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Sense of humor is a universal human trait, enjoyed daily across cultures. However, little is known about the factors that shape individual differences in humor, particularly what contributes to developing a great sense of humor. While previous studies have identified a significant genetic component for various humor attributes, such as humor appreciation and humor styles, no study has looked at the heritability of humor production ability. This study is the first to assess the genetic and environmental influences on humor production ability using a twin study design. Participants included 448 pairs of monozygotic twins and 196 pairs of dizygotic twins (median age 66 years, mostly female) from the Twins UK registry. Twins self-assessed their humor ability, rated the funniness of their co-twin, and completed an objective humor production task by composing funny captions for captionless cartoons. Additionally, they completed a short cognitive ability test and reported their overall health. Findings revealed that self-rated humor ability was influenced by both additive genetic and nonshared environmental factors. In contrast, objective humor production showed no evidence of additive genetic effects. Instead, all individual differences were shaped by shared and nonshared environmental influences, though a small genetic effect cannot be ruled out. These results suggest that humor production may be more complex and difficult to assess than other cognitive abilities. The study also presents intriguing implications for the evolutionary basis of humor.
Threat sensitivity, an individual difference construct reflecting variation in responsiveness to threats of various types, predicts physiological reactivity to aversive stimuli and shares heritable variance with anxiety disorders in adults. However, no research has been conducted yet with youth to examine the heritability of threat sensitivity or evaluate the role of genetic versus environmental influences in its relations with mental health problems. The current study addressed this gap by evaluating the psychometric properties of a measure of this construct, the 20-item Trait Fear scale (TF-20), and examining its phenotypic and genotypic correlations with different forms of psychopathology in a sample of 346 twin pairs (121 monozygotic), aged 9–14 years. Analyses revealed high internal consistency and test-retest reliability for the TF-20. Evidence was also found for its convergent and discriminant validity in terms of phenotypic and genotypic correlations with measures of fear-related psychopathology. By contrast, the TF-20’s associations with depressive conditions were largely attributable to environmental influences. Extending prior work with adults, current study findings provide support for threat sensitivity as a genetically-influenced liability for phobic fear disorders in youth.
Despite the high prevalence of generalized anxiety among young adults, studies investigating factors that shape the course of these symptoms during the twenties are scarce. In addition, generalized anxiety can manifest in different ways, but it is unclear whether symptoms cluster under distinct dimensions in this age group. The current study addressed these gaps using data from the Twins Early Development Study. First, we examined genetic and environmental contributions to continuity and change in generalized anxiety symptoms in young adulthood and the heritability of a latent factor reflecting stability over this period. Next, to explore potential dimensions of generalized anxiety, we investigated the factorial structure of symptoms as well as etiological influences underpinning the different factors.
Methods
The sample comprised 6,429 twin pairs. Generalized anxiety was assessed at six waves (age 23–26 years).
Results
Genetic factors largely accounted for continuity and environmental factors for change in symptom severity. Furthermore, the heritability of stable generalized anxiety (60%) was substantially higher than that at any single time point (39–46%). Regarding the factorial structure of symptoms, we found evidence of two dimensions: worry-avoidance and somatic-distress symptoms. Genetic correlations (rG = 0.77–0.91) between the two dimensions were higher than environmental correlations (rE = 0.26–0.65).
Conclusions
The current findings suggest that extracting temporal stability provides the strongest opportunity to identify genetic influences on generalized anxiety. Moreover, the results indicate that differences between generalized anxiety dimensions are more likely attributable to environmental than genetic effects.
Since the 1970s, twin birth rates have increased sharply in developed countries. In Africa, where the rate is the highest globally, its evolution and variation are poorly understood. This article aims to estimate the twinning rate in sub-Saharan African (SSA) countries throughout 1986–2016 and analyze its spatial, temporal, and ethnic variations. It also seeks to identify social and demographic factors associated with a high probability of twin births and outline a forecast of the twinning rate. We used data from 174 Demographic and Health Surveys from 42 countries. We supplemented them with the UN World Population Prospects (WPP). The twinning rate was calculated by reporting the number of twin births per thousand total births. We used logistic regression to analyze the factors associated with twin births. We projected the twinning rate based on WPP. The overall SSA twinning rate is 17.4 per 1000, but it has changed very little over time, and we expect it will grow a little between 2015 and 2050, increasing at most from 17.4 per 1000 to 18.4 per 1000. We also show significant differences in the twinning rate in SSA according to mother ethnicity. Most ethnic groups with high twinning rates belong to the large Bantu ethnic family. SSA remains the ‘land of twins’, with the twinning rate changing slowly. However, specific health policies must target twin births in SSA to address the public health challenges they present.
