This article argues that a pervasive but confused theory of free will is driving unwarranted resistance to behavioral genetic research and undermining the concept of personal responsibility enshrined in our moral and legal conventions. We call this the theory of ‘free-will-by-subtraction’. A particularly explicit version of this theory has been propounded by the psychologist Eric Turkheimer, who has proposed that human agency can be scientifically quantified as the behavioral variation that remains unexplained after known genetic and environmental causes have been accounted for. This theory motivates resistance to research that suggests genetic differences substantially account for differences in human behavior because that is seen to reduce the scope of human freedom. In academic philosophy, free-will-by-subtraction theory corresponds to a position called ‘libertarian incompatibilism’, which holds that human beings are not responsible for behavior that has extrinsic causes yet maintains that free will nonetheless exists because some fraction of human behavior is self-caused. However, this position is rejected by most professional philosophers. We argue that libertarian incompatibilism is inconsistent with a secular materialist outlook in which all human behavior is understood to have extrinsic causes whether those causes are known to science or not — an outlook Turkheimer shares. We show that Turkheimer sustains this contradiction by adopting an untenable position we call ‘epistemic libertarianism’, which holds that extrinsic causes of our behavior only infringe on our freedom if we know about them. By contrast, the overwhelming majority of secular materialist philosophers support a position called ‘compatibilism’, which maintains that free will is compatible with the comprehensive extrinsic causation of human behavior. We show that compatibilism neutralizes the threat that genetic explanation poses to human agency and rescues a generous conception of personal responsibility that aligns with our moral intuitions.

Childless individuals have historically faced stigma with assumptions that they lack an interest in future generations because they do not directly contribute to genetic lineage. Individuals share approximately half of their genes with siblings, 12.5% with first cousins, and 6.25% with first cousins’ children. Norwegian census data (2005−2023), reflecting similar trends to the US, UK, and other European countries, indicates a moderate difference in the number of siblings (Parents: 2.03 [women and men]; Childless: 1.88 [women], 1.94 [men]) and nieces/nephews (Parents: 3.99 [women], 4.03 [men]; Childless: 3.32 [women], 3.42 [men]) for 514,777 women and 532,834 men, respectively. By linking four generations through grandmothers, both childless and childbearing women had a slightly higher number of biological extended family members (Parents: 9.63 cousins with 15.79 children; Childless: 8.66 cousins with 12.22 children). Linking four generations for men, numbers were similar: Parents: 9.68 cousins with 15.91 children, Childless: 8.83 cousins with 12.44 children. Based on the average number of children who are parents, the childless have an average genetic fitness that is 49% of that for parents for the next generation. Both parents and childless individuals have a stake in future generations through their biological extended family.

Depression, a leading cause of global disability, arises from a multifaceted combination of genetic and environmental components. This study explores the relationship between major depressive disorder (MDD) polygenic scores (PGS), characteristics and symptoms of depression, and community-shared socioeconomic factors derived from postal code data in a cohort of 12,646 individuals from the Australian Genetics of Depression Study (AGDS). Our findings reveal that people living in areas with relatively higher socioeconomic advantages and education/occupation scores are more likely to report experiencing fewer depressive symptoms during their worst depressive period, as well as fewer number of lifetime episodes. Additionally, participants who reported depression onset later in life tend to currently reside in wealthier areas. Interestingly, no significant interaction between genetic and socioeconomic factors was observed, suggesting their independent contribution to depression outcomes. This research underscores the importance of integrating socioeconomic factors into psychiatric evaluation and care, and points to the critical role of public policy in addressing mental health disparities driven by socioeconomic factors. Future research should aim to further elucidate the causal relationships within these associations and explore the potential for integrated genetic and socioeconomic approaches in mental health interventions.

Is general intelligence (g) a reflective construct, representing a latent causal entity underlying subtest performance, or a formative construct, better understood as an aggregate variable shaped by and summarizing variation across subtests? Genetically informative data provide a framework for testing whether a construct is reflective or formative by comparing common pathway and independent pathways structural equation models (SEMs). Previous studies using biometric SEMs have predominantly supported the reflective model, with phenotypic g mediating the effects of additive genetic and environmental influences on lower level abilities. In the current study, four large genetically informed datasets (three from the US and one from the UK) were analyzed to test three competing SEM models — common pathway, independent pathways, and merged — using Confirmatory Factor Analysis (CFA). Genetic g was estimated in each sample as a latent variable derived from polygenic scores indexing educational attainment and cognitive abilities. The models were compared as follows: the common pathway model, consistent with a reflective g, included a direct path from genetic g to phenotypic g; the independent pathways model, consistent with a formative g, featured indirect paths from genetic g to phenotypic g via subtests; and the merged model incorporated both direct and indirect paths. Across all four datasets, the merged model consistently provided the best fit (based on goodness-of-fit and parsimony criteria). Phenotypic g mediated between 31% and 81% of the effects of genetic g on subtests. These findings suggest that g functions as both a reflective and formative entity.

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.

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.

This study aimed to establish normal reference ranges of combined cardiac output (CCO) and umbilical venous flow volume (UVFV) in twin fetuses at 20 to 28 weeks of gestation and to evaluate the differences between monochorionic and dichorionic twins. CCO and UVFV were prospectively measured by ultrasound at two centers. The following exclusion criteria were applied: age <18 years or >45 years, first hospital visit at >16 weeks of gestation, monochorionic monoamniotic twin pregnancy, fetal structural or chromosomal abnormality, fetal growth restriction, twin-twin transfusion syndrome, twin anemia polycythemia sequence, and severe hypertension or renal disease were excluded. The period was divided into three groups: 20–22 weeks of gestation, 23–25 weeks of gestation, and 26–28 weeks of gestation. The CCO and UVFV were measured at least once during each period. CCO and UVFV were collected from 274 and 269 fetuses and were measured 412 and 424 times, respectively. UVFV and CCO levels increased as gestation progressed. The weight-corrected UVFV (UVFV/kg) and CCO (CCO/kg) remained stable. UVFV and CCO did not differ between monochorionic and dichorionic twin fetuses. The mean ± SD of UVFV/kg and CCO/kg were determined as 127.8 ± 31.8 and 439.4 ± 80.1 mL/kg/min, respectively. The UVFV-to-CCO ratio also remained stable from 20 to 28 weeks of gestation, ranging from 27.7% to 31.8%. The values and ranges of UVFV/kg and mean CCO/kg in twins were similar to those in singletons.

Highlights from the International Symposium on Twins, held at the University of Crete on May 23−24, 2025, are summarized. The symposium, organized by Dr Maria Markodimitraki, Professor in the Department of Preschool Education at the University of Crete, attracted scholars and practitioners from Greece and around the world. Meetings with a pair of reunited monozygotic female twins, and a female twin in search of her sister, also from Greece, are described. This review is followed by summaries of twin research on neonatal outcomes, growth discordance and restriction, and romantic partners and alcohol use. Human interest stories include a book documenting the extraordinary lives of identical twins Celia and Mamaine Paget, a museum wing honoring the lost Rockefeller twin, a remarkable conjoined twinning case in India, the death of an Australian sports icon, and a most unusual triplet birth.