The massive global variation in caesarean-section (C-section) rate is usually attributed to socio-economic, medical and cultural heterogeneity. Here, we show that a third of the global variance in current national C-section rate can be explained by the trends of adult body height from the 1970s to the 1990s. In many countries, living conditions have continually improved during the last century, which has led to an increase in both fetal and adult average body size. As the fetus is one generation ahead of the mother, the fetus is likely to experience better environmental conditions during development than the mother did, causing a disproportionately large fetus and an increased risk of obstructed labour. A structural equation model revealed that socioeconomic development and access to healthcare affect C-section rate via multiple causal pathways, but the strongest direct effect on C-section rate was body height change. These results indicate that the historical trajectory of socio-economic development affects-via its influence on pre-and postnatal growth-the intergenerational relationship between maternal and fetal dimensions and thus the difficulty of labour. This sheds new light on historic and prehistoric transitions of childbirth and questions the World Health Organization (WHO) suggestion for a global 'ideal' C-section rate. BackgroundCompared with other mammals, childbirth in humans is strikingly difficult owing to the tight fit between the baby's head and shoulders and the mother's pelvis [1][2][3][4][5]. United States (US) statistics suggest that cephalopelvic disproportion-a mismatch of the fetal head and the maternal birth canal-occurs in 2.3% of infants weighing 3-4 kg at birth and in 5.8% of those weighing more [6]. A number of individual risk factors for cephalopelvic disproportion have been identified, including maternal and paternal body height, obesity and the age of the mother [7][8][9][10][11][12][13][14]. In most countries, however, the rate (i.e. incidence) of caesarean section (C-section) greatly exceeds that of actual anatomical disproportion [15][16][17]. Even if the birth canal can accommodate the fetus, a tight feto-pelvic fit can delay labour and increase the risk of maternal and fetal morbidity, which is often prevented by caesarean intervention. C-section rates have been reported to correlate also with psychological factors such as fear and anxiety, socio-economic factors such as family income and education, as well as with access to healthcare [18][19][20][21][22][23]. As a result, C-section rate varies considerably across social and demographic groups within most countries. At a global level, C-section rate varies even more starkly, ranging from 1-2% in many sub-Saharan African countries, up to about 50% in Egypt, Turkey or Brazil. Even in Europe, which is culturally and socio-economically relatively homogeneous, incidences range from about 15% in Scandinavia to more than 35% in Portugal, Romania and Italy [16,17]. Especially in developing countries, incidences are rising rapidly [16,...
Brain and skull tissues interact through molecular signalling and mechanical forces during head development, leading to a strong correlation between the neurocranium and the external brain surface. Therefore, when brain tissue is unavailable, neurocranial endocasts are often used to approximate brain size and shape. Evolutionary changes in brain morphology may have resulted in secondary changes to neurocranial morphology, but the developmental and genetic processes underlying this relationship are not well understood. Using automated phenotyping methods, we quantified the genetic basis of endocast variation across large genetically varied populations of laboratory mice in two ways: (1) to determine the contributions of various genetic factors to neurocranial form and (2) to help clarify whether a neurocranial variation is based on genetic variation that primarily impacts bone development or on genetic variation that primarily impacts brain development, leading to secondary changes in bone morphology. Our results indicate that endocast size is highly heritable and is primarily determined by additive genetic factors. In addition, a non‐additive inbreeding effect led to founder strains with lower neurocranial size, but relatively large brains compared to skull size; suggesting stronger canalization of brain size and/or a general allometric effect. Within an outbred sample of mice, we identified a locus on mouse chromosome 1 that is significantly associated with variation in several positively correlated endocast size measures. Because the protein‐coding genes at this locus have been previously associated with brain development and not with bone development, we propose that genetic variation at this locus leads primarily to variation in brain volume that secondarily leads to changes in neurocranial globularity. We identify a strain‐specific missense mutation within Akt3 that is a strong causal candidate for this genetic effect. Whilst it is not appropriate to generalize our hypothesis for this single locus to all other loci that also contribute to the complex trait of neurocranial skull morphology, our results further reveal the genetic basis of neurocranial variation and highlight the importance of the mechanical influence of brain growth in determining skull morphology.
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