Despite the decline in mortality rates among children in developing countries, disparities persist between countries, particularly between twins and singletons. This study employed data from nine Demographic and Health Surveys in the Dominican Republic and Haiti to estimate and compare mortality rates for twins and singletons in categories of the under-5 age group (neonatal, postneonatal, and child mortality) and examine the factors associated with excess mortality among twins. From 1996 to 2013, the under-5 mortality rate (U5MR) for singletons in the Dominican Republic declined from 56‰ (95% CI [47, 64) to 30‰ (22–39) and from 108‰ (53–164) to 53‰ (16–89) among twins. In Haiti, between 1994 and 2016, the U5MR declined from 121‰ (109–133) to 77‰ (68–80) for singletons and from 432‰ (327–538) to 204‰ (149–260) among twins. The adjusted risk of neonatal death for twins is 1.4 (1.0–1.9) times higher than for singletons in the Dominican Republic, compared to a risk of 4.3 (3.5–5.3) times higher in Haiti. In the post-neonatal period, the mortality risk for twins in the Dominican Republic was 1.8 (1.0–3.1) times higher than that for singletons, 2.9 (2.3–3.8) in Haiti. The risk of death for twins was not significantly different from that for singletons in both the Dominican Republic and Haiti at ages 1–4 years. Low birth weight, lack of breastfeeding, absence of, or inadequate, antenatal care, noncesarean section birth, and high birth order were associated with excess mortality among twins in both countries.
Vanishing twin syndrome is a miscarriage of multiples where one or more fetuses ‘vanishes’ (i.e., partial or full resorption or via calcification) during pregnancy, often before detection via ultrasound. It affects 30−50% of multifetal pregnancies, with most cases resulting in full resorption within the first trimester. Despite its recognition since 1945 and rising occurrence in both natural and assisted pregnancies, standardized clinical guidelines remain inadequate, leading to inconsistent diagnosis, counseling, and communication from healthcare providers. This study examines the experiences of mothers and gestational carriers diagnosed with VTS, focusing on patient-provider communication, risks, and symptom disclosure. A global online survey collected qualitative and quantitative data from 153 participants across 17 countries. Results show that most patients with formal diagnoses experienced negative interactions with healthcare providers, with an average sentiment score of −0.7 (on a scale from −2 to 2). Over 53.4% rated their communication experience as −1, and the average satisfaction score for the amount of information received was 3.5/10. Additionally, 43% of respondents were not informed about chorionicity, a key factor affecting fetal outcomes. Significant discrepancies in care were observed across different countries. The findings highlight major gaps in patient-provider communication and inconsistent clinical practices regarding VTS. Addressing these issues through improved education, clearer protocols, and standardized guidelines could enhance patient experiences and decision-making. Future research should focus on provider training and evidence-based strategies to improve the management of VTS and other types of miscarriage and death of multiples during pregnancy and postpartum.
Richard Tremblay started his professional career as a clinician with juvenile delinquents and mentally ill offenders. He spent the rest of his career doing longitudinal and experimental studies to identify effective preventive interventions during the preschool and elementary school years. Results from these studies showed that early interventions with at risk children and their parents had very long-term impacts. Within these longitudinal studies, he also studied genetic and epigenetic effects on the development of violent behavior.
We evaluated the prevalence and risk factors for child maltreatment in multiples aged 3 years and compared them to singletons in Japanese population-based data. Records on child maltreatment and health check-ups at 3 years of age from 17,125 singletons, 488 twins and 18 triplets were collected from a Public Health Center between April 2007 and March 2011. The associations of child maltreatment with potential risk factors were analyzed using the logistic regression model. Out of all children, 76 (4.31 per 1000) children had documented maltreatment including 69 (4.03 per 1000) singletons and seven (14.31 per 1000) twins. All of the cases in twins were physical abuse (100%) and nearly half of the cases (43%) included emotional abuse. Among twins, 86% of the biological mothers were suspected. The alleged perpetrators of twins showed a significantly higher rate of maternal depression compared to those of singletons. After adjusting the results for a number of potential biological and social risk factors, twins or triplets had a higher risk for maltreatment than singletons (OR 3.39, 95% CI [1.17, 9.83]). Healthcare providers should be aware that a multiple birth can place considerable stress on a family leading to child maltreatment and should provide appropriate support and intervention for mothers with multiples.
