles
which affect social behaviour towards humans.
We suggest a hitherto unconsidered reason why a separate domesticated population of cats (apart from pedigree breeds) has not yet emerged: the unusual and stringent
nutrient requirements of the cat may historically have militated against successful breeding on a completely human-provided
diet, and led to the retention of the ability to achieve a nutritionally complete diet by scavenging and/or hunting. More recently, the widespread availability
of nutritionally complete manufactured foods and veterinary care in western countries appears to be leading towards a rapid change in the population dynamics and
population genetics of both owned and feral
[Keywords: domestication, feral populations, population dynamics, cat]
The interplay between socioecologlcal and biological processes manifests Itself at the level of individuals, populations, and species. The biology of
Individuals is deeply modified when they are groups; many of the attributes of populations such as size, distribution, composition, etc. are related to social
interactions, and at the level of species, patterns of social relations within groups tend to be structured in ways that influence survival, reproduction, and
exchange among populations.
In one experimental approach to these problems, the social ecology of freely growing populations of mice In large enclosures was related to behavioral,
physiological, and health changes of individuals, to demographic changes and to changes of gene frequencies. Another experiment examined the process and effects of
artificial selection for the same trait in different social environments.
The population enclosures were octagonal structures subdivided Into central and peripheral sections with a total surface area of 13.3 square feet. From a
founder group of mice of known genetic (progeny of a four-way cross among inbred mouse strains C57L/J, SWR/J,
C3HeB/FeJ, 129/J) and environmental background, three equivalent samples of mice were distributed into replicate population enclosures (Pop A and B) and
into standard laboratory cages as randomly mated male-female pairs—the control group (Pop C).
During the first year of study, daily observations of the enclosures were made, and several censuses were performed. Identifiable cohorts, animals born during
each census interval, were established to provide an additional way of analyzing changes in the populations.
In Pop C, reproduction remained constant and mortality was negligible. Marked changes occurred in Pop A and B. The sizes (1000-A and 800-B mice) and densities
(85-A and 60-B mice per square foot) are several times greater than those of any previously reported population of small mammals. However, there would have been
100,000 mice in each enclosure at the end of a year had the populations continued to grow as they did at first. Changes of reproductive physiology constituted
prominent aspects of self-regulation in the enclosures. Peak demographic input rates occurred during the third month, but were already associated with decreased
productivity per adult female. Analysis of maturation and reproduction pointed to inhibition of reproduction in sexually mature females as the most important
factor in the decline of productivity. Pregnancy rates fell steadily and inhibition of full-term gestation occurred. Gonads and reproductive cells of males were
adult, but a large proportion of males showed little sexual activity.
Neonatal mortality was particularly striking in Pop B, where 30% of females showed advanced pregnancy during the last 5.5 months with no newborns surviving.
About 25% of the mice in the enclosures died during the year. Highest weekly death rates occurred during the first half of the year before peak numbers were
present. Autopsies of mice of Pop A revealed little in the way of abnormal findings.
Biomass either paralleled or increased more rapidly than numbers in both enclosures, contrasting with some other population: studies in which growth was
impaired with crowding.
Changes of behavior included: 1. disappearance of circadian activity peaks, 2. decline in frequency of fighting per male but an increase in unusual
aggressiveness, 3. aberrations of sexual behavior, 4. deterioration of maternal care, 5. cannibalism, 6. striking decrease in social responsiveness.
Cohorts in the populations were biologically distinguishable sub-units in contrast to control cohorts, which showed no such differentiation. Cohorts in Pop A
and B differed with respect to reproduction physiology, mortality, and behavior, and intercohort differences persisted at all levels of population density.
Many of the properties of Pop A and B mice changes when the mice were placed in different social environments, attesting to the specificity of the influence of
social factors. For example, mice of Pop A, randomly paired in control cages, showed a marked rise in reproduction, and cohorts reproductively inhibited before
were most productive in the new social environment. Behavioral tests performed outside the enclosure environment revealed: 1. intercohort differences among Pop A
mice contrasted with stereotyped behavior of Pop C mice, and 2. changes in behavior of Pop A mice both immediately after removal from the population and after six
weeks in new social conditions. Pop B mice changed their social environment by emigrating into the empty interconnected enclosure of Pop A. Two distinctive
sub-populations formed. Greater changes in reproduction, mortality, and behavior occurred in the emigrant subpopulation, which underwent more extensive social
reorganization. Immediately following reunion of the two subpopulations, a population crash occurred, possibly related to the sudden changes of social
Use of genetically defined animals made feasible the study of gene frequency changes. Polymorphism of alleles at the C locus affecting coat color differed
between Pop A and B on the one hand and Pop C on the other. Although the magnitude of the upward change of recessive c in Pop A and B was not large, the
consistency and similarity of the change in Pop A and B and lack of change in Pop C suggested the action of systematic processes and the probable adaptiveness of
the changes. There was little evidence of differential adult reproduction or mortality among the phenotypes but there were suggestions of differential neonatal
survival. The relatively slow rate of change of the alleles after the first generation suggested the establishment of a state of balanced polymorphism at the C
locus. Hemoglobin allele and genotype frequencies of mice of Pop A alive at the end of the year did not deviate from what might have been predicted on the basis of
Selection for the same trait in varied environments tends to involve genetic and physiological differences. The question of adaptability to different social
environments was studied; heavy body weight at sexual maturity was chosen as the trait for selection; groups of different sizes—pairs or groups of 20–30 mice—were
the environmental variables. Sexes were kept separate between weaning and sexual maturity. A within-litter selection method was used.
Crowding depressed weight at sexual maturity but equal improvement with selection occurred in both social environments. Heritability was also equal in crowded
and uncrowded groups. Environmental exchange carried out in the sixth and seventh generation suggested that mice selected in crowded environments performed
slightly better in both crowded and uncrowded environments.
The large sizes and unusual degree of crowding attained by the freely growing populations in this study compared with previous studies may be related to the
types of animals used, to the number of individuals in the founder nuclei, and to the physical structure of the enclosures. Extreme crowding was compatible with
general physical health. The decline of fertility and fecundity, the decreased survival of newborns, and the appearance of behavioral aberrations—rather than
disease or an increase in adult mortality—represented the major self-regulatory mechanisms that eventually limited population growth. The growth of individuals was
not inhibited. Social withdrawal and the decline of social interaction rather than a rise of interaction characterized the populations. Such findings cast doubt
about the generality of the so-called “Stress” theory of social ecology that emphasizes increased interaction and pituitary-adrenal hyperactivity as the principal
mechanisms involved in self-regulation of vertebrate populations.
Other formulations of mammalian social ecology, such as those that focus on the importance of early development, of spatial requirements, of neurophysiological
reactivity, and of communications, constitute additional explanations of the interplay of social and biological processes in crowded populations.
Although man’s potential reactions are more complex and variable than those of lower vertebrates and give prominence to the role of symbols and culture, his
social environment is even more fundamental to his entire existence. This, if anything, increases the importance of the interplay of socioecological and biological
processes for man.