Past studies indicate daily increases in estrogen across the menstrual cycle protect against binge-eating (BE) phenotypes (e.g. emotional eating), whereas increases in progesterone enhance risk. Two previous studies from our laboratory suggest these associations could be due to differential genomic effects of estrogen and progesterone. However, these prior studies were unable to directly model effects of daily changes in hormones on etiologic risk, instead relying on menstrual cycle phase or mean hormone levels. The current study used newly modified twin models to examine, for the first time, the effects of daily changes in estradiol and progesterone on genetic/environmental influences on emotional eating in our archival twin sample assessed across 45 consecutive days.
Methods
Participants included 468 female twins from the Michigan State University Twin Registry. Daily emotional eating was assessed with the Dutch Eating Behavior Questionnaire, and daily saliva samples were assayed for ovarian hormone levels. Modified genotype × environment interaction models examined daily changes in genetic/environmental effects across hormone levels.
Results
Findings revealed differential effects of daily changes in hormones on etiologic risk, with increasing genetic influences across progesterone levels, and increasing shared environmental influences at the highest estradiol levels. Results were consistent across primary analyses examining all study days and sensitivity analyses within menstrual cycle phases.
Conclusions
Findings are significant in being the first to identify changes in etiologic risk for BE symptoms across daily hormone levels and highlighting novel mechanisms (e.g. hormone threshold effects, regulation of conserved genes) that may contribute to the etiology of BE.
Suppose you are running a company that provides proofreading services to publishers. You employ people who sit in front of screens, correcting written text. Spelling errors are the most frequent problem, so you are motivated to hire proofreaders who are excellent spellers. Therefore, you decide to give your job applicants a spelling test. It isn’t hard: throw together 25 words, and score everyone on a scale of 0–25. You are now a social scientist, a specialist called a psychometrician, measuring “spelling ability.”
The reader should be officially informed that in this chapter I take leave of the widely accepted consensus about nature–nurture. This is not a textbook, and everything that I have said up to now has been very much my own take on things, but for the most part I have not strayed far from what most scientists would say about the intellectual history of nature and nurture. Not everyone perhaps, but most people agree that Galton was a racist, eugenics a moral and scientific failure, heritability of behavioral differences nearly universal, heritability a less than useful explanatory concept, twin studies an interesting but ultimately limited research paradigm, and linkage and candidate gene analysis of human behavior decisive failures.
Has it always been the case that living people must struggle with the moral failings of their dead ancestors, or is that a special burden that has been placed on the shoulders of citizens and scientists living in contemporary Europe and North America? Recently, the culture feels as though it is being torn apart by this question. I was taught in grade school that the United States is the greatest country in the world, the land of the free and the home of the brave, where anyone could be a millionaire or president if they put in the effort. It is hardly radical to recognize that this is less than true today and isn’t even close to true historically, especially if one is not white, Christian, and male.
Notwithstanding Galton’s admonition to count everything, counting is just a tool; it is no more science than hammering is architecture. One hundred years after Galton, Robert Hutchins remarked, contemptuously, that a social scientist is a person who counts telephone poles. The obvious way to turn counting into science is by conducting experiments, that is by manipulating nature and observing what the consequences are for whatever one is counting. Gregor Mendel, for example, was certainly a counter – he counted the mixtures of smooth and wrinkled peas in the progeny of the pea plants he intentionally crossed. What made Mendel’s work science was the intentional crossing of the plants, not the counting itself. It would have been much more difficult – perhaps impossible – to observe the segregation and independent assortment of traits by counting smooth and wrinkled peas in the wild.
Why is divorce heritable? It’s clear that it is heritable, in the rMZ > rDZ sense. I hope I have convinced you that the heritability of divorce doesn’t mean that there are “divorce genes,” or that divorce is passed down genetically from parents to children, but seriously: how does something like that happen? I am aware that my constant minimizing of the implications of heritability can seem as though I am keeping my finger in the dike against an inevitable onslaught of scientifically based genetic determinism, the final Plominesque realization that our genes make us who we are, the apotheosis of Galton’s proclamation in 1869: “I propose to show … that a man’s natural abilities are derived by inheritance, under exactly the same limitations as are the form and physical features of the whole organic world” (Hereditary Genius, p. 1).
Robert Plomin, whose name has come up a few times already, is unquestionably the most important psychological geneticist of our time. Trained in social and personality psychology at the University of Texas at Austin in the 1970s (my graduate alma mater, though we didn’t overlap), he went on to faculty positions at the University of Colorado and the Pennsylvania State University (both major American centers for behavior genetics) before moving to London to take a position at the Institute of Psychiatry. Plomin’s career has embodied the integration of behavioral genetics into mainstream social science and psychology. Everywhere Plomin has been, he has initiated twin and adoption studies, many of which continue to make contributions today. Although genetics has always played a central role in Plomin’s research, you would never mistake his work for that of a biologist or quantitative geneticist: he (like me) has always been first and foremost a psychologist.
The Second World War marked a turning point for what was considered acceptable in genetics and its implications for eugenic and racially motivated social policies. To be sure, the change in attitude was not quick or decisive. Tens of thousands of Americans were sterilized involuntarily after the war. Anti-black racism, antisemitism, and anti-immigrant sentiment, needless to say, persisted for a long while and have not yet been eliminated; interracial marriage was still illegal in much of the country during my lifetime. But – and despite the foot-dragging, I think this needs to be recognized as an advance – it slowly became less and less acceptable to adopt openly eugenic or racist opinions in public or to justify them based on science. Retrograde attitudes about such things persist to this day, but they have mostly been relegated to the fringes of scientific discourse.
Many people outside of psychology and biology come to the subject of nature–nurture because of an interest in race. That is unfortunate, but I get it. People, especially in the United States, are obsessed with race, for obvious reasons: American history is indelibly steeped in racial categories. The two foundational failures of the American experience – genocide of Indigenous Americans and enslavement of Africans – happened because of race and racism. Even today in the United States, people of all persuasions think about race all the time, whether as hereditarian racists convinced that there are essential biological differences among ancestral groups, progressives fascinated by personal identity and the degradations that non-white people still experience, or the dozens of racial and ethnic categories obsessively collected by the U.S. census.
Let’s summarize where the nature–nurture debate stood as the twentieth century drew to a close. When the century began, thinkers were faced for the first time with the hard evolutionary fact that human beings were not fundamentally different biologically than other evolved organisms. Galton and his eugenic followers concluded that even those parts of human experience that seemed to be unique – social, class, and cultural differences; abilities, attitudes, and personal struggles – were likewise subsumed by evolution and the mammalian biology it produced. People and societies could therefore be treated like herds of animals, rated on their superior and inferior qualities, bred to maintain them, treated to fix them, and culled as necessary for the good of the herd. Not every mid-century moral disaster that followed resulted from their misinterpretation of human evolution, but it played a role. Society has been trying to recover from biologically justified racism, eugenics, and genocide ever since.
The theory of evolution, as espoused by Charles Darwin in The Origin of Species in 1859, was difficult to accept for religious believers whose assumptions about the world were shattered by it, but Darwin’s The Descent of Man, published 12 years later, posed even greater challenges to people who did accept it, and those challenges continue today. It has often been noted that a disorienting consequence of the Enlightenment was to force people to recognize that humans were not created at the center of the universe in the image of God, but instead on a remote dust-speck of a planet, in the image of mold, rats, dogs, and chimps. For the entirety of recorded history, moral beliefs about humans had been based on the idea that people were in some fundamental sense apart from the rest of nature. Darwin disabused us of that notion once and for all. The scientific and social upheaval that has occurred since Darwin has been an extended process of coming to terms with a unification of humans and the rest of the natural world.
Natural selection should favour litter sizes that optimise trade-offs between brood-size and offspring viability. Across the primate order, the modal litter size is one, suggesting a deep history of selection favouring minimal litters in primates. Humans, however – despite having the longest juvenile period and slowest life-history of all primates – still produce twin births at appreciable rates, even though such births are costly. This presents an evolutionary puzzle. Why is twinning still expressed in humans despite its cost? More puzzling still is the discordance between the principal explanations for human twinning and extant empirical data. Such explanations propose that twinning is regulated by phenotypic plasticity in polyovulation, permitting the production of larger sib sets if and when resources are abundant. However, comparative data suggest that twinning rates are actually highest in poorer economies and lowest in richer, more developed economies. We propose that a historical dynamic of gene–culture co-evolution might better explain this geographic patterning. Our explanation distinguishes geminophilous and geminophobic cultural contexts, as those celebrating twins (e.g. through material support) and those hostile to twins (e.g. through sanction of twin-infanticide). Geminophilous institutions, in particular, may buffer the fitness cost associated with twinning, potentially reducing selection pressures against polyovulation. We conclude by synthesising a mathematical and empirical research programme that might test our ideas.